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Pubmed Article
HIV due to female sex work: regional and global estimates.
PLoS ONE
PUBLISHED: 01-01-2013
Female sex workers (FSWs) are at high risk of HIV infection. Our objective was to determine the proportion of HIV prevalence in the general female adult population that is attributable to the occupational exposure of female sex work, due to unprotected sexual intercourse.
Authors: Jennifer A. Juno, Genevieve Boily-Larouche, Julie Lajoie, Keith R. Fowke.
Published: 07-06-2014
ABSTRACT
Despite the public health importance of mucosal pathogens (including HIV), relatively little is known about mucosal immunity, particularly at the female genital tract (FGT). Because heterosexual transmission now represents the dominant mechanism of HIV transmission, and given the continual spread of sexually transmitted infections (STIs), it is critical to understand the interplay between host and pathogen at the genital mucosa. The substantial gaps in knowledge around FGT immunity are partially due to the difficulty in successfully collecting and processing mucosal samples. In order to facilitate studies with sufficient sample size, collection techniques must be minimally invasive and efficient. To this end, a protocol for the collection of cervical cytobrush samples and subsequent isolation of cervical mononuclear cells (CMC) has been optimized. Using ex vivo flow cytometry-based immunophenotyping, it is possible to accurately and reliably quantify CMC lymphocyte/monocyte population frequencies and phenotypes. This technique can be coupled with the collection of cervical-vaginal lavage (CVL), which contains soluble immune mediators including cytokines, chemokines and anti-proteases, all of which can be used to determine the anti- or pro-inflammatory environment in the vagina.
20 Related JoVE Articles!
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Measuring Frailty in HIV-infected Individuals. Identification of Frail Patients is the First Step to Amelioration and Reversal of Frailty
Authors: Hilary C. Rees, Voichita Ianas, Patricia McCracken, Shannon Smith, Anca Georgescu, Tirdad Zangeneh, Jane Mohler, Stephen A. Klotz.
Institutions: University of Arizona, University of Arizona.
A simple, validated protocol consisting of a battery of tests is available to identify elderly patients with frailty syndrome. This syndrome of decreased reserve and resistance to stressors increases in incidence with increasing age. In the elderly, frailty may pursue a step-wise loss of function from non-frail to pre-frail to frail. We studied frailty in HIV-infected patients and found that ~20% are frail using the Fried phenotype using stringent criteria developed for the elderly1,2. In HIV infection the syndrome occurs at a younger age. HIV patients were checked for 1) unintentional weight loss; 2) slowness as determined by walking speed; 3) weakness as measured by a grip dynamometer; 4) exhaustion by responses to a depression scale; and 5) low physical activity was determined by assessing kilocalories expended in a week's time. Pre-frailty was present with any two of five criteria and frailty was present if any three of the five criteria were abnormal. The tests take approximately 10-15 min to complete and they can be performed by medical assistants during routine clinic visits. Test results are scored by referring to standard tables. Understanding which of the five components contribute to frailty in an individual patient can allow the clinician to address relevant underlying problems, many of which are not evident in routine HIV clinic visits.
Medicine, Issue 77, Infection, Virology, Infectious Diseases, Anatomy, Physiology, Molecular Biology, Biomedical Engineering, Retroviridae Infections, Body Weight Changes, Diagnostic Techniques and Procedures, Physical Examination, Muscle Strength, Behavior, Virus Diseases, Pathological Conditions, Signs and Symptoms, Diagnosis, Musculoskeletal and Neural Physiological Phenomena, HIV, HIV-1, AIDS, Frailty, Depression, Weight Loss, Weakness, Slowness, Exhaustion, Aging, clinical techniques
50537
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Oscillation and Reaction Board Techniques for Estimating Inertial Properties of a Below-knee Prosthesis
Authors: Jeremy D. Smith, Abbie E. Ferris, Gary D. Heise, Richard N. Hinrichs, Philip E. Martin.
Institutions: University of Northern Colorado, Arizona State University, Iowa State University.
The purpose of this study was two-fold: 1) demonstrate a technique that can be used to directly estimate the inertial properties of a below-knee prosthesis, and 2) contrast the effects of the proposed technique and that of using intact limb inertial properties on joint kinetic estimates during walking in unilateral, transtibial amputees. An oscillation and reaction board system was validated and shown to be reliable when measuring inertial properties of known geometrical solids. When direct measurements of inertial properties of the prosthesis were used in inverse dynamics modeling of the lower extremity compared with inertial estimates based on an intact shank and foot, joint kinetics at the hip and knee were significantly lower during the swing phase of walking. Differences in joint kinetics during stance, however, were smaller than those observed during swing. Therefore, researchers focusing on the swing phase of walking should consider the impact of prosthesis inertia property estimates on study outcomes. For stance, either one of the two inertial models investigated in our study would likely lead to similar outcomes with an inverse dynamics assessment.
Bioengineering, Issue 87, prosthesis inertia, amputee locomotion, below-knee prosthesis, transtibial amputee
50977
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The α-test: Rapid Cell-free CD4 Enumeration Using Whole Saliva
Authors: Cynthia L. Bristow, Mariya A. Babayeva, Rozbeh Modarresi, Carole P. McArthur, Santosh Kumar, Charles Awasom, Leo Ayuk, Annette Njinda, Paul Achu, Ronald Winston.
Institutions: Weill Cornell Medical College , University of Missouri-Kansas City-School of Dentistry, University of Missouri Kansas City- School of Pharmacy, Bamenda, NWP, Cameroon, Mezam Polyclinic HIV/AIDS Treatment Center, Cameroon, Institute for Human Genetics and Biochemistry.
There is an urgent need for affordable CD4 enumeration to monitor HIV disease. CD4 enumeration is out of reach in resource-limited regions due to the time and temperature restrictions, technical sophistication, and cost of reagents, in particular monoclonal antibodies to measure CD4 on blood cells, the only currently acceptable method. A commonly used cost-saving and time-saving laboratory strategy is to calculate, rather than measure certain blood values. For example, LDL levels are calculated using the measured levels of total cholesterol, HDL, and triglycerides1. Thus, identification of cell-free correlates that directly regulate the number of CD4+ T cells could provide an accurate method for calculating CD4 counts due to the physiological relevance of the correlates. The number of stem cells that enter blood and are destined to become circulating CD4+ T cells is determined by the chemokine CXCL12 and its receptor CXCR4 due to their influence on locomotion2. The process of stem cell locomotion into blood is additionally regulated by cell surface human leukocyte elastase (HLECS) and the HLECS-reactive active α1proteinase inhibitor (α1PI, α1antitrypsin, SerpinA1)3. In HIV-1 disease, α1PI is inactivated due to disease processes 4. In the early asymptomatic categories of HIV-1 disease, active α1PI was found to be below normal in 100% of untreated HIV-1 patients (median=12 μM, and to achieve normal levels during the symptomatic categories4, 5. This pattern has been attributed to immune inactivation, not to insufficient synthesis, proteolytic inactivation, or oxygenation. We observed that in HIV-1 subjects with >220 CD4 cells/μl, CD4 counts were correlated with serum levels of active α1PI (r2=0.93, p<0.0001, n=26) and inactive α1PI (r2=0.91, p<0.0001, n=26) 5. Administration of α1PI to HIV-1 infected and uninfected subjects resulted in dramatic increases in CD4 counts suggesting α1PI participates in regulating the number of CD4+ T cells in blood 3. With stimulation, whole saliva contains sufficient serous exudate (plasma containing proteinaceous material that passes through blood vessel walls into saliva) to allow measurement of active α1PI and the correlation of this measurement is evidence that it is an accurate method for calculating CD4 counts. Briefly, sialogogues such as chewing gum or citric acid stimulate the exudation of serum into whole mouth saliva. After stimulating serum exudation, the activity of serum α1PI in saliva is measured by its capacity to inhibit elastase activity. Porcine pancreatic elastase (PPE) is a readily available inexpensive source of elastase. PPE binds to α1PI forming a one-to-one complex that prevents PPE from cleaving its specific substrates, one of which is the colorimetric peptide, succinyl-L-Ala-L-Ala-L-Ala-p-nitroanilide (SA3NA). Incubating saliva with a saturating concentration of PPE for 10 min at room temperature allows the binding of PPE to all the active α1PI in saliva. The resulting inhibition of PPE by active α1PI can be measured by adding the PPE substrate SA3NA. (Figure 1). Although CD4 counts are measured in terms of blood volume (CD4 cells/μl), the concentration of α1PI in saliva is related to the concentration of serum in saliva, not to volume of saliva since volume can vary considerably during the day and person to person6. However, virtually all the protein in saliva is due to serum content, and the protein content of saliva is measurable7. Thus, active α1PI in saliva is calculated as a ratio to saliva protein content and is termed the α1PI Index. Results presented herein demonstrate that the α1PI Index provides an accurate and precise physiologic method for calculating CD4 counts.
Medicine, Issue 63, CD4 count, saliva, antitrypsin, hematopoiesis, T cells, HIV/AIDS, clinical
3999
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A Noninvasive Method For In situ Determination of Mating Success in Female American Lobsters (Homarus americanus)
Authors: Jason S Goldstein, Tracy L Pugh, Elizabeth A Dubofsky, Kari L Lavalli, Michael Clancy, Winsor H Watson III.
Institutions: University of New Hampshire, Massachusetts Division of Marine Fisheries, Boston University, Middle College.
Despite being one of the most productive fisheries in the Northwest Atlantic, much remains unknown about the natural reproductive dynamics of American lobsters. Recent work in exploited crustacean populations (crabs and lobsters) suggests that there are circumstances where mature females are unable to achieve their full reproductive potential due to sperm limitation. To examine this possibility in different regions of the American lobster fishery, a reliable and noninvasive method was developed for sampling large numbers of female lobsters at sea. This method involves inserting a blunt-tipped needle into the female's seminal receptacle to determine the presence or absence of a sperm plug and to withdraw a sample that can be examined for the presence of sperm. A series of control studies were conducted at the dock and in the laboratory to test the reliability of this technique. These efforts entailed sampling 294 female lobsters to confirm that the presence of a sperm plug was a reliable indicator of sperm within the receptacle and thus, mating. This paper details the methodology and the results obtained from a subset of the total females sampled. Of the 230 female lobsters sampled from George's Bank and Cape Ann, MA (size range = 71-145 mm in carapace length), 90.3% were positive for sperm. Potential explanations for the absence of sperm in some females include: immaturity (lack of physiological maturity), breakdown of the sperm plug after being used to fertilize a clutch of eggs, and lack of mating activity. The surveys indicate that this technique for examining the mating success of female lobsters is a reliable proxy that can be used in the field to document reproductive activity in natural populations.
Environmental Sciences, Issue 84, sperm limitation, spermatophore, lobster fishery, sex ratios, sperm receptacle, mating, American lobster, Homarus americanus
50498
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Dissection of Oenocytes from Adult Drosophila melanogaster
Authors: Joshua J. Krupp, Joel D. Levine.
Institutions: University of Toronto.
In Drosophila melanogaster, as in other insects, a waxy layer on the outer surface of the cuticle, composed primarily of hydrocarbon compounds, provides protection against desiccation and other environmental challenges. Several of these cuticular hydrocarbon (CHC) compounds also function as semiochemical signals, and as such mediate pheromonal communications between members of the same species, or in some instances between different species, and influence behavior. Specialized cells referred to as oenocytes are regarded as the primary site for CHC synthesis. However, relatively little is known regarding the involvement of the oenocytes in the regulation of the biosynthetic, transport, and deposition pathways contributing to CHC output. Given the significant role that CHCs play in several aspects of insect biology, including chemical communication, desiccation resistance, and immunity, it is important to gain a greater understanding of the molecular and genetic regulation of CHC production within these specialized cells. The adult oenocytes of D. melanogaster are located within the abdominal integument, and are metamerically arrayed in ribbon-like clusters radiating along the inner cuticular surface of each abdominal segment. In this video article we demonstrate a dissection technique used for the preparation of oenocytes from adult D. melanogaster. Specifically, we provide a detailed step-by-step demonstration of (1) how to fillet prepare an adult Drosophila abdomen, (2) how to identify the oenocytes and discern them from other tissues, and (3) how to remove intact oenocyte clusters from the abdominal integument. A brief experimental illustration of how this preparation can be used to examine the expression of genes involved in hydrocarbon synthesis is included. The dissected preparation demonstrated herein will allow for the detailed molecular and genetic analysis of oenocyte function in the adult fruit fly.
Developmental Biology, Issue 41, Drosophila, oenocytes, metabolism, cuticular hydrocarbons, chemical senses, chemical communication, pheromones, adult
2242
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Specific Marking of HIV-1 Positive Cells using a Rev-dependent Lentiviral Vector Expressing the Green Fluorescent Protein
Authors: Jia Guo, Clinton Enos, Yuntao Wu.
Institutions: George Mason University.
Most of HIV-responsive expression vectors are based on the HIV promoter, the long terminal repeat (LTR). While responsive to an early HIV protein, Tat, the LTR is also responsive to cellular activation states and to the local chromatin activity where the integration has occurred. This can result in high HIV-independent activity, and has restricted the usefulness of LTR-based reporter to mark HIV positive cells 1,2,3. Here, we constructed an expression lentiviral vector that possesses, in addition to the Tat-responsive LTR, numerous HIV DNA sequences that include the Rev-response element and HIV splicing sites 4,5,6. The vector was incorporated into a lentiviral reporter virus, permitting highly specific detection of replicating HIV in living cell populations. The activity of the vector was measured by expression of the green fluorescence protein (GFP). The application of this vector as reported here offers a novel alternative approach to existing methods, such as in situ PCR or HIV antigen staining, to identify HIV-positive cells. The vector can also express therapeutic genes for basic or clinical experimentation to target HIV-positive cells.
Infectious Disease, Issue 43, HIV-1, Rev, GFP, lentiviral vector, RRE
2198
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Development of Cell-type specific anti-HIV gp120 aptamers for siRNA delivery
Authors: Jiehua Zhou, Haitang Li, Jane Zhang, Swiderski Piotr, John Rossi.
Institutions: Beckman Research Institute of City of Hope, Beckman Research Institute of City of Hope, Beckman Research Institute of City of Hope.
The global epidemic of infection by HIV has created an urgent need for new classes of antiretroviral agents. The potent ability of small interfering (si)RNAs to inhibit the expression of complementary RNA transcripts is being exploited as a new class of therapeutics for a variety of diseases including HIV. Many previous reports have shown that novel RNAi-based anti-HIV/AIDS therapeutic strategies have considerable promise; however, a key obstacle to the successful therapeutic application and clinical translation of siRNAs is efficient delivery. Particularly, considering the safety and efficacy of RNAi-based therapeutics, it is highly desirable to develop a targeted intracellular siRNA delivery approach to specific cell populations or tissues. The HIV-1 gp120 protein, a glycoprotein envelope on the surface of HIV-1, plays an important role in viral entry into CD4 cells. The interaction of gp120 and CD4 that triggers HIV-1 entry and initiates cell fusion has been validated as a clinically relevant anti-viral strategy for drug discovery. Herein, we firstly discuss the selection and identification of 2'-F modified anti-HIV gp120 RNA aptamers. Using a conventional nitrocellulose filter SELEX method, several new aptamers with nanomolar affinity were isolated from a 50 random nt RNA library. In order to successfully obtain bound species with higher affinity, the selection stringency is carefully controlled by adjusting the conditions. The selected aptamers can specifically bind and be rapidly internalized into cells expressing the HIV-1 envelope protein. Additionally, the aptamers alone can neutralize HIV-1 infectivity. Based upon the best aptamer A-1, we also create a novel dual inhibitory function anti-gp120 aptamer-siRNA chimera in which both the aptamer and the siRNA portions have potent anti-HIV activities. Further, we utilize the gp120 aptamer-siRNA chimeras for cell-type specific delivery of the siRNA into HIV-1 infected cells. This dual function chimera shows considerable potential for combining various nucleic acid therapeutic agents (aptamer and siRNA) in suppressing HIV-1 infection, making the aptamer-siRNA chimeras attractive therapeutic candidates for patients failing highly active antiretroviral therapy (HAART).
Immunology, Issue 52, SELEX (Systematic Evolution of Ligands by EXponential enrichment), RNA aptamer, HIV-1 gp120, RNAi (RNA interference), siRNA (small interfering RNA), cell-type specific delivery
2954
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Community-based Adapted Tango Dancing for Individuals with Parkinson's Disease and Older Adults
Authors: Madeleine E. Hackney, Kathleen McKee.
Institutions: Emory University School of Medicine, Brigham and Woman‘s Hospital and Massachusetts General Hospital.
Adapted tango dancing improves mobility and balance in older adults and additional populations with balance impairments. It is composed of very simple step elements. Adapted tango involves movement initiation and cessation, multi-directional perturbations, varied speeds and rhythms. Focus on foot placement, whole body coordination, and attention to partner, path of movement, and aesthetics likely underlie adapted tango’s demonstrated efficacy for improving mobility and balance. In this paper, we describe the methodology to disseminate the adapted tango teaching methods to dance instructor trainees and to implement the adapted tango by the trainees in the community for older adults and individuals with Parkinson’s Disease (PD). Efficacy in improving mobility (measured with the Timed Up and Go, Tandem stance, Berg Balance Scale, Gait Speed and 30 sec chair stand), safety and fidelity of the program is maximized through targeted instructor and volunteer training and a structured detailed syllabus outlining class practices and progression.
Behavior, Issue 94, Dance, tango, balance, pedagogy, dissemination, exercise, older adults, Parkinson's Disease, mobility impairments, falls
52066
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Mass Production of Genetically Modified Aedes aegypti for Field Releases in Brazil
Authors: Danilo O. Carvalho, Derric Nimmo, Neil Naish, Andrew R. McKemey, Pam Gray, André B. B. Wilke, Mauro T. Marrelli, Jair F. Virginio, Luke Alphey, Margareth L. Capurro.
Institutions: Oxitec Ltd, Universidade de São Paulo, Universidade de São Paulo, Moscamed Brasil, University of Oxford, Instituto Nacional de Ciência e Tecnologia em Entomologia Molecular (INCT-EM).
New techniques and methods are being sought to try to win the battle against mosquitoes. Recent advances in molecular techniques have led to the development of new and innovative methods of mosquito control based around the Sterile Insect Technique (SIT)1-3. A control method known as RIDL (Release of Insects carrying a Dominant Lethal)4, is based around SIT, but uses genetic methods to remove the need for radiation-sterilization5-8. A RIDL strain of Ae. aegypti was successfully tested in the field in Grand Cayman9,10; further field use is planned or in progress in other countries around the world. Mass rearing of insects has been established in several insect species and to levels of billions a week. However, in mosquitoes, rearing has generally been performed on a much smaller scale, with most large scale rearing being performed in the 1970s and 80s. For a RIDL program it is desirable to release as few females as possible as they bite and transmit disease. In a mass rearing program there are several stages to produce the males to be released: egg production, rearing eggs until pupation, and then sorting males from females before release. These males are then used for a RIDL control program, released as either pupae or adults11,12. To suppress a mosquito population using RIDL a large number of high quality male adults need to be reared13,14. The following describes the methods for the mass rearing of OX513A, a RIDL strain of Ae. aegypti 8, for release and covers the techniques required for the production of eggs and mass rearing RIDL males for a control program.
Basic Protocol, Issue 83, Aedes aegypti, mass rearing, population suppression, transgenic, insect, mosquito, dengue
3579
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Sex Stratified Neuronal Cultures to Study Ischemic Cell Death Pathways
Authors: Stacy L. Fairbanks, Rebekah Vest, Saurabh Verma, Richard J. Traystman, Paco S. Herson.
Institutions: University of Colorado School of Medicine, Oregon Health & Science University, University of Colorado School of Medicine.
Sex differences in neuronal susceptibility to ischemic injury and neurodegenerative disease have long been observed, but the signaling mechanisms responsible for those differences remain unclear. Primary disassociated embryonic neuronal culture provides a simplified experimental model with which to investigate the neuronal cell signaling involved in cell death as a result of ischemia or disease; however, most neuronal cultures used in research today are mixed sex. Researchers can and do test the effects of sex steroid treatment in mixed sex neuronal cultures in models of neuronal injury and disease, but accumulating evidence suggests that the female brain responds to androgens, estrogens, and progesterone differently than the male brain. Furthermore, neonate male and female rodents respond differently to ischemic injury, with males experiencing greater injury following cerebral ischemia than females. Thus, mixed sex neuronal cultures might obscure and confound the experimental results; important information might be missed. For this reason, the Herson Lab at the University of Colorado School of Medicine routinely prepares sex-stratified primary disassociated embryonic neuronal cultures from both hippocampus and cortex. Embryos are sexed before harvesting of brain tissue and male and female tissue are disassociated separately, plated separately, and maintained separately. Using this method, the Herson Lab has demonstrated a male-specific role for the ion channel TRPM2 in ischemic cell death. In this manuscript, we share and discuss our protocol for sexing embryonic mice and preparing sex-stratified hippocampal primary disassociated neuron cultures. This method can be adapted to prepare sex-stratified cortical cultures and the method for embryo sexing can be used in conjunction with other protocols for any study in which sex is thought to be an important determinant of outcome.
Neuroscience, Issue 82, male, female, sex, neuronal culture, ischemia, cell death, neuroprotection
50758
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A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Authors: Daniel T. Claiborne, Jessica L. Prince, Eric Hunter.
Institutions: Emory University, Emory University.
The protective effect of many HLA class I alleles on HIV-1 pathogenesis and disease progression is, in part, attributed to their ability to target conserved portions of the HIV-1 genome that escape with difficulty. Sequence changes attributed to cellular immune pressure arise across the genome during infection, and if found within conserved regions of the genome such as Gag, can affect the ability of the virus to replicate in vitro. Transmission of HLA-linked polymorphisms in Gag to HLA-mismatched recipients has been associated with reduced set point viral loads. We hypothesized this may be due to a reduced replication capacity of the virus. Here we present a novel method for assessing the in vitro replication of HIV-1 as influenced by the gag gene isolated from acute time points from subtype C infected Zambians. This method uses restriction enzyme based cloning to insert the gag gene into a common subtype C HIV-1 proviral backbone, MJ4. This makes it more appropriate to the study of subtype C sequences than previous recombination based methods that have assessed the in vitro replication of chronically derived gag-pro sequences. Nevertheless, the protocol could be readily modified for studies of viruses from other subtypes. Moreover, this protocol details a robust and reproducible method for assessing the replication capacity of the Gag-MJ4 chimeric viruses on a CEM-based T cell line. This method was utilized for the study of Gag-MJ4 chimeric viruses derived from 149 subtype C acutely infected Zambians, and has allowed for the identification of residues in Gag that affect replication. More importantly, the implementation of this technique has facilitated a deeper understanding of how viral replication defines parameters of early HIV-1 pathogenesis such as set point viral load and longitudinal CD4+ T cell decline.
Infectious Diseases, Issue 90, HIV-1, Gag, viral replication, replication capacity, viral fitness, MJ4, CEM, GXR25
51506
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Assessing Differences in Sperm Competitive Ability in Drosophila
Authors: Shu-Dan Yeh, Carolus Chan, José M. Ranz.
Institutions: University of California, Irvine.
Competition among conspecific males for fertilizing the ova is one of the mechanisms of sexual selection, i.e. selection that operates on maximizing the number of successful mating events rather than on maximizing survival and viability 1. Sperm competition represents the competition between males after copulating with the same female 2, in which their sperm are coincidental in time and space. This phenomenon has been reported in multiple species of plants and animals 3. For example, wild-caught D. melanogaster females usually contain sperm from 2-3 males 4. The sperm are stored in specialized organs with limited storage capacity, which might lead to the direct competition of the sperm from different males 2,5. Comparing sperm competitive ability of different males of interest (experimental male types) has been performed through controlled double-mating experiments in the laboratory 6,7. Briefly, a single female is exposed to two different males consecutively, one experimental male and one cross-mating reference male. The same mating scheme is then followed using other experimental male types thus facilitating the indirect comparison of the competitive ability of their sperm through a common reference. The fraction of individuals fathered by the experimental and reference males is identified using markers, which allows one to estimate sperm competitive ability using simple mathematical expressions 7,8. In addition, sperm competitive ability can be estimated in two different scenarios depending on whether the experimental male is second or first to mate (offense and defense assay, respectively) 9, which is assumed to be reflective of different competence attributes. Here, we describe an approach that helps to interrogate the role of different genetic factors that putatively underlie the phenomenon of sperm competitive ability in D. melanogaster.
Developmental Biology, Issue 78, Molecular Biology, Cellular Biology, Genetics, Biochemistry, Spermatozoa, Drosophila melanogaster, Biological Evolution, Phenotype, genetics (animal and plant), animal biology, double-mating experiment, sperm competitive ability, male fertility, Drosophila, fruit fly, animal model
50547
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An Affordable HIV-1 Drug Resistance Monitoring Method for Resource Limited Settings
Authors: Justen Manasa, Siva Danaviah, Sureshnee Pillay, Prevashinee Padayachee, Hloniphile Mthiyane, Charity Mkhize, Richard John Lessells, Christopher Seebregts, Tobias F. Rinke de Wit, Johannes Viljoen, David Katzenstein, Tulio De Oliveira.
Institutions: University of KwaZulu-Natal, Durban, South Africa, Jembi Health Systems, University of Amsterdam, Stanford Medical School.
HIV-1 drug resistance has the potential to seriously compromise the effectiveness and impact of antiretroviral therapy (ART). As ART programs in sub-Saharan Africa continue to expand, individuals on ART should be closely monitored for the emergence of drug resistance. Surveillance of transmitted drug resistance to track transmission of viral strains already resistant to ART is also critical. Unfortunately, drug resistance testing is still not readily accessible in resource limited settings, because genotyping is expensive and requires sophisticated laboratory and data management infrastructure. An open access genotypic drug resistance monitoring method to manage individuals and assess transmitted drug resistance is described. The method uses free open source software for the interpretation of drug resistance patterns and the generation of individual patient reports. The genotyping protocol has an amplification rate of greater than 95% for plasma samples with a viral load >1,000 HIV-1 RNA copies/ml. The sensitivity decreases significantly for viral loads <1,000 HIV-1 RNA copies/ml. The method described here was validated against a method of HIV-1 drug resistance testing approved by the United States Food and Drug Administration (FDA), the Viroseq genotyping method. Limitations of the method described here include the fact that it is not automated and that it also failed to amplify the circulating recombinant form CRF02_AG from a validation panel of samples, although it amplified subtypes A and B from the same panel.
Medicine, Issue 85, Biomedical Technology, HIV-1, HIV Infections, Viremia, Nucleic Acids, genetics, antiretroviral therapy, drug resistance, genotyping, affordable
51242
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Protein WISDOM: A Workbench for In silico De novo Design of BioMolecules
Authors: James Smadbeck, Meghan B. Peterson, George A. Khoury, Martin S. Taylor, Christodoulos A. Floudas.
Institutions: Princeton University.
The aim of de novo protein design is to find the amino acid sequences that will fold into a desired 3-dimensional structure with improvements in specific properties, such as binding affinity, agonist or antagonist behavior, or stability, relative to the native sequence. Protein design lies at the center of current advances drug design and discovery. Not only does protein design provide predictions for potentially useful drug targets, but it also enhances our understanding of the protein folding process and protein-protein interactions. Experimental methods such as directed evolution have shown success in protein design. However, such methods are restricted by the limited sequence space that can be searched tractably. In contrast, computational design strategies allow for the screening of a much larger set of sequences covering a wide variety of properties and functionality. We have developed a range of computational de novo protein design methods capable of tackling several important areas of protein design. These include the design of monomeric proteins for increased stability and complexes for increased binding affinity. To disseminate these methods for broader use we present Protein WISDOM (https://www.proteinwisdom.org), a tool that provides automated methods for a variety of protein design problems. Structural templates are submitted to initialize the design process. The first stage of design is an optimization sequence selection stage that aims at improving stability through minimization of potential energy in the sequence space. Selected sequences are then run through a fold specificity stage and a binding affinity stage. A rank-ordered list of the sequences for each step of the process, along with relevant designed structures, provides the user with a comprehensive quantitative assessment of the design. Here we provide the details of each design method, as well as several notable experimental successes attained through the use of the methods.
Genetics, Issue 77, Molecular Biology, Bioengineering, Biochemistry, Biomedical Engineering, Chemical Engineering, Computational Biology, Genomics, Proteomics, Protein, Protein Binding, Computational Biology, Drug Design, optimization (mathematics), Amino Acids, Peptides, and Proteins, De novo protein and peptide design, Drug design, In silico sequence selection, Optimization, Fold specificity, Binding affinity, sequencing
50476
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Barnes Maze Testing Strategies with Small and Large Rodent Models
Authors: Cheryl S. Rosenfeld, Sherry A. Ferguson.
Institutions: University of Missouri, Food and Drug Administration.
Spatial learning and memory of laboratory rodents is often assessed via navigational ability in mazes, most popular of which are the water and dry-land (Barnes) mazes. Improved performance over sessions or trials is thought to reflect learning and memory of the escape cage/platform location. Considered less stressful than water mazes, the Barnes maze is a relatively simple design of a circular platform top with several holes equally spaced around the perimeter edge. All but one of the holes are false-bottomed or blind-ending, while one leads to an escape cage. Mildly aversive stimuli (e.g. bright overhead lights) provide motivation to locate the escape cage. Latency to locate the escape cage can be measured during the session; however, additional endpoints typically require video recording. From those video recordings, use of automated tracking software can generate a variety of endpoints that are similar to those produced in water mazes (e.g. distance traveled, velocity/speed, time spent in the correct quadrant, time spent moving/resting, and confirmation of latency). Type of search strategy (i.e. random, serial, or direct) can be categorized as well. Barnes maze construction and testing methodologies can differ for small rodents, such as mice, and large rodents, such as rats. For example, while extra-maze cues are effective for rats, smaller wild rodents may require intra-maze cues with a visual barrier around the maze. Appropriate stimuli must be identified which motivate the rodent to locate the escape cage. Both Barnes and water mazes can be time consuming as 4-7 test trials are typically required to detect improved learning and memory performance (e.g. shorter latencies or path lengths to locate the escape platform or cage) and/or differences between experimental groups. Even so, the Barnes maze is a widely employed behavioral assessment measuring spatial navigational abilities and their potential disruption by genetic, neurobehavioral manipulations, or drug/ toxicant exposure.
Behavior, Issue 84, spatial navigation, rats, Peromyscus, mice, intra- and extra-maze cues, learning, memory, latency, search strategy, escape motivation
51194
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Choice and No-Choice Assays for Testing the Resistance of A. thaliana to Chewing Insects
Authors: Martin De Vos, Georg Jander.
Institutions: Cornell University.
Larvae of the small white cabbage butterfly are a pest in agricultural settings. This caterpillar species feeds from plants in the cabbage family, which include many crops such as cabbage, broccoli, Brussel sprouts etc. Rearing of the insects takes place on cabbage plants in the greenhouse. At least two cages are needed for the rearing of Pieris rapae. One for the larvae and the other to contain the adults, the butterflies. In order to investigate the role of plant hormones and toxic plant chemicals in resistance to this insect pest, we demonstrate two experiments. First, determination of the role of jasmonic acid (JA - a plant hormone often indicated in resistance to insects) in resistance to the chewing insect Pieris rapae. Caterpillar growth can be compared on wild-type and mutant plants impaired in production of JA. This experiment is considered "No Choice", because larvae are forced to subsist on a single plant which synthesizes or is deficient in JA. Second, we demonstrate an experiment that investigates the role of glucosinolates, which are used as oviposition (egg-laying) signals. Here, we use WT and mutant Arabidopsis impaired in glucosinolate production in a "Choice" experiment in which female butterflies are allowed to choose to lay their eggs on plants of either genotype. This video demonstrates the experimental setup for both assays as well as representative results.
Plant Biology, Issue 15, Annual Review, Plant Resistance, Herbivory, Arabidopsis thaliana, Pieris rapae, Caterpillars, Butterflies, Jasmonic Acid, Glucosinolates
683
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Injection of dsRNA into Female A. aegypti Mosquitos
Authors: Brian M. Luna, Jennifer Juhn, Anthony A. James.
Institutions: University of California, Irvine (UCI), University of California, Irvine (UCI).
Reverse genetic approaches have proven extremely useful for determining which genes underly resistance to vector pathogens in mosquitoes. This video protocol illustrates a method used by the James lab to inject dsRNA into female A. aegypti mosquitoes, which harbor the dengue virus. The technique for calibrating injection needles, manipulating the injection setup, and injecting dsRNA into the thorax is illustrated.
Cellular Biology, Issue 5, mosquito, malaria, genetics, injection
215
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Using Micro-Electro-Mechanical Systems (MEMS) to Develop Diagnostic Tools
Authors: Utkan Demirci.
Institutions: Brigham and Women's Hospital.
Cellular Biology, Issue 8, microfluidics, diagnostics, capture, blood, HIV, bioengineering
314
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Molecular Evolution of the Tre Recombinase
Authors: Frank Buchholz.
Institutions: Max Plank Institute for Molecular Cell Biology and Genetics, Dresden.
Here we report the generation of Tre recombinase through directed, molecular evolution. Tre recombinase recognizes a pre-defined target sequence within the LTR sequences of the HIV-1 provirus, resulting in the excision and eradication of the provirus from infected human cells. We started with Cre, a 38-kDa recombinase, that recognizes a 34-bp double-stranded DNA sequence known as loxP. Because Cre can effectively eliminate genomic sequences, we set out to tailor a recombinase that could remove the sequence between the 5'-LTR and 3'-LTR of an integrated HIV-1 provirus. As a first step we identified sequences within the LTR sites that were similar to loxP and tested for recombination activity. Initially Cre and mutagenized Cre libraries failed to recombine the chosen loxLTR sites of the HIV-1 provirus. As the start of any directed molecular evolution process requires at least residual activity, the original asymmetric loxLTR sequences were split into subsets and tested again for recombination activity. Acting as intermediates, recombination activity was shown with the subsets. Next, recombinase libraries were enriched through reiterative evolution cycles. Subsequently, enriched libraries were shuffled and recombined. The combination of different mutations proved synergistic and recombinases were created that were able to recombine loxLTR1 and loxLTR2. This was evidence that an evolutionary strategy through intermediates can be successful. After a total of 126 evolution cycles individual recombinases were functionally and structurally analyzed. The most active recombinase -- Tre -- had 19 amino acid changes as compared to Cre. Tre recombinase was able to excise the HIV-1 provirus from the genome HIV-1 infected HeLa cells (see "HIV-1 Proviral DNA Excision Using an Evolved Recombinase", Hauber J., Heinrich-Pette-Institute for Experimental Virology and Immunology, Hamburg, Germany). While still in its infancy, directed molecular evolution will allow the creation of custom enzymes that will serve as tools of "molecular surgery" and molecular medicine.
Cell Biology, Issue 15, HIV-1, Tre recombinase, Site-specific recombination, molecular evolution
791
Play Button
Interview: HIV-1 Proviral DNA Excision Using an Evolved Recombinase
Authors: Joachim Hauber.
Institutions: Heinrich-Pette-Institute for Experimental Virology and Immunology, University of Hamburg.
HIV-1 integrates into the host chromosome of infected cells and persists as a provirus flanked by long terminal repeats. Current treatment strategies primarily target virus enzymes or virus-cell fusion, suppressing the viral life cycle without eradicating the infection. Since the integrated provirus is not targeted by these approaches, new resistant strains of HIV-1 may emerge. Here, we report that the engineered recombinase Tre (see Molecular evolution of the Tre recombinase , Buchholz, F., Max Planck Institute for Cell Biology and Genetics, Dresden) efficiently excises integrated HIV-1 proviral DNA from the genome of infected cells. We produced loxLTR containing viral pseudotypes and infected HeLa cells to examine whether Tre recombinase can excise the provirus from the genome of HIV-1 infected human cells. A virus particle-releasing cell line was cloned and transfected with a plasmid expressing Tre or with a parental control vector. Recombinase activity and virus production were monitored. All assays demonstrated the efficient deletion of the provirus from infected cells without visible cytotoxic effects. These results serve as proof of principle that it is possible to evolve a recombinase to specifically target an HIV-1 LTR and that this recombinase is capable of excising the HIV-1 provirus from the genome of HIV-1-infected human cells. Before an engineered recombinase could enter the therapeutic arena, however, significant obstacles need to be overcome. Among the most critical issues, that we face, are an efficient and safe delivery to targeted cells and the absence of side effects.
Medicine, Issue 16, HIV, Cell Biology, Recombinase, provirus, HeLa Cells
793
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Policies | License Agreement | ISSN 1940-087X
simple hit counter
What is Visualize?
JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.
How does it work?
We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.
Video X seems to be unrelated to Abstract Y...
In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.
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ALB's Materials Website: www.albmaterials.com
A Brief Introduction of DM1 and DM1-SMCC
What's DM1, DM1-SMCC?
DM1 is abbr. of N2’-Deacetyl-N2’-(3-mercapto-1-oxopropyl)-maytansine, which is a maytansinoid cytotoxic agent used in trastuzumab emtansine and additional antibody-drug conjugates (ADC) in development.
DM1-SMCC, also called SMCC-DM1. It’s DM1 linked with SMCC (4-(3-mercapto-2,5-dioxo-1-pyrrolidinylmethyl)-cylohexanecarboxylic acid) linker. DM1-SMCC can react with amino group in MAB(monoclonal antibodies) directly with SMCC.
Structure of DM1 and DM1-SMCC:
Please refer to: DM1 | Tubulin-Binders
Please refer to: DM1-SMCC | Tubulin-Binders
DM1 Synonyms: N2' -deacetyl-N2' -(3-Mercapto-1-oxopropyl)-Maytansine; Maytansinoid DM 1
Toxicity of DM1:
IC50 of proliferation/viability of tumor cell lines are in the range of 10-10–10-12 M for DM1/DM4 maytansinoid derivatives.
DM1 mechanism of action:
DM1, and other Maytansine analogs are a microtubule-targeted drug that binds to tubulin at the vinca binding site, it can depolymerize microtubules and arrest cells in mitosis.
FDA approved ADCs drugs with DM1:
Kadcyla ® (ado-trastuzumab emtansine or T-DM1, Genentech) is an ADC comprised of trastuzumab conjugated through lysines to DM1, via a non-cleavable thioether linker (N-succinimidyl 4-(N-maleimidomethyl) cyclohexane-1-carboxylate, SMCC), with an average DAR of 3.5. The conjugate is abbreviated T-DM1.
The FDA approval of Kadcyla ® in 2013. Kadcyla ® Glossary is approved to treat HER2-positive breast cancer that has spread to other parts of the body (metastatic breast cancer) after prior treatment with trastuzumab (Herceptin) and a taxane. Prior treatment could have been for the initial treatment of breast cancer or for the treatment of cancer that had spread to other parts of the body. Trastuzumab alone stops growth of cancer cells by binding to the HER2/neu receptor, whereas DM1 enters cells and destroys them by binding to tubulin. Because the monoclonal antibody targets HER2, and HER2 is only over-expressed in cancer cells, the conjugate delivers the toxin specifically to tumor cells.
Commercial Availability of DM1:
DM1 and DM1-SMCC(SMCC-DM1) are commercial available from ALB Technology.
ALB Technology Limited is a professional ADCs drugs and linkers supplier. ALB Technology Limited's featured ADCs products include MMAEMMAFDM1DM1-SMCC, MaytansinolFmoc-Val-Cit-PAB-MMAE, Fmoc-Val-Cit-PAB-MMAF, MC-Val-Cit-PAB-MMAEMC-Val-Cit-PAB-MMAF,Val-Cit-PABFmoc-Val-Cit-PABFmoc-Val-Cit-PAB-PNP ect.
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Anti Narcoleptics Drugs > Anti Narcoleptic Articles > Modapro helps military during operations
Modapro helps military during operations
Modapro is received for…
…making much better a state of wakefulness by patients with inordinate sleepiness caused by narcolepsy disease or other various sleep disorders. The drug may also be received for many other conditions and purposes as prescribed by your doctor medication. Modapro is an agent promoting the state of wakefulness. It can be taken by the students preparing for exams, businessmen and managers for improving the capabilities and their physical stamina, people who often visit night clubs and passengers flying to distant time zones (jet lags).
So you can buy Modapro according to your own goals at the nearest drugstore if you are a resident of the US, Australia and European countries even without a prescription of your doctor. There are also many reliable online pharmacies where you can order Modapro and the drug will be delivered right to your front door. Exactly how the medication works has not actually been found out yet, but it is assumed to work by changing the natural chemicals (also called neurotransmitters) in the human brain.
Does Modapro have any significant side effects?
Not every side effect of Generic Modapro may be described. So you should always ask your doctor, pharmacist or healthcare professional for their medical advice. Moreover, in addition to the needed effects of the given drug, some undesirable side effects may be noticed. In case that any of the mentioned side effects do appear, you may require medical checkup and attention. There might be anxiety, overexcitement, nausea and a little headache. The symptoms of overdose with the medication are agitation, fast and pounding heartbeat, a bit increased blood pressure and some trouble with sleeping.
Some of these little side effects may not even need the medical attention. When your body adjusts to Modapro during the treatment, the mentioned above side effects will just go away. Your doctor or pharmacist may also tell you about means for reducing or preventing some of the given side effects. So if any of the given side effects keep occurring, bother you or if you have any questions about reception of the medication, consult your personal doctor.
Indications and usage.
Tablets that contain Modapro are intended to improve the state of wakefulness by adult patients who have inordinate sleepiness during the day connected with suffering from narcolepsy, obstructive sleep apnea or shift work disorder. Limitations for usage: tablets are designed in order to successfully treat unreasonable sleepiness and are not used as treatment for the underlying obstruction.
The usual recommended dosage of the drug used in tablets for patients with the disease of narcolepsy is about 200 mg received orally once a day as the one dose early in the morning. Doses that are up to 400 mg a day, are taken as the one dose, have been well treated by the patients, but there is no certain evidence that this dose has additional benefit beyond that one of the 200 mg a day dose.
Why the drug is so popular for military?
Researchers recently have had the opportunity to compare a group of people with and without taking the drug. The test was conducted using elite F-117A Nighthawk pilots. F117-A Nighthawk is one of those black triangular stealth attack aircraft used with surgical precision by the US air force in all recent wars. The test group consisted of the people who flew on these aircraft - people who pushed the limits of performance of a person nowadays using one of the most expensive and sophisticated aircraft in the world. The research found out that a group that was taking Modapro was doing much better than the one which was not.
Modapro is the one of newest and modern means in combating unreasonable sleepiness during a day and helping healthy people stay awake for longer.
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3 Ways Your Hydration Status Changes As You Age
3 Ways Your Hydration Status Changes As You Age
Human life expectancy is increasing rapidly, with some current predictions suggesting that women will pass the 90-year mark relatively soon (well, those lucky enough to be born in South Korea in 2030 anyway). This is amazing when you think that just less than a century ago the average life expectancy in the U.K. in 1921 was 59 for women and just 55 for men.
The fact that we’re living much longer (combined with increases in free leisure time) has meant that more and more older adults are taking part in serious sporting events and achieving things that would not have seemed possible even a few generations ago.
Like Rob Barel winning the men’s 60-64 age group at the 2017 IRONMAN World Championship in Kona in a staggering 9 hours and 46 minutes—a time that would have placed him in the top 10 of the race overall well into the mid 1980s!
It’s great to see more and more older athletes taking part in endurance events, but how does age affect things like recovery, nutritional and hydration requirements? I’m going to look at that last one in particular and discuss three common traits of ageing that mean getting your hydration strategy right all the more important as the years go by.
1. You have less water on board to start with, so dehydration is more of a risk
Around 60 to 70 percent of your total body water is locked inside your cells in the intra-cellular compartment ( ICF), with the remainder sloshing around outside them as extra-cellular fluid (ECF).
Because your muscle cells contain a large amount of your ICF volume, the amount of muscle mass you have has a big influence on your total body water levels. Losing lean muscle tissue is an inevitable consequence of getting older (especially past the age of 50), so it follows that your total body water content declines as you age.
I’ve seen it reported that losing four to six liters of total body water between the ages of 20 and 80 is in the normal range, though there’s not a complete consensus in this area and my guess is that this may well vary considerably from individual to individual.
Although training (especially lifting weights) can help to reduce the loss of muscle mass with ageing to a certain degree, it’s basically impossible to halt it altogether. With this loss of muscle you also lose a significant chunk of your “reservoir” of fluids as you age, meaning that dehydration when you’re sweating a lot can occur more rapidly than it can for younger athletes.
2. You tend to lose more water through urine, so dehydration is more of a risk
Another thing that impacts hydration levels in older people is the fact that kidney function tends to deteriorate as you get older as well. Reduced kidney function means less concentrated urine can be produced and, as a result, more free water is lost when you pee.
This may be compounded in some by a reduction in levels of aldosterone, a hormone responsible for helping your body hold onto water more effectively.
3. Your sensation of thirst is diminished, so, you guessed it—dehydration is more of a risk!
A study published in 2001 clearly demonstrated that, whilst adults over 65 tended to drink sufficient fluids to maintain normal hydration status on a day to day basis, when their hydration levels were challenged by periods of sweating, their sensation of thirst—and therefore their tendency to rehydrate effectively—was compromised when compared with younger people.
The participants tended to correct this dehydration eventually, but possibly more slowly than would be compatible with optimal recovery from performance in high intensity sport.
These three factors suggest that older athletes need to be a bit more diligent with their hydration practices than younger people as the margin for error is reduced and the risk of dehydration is increased.
What can older athletes do to stay hydrated?
1. Be aware that you probably need to drink a bit more
This would be a good start. But, beware, I’ve written about the perils of dramatically over-consuming fluids before. In a nutshell, hyponatremia is a very real risk and this can really impact your performance and make you pretty ill, so that advice needs to be handled with common sense and care.
2. Take in additional sodium with your fluids when you’re sweating
Sodium helps you hold onto more water in your extra-cellular fluid and bloodstream and this reduces cardiovascular strain, helping you maintain your performance. It can also help you avoid cramp.
The concentrations of sodium in your body fluids are finely balanced by various mechanisms, so it can be a sensible idea to add a bit of extra salt to your food, and/or some sodium supplements in your drinks, at times when you know your hydration levels might be challenged. Increasing your sodium intake also increases thirst, which should urge you to drink more too.
As an aside, it’s worth noting that the 1,000mg/l and 1,500mg/l electrolyte supplements we make at Precision Hydration are 2x and 3x stronger than typical sports drinks, so they’re often very popular with older athletes who’re struggling to stay properly hydrated with water or weak hydration supplements alone.
Finally, it’s very important for older athletes to start training or events properly hydrated and to ensure they rehydrate effectively after they’ve finished.
If you’re an older athlete who struggles with hydration issues like dehydration or cramp after longer period of sweating, it’s worth taking Precision Hydration’s free online Sweat Test to help you get started with personalising your hydration strategy. And, if you have any questions at all, just drop me an email.
Andy Blow
Andy Blow has a few top 10 Ironman and 70.3 finishes and an Xterra World Age Group title to his name. He founded Precision Hydration to help athletes solve their hydration issues. He has a degree in Sport and Exercise Science and was once the Team Sports Scientist for Benetton and Renault F1 teams.
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5eff3d1f6f98e57329caed0ceb9053d3
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5,160,946,254,349,826,000
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Arterial Ulcers
Abstract
Oxygen is delivered to tissue by way of arterial circulation. When there is inadequate oxygen delivery to the tissue it starts to become stressed and when oxygen delivery becomes critically low the tissue begins to die. This condition is known as an arterial leg ulcer and it is estimated that there are approximately 500,000 of these types of wounds in the United States per year,. Of note, these wounds are specifically not inclusive of “neuro-ischemic” diabetic foot ulcers (which are discussed in the Diabetic Foot Ulcer session). In patients with arterial leg ulcers there are three significant clinical interventions that need to occur. First, the effected area needs to be re-vascularized; this can occur using several types of procedures, in particular endovascular or open. However, in approximately 15 percent of all patients this initial step cannot be adequately accomplished. In patients that cannot be re-vascularized there is a 50 percent chance of losing the limb within six months of initial presentation. Once re-vascularization has occurred, the second phase is to debride the wound to promote healing through the formation of a healthy tissue matrix. There are a variety of diagnostic tests to determine if the tissue has adequate circulation to heal; including physical examination and the use of a hand held Doppler probe and blood pressure cuff. Known as the ankle brachial index, this method is preferable in determining adequate circulation in an arterial leg ulcer. Tissue viability is determined by looking at the blood pressure ratio between the arteries of the foot and leg and the brachial blood pressure of the arm. Finally, if necessary, reconstruction of the effected area, to promote complete wound closure, is required. This reconstruction can be either surgical (full-thickness flap procedure) or medical (implanting artificial skin matrices and/or negative pressure therapy).
References
Federman DG, Ladiiznski B, Dardik A, Kelly M, Shapshak D, Ueno CM, et al. Wound healing society 2014 update on guidelines for arterial ulcers. Wound Repair Regen. 2016;24(1): 127–35
The society for vascular surgery lower extremity threatened limb classification system: risk stratification based on wound, ischemia, and foot infection (WIfI). J Vasc Surg. 2014;59:220–34
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5eff3d1f6f98e57329caed0ceb9053d3
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%0 Journal Article %A Uehahara, Shotaro %A Ishii, Sakura %A Uno, Yasuhiro %A Inoue, Takashi %A Sasaki, Erika %A Yamazaki, Hiroshi %T Regio- and stereo-selective oxidation of a cardiovascular drug metoprolol mediated by cytochrome P450 2D and 3A enzymes in marmoset livers %D 2017 %R 10.1124/dmd.117.075630 %J Drug Metabolism and Disposition %P dmd.117.075630 %X A β-blocker metoprolol is one of the in vivo probes for human cytochrome P450 (P450) 2D6. Investigation of non-human primate P450 enzymes helps improve accuracy of the extrapolation of pharmacokinetic data from animals into humans. Common marmosets (Callithrix jacchus) are a potential primate model for preclinical research, but detailed roles of marmoset P450 enzymes in metoprolol oxidations remained unknown. In this study, regio- and stereo-selectivity of metoprolol oxidations by a variety of P450 enzymes in marmoset and human livers were investigated in vitro. Although liver microsomes from cynomolgus monkeys and rats preferentially mediated S-metoprolol O-demethylation and R-metoprolol α-hydroxylation, respectively, those from humans, marmosets, minipigs, and dogs preferentially mediated R-metoprolol O-demethylation, in contrast to slow rates of R- and S-metoprolol oxidations in mouse liver microsomes. R- and S-metoprolol O-demethylation activities in marmoset livers were strongly inhibited by quinidine and ketoconazole, and were significantly correlated with bufuralol 1'-hydroxylation and midazolam 1'-hydroxylation activities and also with P450 2D and 3A4 contents, different from the cases in human livers which did not have any correlations with P450 3A-mediated midazolam 1'-hydroxylations. Recombinant human P450 2D6 enzyme and marmoset P450 2D6/3A4 enzymes effectively catalyzed R-metoprolol O-demethylation, comparable to the activities of human and marmoset liver microsomes, respectively. These results indicated that the major roles of P450 2D enzymes for the regio- and stereo-selectivity of metoprolol oxidations were similar between human and marmoset livers, but the minor roles of P450 3A enzymes were unique to marmosets. %U http://dmd.aspetjournals.org/content/dmd/early/2017/05/11/dmd.117.075630.full.pdf
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702,230,459,117,646,500
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skin-hair-icon
Swelling around the eye
There is a redness on my left eye lid and below my eye. It's swelled up and it burns when you touch it. There are little bubbles of skin formed too now. And skin is drying up there. Please tell me what is it and what to do. It hurts.
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Probably its herpes or allergic reaction. Get evaluation done at nearby physician.
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ICD-10-CM Code F06
Other mental disorders due to known physiological condition
Version 2021 Non-Billable Code
Not Valid for Submission
F06 is a "header" nonspecific and non-billable code code, consider using a code with a higher level of specificity for a diagnosis of other mental disorders due to known physiological condition. The code is NOT valid for the year 2021 for the submission of HIPAA-covered transactions.
ICD-10:F06
Short Description:Other mental disorders due to known physiological condition
Long Description:Other mental disorders due to known physiological condition
Consider the following ICD-10 codes with a higher level of specificity:
• F06.0 - Psychotic disorder with hallucinations due to known physiological condition
• F06.1 - Catatonic disorder due to known physiological condition
• F06.2 - Psychotic disorder with delusions due to known physiological condition
• F06.3 - Mood disorder due to known physiological condition
• F06.30 - Mood disorder due to known physiological condition, unspecified
• F06.31 - Mood disorder due to known physiological condition with depressive features
• F06.32 - Mood disorder due to known physiological condition with major depressive-like episode
• F06.33 - Mood disorder due to known physiological condition with manic features
• F06.34 - Mood disorder due to known physiological condition with mixed features
• F06.4 - Anxiety disorder due to known physiological condition
• F06.8 - Other specified mental disorders due to known physiological condition
Tabular List of Diseases and Injuries
The Tabular List of Diseases and Injuries is a list of ICD-10 codes, organized "head to toe" into chapters and sections with guidance for inclusions, exclusions, descriptions and more. The following references are applicable to the code F06:
Includes
Includes
This note appears immediately under a three character code title to further define, or give examples of, the content of the category.
• mental disorders due to endocrine disorder
• mental disorders due to exogenous hormone
• mental disorders due to exogenous toxic substance
• mental disorders due to primary cerebral disease
• mental disorders due to somatic illness
• mental disorders due to systemic disease affecting the brain
Code First
Code First
Certain conditions have both an underlying etiology and multiple body system manifestations due to the underlying etiology. For such conditions, the ICD-10-CM has a coding convention that requires the underlying condition be sequenced first followed by the manifestation. Wherever such a combination exists, there is a "use additional code" note at the etiology code, and a "code first" note at the manifestation code. These instructional notes indicate the proper sequencing order of the codes, etiology followed by manifestation.
• the underlying physiological condition
Type 1 Excludes
Type 1 Excludes
A type 1 excludes note is a pure excludes note. It means "NOT CODED HERE!" An Excludes1 note indicates that the code excluded should never be used at the same time as the code above the Excludes1 note. An Excludes1 is used when two conditions cannot occur together, such as a congenital form versus an acquired form of the same condition.
• unspecified dementia F03
Type 2 Excludes
Type 2 Excludes
A type 2 excludes note represents "Not included here". An excludes2 note indicates that the condition excluded is not part of the condition represented by the code, but a patient may have both conditions at the same time. When an Excludes2 note appears under a code, it is acceptable to use both the code and the excluded code together, when appropriate.
• delirium due to known physiological condition F05
• dementia as classified in F01 F02
• other mental disorders associated with alcohol and other psychoactive substances F10 F19
Code Classification
• Mental and behavioural disorders (F00–F99)
• Mental disorders due to known physiological conditions (F01-F09)
• Other mental disorders due to known physiological condition (F06)
Code History
• FY 2016 - New Code, effective from 10/1/2015 through 9/30/2016
(First year ICD-10-CM implemented into the HIPAA code set)
• FY 2017 - No Change, effective from 10/1/2016 through 9/30/2017
• FY 2018 - No Change, effective from 10/1/2017 through 9/30/2018
• FY 2019 - No Change, effective from 10/1/2018 through 9/30/2019
• FY 2020 - No Change, effective from 10/1/2019 through 9/30/2020
• FY 2021 - No Change, effective from 10/1/2020 through 9/30/2021
Information for Patients
Mental Disorders
Also called: Mental illness
What are mental disorders?
Mental disorders (or mental illnesses) are conditions that affect your thinking, feeling, mood, and behavior. They may be occasional or long-lasting (chronic). They can affect your ability to relate to others and function each day.
What are some types of mental disorders?
There are many different types of mental disorders. Some common ones include
• Anxiety disorders, including panic disorder, obsessive-compulsive disorder, post-traumatic stress disorder, and phobias
• Depression, bipolar disorder, and other mood disorders
• Eating disorders
• Personality disorders
• Psychotic disorders, including schizophrenia
What causes mental disorders?
There is no single cause for mental illness. A number of factors can contribute to risk for mental illness, such as
• Your genes and family history
• Your life experiences, such as stress or a history of abuse, especially if they happen in childhood
• Biological factors such as chemical imbalances in the brain
• A traumatic brain injury
• A mother's exposure to viruses or toxic chemicals while pregnant
• Use of alcohol or recreational drugs
• Having a serious medical condition like cancer
• Having few friends, and feeling lonely or isolated
Mental disorders are not caused by character flaws. They have nothing to do with being lazy or weak.
Who is at risk for mental disorders?
Mental disorders are common. More than half of all Americans will be diagnosed with a mental disorder at some time in their life.
How are mental disorders diagnosed?
The steps to getting a diagnosis include
• A medical history
• A physical exam and possibly lab tests, if your provider thinks that other medical conditions could be causing your symptoms
• A psychological evaluation. You will answer questions about your thinking, feelings, and behaviors.
What are the treatments for mental disorders?
Treatment depends on which mental disorder you have and how serious it is. You and your provider will work on a treatment plan just for you. It usually involves some type of therapy. You may also take medicines. Some people also need social support and education on managing their condition.
In some cases, you may need more intensive treatment. You may need to go to a psychiatric hospital. This could be because your mental illness is severe. Or it could be because you are at risk of hurting yourself or someone else. In the hospital, you will get counseling, group discussions, and activities with mental health professionals and other patients.
• Adjustment disorder (Medical Encyclopedia)
• Conversion disorder (Medical Encyclopedia)
• Illness anxiety disorder (Medical Encyclopedia)
• Somatic symptom disorder (Medical Encyclopedia)
[Learn More]
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The Connection Between Gum Disease and Heart Disease
Most people believe that a little bleeding while brushing their teeth is normal. It is such myths and misconceptions that have resulted in more than 80% of the population with gum disease. Periodontal disease (gum disease) is an infection that causes chronic inflammation of the gums, with one of it’s signs being bleeding while brushing or flossing. Recent studies have found that there is a direct correlation between heart disease and gum disease. The understanding of this relationship and what to do about it is a matter of life and death.
Research describes the affect of gum disease and heart disease at least as strong as the link of heart disease to cholesterol, smoking or body weight. These recent studies have found blood clots escape into the bloodstream, increasing the risk of heart attacks and stroke. These same blood clots were found to contain the most common strain of bacteria in dental plaque.
Unfortunately, there are no early warning signs to gum disease, it progresses silently, often without pain. Since there is no pain or discomfort present during the initial stages, people often ignore the signs and symptoms, believing them to be normal occurrences. The disease eventually destroys the gum and supporting bone that holds the teeth in place.
What is alarming is that other health concerns are also being found to relate to gum disease. Bacteria in plaque have also been found to have a link in a weakened immune system that can slow wound healing; higher risk of premature; low birth weight infants; stroke; and lung infection in people with chronic lung diseases.
The mouth is an extremely important organ and is the doorway to the body. Digestion begins here, many diseases, such as diabetes and AIDS show initial signs here, and our confidence in how willing we are to smile, depends on how we feel about the appearance of our teeth. The teeth are made to last a lifetime and even after;, as seen in excavated ancient skulls. It is a myth to think that with age, teeth become loose and are lost. Many factors affect tooth loss: heredity, diet and nutrition, stress, and the health of the gums. We have no control over heredity, but we can counteract any week links in our genes with the other factors.
Numerous studies have established the importance of diet and nutrition, stress management and exercize for a healthy body. The same rules apply to the health of the oral cavity. Fresh food free of chemicals, preservatives and additives are essential for prevention of disease. However, stress can deplete our body of vital nutrients if supplements are not taken to replace those needed vitamins and minerals. Bleeding gums have been associated with defficiency of vitamin C. Calcium and it’s importance for healthy teeth and bone is well documented. During menopause, a woman’s body decreases the production of the hormone estrogen, which helps bones absorb and retain calcium. If calcium supplements are not taken (at least 1200-1500 mg/ day) the first place the needed calcium is taken from is the jaw bone. This may lead to loose teeth.
Proper oral hygiene is the other factor which may counteract any bad genes passed down for gum disease. There are may tools available to take responability towards good daily hygiene. Of course, brushing and flossing are the main part of daily hygiene, however, if deep gum pockets exist, it will be almost impossible to floss those areas. In that case, water irrigators are useful. Proxi-brushes are very small, brushes that resemble pipe cleaners. They are used to clean between exposed roots of back teeth and deep gum pockets.
If the basic rules for a healthy body are practiced daily, with added good oral hygiene, you need never be afraid of going to the dentist or of loosing your teeth.
Invalid OAuth access token.
Avatar Written by Flora Parsa Stay DDS
Explore Wellness in 2021
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Small molecule analogues of an immunomodulatory helminth product provide a novel approach to dissecting macrophage signal transduction pathways : Poster abstract
Al-Riyami, Lamyaa and Rzepecka, Justyna and Khalaf, Abedawn and Suckling, Colin and Harnett, M. and Harnett, William (2010) Small molecule analogues of an immunomodulatory helminth product provide a novel approach to dissecting macrophage signal transduction pathways : Poster abstract. Immunology, 131 (Supple). p. 164. ISSN 0019-2805
Full text not available in this repository.Request a copy from the Strathclyde author
Abstract
ES-62 is an immunomodulatory phosphorylcholine (PC)-containing protein that is actively secreted by the rodent filarial nematode Acanthocheilonema viteae during parasitism of the vertebrate host. The net effect of ES-62¢s interaction with the immune system is the generation of an anti-inflammatory immunological phenotype. ES-62 acts to inhibit the inflammatory response by selectively targeting key MAPkinase and NF-jB signalling cassettes in a number of cells of the immune system. The activity of ES-62 is dependent on its PC moieties and therefore we tested a range of small PC-containing compounds for comparable activity to the parent molecule, in in vitro assays of inflammation employing mouse macrophages. Some of the compounds examined were indeed found to mimic the anti-inflammatory effects of ES-62 but of particular interest was the observation that some selectivity of action was demonstrated, with certain compounds differentially inhibiting distinct functional components of the inflammatory response. This raises the exciting possibility of employing such small compounds to dissect the network of key signalling pathways underlying immune cell responsiveness. In particular, we are focusing on molecular signals involved in differentially regulating inflammatory cytokines including IL-12p40, TNF-a and IL-6 produced by macrophages.
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Text Size
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Giving Fish Versus Teaching To Fish: Which is More Effective In Treating Anxiety?
anonymous anonymous
Hello. I have social anxiety disorder and I've just changed my therapist, because I moved to a different city. I already had 3 sessions with my new therapist, but he's really different than my old one. I liked the old one more mostly because, when I told him that I‘m afraid of not knowing what people actually think of the things I say or do, he understood what I wanted from him and he‘d never (or at least almost never) beat around the bush. And even though I told this one the same thing, it still feels like sometimes he hides something that he‘d otherwise say just to not "insult“ me, I guess. He just makes the confused look for a second and says something really non-straightforward, which is pretty hard for me to understand. I talked about this thing with my friend and he didn‘t really agree that the old therapist was better, he said that he wasn‘t acting professional, because I should understand things myself and he shouldn‘t say his opinion and I feel like I really don‘t agree with her. It wasn‘t like the old therapist would just say his opinion and present it like a fact or made me do the things that he suggested me, he just said what he thought about the situation and suggested what could be the best solution for me, when I couldn't figure it out myself and I really appreciated that. I really want the new one to not be so overly nice, because I feel like it's not going to get me anywhere. But I‘m not sure how to talk with him about that.
Dr. Richard Schultz Says...
Hello, and thank you so very much for addressing this question to me.
I find your question valuable for two reasons. First, it regards the treatment of Anxiety, of the Social variety, which is a specialty of mine. Second, it portrays the type of care NOT usually effective in such treatment, and third, your question is about the issue of communicating effectively with your therapist in order to yield the best outcome possible. Important issues all.
You may not have known this before, but you sure know it now; the "fit" between client and therapist, particularly from the perspective of the client, is a very significant predictor of therapeutic outcome. So, all in all, it is best to work with a therapist by whom you feel understood, valued, and whom you feel you can trust (trust that they are working with your best interests in mind and that they are highly skilled).
So, it seems we have a little dilemma here. Technically, and purely based on your description ("he understood what I wanted and never hesitated to give it to me"), your former therapist was treating your social anxiety by "giving you fish." In this case, "reassurance" is the fish. Perhaps you had a negative thought about how you might be seen at an upcoming social event, or perhaps you thought your therapist was critical of your sounding a bit scattered in session; in both scenarious, it sounds like the good old therapist was quick to correct your fortune telling and mind reading, and to promptly REASSURE you.
What's wrong with reassurance? In general, nothing. However, when it is elicited or sought in order to reduce anxiety, REASSURANCE ACTUALLY LEADS TO THE PERSISTENCE AND WORSENING OF ANXIETY! (based on the principle of "Negative Reinforcement" - Google it). Because although reassurance for an anxious person may yield a slight reduction in distress, it's really like a hit of "crack." It might feel great for a minute or two, or even 30 minutes or an hour, depending on how much reassurance/crack you can get, but the effects of both are terribly short-lived. They are like "temporaries stays of execution." But with each new day, the firing squad appears to line up yet again, and the anxiety is off and running, once again.
The problem with being given nice, fresh fish every day, is that never actually learn to bait a hook, drop it in the water, and try to catch a fish! And once you learn, you won't feel NEARLY so dependent on others for reassurance (which they don't ALWAYS give, right?). You will no longer have to worry about "whether or not there will be fish," or whether your therapist will give you any. The solution to this dilemma is to NOT seek fish, but to learn to fish. And indeed, as in leanring any new skill, there will be hits and misses on your way to a new set of skills. When someone hands you a fish, that all seems completely unnecessary, BUT IT DOESN'T LEAD TO CHANGE! Besides, most of us like to see ourselves as having a strong sense of agency and will and mastery in life, not as waiting for crumbs of crack to get through the day.
Ultimately, I suppose I would ask you how long you worked with the previous therapist, and during that time, by what percentage did your symptoms of social anxiety reduce? Approximately, of course. By 10%? 20%? 30%? Was the symptom severity ever measured and tracked from session to session? Were you given assignments to complete outside of session? Readings? Thought records? Exposures? These latter tools are DE RIGEUR when it comes to treating social anxiety.
So, what happens when you can't get reassurance from your therapist? Or from anyone else? THAT is precisely the right question to be asking in the treatment of social anxiety, because the answer to it is your only real long term, "inside job" solution. You learn a variety of VERY DIFFERENT ways of "greeting" anxiety (after all, it comes from inside you, so it's best to treat it as a friend and not an enemy).
My guess is that the new therapist MIGHT be trying indeed to teach you to fish, versus simply serving them up, but it is also clear that the rational for the new therapist's approach has NOT been made adequately clear to you. It is therefore quite understandable for you to feel disconnected from your therapist when you are not sure what he is saying, or why he is saying it. Anyone else in your shoes would likely have a similar reaction, especially given what you had been accustomed to.
How to deal with this? Easy! My number one recommendation to you is that you bring your original letter to me, and my response to you, with you to your very next session. Put your cards on the table and express your concerns, your disappointments, your confusion about what he's really thinking, etc. Whether or not you like the answer, you will be treating the anxiety SIMPLY by being willing to have the uncomfortable conversation. Its YOUR therapy, and YOUR LIFE that is being burdened by anxiety. It's also YOUR MONEY and YOUR TIME. Don't you think you deserve to use it as you wish? Perhaps not, and if so, this needs to go on the list of automatic thoughts ("I don't deserve to disagree with professionals, even if I'm paying; that is wrong, disrespectful, and could lead to an uncomfortable conflict or discussion"). That belief will then be subject to evaluation, and YOU will lead the charge!
Ideally, you will ultimately want to work with a psychologist well-trained and experienced with the treatment of anxiety in general, and of social anxiety in particular. They should have a strong grounding in cognitive-behavioral therapy, which is the most effective approach for this condition. Your new therapist may very well be coming from this perspective, and that may come out in the discussion I am proposing you initiate at YOUR VERY NEXT SESSION.
Your primary challenge is to relate to anxiety as a friend or as an assistant; it is not your master although you treat it as such. With self-acceptance, you need no reassurance, and without it, all of the reassurance in the world won't help you.
Please feel free to review my replies to many other questions about social anxiety, and my guess is that you will benefit from doing so.
Please do also let me know if I can be of further assistance to you, and updates on your progress would be so very welcome.
Sincerely,
Richard E. Schultz, Ph.D.
Drschultz.org
MindsetDoc.com
@mindsetdoc (Twitter and IG)
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Radiation Tooth Decay in Elderly Cancer Patients
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Tooth decay from radiation therapy, known as radiation caries, is a rampant form dental decay that may occur in individuals undergoing radiation therapy for cancer in the head and neck region. It is one of the many side effects associated with radiation therapy. The elderly who are at a greater risk of many different types of cancer are more likely to have to deal with these consequences of undergoing radiation therapy. However, it should not detract from the fact that the benefits of radiation therapy in the treatment of cancer often outweighs these side effects.
Why does radiation cause tooth decay?
The radiation therapy reduces the flow of saliva as it causes damage to major and minor salivary glands. The altered salivary flow makes the teeth susceptible to develop new points of decay or worsens pre-existing decay. The lesions defer from normal dental decay as they are rapidly progressing and follow unusual patterns.
Types of Radiation Tooth Decay
Clinically radiation caries can be categorized in three types :
The first type is the widespread superficial lesions that attack all surfaces of the teeth. Unlike carious lesions in non-irradiated individuals the radiation caries tend to involve the incisal edges of the crowns and cusp tips of canines and molars.
The second type is the encircling type of caries that occur over the root surface (cementum caries) and dentin. The destruction generally begins at the cervical third of the teeth. The lesion may aggressively encircle the tooth causing the entire crown to be lost with only root stumps remaining within the tooth sockets.
The third type is associated with pigmented lesion over the entire crown of the teeth. Generally dark spots are seen on the crown at the surfaces adjacent to the gums
Combination of all three types may also be seen in some individuals. Lesions associated with radiation caries progress rapidly involving dental pulp and may lead to complications during the course of radiotherapy.
How does radiation therapy lead to decay?
Radiation caries is a side effect of ionizing radiation. During radiation therapy the salivary gland tissue damaged due to free radicals generated by radiation. The damage to the salivary glands not only reduces the amount of saliva produced but also alters the pH and composition of saliva. Normally saliva has an antimirobial action but the altered saliva is not as effective as normal saliva against the bacteria causing dental decay. Therefore patients undergoing radiation therapy have increase amounts of cariogenic bacteria such as Streptococcus mutans and Lactobacilli.
The altered saliva composition also reduces the ability of the saliva to re-mineralize the initial carious lesions. The reduced re-mineralization activity makes the carious lesion rapidly progressive. The lack of saliva also causes food and debris accumulation leading to an increase in cavities.
Treatment for Radiation Decay
The best way to treat radiation caries is by minimizing the risk factors before initiation of radiation therapy. The possibility of decay arising should not stop a person from undergoing radiation therapy. Existing decay lesions, deep pits, fissures, abnormal grooves on the tooth surface or sites more prone to develop decay should be restored before the radiation therapy. All additional dental work should also be ideally completed before the onset of therapeutic radiation dosage.
Radiation therapy patients are advised to maintain strict oral hygiene practices to reduce the incidence of tooth decay. Using mouthwashes, fluoride-containing gels and toothpastes and flossing is highly beneficial. Dietary changes to avoid carbonated drinks, sugary food and fermentable carbohydrates are also recommended. The patient is advised to refrain from alcohol and smoking.
The lack of saliva can be managed by artificial salivary supplements (carboxymethyl cellulose saliva substitute) or drugs inducing saliva secretions (pilocarpine). The patient is also advised to sip non-carbonated sugarless fluids and xylitol-containing chewing gums.
Copyright © 2019 SeniorHealth365.com. All rights reserved.
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Do Superfoods Really Work?
Recent dietary research has uncovered 14 different nutrient-dense foods that time and again promote good overall health.
Coined “superfoods,” they tend to have fewer calories, higher levels of vitamins and minerals, and many disease-fighting antioxidants.
Beans (legumes), berries (especially blueberries), broccoli, green tea, nuts (especially walnuts), oranges, pumpkin, salmon. soy, spinach, tomatoes, turkey, whole grains and oats, and yogurt can all help stop and even reverse diseases such as hypertension, diabetes, Alzheimer’s, and some forms of cancer.
And where one might have an effect on a certain part of the body, it can also affect the health of other body functions and performance, since the whole body is connected.
With these 14 foods as the base of a balanced, solid diet, weight loss gimmicks and other fly-by-night programs can become a thing of the past in your life.
Conversely, the ill-effects of an unbalanced diet are several and varied. Low energy levels, mood swings, tired all the time, weight change, uncomfortable with your body are just a few signs that your diet is unbalanced.
An unbalanced diet can cause problems with maintenance of body tissues, growth and development, brain and nervous system function, as well as problems with bone and muscle systems.
Symptoms of malnutrition include lack of energy, irritability, a weakened immune system leading to frequent colds or allergies, and mineral depletion that can trigger a variety of health concerns including anemia.
And since the body is connected, realising that an unhealthy body will result in a low mood only makes sense. When we nourish our body with these superfoods and complement them with other nutrient-dense and healthy fresh foods, our mood will be vitalized and healthy as a direct result.
Many modern diets based on prepackaged convenience foods are sorely lacking in many vitamins and minerals, which can affect our mental capacities as well, and cause irritability, confusion, and the feeling of ‘being in a fog’ all the time.
Superfoods can be the basis of a sound, healthy, nutritious solution to curing many of these ailments and more.
Chris, myHealthCoach
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Queston #13751Note
Kluver-Bucy syndrome present with sexual behavior (increased lipido, sexually suggestive speech), hyperorality, seizures, and overall decreased inhibitions.
The most common causes of Kluver-Bucy syndrome include head trauma, infection (HSV-1 encephalitis), and malignancy.
The pathophysiology involves bilateral damage to the medial and anterior temporal lobes, often involving the amygdala and/or hippocampus.
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Mindfulness-based stress reduction for solid organ transplant recipients: a randomized controlled trial.
Cynthia R. Gross, Mary Jo Kreitzer, William Thomas, Maryanne Reilly-Spong, Michel Cramer-Bornemann, John A. Nyman, Patricia Frazier, Hassan N. Ibrahim
Research output: Contribution to journalArticle
73 Scopus citations
Abstract
CONTEXT: Patients who have received solid organ transplants continue to experience a myriad of complex symptoms related to their underlying disease and to chronic immunosuppression that reduce the quality of life. Beneficial nonpharmacologic therapies to address these symptoms have not been established in the transplant population. OBJECTIVE: Assess the efficacy of mindfulness-based stress reduction (MBSR) in reducing symptoms of anxiety, depression, and poor sleep in transplant patients. DESIGN, SETTING, AND PATIENTS: Controlled trial with a two-staged randomization. Recipients of kidney, kidney/pancreas, liver, heart, or lung transplants were randomized to MBSR (n=72) or health education (n=66) initially or after serving in a waitlist. Mean age was 54 years (range 21-75); 55% were men, and 91% were white. INTERVENTIONS: MBSR, a mindfulness meditation training program consisting of eight weekly 2.5-hour classes; health education, a peer-led active control. PRIMARY OUTCOME MEASURES: Anxiety (State-Trait Anxiety Inventory), depression (Center for Epidemiologic Studies Depression Scale), and sleep quality (Pittsburgh Sleep Quality Index) scales assessed by self-report at baseline, 8 weeks, 6 months, and 1 year. RESULTS: Benefits of MBSR were above and beyond those afforded by the active control. MBSR reduced anxiety and sleep symptoms (P < .02), with medium treatment effects (.51 and .56) at 1 year compared to health education in intention-to-treat analyses. Within the MBSR group, anxiety, depression, and sleep symptoms decreased and quality-of-life measures improved by 8 weeks (P < .01, all), and benefits were retained at 1 year (P < .05, all). Initial symptom reductions in the health education group were smaller and not sustained. Comparisons to the waitlist confirmed the impact of MBSR on both symptoms and quality of life, whereas health education improvements were limited to quality-of-life ratings. CONCLUSIONS: MBSR reduced distressing symptoms of anxiety, depression, and poor sleep and improved quality of life. Benefits were sustained over 1 year. A health education program provided fewer benefits, and effects were not as durable. MBSR is a relatively inexpensive, safe, and effective community-based intervention.
Original languageEnglish (US)
Pages (from-to)30-38
Number of pages9
JournalAlternative therapies in health and medicine
Volume16
Issue number5
StatePublished - Sep 1 2010
Fingerprint Dive into the research topics of 'Mindfulness-based stress reduction for solid organ transplant recipients: a randomized controlled trial.'. Together they form a unique fingerprint.
• Cite this
Gross, C. R., Kreitzer, M. J., Thomas, W., Reilly-Spong, M., Cramer-Bornemann, M., Nyman, J. A., Frazier, P., & Ibrahim, H. N. (2010). Mindfulness-based stress reduction for solid organ transplant recipients: a randomized controlled trial. Alternative therapies in health and medicine, 16(5), 30-38.
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Tag Archives: doing crunches
Keep A Fit And Healthy Body With These Fitness Tips
With so many different fitness options available, it is easy to find a workout that you enjoy and that will keep you motivated to reach your goals. Follow these fitness tips to stay motivated.
To get in shape, many people turn to weight lifting at the gym. Basically you need on six easy exercises in order to stay fit, they are push ups, pull ups, bridges, leg raises, squats, and handstand push ups.
To motivate yourself for proper fitness, create some personal goals. It helps you to keep focus on obstacles as opposed to losing your motivation due to their difficulty. In addition, it helps prevent you from giving up because you are forced to consider your fitness regimen as a continuing process.
A few different exercises are recommended if you want to spice up a workout routine. Doing so will make your fitness plan less boring, helping to maintain your motivation to continue your workouts on a daily basis. Your body will also not benefit as much if you do the same thing every day.
Abdominal Muscles
When working on your abdominal muscles you should never put your entire focus on doing crunches. A university study has shown that it takes a quarter million crunches to burn a single pound of fat. You really are not doing as much exercise as you thought if you are just doing crunches. Find other, more strenuous ways, to work those abdominal muscles.
Flexing your glutes when you do a rep is recommended when lifting weights over your head. This habit will improve your weight-lifting form and reduce the chance of injury; it also provides a little bit of exercise to help tone up your butt. This provides your spine with more stabilization.
m routine To make it easier, start by awakening 15 minutes earlier than you normally would, and spend that 15 minutes walking, doing calisthenics or skipping rope. Doing this starts your day on the right food and also disciplines your life with healthy habits.
When using a work out bench you are not familiar with for the first time, you should test to make sure the padding is up to your specifications. Simply apply pressure to the cushion with your thumb to see what it’s made of. If you feel wood or metal that is under the bench, get another seat.
You should schedule your day and plan on eating and exercising at specific times. If you are busy at lunchtime, you may end up choosing something unhealthy, like fast food or snacks from a vending machine. You can get your daily exercise and eat healthy foods every day by taking the time to plan ahead.
When trying to get yourself in good running shape, follow the way a Kenyan trains. The typical Kenyan runner paces very slowly for the first part of the run, about one third. You should gradually increase your pace throughout the run. When you get to the middle third of your run, increase your pace to your normal speed. When you are on your last leg, sprint! If you do this on a regular basis, you will have noticeable differences in your speed and endurance.
Your dog can make a great workout partner. You dog will love to go on these walks and he won’t get tired of it no matter how frequent they are. Don’t go all out at the beginning. Cover a block or two in your first walk, and than you can add more distance over time. This is a benefit of having a canine companion.
One easy way to increase your fitness is through yard work. It’s highly likely that your yard could use the work anyway, and you certainly need to keep yourself moving. This is a wonderful pairing. You can improve your house and your living environment at the same time, while also providing yourself with physical activity. Working in your yard is a great way to improve both your property and your body.
Use these suggestions to get your fitness routine under way. The importance of being physically active everyday cannot be overemphasized. By living a healthier way of life, you will not only have increased energy, you will also be able to deal with any problem life throws at you.
Out Of Shape? Get Fit With These Tips!
Fitness should not seem like a far off goal. Don’t avoid getting started today. Exercise doesn’t have to disrupt your life, either. All you need to do is make some small changes in your lifestyle. The below article will show you how.
You may wish to consider scheduling a few sessions with a trusted personal trainer if you are unaccustomed to a regular workout routine. Your trainer can help you to set up a suitable program so that you can reach your goals easily. For a beginner, the gym can be intimidating; a trainer can help by showing you around and giving you instructions. Getting professional help building a custom plan will give you a leg up on your fitness goals.
Smaller Muscles
When working with weights, start with smaller machines first. The smaller muscles in your body get tired out before the larger muscles, so begin with lower-weight dumbbells and then move up to tougher-weight machines. This way, when you’re working out those larger muscles, the smaller muscles can rest a bit.
You can get strong thighs, which will protect your knees. It’s very common for athletes and people that workout to tear the ligament behind their kneecap. To protect your knees, you must do exercises for your hamstrings and your quadriceps. You can accomplish doing this by doing leg curls and also leg extensions.
Crunches alone won’t help you build abs. A prominent university found that only one pound of fat gets burned even after 250,000 crunches. You really are not doing as much exercise as you thought if you are just doing crunches. Use other exercises to get the best results on your abs.
There are lots of different types of exercise routines and classes that keep you feeling energized and motivated. Rotating among different types of exercises can give you the opportunity to find several that you love and keep you going back for more. If you have not yet, try a dance or yoga class to mix it up. Try kickboxing or boot-camp classes. The great thing about trying different classes is that you need not return to any you don’t like, and you’ll still be working out productively throughout the trial process.
If you want to build muscle, you need lift heavy for fewer repetitions. Focus on one muscle group at a time: start with your chest for instance. Begin with a warm-up set using lighter weights. You should be able to do 15-20 reps at your warm-up weight. The next set should be weights that are heavy enough that you can only complete 6 to 8 reps. Add another five pounds and do your third set.
Some people are perfectly content using fitness equipment in a gym, but running outside is better overall. A great run through a city park or down a country road is both scenic and exhilarating so save the treadmill for inclement weather when getting out is impossible.
You need to have good footwear when you are working out. If you don’t wear shoes which are properly created for specific activities, you increase your risks of incurring injury to your legs and feet. You can also cause foot discomfort post-workout which can prevent you from exercising later.
Set a schedule for exercise if you don’t work out regularly or avoid it altogether. You should spread your workouts out over the course of the week, fixing them on specific days, and committing yourself to completing them. If you have to miss a work out ensure that you make it up.
You can enhance your workouts effectively by learning how to control your breathing properly. While doing crunches or situps, exhale as your shoulders reach their highest point. Your muscles have to work harder if you exhale deeply.
Never attempt to move out of the bed and workout when you are under the weather. If you are ill, the body dedicates its resources to self-preservation and healing. It’s difficult or impossible for your body to get stronger or build muscles while it’s doing this. So, you should refrain from working out until your body has recovered from illness. While you are waiting, you can eat, sleep, and build up your strength.
The following article is your ticket to a fitter, more beautiful you. You may have already formed a workable fitness routine, but adding some of these ideas might improve your results or change up your regimen a little. You will find that it is a journey to becoming a more fit person.
Great Tips For Losing Weight And Keeping It Off!
Finding the best fitness information online is not always the most straightforward task. The sheer volume of available information can overwhelm you, and leave you wondering if you will ever get around to actually exercising. Luckily, the very best tips are in this article, and you can read them below.
Walking will help to increase fitness and is a fantastic workout. Be sure that you are getting the most out of the time by walking briskly and squeezing your muscles as you go, placing your heel down first. You can also incorporate your arms so that you are working your whole body, burning even more calories with each step.
If you are looking to get as physically fit as possible, search for an exercise routine that tones muscles while simultaneously adding flexibility. Look for local classes.
Doing Crunches
When working on your abdominal muscles you should never put your entire focus on doing crunches. Studies show that after 250,000 crunches only a pound of fat is burned. You really are not doing as much exercise as you thought if you are just doing crunches. You should also work out the abs in various different ways.
When doing any workout, you should make sure to exhale after every repetition of the given weight. This lets your body use more energy and intake more air so that you can work out with better energy levels.
If you truly want to do everything in your power to get into shape then you are going to want to invest money into hiring a personal trainer. Personal trainers can help you optimize your workout so that you get the most out of it, and also keep your motivation up when it flags. A personal trainer will ensure you see results, although they are not for everyone.
One simple way to increase your muscle mass is to lift lots of weight just a few times. Choose the muscle group you wish to target. Warm up by lifting lighter, easier to lift weights. Your warm up should included 15 to 20 reps. Change to a heavier weight for the next set. You should only be able to do 6 to 8 repetitions at this weight. Add about five more pounds and repeat.
One way to quickly build up strength in your legs is to do “wall sits.” Start by selecting an area of empty wall space that will accommodate your body in motion. With your back facing the wall, position yourself approximately 18 inches from it. As you bend your knees, lean backwards against the wall until your back makes full contact with the wall. Keep squatting down to the point where you are in a sitting position with your thighs perfectly parallel to the floor. Hold this stance until you can’t stand it anymore.
Muscle Mass
If you are looking to gain muscle mass, then do more reps with a lesser weight to achieve this. You want to build endurance to build muscle mass. Many people are known to use this method and it works.
As discussed at the beginning of this article, getting the best information, and applying it to your own fitness goals, is not the most simple task. Keeping yourself educated, however, is one of the key parts of reaching your goals. Use the tips you learned here, and success will come easy.
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A woman looking at a meter
While there’s a long list of things that need to happen, at the right time, in the right place, in order for a woman to get pregnant, ovulation is definitely one of the most important pieces of the puzzle. Ovulation is the typically once-monthly process by which an egg, beginning in the follicle, matures and releases into the fallopian tubes, where it can be fertilized. Without ovulation, there’s no egg—and therefore no pregnancy.
Learn more about ovulation.
So what can affect ovulation, and therefore your chance of getting pregnant—or not getting pregnant, if that’s where you’re at?
Age.
If we’ve said it once, we’ve said it a thousand times: age is the primary factor affecting fertility, and can affect both ovulation and the viability of a woman’s eggs. A woman is born with all the eggs she’ll ever have—at birth, that’s about a million. As she gets older, she has fewer eggs in her ovarian reserve (egg count); plus, a higher percentage of those eggs become genetically abnormal due to natural aging (egg quality).
Contact Us to Chat with a Fertility Advisor
Let’s Talk
Learn more about the top 6 factors affecting female fertility.
Age can affect ovulation as a woman’s egg count gets particularly low, in the period known as “perimenopause.” During that time, which typically predates the “actual” menopause by several years,she may experience irregular ovulation, the telltale signs of which are irregular menstrual periods or wonky results when using ovulation predictor kits. Around age 51, on average, women enter menopause, considered the official end of ovulation.
However, it’s important to remember that egg count is only one factor in fertility; egg quality, which declines gradually as a woman ages, is much more important, and can impact a woman’s ability to get pregnant long before age can affect ovulation.
A proactive fertility assessment and ovarian reserve testing, like we offer here at Extend Fertility, can help women understand if they’re at risk for premature diminished ovarian reserve (DOR), premature menopause, or other conditions that can affect ovulation.
Learn more about what ovarian reserve testing can tell us.
Hormonal birth control.
Hormonal birth control, such as pills, patches, rings, and injections, are formulated so that they can affect ovulation in a way that prevents the user from getting pregnant. Ovulation begins in the hypothalamus, a region of the brain that releases a hormone—gonadotropin-releasing hormone—that kicks off the ovulatory cycle. That hormone then triggers the pituitary gland, also in the brain, to produce other hormones (luteinizing hormone and follicle-stimulating hormone), which stimulate your ovaries to produce still other hormones (estrogen and progesterone) that prompt ovulation.
Learn more about birth control and fertility.
Hormonal birth control uses synthetic versions of progesterone and/or estrogen to interrupt this process and prevent ovulation. For women who decide they’re ready to get pregnant, the good news is that hormonal birth control can affect ovulation for only as long as it’s in your bloodstream; for most types of birth control, that’s only about two to three months, maximum, after you stop taking it. (The exception to this is the birth control “Depo” shot, which is intended to be a longer-acting form of birth control and can affect ovulation for a longer period.) Hormonal birth control doesn’t have a long-term effect on fertility.
Polycystic ovary syndrome.
While the cause of polycystic ovary syndrome (PCOS) is unknown, it’s characterized by the presence of two or three clinical signs: infrequent, irregular, or prolonged menstrual cycles; elevated levels of male hormones (androgens), that sometimes cause excess facial and body hair or acne; and polycystic ovaries, meaning the ovaries have an overabundance of immature egg follicles (cysts) but fail to regularly release eggs (ovulate). These cysts often appear arranged around the periphery of the ovary, in what’s known as a “pearl necklace” formation.
We also know that carbohydrate metabolism, or the body’s ability to break down and process the carbohydrates you eat, play a role in PCOS. Insulin, a hormone produced in the pancreas, allows cells to use sugar, the body’s primary energy supply. If cells become resistant to the action of insulin, blood sugar levels can rise, and the body might produce more insulin to compensate. Studies suggest that excess insulin increases androgen production, which can affect ovulation and cause the symptoms of PCOS.
The good news is that, because PCOS is connected to insulin levels, it can respond to simple, non-medical interventions, such as improved diet, exercise, and weight loss. Hormonal birth control can also help manage the symptoms of PCOS for women who aren’t looking to get pregnant. Because PCOS can affect ovulation, it’s a common cause of female infertility; in addition to lifestyle changes, there are several medication options that can help women with PCOS get pregnant by medically inducing ovulation.
Endometriosis.
Endometriosis is a condition in which the tissue that lines the uterus, known as the “endometrium,” begins to grow on other organs inside a woman’s body, like the ovaries, the outside of the uterus, or Fallopian tubes. These tissues grow, thicken, breakdown, and bleed just like the endometrium inside the uterus, except because they’re outside, this cycle can cause irritation or inflammation in surrounding organs or even produce scar tissue, known as “adhesions,” that can cause organs to attach to each other. Endometriosis is a common cause of fertility issues, and can be painful or even debilitating.
Endometriosis can cause fertility issues by producing a physical blockage to the reproductive system. The disease can also damage the egg supply in the ovaries, and the resulting inflammation—as well as diminished ovarian reserve—can affect ovulation, as well. As endometriosis expert Dr. Iris Orbuch explains, the condition both “decreases a woman’s ovarian reserve [and] decreases fertility by either an anatomical distortion or via inflammation.”
Additionally, while surgical treatment of endometriosis, known as laparoscopy, offers long-term pain relief, studies show that it can reduce ovarian reserve (and therefore can affect ovulation) by inadvertently removing healthy ovarian tissue or cutting off blood supply to the ovary. It’s also possible that endometriosis may reduce egg quality, possibly by creating an inflammatory environment in the reproductive system; this is a matter of debate in the scientific literature. Concerns regarding the effect of endometriosis on egg quality and quantity have prompted many experts to recommend that women with endometriosis freeze their eggs.
Learn more about endometriosis, fertility, and egg freezing.
Body weight.
Being too overweight or too underweight can affect ovulation.
According to an article in the journal Reproduction exploring the well-supported relationship between obesity and infertility, excess body weight can affect ovulation by throwing off the delicate balance of hormones required for a healthy menstrual cycle. How? One theory is that an excess of adipose (fat) tissue, an important site of steroid production, has been shown to increase the levels of certain steroids in overweight women. This steroid increase can reduce the ability of important reproductive hormones, such as estrogen, to get where they need to go, which can affect ovulation. Obesity may also be related to insulin resistance, which, as in PCOS, can affect reproductive hormone levels.
On the other hand, though, being significantly underweight, having a very low body fat percentage, or vigorously exercising over 60 minutes per day can also affect ovulation. Ovulation and menstruation require a lot of energy from a woman’s body. When someone is very underweight, their body attempts to conserve energy by putting a pause on certain functions, like ovulation. (This is why women with eating disorders like anorexia nervosa typically lose their menstrual periods.) It’s also believed that—again, because body fat affects steroid levels, and steroid levels affect the flow of reproductive hormones like estrogen—too little adipose tissue, just like too much, can affect ovulation by preventing hormones from getting from the brain to the ovaries.
Endocrine disorders.
If we’ve learned anything by now in this post, it’s this: the human body is a complex, interconnected network that requires a pretty specific balance in order to function properly. That’s exemplified perfectly by the fact that disorders of far-flung parts of endocrine system (like the hypothalamus, thyroid, or pituitary gland) can affect ovulation, which happens in the ovaries.
The fact is, as organs which produce hormones, the ovaries are part of the endocrine system, and are in constant communication with its other parts. So if another organ in the system is working too hard—or not hard enough—it can affect ovulation and other functions of the ovaries.
One example is the thyroid, which produces thyroid hormones that control the metabolism of every cell in our bodies. Both an overactive (hyper) or underactive (hypo) thyroid can affect ovulation and are associated with reduced fertility and irregular menstruation. And, in some cases, thyroid disorder and ovulatory disorder may both be related to a problem in the hypothalamus or pituitary glands, which control them both!
Sleep disruption.
While research into the connection between sleep and fertility is still a work in progress, disrupted sleep cycles has been correlated with menstrual irregularities, increased instances of PCOS, dysmenorrhea, and increased time to, and reduced rates for, conception—among other negative reproductive health outcomes—in several studies. Primarily a concern for people who work late nights or irregular shifts (or who experience sleep disorders like insomnia), it’s thought that sleep disruption can affect ovulation because sleep may be a factor in the body’s regulation of:
• TSH, explained above
• Luteinizing hormone (LH), which triggers ovulation
• Follicle-stimulating hormone (FSH), which helps ovarian follicles mature
• Progesterone
• Or other important hormones that can affect ovulation.
Since research is still limited, it may not be that sleep disruption can affect ovulation—it may be that both sleep and ovulation are being affected by some other imbalance. What is clear is that healthy sleep is pretty crucial for health, in general—so making regular shut-eye a priority definitely can’t hurt.
Have more questions about what can affect ovulation, fertility, or egg freezing success?
Contact us.
Share
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Got Acne Scars? || Identifying And Healing The 2 Types Of Facial Scarring
Acne Scars
Fact: Roughly 6 percent of all the pimples that appear on your skin will leave scarring behind.. And while acne prevention comes in as the best case scenario in the quest for avoiding scarring as a result, it might not be the case most of the time.. Moreover, the nasty habit of picking, squeezing and trying to aggressively pop existing pimples, makes things much worse than what you may think..
Acne scars come in two types which can easily be identified visually.. And while the culprit is the same, the results might vary.. Identifying the type of scar you could develops halfway into dealing with them afterwards..
1 || Hyper-pigmentation Scarring
Acne Scars
Hyper-pigmentation involves the appearance of brown or red marks that replace the blemish spot.. Those are different from one another. The brownish markings left behind are affectionately known as post-inflammatory hyper-pigmentation (PIH), whereas red or pink markings are known as post-inflammatory erythema (PIE).
These scars are all typically expected to go away on their own over the course of several weeks to a couple months, and there are definite ways to speed that process along.
2 || Indented or Depressed Scarring
Acne Scars
Just as their name implies, yes indented scars are in fact depressing! Those types of scars are the blemishes that actually form topographical cavities on the surface of skin. The indentations in the skin are caused by damage to collagen, the sad news is and contrary to the hyper-pigmentation scars, they won’t disappear on their own.
There are three different types of scars that fall within the “indented” category: ice pick scars, box scars and rolling scars. Ice pick scars as narrow indentations that are smaller than 2mm wide, and extend deep into the skin, giving the appearance of small holes. A box scar looks like a punched hole that can be either round or linear but has distinctive lines. Lastly, the rolling scar has gentle, sloping edges that disappear when skin is stretched.
How to Deal With Each Type Of Acne Scarring…
1 || For the hyper-pigmentation scars the best healing process includes chemical exfoliation and vitamin C.
2 || Chemical exfoliants like salicylic and azelaic acid are incredibly helpful when it comes to dark marks, since they break down the bonds between skin cells, in turn making it easier to slough off dull or pigmented surface cells. Salicylic acid is considered a beta hydroxy acid (BHA) and penetrates deeper into the skin than alpha hydroxy acids (AHA), such as azelaic, so the quicker you want that mark gone, the more heavily you may want to rely on salicylic, if your skin can hold up to that level of exfoliation.
Acne Scars
A powerful ingredient most dermatologists turn to in order to fade acne scars.. This world-wide loved antioxidant can repair damage to skin, including hyperpigmentation.
Acne Scars
When infused with vitamin C, vitamin E is highly recommended since it also helps to protect skin and bolster it against damaging free-radicals.
# Sunscreen.. Should go without saying..
2 || For the Depressed Scars..
These indented types of scars can be improved upon with the right treatment strategy. A topical retinoid initially comes to mind to stimulate the damaged collagen and spur the production new, plump skin that fills out the scar.
Acne Scars
# Fraxel A laser treatment which punches microscopic holes in your skin to create a controlled wound that will heal itself in a more cosmetically appealing manner.
Acne Scars
# Microneedling Like Fraxel, microneedling creates small wounds in the skin that encourage collagen production and new skin healing. Unlike Fraxel, microneedling is done with physical metal points rather than laser. If your scars are very deep speak to your dermatologist about dermal fillers, injectibles which can soften the look of ice pick, boxed and rolling scars.
Acne Scars
Bottom line? Patience and commitment are key to healing acne scars — no matter what type.
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2,190,515,257,519,161,000
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Impact Factor 3.508
2017 JCR, Clarivate Analytics 2018
Frontiers journals are at the top of citation and impact metrics
Original Research ARTICLE
Front. Neurol., 03 October 2016 | https://doi.org/10.3389/fneur.2016.00162
Vestibular Perceptual Thresholds Increase above the Age of 40
• 1Harvard Medical School, Boston, MA, USA
• 2Jenks Vestibular Physiology Laboratory, MEEI, Boston, MA, USA
• 3University of Colorado at Boulder, Boulder, CO, USA
• 4Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA
We measured vestibular perceptual thresholds in 105 healthy humans (54F/51M) ranging from 18 to 80 years of age. Direction-recognition thresholds were measured using standard methods. The motion consisted of single cycles of sinusoidal acceleration at 0.2 Hz for roll tilt and 1.0 Hz for yaw rotation about an earth-vertical axis, inter-aural earth-horizontal translation (y-translation), inferior–superior earth-vertical translation (z-translation), and roll tilt. A large subset of this population (99 of 105) also performed a modified Romberg test of standing balance. Despite the relatively large population (54F/51M), we found no difference between thresholds of male and female subjects. After pooling across sex, we found that thresholds increased above the age of 40 for all five motion directions investigated. The data were best modeled by a two-segment age model that yielded a constant baseline below an age cutoff of about 40 and a threshold increase above the age cutoff. For all subjects who passed all conditions of the balance test, the baseline thresholds were 0.97°/s for yaw rotation, 0.66°/s for 1-Hz roll tilt, 0.35°/s for 0.2-Hz roll tilt, 0.58 cm/s for y-translation, and 1.24 cm/s for z-translation. As a percentage of the baseline, the fitted slopes (indicating the threshold increase each decade above the age cutoff) were 83% for z-translation, 56% for 1-Hz roll tilt, 46% for y-translation, 32% for 0.2-Hz roll tilt, and 15% for yaw rotation. Even taking age and other factors into consideration, we found a significant correlation of balance test failures with increasing roll-tilt thresholds.
Introduction
Data suggest that, on average, females and males have a significantly different number of vestibular afferent fibers (1) and that a significant difference in the size of the vestibular labyrinth exists (2). Such anatomical differences could contribute to behavioral differences, but studies utilizing standard clinical vestibular assays (38) have found no significant sex effects. Nonetheless, differences could exist. Wall and colleagues reported a very small, but significant, difference in the VOR phase at 0.005 Hz in a population of 25 males and 25 females (9). Benson reported perceptual translation thresholds (i.e., the smallest motion that can be reliably perceived as leftward or rightward) for females that were roughly 40% lower than for males for each of the three translation directions (7), but this difference was not statistically significant. Similarly, yaw rotation thresholds were reported to be about 20% lower in females than males (8), but again, this difference was not statistically significant. Given these data, we felt that a sex effect deserved study using a larger sample.
We chose to measure vestibular thresholds for a variety of reasons. (1) Threshold testing uses small motions that typically are well tolerated. (2) Like other threshold measures (e.g., auditory thresholds), vestibular thresholds have direct functional relevance. (3) Thresholds have been shown to be a sensitive measure of vestibular function that has been shown to identify specific peripheral vestibular deficits (10). (4) Thresholds have shown great promise to help diagnose central disorders such as vestibular migraine (11, 12), which may be the most prevalent vestibular disorder. (5) Unlike other vestibular responses such as the VOR, one previous study was unable to demonstrate adaptive perceptual threshold changes even following substantial training efforts (13) – possibly because the brain receives little information to drive adaptation during threshold-level motion. (6) Thresholds can provide a comprehensive assay of many aspects of vestibular function – including perception, all peripheral end organ pairs, central vestibular functions, etc. – that are straightforward to interpret and can be compared across motion types (i.e., translation, tilt, and rotation) relative to normal.
Earlier vestibular threshold studies have come to different conclusions regarding the effect of age on rotation thresholds and translation thresholds. One study (14) measured thresholds for yaw rotation in a group of 19 younger subjects, aged 20–26, and a group of 16 older subjects, aged 63–84, and found no significant effect of age. Similarly, Seemungal and colleagues (15) reported no difference in yaw rotation thresholds between a group of 14 young (mean age of 23) and 9 older (mean age of 63) normal subjects. Each of these reports is consistent with another study (16) of 24 normal subjects between the ages of 21 and 60 that found no effect of age on yaw rotation thresholds.
While published studies do not show a significant correlation of yaw rotation thresholds with age, there is evidence to suggest that translational thresholds do correlate with age. However, one of the studies that did not find a correlation of yaw rotation threshold with age (16) did report a correlation with age for thresholds measured using naso-occipital (x-axis) and inter-aural (y-axis) translations. Furthermore, Agrawal and colleagues (17) reported that thresholds of 42 normal subjects demonstrated a significant positive correlation with age for naso-occipital (x-axis) and inferior–superior (z-axis) translation but not for inter-aural (y-axis) translation, and another recent paper (18) reported that translation thresholds for 42 normal subjects were significantly correlated with age for naso-occipital (x-axis), inferior–superior (z-axis), and inter-aural (y-axis) translations. Finally, Kingma (19) reported that for a population of 28 healthy subjects between the ages of 22 and 60 (7 subjects/decade), thresholds increased linearly with age for naso-occipital (x-axis) translation but found no correlation for inter-aural (y-axis) translation thresholds.
Before proceeding, we also note that non-vestibular cues (e.g., somatosensory and proprioceptive) may contribute to these thresholds, but a previous study showed bilateral vestibular defective patients have significantly higher thresholds (20), suggesting a predominant influence of the vestibular cues.
Given the earlier findings, we decided to include a larger number of healthy normal subjects (54 females and 51 males) than reported in previous investigations. We specifically targeted our recruitment to obtain age- and gender-matched subjects for each decade spanning an age range between 18 and 80. We measured direction-recognition thresholds in the dark for (a) yaw rotations – transduced primarily by the lateral semicircular canals, (b) superior–inferior (z-axis) translations – transduced primarily by the saccular organs, (c) inter-aural (y-axis) translations – transduced primarily by the utricular organs, and (d) roll tilts – transduced primarily by the vertical canals and the utricular organs. We emphasize that this study is the first to look at age effects for roll-tilt thresholds; the importance of this is emphasized by recent reports of lowered thresholds in patients suffering vestibular migraine (11, 12).
Materials and Methods
Perceptual thresholds were sampled in 105 subjects, 54 females and 51 males, between the ages of 18 and 80. All subjects filled out a general health questionnaire to confirm that they qualified to participate, including the absence of vestibular symptoms. Menstrual cycle status and diagnosis of migraine were determined via two separate questionnaires. A standing balance test was used to objectively evaluate balance function. Threshold data collection methods generally mimicked those used by Valko and colleagues (20), but data were collected for only a small subset of the frequencies sampled in that earlier study. Specifically, for each subject, yaw rotations were applied about an earth-vertical axis at 1 Hz, y-translations were applied along an earth-horizontal axis at 1 Hz, z-translations were applied along the earth-vertical axis at 1 Hz, and roll tilts about a head-centered earth-horizontal axis were applied at 0.2 and 1 Hz. Participation in the study took about 3 h including at least two breaks. Informed consent was obtained from all subjects as dictated by the Declaration of Helsinki, and the study was approved by the MEEI Human Use Committee.
Questionnaires
A short health questionnaire was administered to all subjects for screening purposes. History of current and previous diseases, with an emphasis in neurological, otologic, vestibular, and chronic uncontrolled diseases, and medications was obtained. Acting conservatively, subjects diagnosed with any major health problem or under medications that could potentially affect vestibular function or decision making were excluded, as were subjects with any history of vestibular symptoms. As just one example, subjects with vestibular migraine would typically have been excluded because of their occasional symptoms.
Women were asked to fill out a separate questionnaire to establish menstrual cycle status (premenopausal, postmenopausal, or other). For premenopausal women, length and regularity of cycles, start of current cycle (i.e., first day of menstrual bleeding), and current use of hormonal contraception was recorded.
Because prevalence of migraine is known to be higher in females (21), we considered migraine as a potential confounding factor for our analyses. The Migraine Screen Questionnaire (MS-Q) developed and validated by Láinez et al. (22, 23) was administered to confirm history of migraine and/or to detect hidden migraine. A MS-Q score ≥4 was considered positive.
Balance Testing
To assess balance function, the modified Romberg test of standing balance on firm and compliant support surfaces (24) was performed. This balance test consists of four steps. Each step must be passed in order to move to the next step. All steps are performed standing with feet together and arms crossed. To pass the first step, each participant had to stand on the floor for 15 s with eyes open. To pass the second step, they had to stand on the floor for 15 s with eyes closed. To pass the third step, they had to stand on memory foam with eyes open for 30 s. To pass the final step, they had to stand on the foam with eyes closed for 30 s. This final test condition primarily assesses vestibular function (24, 25), since visual contributions are eliminated and the foam makes kinesthetic cues unreliable. The balance test was scored on a pass/fail basis. Failure was defined as participants needing to open their eyes or arms or move their feet to maintain stability before the end of the trial. All subjects were allowed two trials at each step.
Motion Stimuli and Psychophysical Threshold Tests
The motion paradigms and psychophysical tests employed to measure perceptual thresholds for this study have been previously published in detail (26, 27), so are described briefly herein. Motion stimuli were generated with a Moog 6DOF motion platform. Motion stimuli were single cycles of sinusoidal acceleration (either linear acceleration or angular acceleration) [a(t)=Asin(2πft)=Asin(2πtT), where A is the acceleration amplitude and f is the motion frequency]. We present thresholds using the peak velocity of each stimulus. As shown in earlier papers [e.g., Ref. (8, 26)], this yields bell-shaped velocity trajectories having a maximum velocity of vmax = A/(πf).
Subjects were seated in an upright position, held via an adjustable five-point harness and a helmet. To minimize other sensory cues, motions were performed in the dark in a light-tight room, all skin surfaces except the face and hands were covered, and noise-canceling headphones played constant amplitude white noise during the motions to mask any auditory cues and to indicate the time period when each motion occurred.
A three-down/one-up (3D/1U) adaptive staircase was used to target stimuli near threshold (28, 29). To minimize training effects, suprathreshold practice trials were administered until each subject understood and was comfortable with the task before each set of trials. Each block consisted of 100 trials, where a single motion stimulus was provided per trial. One hundred trials was considered adequate because an earlier study (29) showed that 100 trials yielded methodological threshold variations of just 18% – much less than the intra-subject variations reported previously by Benson (7, 8). Furthermore, 200 trials, while roughly doubling test time, yielded just an incremental improvement in threshold precision (from 18 to 13%). Until the first mistake, the stimulus was halved after three correct responses at each level. From this point onward, the size of the change in stimulus magnitude was determined using parameter estimation by sequential testing (PEST) rules (30). For all conditions, initial stimuli were set at a level that was suprathreshold for the vast majority of subjects. Yaw rotations began at a vmax = 4°/s, y-translations at vmax = 4 cm/s, z-translations at vmax = 16 cm/s, and roll tilts at vmax = 3°/s for 1-Hz stimuli and vmax = 2°/s for 0.2 Hz. No feedback was provided as to the correctness of the responses after each trial. On only one test (1-Hz roll tilt) did the subject increase the stimulus amplitude beyond the motion device motion capabilities (1 out of more than 500 successful tests). When this occurred, since we thought that the subject may not have understood how to indicate the tilt direction, the subject was instructed again and given a second chance and then successfully completed the testing.
As a subtle enhancement to the published methods, all subjects used a two-stage task on an iPad to indicate responses. The iPad backlight illumination was off during all motion stimuli. Subjects were instructed to first tap the left (top) side of the screen if they perceived a leftward (upward) motion or to tap the right (bottom) side for rightward (downward) motion. Each tap was followed by feedback confirming the selection. Subjects were instructed that they must provide an answer. These instructions mimicked our earlier instructions, with the only difference as the use of an iPad instead of buttons to provide the binary indications. These standard binary data are used for all analyses presented herein.
After indicating perceived motion direction, subjects were instructed to indicate whether they were uncertain or not uncertain. If uncertain, subjects pressed the left and right sides of the iPad screen simultaneously. Otherwise, they pressed the same side of the screen again (e.g., right side twice for a right/certain response). These certainty/uncertainty data are not presented herein and are described here only to report our exact procedures.
As noted by others (13), testing at different frequencies could yield different results, especially since thresholds vary with frequency [e.g., Ref. (7, 8, 20, 26, 3133)]. Roll tilts at 0.2 Hz were chosen to assess sensory integration between canal and otolith cues (34), but we chose 1-Hz stimuli for most testing because (1) subjects report that tasks using 1-Hz stimuli are easier than both (a) higher frequency (e.g., 5 Hz) stimuli that require high alertness to avoid missing brief stimuli and (b) lower frequency (e.g., 0.1 Hz) stimuli that require extended periods of attention and (2) they require just 1 s, so 100 trials can be accomplished in less than 10 min (including time for responses and pauses between trials).
Data Analysis
For all conditions, the threshold (σ, sometimes called the psychometric width parameter) was determined by fitting a psychometric curve to the binary (e.g., left/right) experimental data. Specifically, a Gaussian cumulative distribution psychometric function defined by the parameters σ and μ was fit using a maximum likelihood estimate via a bias-reduced generalized linear model (BRGLM) (35) and probit link function (36). Fits were performed in MATLAB using the Statistic Toolbox version 8.3.
Geometric means were calculated for across subject averages, because, consistent with earlier reports (7, 8), data demonstrated a lognormal distribution across subjects for all conditions (Kolmogorov–Smirnov goodness-of-fit for lognormal distribution, p > 0.25). Both non-parametric and parametric analyses (using data in logarithmic units) were used. Multiple logistic regression was used to estimate the odds of failing the balance test associated with thresholds and age. A Pearson correlation was used to test for correlation between thresholds in different axes. Analyses were performed using SAS statistical software (SAS Institute Inc., Cary, NC, USA).
Data in other sensory domains [e.g., odor identification (37), visual acuity (38), and speech intelligibility (39)] suggest thresholds vary with age in a piecewise manner – with a flat plateau below an age cutoff and decreasing sensitivity above the same age cutoff. As our data shown in Figure 1 also suggest a similar piecewise linear pattern, we hypothesize thresholds remain relatively constant (i.e., no effect of age) up until some age cutoff at which point they increase (for simplicity, we assume this increase is linear). For each motion condition, the following continuous, piecewise linear model was fit to each subject’s threshold (σi) data with three parameters: (1) an “age cutoff” (a^cutoff), (2) a “baseline” level (σ^baseline) that represents the average threshold for ages less than the age cutoff, and (3) a “slope” (m^) that represents the rate of threshold increase above the age cutoff, where ai is each subject’s age in years rounded to the nearest integer at the time of testing was (e.g., 38 years of age). We present slope per decade (i.e., 10 years) throughout, since decades provide a more meaningful timescale for such changes.
σi=f(ai)={σ^baselineif aia^cutoffm^(aia^cutoff)+σ^baselineif ai>a^cutoff}
FIGURE 1
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Figure 1. Average (geometric mean) vestibular perceptual thresholds when grouped into five age ranges; error bars represent SD. (A,B) Top row shows thresholds for 1-Hz yaw rotation (blue triangle), 1-Hz roll tilt (green circle), 0.2-Hz roll tilt (red square); (C,D) bottom row shows thresholds for 1-Hz z-translation (magenta triangle) and 1-Hz y-translation (cyan diamond). (A,C) Left column, with solid lines and filled symbols, represents data from all 105 subjects. (B,D) Right column, with dashed lines and open symbols, represents data from 79 subjects who completed and passed all steps of the balance test. For clarity, data points are offset left/right slightly to minimize overlap. Inset cartoons indicating motion direction are reprinted with permission from Wolfe et al. (40).
As previously discussed, the thresholds were lognormally distributed; thus, the threshold data were log transformed and then a log-transformed version of the above age model was fit using a least-squared Nelder–Mead non-linear minimization routine (MATLAB fminsearch.m). Residuals were analyzed to assess the appropriateness of the fits. A parametric bootstrap approach (41), with M = 2,000 simulated data sets, was used to estimate the 95% confidence intervals of each fit parameter.
As shown in Figure 1, the age cutoffs were found to be similar across motion conditions. To quantify a single overall age cutoff, a comprehensive model (same piecewise form as above) was fit to the thresholds across all motion conditions. The model consisted of 11 parameters: 1 overall age cutoff, 5 baseline levels, and 5 slopes (corresponding to each of the 5 motion conditions). Each individual threshold data point was first log transformed, then standardized by the motion condition using the respective mean and SD prior to fitting a log-transformed version of the linear age model described above to each of the five data sets simultaneously. The standardization and log transformation processes were reversed to present model fit parameters and curves in the original physical units. We used likelihood ratio tests and Bayesian information criteria (BIC) to assess goodness-of-fit for the proposed piecewise two-segment linear models compared to alternative simple linear and average models.
Results
Thresholds
Our data do not suggest any threshold differences between males and females (Table 1). Statistical tests fail to demonstrate any significant effect of sex on thresholds. Even when we included migraine status, age, and balance test results as factors in multivariate analyses, no significant sex effect was found (p > 0.4, for each motion condition).
TABLE 1
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Table 1. Thresholds for males and females (95% CI) for each of the five motion conditions.
We also looked for a potential difference between premenopausal women under hormonal contraception and normal cycling women (Table 2). In all conditions, women taking hormonal birth control had higher thresholds. This difference did not appear significant except for yaw rotation thresholds (Wilcoxon rank sum, p = 0.037). Given multiple comparisons, we do not treat this difference as significant.
TABLE 2
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Table 2. Thresholds for females who are and are not taking hormonal birth control for each of the five motion conditions.
Furthermore, given that the association between hormonal contraception and yaw rotation thresholds could be explained by shared associations with other factors such as age, migraine status, or balance test results, we included all these factors in a multivariate analysis and found no significant effect of hormonal contraception on yaw rotation thresholds (p = 0.68) or for any of our other motion conditions.
In our sample, participants with migraine, defined as a MS-Q score of 4 or more (23), had lower thresholds for 4 of the 5 conditions – all but yaw rotation – than all other subjects. After correcting for multiple comparisons, that potential difference was not significant (Table 3). Because the sample size for migraine sufferers was so low (N = 5), this is noted as interesting but was not further explored herein.
TABLE 3
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Table 3. Threshold dependent on migraine status (95% CI) for each of the five motion conditions.
Table 4 shows the velocity threshold geometric mean for each motion condition separated into five age groups. As previously reported (7), z-translation thresholds were significantly higher (typically ~2× higher) than y-translation thresholds (paired t test, p < 0.0001). Yaw rotation thresholds were higher than roll tilt 1-Hz thresholds (paired t test, p = 0.0028), and roll tilt 0.2-Hz thresholds were significantly lower than both yaw rotation and roll tilt 1-Hz thresholds (paired t test, p < 0.0001 each). All five motion conditions showed an increase of threshold (poorer direction-recognition performance) with age (Figure 1). We note that all five subplots show a relatively flat threshold plateau below the age of 40–49 and also show increasing thresholds above that same age cutoff.
TABLE 4
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Table 4. Mean threshold by age group for each of the motion conditions, with a 95% confidence interval.
When each of the five motion conditions was analyzed separately, this age effect was significant, even following multiple comparisons correction, for four of the five motions tested (Kruskal–Wallis, p < 0.005) – all but yaw rotation. A similar trend with age was evident in the yaw rotation data, but this trend was not statistically significant (Kruskal–Wallis, p = 0.087). Figures 2 and 3 show these data.
FIGURE 2
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Figure 2. Threshold data for all subjects are plotted versus age for (A) 1-Hz yaw rotation, (B) 1-Hz roll tilt, and (C) 0.2-Hz roll tilt. Closed circles (●) show data for subjects who passed the balance test. Cross mark (X) show data for 20 subjects who passed conditions 1–3 but did not pass condition 4 of the balance test. Open circles (○) show data for six subjects who did not attempt the balance test. Triangles (Δ) show data for five migraineurs. Inset cartoons indicating motion direction are reprinted with permission from Wolfe et al. (40).
FIGURE 3
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Figure 3. Threshold data for all subjects are plotted versus age for (A) 1-Hz y-translation and (B) 1-Hz z-translation. Closed circles (●) show data for subjects who passed the balance test. Cross mark (X) show data for 20 subjects who passed condition 3 but did not pass condition 4 of the balance test. Open circles (○) show data for six subjects who did not attempt the balance test. Triangles (Δ) show data for five migraineurs. Inset cartoons indicating motion direction are reprinted with permission from Wolfe et al. (40).
Having established that there is an age effect that is independent of other factors, we evaluated whether there is an age cutoff above which threshold increases accumulate by fitting a two-piece linear model to the data. To minimize the impact of undiagnosed vestibular dysfunction, this model fit was first performed only on data from subjects who passed the balance test. Fitting this model to the data set for each motion individually (Table 5), we found an average age cutoff of 42.6 years. The residuals were consistent with a normal distribution (KS tests, p > 0.4).
TABLE 5
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Table 5. Fit parameters determined by fitting each motion condition individually for subjects who passed the balance test.
Given that the fitted “age cutoff” was similar across the motion conditions, we also fit a model having 11 parameters that fit a single age cutoff across all 5 threshold data sets while simultaneously fitting 2 parameters (slope above cutoff age, baseline below cutoff age) to each of the 5 motion conditions. This fit was performed twice – once with all of the data and once with data obtained from subjects who passed the balance test. Table 6 shows the results from this fit. As can be seen in Figures 2 and 3 and Table 6, the two fits yielded similar curves. The overall age cutoff when fit simultaneously across all motion conditions was 42.1 years for all subjects and 42.7 years for all subjects who passed the balance test. Each of the slope values shown in Table 6 was significantly greater than 0 (p < 0.05) corresponding to an increase in threshold (worse performance) with increasing age above ~40 years.
TABLE 6
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Table 6. Fit parameters determined via single simultaneous fit of all threshold data.
Table 7 shows fitted degrees of freedom (DOF), variance explained, −2 × log(likelihood), and BIC for each of the four different models presented: mean model, simple linear model, simultaneous two-segment linear model, and the independent two-segment linear model. To allow us to provide a single estimate of variance and BIC for each fitting method, we emphasize that each of the five data sets were standardized using customary calculations (i.e., the mean was subtracted from each data point and then divided by SD) described earlier in the methods, which yields two benefits. First, it makes all parameters dimensionless, which allows us to combine variance across different motion conditions. Second, it makes the variance for each of our five motion dimensions the same, which provides even weighting across the five measures (Otherwise, the variance could be dominated by the measure having the greatest variance).
TABLE 7
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Table 7. Degrees of freedom (DOF), variance explained, −2 × log(likelihood) – which is sometimes called deviance and was calculated using the natural log – and Bayesian information criteria (BIC) scores are shown for the four different models presented herein.
As one would expect, more fit parameters (i.e., more DOF) yields variance reductions, but the 11-parameter 2-segment model explains roughly twice the variance of the 10-parameter model. In other words, adding a single age cutoff parameter to the linear regression model doubles the variance explained.
Likelihood ratio testing was used to test the nested models (mean, simultaneous two-segment, and independent two-segment) and showed that the proposed simultaneous two-segment linear model was significantly better than the mean model for both the full data set (χ2 statistic = 121.8, DOF = 6, p < 0.0001) and the 79 subjects who passed the balance test (χ2 statistic = 88.6, DOF = 6, p < 0.0001). Likelihood ratio testing also showed the simultaneous two-segment linear model is not significantly different from the independent two-segment linear model for both the full data set (χ2 statistic = 0.9, DOF = 4, p = 0.92) and the 79 subjects who passed the balance test (χ2 statistic = 1.0, DOF = 4, p = 0.91).
Bayesian information criteria statistics showed that this model was substantially better than the other models considered, including the simple linear model. In fact, this analysis showed that the simultaneous two-segment model had the smallest BIC for both the full data set and for the 79 subjects who passed the balance test. The BIC for the 11-parameter 2-segment model was always more than 20 points lower than for any other model. For context, BIC differences greater than 10 are considered “very strong” evidence for the model with the lower BIC (42).
The two simple models – the mean and linear regression models – do not match our data well. The mean model cannot capture the fact that thresholds increase above the age of about 40, and the linear regression model cannot capture the fact that thresholds are relatively constant below the age of about 40 (e.g., Figure 1).
Bias
For our direction-recognition task, the fitted bias parameter represents the stimulus magnitude at which a subject is equally likely to respond right (up) or left (down) (43). It is poorly understood because it could originate from any of the three sources: (a) a bias in the information, (b) a bias in the placement of the decision boundary (43), or (c) a bias in the noise distribution. We evaluated bias and normalized bias; normalized bias is simply the fitted bias divided by the fitted threshold. This dimensionless parameter has the advantage that it is readily comparable across motion conditions.
Neither the mean value of the bias nor the mean value of normalized bias was significantly different from 0 for any of the 5 motion conditions. This was true across all 105 subjects as well as for the 79 subjects who passed the balance test (t test, p > 0.05 for all 20 conditions tested after correction for multiple comparisons).1 Furthermore, correlation coefficients for either bias or normalized bias versus age were not significantly different from 0 for any of the 5 motion conditions. Again, this was true for all subjects as well as for those who passed the balance test (Kruskal–Wallis, p > 0.1 for all 20 conditions tested).
Figures 4 and 5 show scatterplots of the normalized bias values for all the motion conditions. Consistent with correlation analyses reported above, no significant or consistent trends are evident.
FIGURE 4
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Figure 4. Normalized bias data for all subjects are plotted versus age for (A) 1-Hz yaw rotation, (B) 1-Hz roll tilt, and (C) 0.2-Hz roll tilt. Closed circles (●) show data for subjects who passed the balance test. Cross mark (X) show data for 20 subjects who passed condition 3 but did not pass condition 4 of the balance test. Open circles (○) show data for six subjects who did not attempt the balance test. Triangles (Δ) show data for five migraineurs. Format mimics Figure 2.
FIGURE 5
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Figure 5. Normalized bias data for all subjects are plotted versus age for (A) 1-Hz y-translation and (B) 1-Hz z-translation. Closed circles (●) show data for subjects who passed the balance test. Cross mark (X) show data for 20 subjects who passed condition 3 but did not pass condition 4 of the balance test. Open circles (○) show data for six subjects who did not attempt the balance test. Triangles (Δ) show data for five migraineurs. Format mimics Figure 3.
Relationship between Thresholds and Romberg Balance Testing
Given that vestibular information is a fundamental contributor to balance control, we looked for associations between thresholds and performance on the modified Romberg test. A subsample of 99 subjects performed the balance test. Not a single participant failed the test in conditions 1, 2, or 3, but 20% (20 of 99) failed in condition 4. Thresholds were significantly greater for participants who failed the final balance test condition (i.e., the Romberg test condition focused primarily on vestibular function) for all motion axes (Table 8).
TABLE 8
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Table 8. Mean thresholds for subjects who passed and failed the balance test.
Consistent with earlier findings (25), the proportion of balance test failures increased with age group (Fisher exact test, p < 0.0001). To test whether the observed difference between the pass and fail group may be due to an age effect or to the influence of other confounding factors, we adjusted for age, gender, and migraine using a mixed model. The significant association of balance test failure with increasing threshold remained persistent for roll tilt at both 0.2 and 1 Hz (p = 0.003 and p = 0.02, respectively) but was not significantly correlated for increasing yaw rotation (p = 0.09), y-translation (p = 0.50), and z-translation (p = 0.09) thresholds. The age effect was unchanged for all motion paradigms – remaining significant for y-translation, z-translation, and roll tilt at 1 Hz (each p < 0.0001) and roll tilt at 0.2 Hz (p = 0.0007) and not significant for yaw rotation (p = 0.12).
Odds of failing the balance test have been associated with significantly increased odds of falling, for American adults 40 years and older (25). Our data show that a 1 unit increase in roll-tilt thresholds at 0.2 Hz (following transformation in SAS using natural log) were associated with a 5.6-fold increase in the odds of failing the balance test (odds ratio, 5.6; 95% confidence interval, 1.6–18.9) in a multiple logistic regression adjusted for age. One-unit increase in roll-tilt thresholds at 1 Hz (log-transformed version) was associated with a 3.7-fold increase in the odds of balance testing failure (odds ratio, 3.7; 95% confidence interval, 1.1–12.9).
Discussion
In this study, we attempted to determine whether sex or age affected perceptual thresholds of vestibular functioning. To do this, we asked subjects to indicate the direction of movement they perceived in 5 blocks of 100 trials each for the following motion conditions: yaw rotation, y-translation, z-translation, roll tilt at 1 Hz, and roll tilt also at 0.2 Hz. One primary finding was that thresholds increased with age for all motion directions above the age of about 40. This finding is consistent with a number of earlier threshold studies that had reported similar effects of age x-axis translation (16, 19) and y-axis translation (16) but inconsistent with a few earlier studies that reported no such age effects for yaw rotation (1416). We note that the yaw rotation age effect was the smallest that we observed and our study had a larger total number of subjects than the earlier studies; these differences likely explain why we found a significant effect of aging in contrast to earlier studies.
We explicitly note that our finding of a statistically significant effect of age on yaw rotation thresholds required both our two-segment model and more than 50 subjects. Our translation threshold findings showed more substantial age effects. These findings are consistent with earlier findings that translation thresholds increase with age (1619). No previous studies have examined roll-tilt thresholds, which is a focus of our study (i.e., 40% of the data reported).
The second primary finding was that increasing roll-tilt threshold was correlated with failure to complete the Romberg foam balance test. Since we know of no mechanism by which balance would impact vestibular thresholds, and since we know that balance depends on vestibular function [e.g., Ref. (44)] and that falls correlate with failure to complete the Romberg foam balance test (25), it is reasonable to suggest that this correlation shows that fall risk is substantially impacted by vestibular function. We emphasize that this was true even when measured in a healthy population chosen without any evidence of specific vestibular disorders.
Finally, while we did not report a full analysis of the within subject correlations between thresholds in different axes, our initial analyses showed that 9 of the 10 pairwise comparisons (all but the correlation of yaw rotation thresholds with y-translation thresholds) of the 5 threshold measurements were correlated (p < 0.05); we plan to make this topic the focus of a future manuscript as soon as we complete extensive analyses of these correlations. A more detailed discussion of our findings and the implications are presented below.
Sex Differences and Individual Differences
One goal when conducting this study was to determine whether there were sex differences in vestibular perceptual thresholds. According to our findings, there were no differences between males and females in their perceptual thresholds; this finding is in line with other studies comparing sex differences (8, 16, 17, 26).
Benson and colleagues previously published a pair of comprehensive threshold studies (7, 8). These studies looked at rotational thresholds (8) and translational thresholds (7). For the 4 motions studied with 24 or more subjects, all demonstrated a range of thresholds with a ratio of roughly 10 for all 4 motions (i.e., the maximum threshold divided by the minimum threshold was about 10). In decibel units, Benson reported SDs of 4.40 (yaw rotation), 4.63 (X-translation), 3.98 (Y-translation), and 6.10 (Z-translation). When converted to decibels our experimental SDs were 4.11 (yaw rotation), 5.23 (Y-translation), 6.47 (Z-translation), 4.62 (1.0-Hz roll tilt), and 4.36 (0.2-Hz roll tilt), which appear similar to Benson’s. These similar empiric variations reported by both studies are most likely due to intersubject differences since variations due to sampling and other methodological details have been shown to be an order of magnitude smaller for 100 binary forced-choice trials (29) than these empirical variations.
Motion Differences
Next, we looked at differences in perceptual thresholds for the various motion stimuli. We found differences in several of the motion thresholds that we tested. Namely, we found that the threshold for y-translation was less than the threshold for z-translation, by approximately a factor of 2. This finding is consistent with MacNeilage et al. who indicated that utricles may have a greater sensitivity to perceive horizontal motion compared to the saccules’ sensitivity to perceive vertical motion (45). This suggestion carries more weight when we also consider that the utricles have a greater density of hair cells compared to the saccules (46). It is possible that the additional hair cells in the utricles could contribute to their sensitivity and therefore lower the y-threshold. Furthermore, Valko et al. suggest that earth-vertical movement is more difficult to discriminate as the otolith must determine whether the gravitational force increases or decreases, whereas for an earth-horizontal movement, the body and brain have access to a greater amount of non-vestibular cues to aid in determining the direction of a particular motion (20). Overall, there are many differences between earth-vertical and earth-horizontal movements; it is possible that the amount of information (e.g., tactile) available during earth-horizontal movement provides easier perception and recognition of the motion direction compared to the amount of information available when moving along the z-axis.
When we divided the data by age group, the threshold velocity for roll tilt at 0.2 Hz was less than the threshold velocity for 1-Hz roll tilt. This is consistent with Valko et al.’s study, where the researchers found that roll-tilt thresholds, expressed as peak velocity, decreased at lower frequencies in healthy subjects (20).
Furthermore, the threshold for roll tilt at 1 Hz was also lower than the yaw threshold. Because roll tilt is perceived by an integration of otolith and semicircular canals, the amount of information available to the vestibular system may facilitate the perception of motion compared to the yaw rotation which primarily relies on the semicircular canals.
Ages for Perceptual Cutoffs
Finally, because we saw that thresholds for each motion condition increased from decade to decade after about age 40, we thought it would be interesting to determine whether there was one specific age at which the perceptual thresholds began to increase for all five motion paradigms. By modeling the data we collected in this study, we found that we were able to separate vestibular thresholds into two categories, namely, “younger” and “older” adults, where younger adults’ thresholds were stable until about 40 years of age, at which point “older” adult vestibular performance began to decline (i.e., thresholds began to increase) at a steady rate for each of the motion thresholds. Between this finding and findings from other studies (16, 18, 47), we can directly assert that changes in vestibular function occur with age. While increasing age above the age cutoff was associated with an increase in threshold in each motion condition, some conditions were impacted more than others: z-translation thresholds increased by ~83% of the baseline per decade after the age cutoff, roll tilt 1 Hz by 56%/decade, y-translation by 46%/decade, roll tilt 0.2 Hz 32%/decade, and yaw rotation 15%/decade. These rates of increased thresholds with aging are for the subset of subjects that passed the balance test, but the values when including all subjects are similar.
Vestibular System Aging
Vestibular functioning can decline for any number of reasons including neurodegenerative disease, peripheral loss, and even medications and their side effects. Age is an important factor that influences the vestibular system and vestibular function. While the mechanisms behind aging remain disputed, it is an important and relevant issue to address here. While others have considered the mechanisms of aging and its particular effect on the vestibular system (48), we would like to expand on what has previously been proposed by comparing age-related changes in the vestibular system to other systems, by discussing potential mechanisms, and consider why little or no threshold difference occur before the age of 40.
Comparison to Other Modalities
We report that – for five different tests of vestibular function – perceptual thresholds appeared constant between the ages of 20 and 40 and increased linearly above the age of 40. A roughly similar pattern has been reported for other sensory systems but with the functional performance plateau lasting until the age of 60. For example, average odor identification shows a plateau until about the age of 60 with functional declines evident above the age of 60 (37). As shown in Figure 2 of Doty, visual acuity (38) and speech intelligibility (39) show similar patterns including declines above the age of about 60. It is interesting to note that the functional decline appears to begin about two decades earlier for vestibular function than for smell, vision, or speech intelligibility. This may indicate that vestibular function is preferentially targeted by whatever mechanism(s) causes functional sensory loss with age (e.g., vestibular threshold increases with age).
Mechanism
The threshold variations were qualitatively similar across all conditions; this suggests at least one shared common cause. The fact that the functional decline pattern (i.e., roughly linear threshold increase begins to occur around age 40 for all conditions) is about the same for all conditions tested weighs against an “overstimulation” cause like that reported for hearing loss (4951), though that certainly does not mean that hearing loss and functional vestibular loss cannot share another (or other) mechanism(s).
No explanation, including our common cause explanation, can explain the quantitative differences across motions (e.g., why do z-translation thresholds demonstrate a slope of more 80% while yaw rotation a 15% slope?) at this time. One simple explanation is that these do not share a common cause. Alternatively, these deficits could reflect a common cause with the quantitative differences due to (a) the amount of available redundancy, which may vary for different motions, (b) the baseline, which obviously impacts this relative slope measure, and/or (c) other mechanisms in addition to a cause common to all motions.
Several studies have reported human vestibular hair cell and vestibular afferent neuron counts as a function of age (46, 52). Vestibular hair cell loss has been reported to show a linear decline with age from birth through 100 years of age that does not directly match our threshold data, especially the constant threshold plateau we report below age 40. This argues against hair cell loss in isolation being a direct explanation of the threshold age pattern we report. Similarly, the loss of afferent neurons does not in isolation match the threshold age pattern we report.
Therefore, we will briefly consider another (possibly related) cause – the free radical theory of aging, which is probably the most persistent theory of aging and could explain why performance declines begin to be evident for vestibular thresholds around the age of 40 but later for some other sensory functions. Specifically, we note that in primates, the average firing rate of peripheral afferent neurons is nearly 100 spikes per second, with the resting rate reported as averaging 91.3 spikes per second for the semicircular canals (53) and 62.7 spikes per second for the otolith organs – 79.1 for superior nerve and 47.0 for inferior nerve (54). These resting rates average between 50 and 100 spikes per second across about 40,000 vestibular afferent neurons (40) and, hence, assert a substantial metabolic load. While the resting rate for individual neurons in the vestibular nuclei is a bit lower, the central vestibular system similarly asserts a substantial metabolic load [e.g., Ref. (55)].
A metabolic-related cascade that could lead to age-related vestibular threshold increases is sketched in the following paragraphs. The heavy metabolic load of the vestibular system – both central and peripheral vestibular systems – requires extensive ATP production via mitochondria. Since mitochondria are the biggest contributors of oxidative load (i.e., free radicals) to the body, this leads directly to a relatively large oxidative stress. Many of these free radicals are quenched. Others escape and cause damage distributed elsewhere. But some of these free radicals cause local damage. This local damage can lead to dysfunctional central and/or peripheral function. This proposed mechanism would be consistent with studies showing oxidative contributions to peripheral cochlear dysfunction [e.g., Ref. (56)]. When the vestibular functional loss (i.e., neuronal cell death and/or dysfunction) leads to more “signal” loss than “noise” loss, it would lead to increased perceptual thresholds.
A review of the evidence for/against the free radical theory of aging and other theories of aging is beyond the scope of this paper but can be found in various books/reviews [e.g., Ref. (5759)] We simply note here that the most recent incarnation (60, 61) of the free radical theory of aging (59, 62, 63) would be consistent with the cascade described above. If the free radical theory of aging is the major contributor to the deficit observed in thresholds above the age of 40, this could make vestibular threshold changes a relatively simple, sensitive, non-invasive behavioral biomarker for aging in humans above the age of 40, especially, since, as noted earlier, the age effects for vestibular function appear earlier than for odor discrimination, visual acuity, or speech intelligibility.
Why Are No Threshold Changes Evident below the Age 40?
Small threshold changes below the age of 40 may be evident for an individual but were masked by intersubject variability, since our study was not longitudinal. Long-term longitudinal studies would likely show whether threshold changes occur in individual humans before the age of 40.
While speculative, the free radical mechanism described earlier could also be consistent with the relative threshold constancy before age 40. Let us assume that vestibular contributions are crucial and that oxidative neuronal cell loss due to cell death or neuronal dysfunction is inevitable. If true, one reasonable evolutionary strategy would be to have an excess of neurons at least till reproductive vigor started to wane. In other words, some neuronal cell loss occurs before age 40, but the available excess of vestibular neurons yields redundancy such that the incremental decrease in overall signal matches the incremental decrease in overall noise for each vestibular neuron lost due to dysfunction or death. But around age 40, the vestibular cell counts reduce to the point that each neuron loss causes more incremental signal loss than noise loss. If true, this would suggest that we have on the order of 40,000 vestibular afferent neurons to provide some redundancy to fend off functional impact of peripheral vestibular loss. Such peripheral redundancy could also explain why thresholds as a function of age do not match the aging patterns shown by vestibular afferent neuron counts (52, 64) or vestibular hair cell counts as a function of age (46, 64). Furthermore, this hypothesis could account for different quantitative aging patterns reported herein (i.e., Z-translation slope much greater than yaw rotation slope relative to baseline) for different movements.
Implications
Our threshold data showed that vestibular thresholds broadly increased with age above the age of 40 (by 15–83% per decade depending upon the motion condition, p < 0.05 for all five threshold measures). Furthermore, our data showed that balance test failures increased significantly as roll-tilt thresholds increased – even when age and other factors were fully considered by our mixed-model analysis. This latter finding is important because an earlier study showed that failure to complete the Romberg foam balance test correlates highly with falls (25). More specifically, data from a National Health and Nutrition Examination Survey (NHANES) were analyzed to show that 35.4% of American subjects above the age of 40 were unable to stand on foam with their eyes closed – the exact same failure that we showed to be significantly correlated with increasing roll-tilt thresholds. The earlier study (25) also reported increased odds of falling – an odds ratio of 6.3 – for such individuals with subclinical vestibular dysfunction relative to those without dysfunction (i.e., individuals who were able to complete the balance testing successfully).
Given different definitions and different methods, these American findings are neither far from the findings of a German study that estimated prevalence of vertigo to be 22.9% (65) nor from self-reported vertigo prevalence rates of about 20% (66, 67). In fact, self-reported dizziness for the American study was 27.0% – certainly in line with the earlier estimates. For the fraction of such symptomatic individuals with measured vestibular dysfunction, the American study reported increased odds of falling – i.e., an odds ratio of 12.3. Our findings of a decrement in vestibular function – directly assessed via vestibular thresholds – above the age of 40 could certainly help explain why 35% of the NHANES population above the age of 40 demonstrated balance dysfunction.
Given the clear evidence presented herein that vestibular function declines with age above the age of 40 and given the relative consistency of the earlier estimates of vestibular and balance dysfunction (25, 6567), it seems reasonable to try to make a conservative estimate of the number of people who might die each year due to vestibular dysfunction. For example, it seems likely that at least some of the transportation accidents (e.g., car crashes) that lead to the death of about 50,000 Americans each year (39) are due to vestibular dysfunction, but, unfortunately, we were unable to find enough relevant data at this time to estimate the contributions of vestibular dysfunction to motor vehicle accidents. On the other hand, available data do allow us to conservatively estimate the number of deaths each year caused by falls related to vestibular dysfunction. These calculations are provided in detail in Appendix A. Table A1 in Appendix provides a range of estimates – some more conservative and some less so. The annual death estimates correlated with vestibular dysfunction range from 48,000 to 152,000.2 While the largest estimate of nearly 152,000 deaths per year may prove inaccurate, it is worth noting that this would be placed third in the US behind only heart disease and cancer. Even the lowest estimate of ~48,000 deaths per year – which would place this as the tenth largest cause of death in the US – conveys the gravity of the problem.
We emphasize that estimating death rates was not a goal of our study but rather an implication of the finding – even after correcting for age effects – that the proportion of balance test failures increased with roll-tilt thresholds, especially at 0.2 Hz (p = 0.0007); 1 unit increase in roll-tilt thresholds (log-transformed version) corresponded to a 5.6-fold increase in the odds of failing the balance test. We further emphasize that extrapolating the current data to fall risk has limitations. Nonetheless, the range of estimated deaths potentially due to vestibular dysfunction (Table A1 in Appendix) suggests the scope of the problem and highlights the need for broader epidemiologic studies focused on mortality associated with vestibular dysfunction.
We close this implications section by juxtaposing some facts discussed above. (1) Data showed that vestibular thresholds, including roll-tilt thresholds, broadly increased with age above the age of 40 (by 15–83% per decade depending upon the motion condition). (2) Analyses showed that balance test failures, which have previously been shown to correlate highly with falls (25), increased significantly as roll-tilt thresholds increased. (3) Calculations suggested that vestibular dysfunction could possibly be ranked somewhere between the third and tenth biggest killer of Americans. Even in isolation, this is alarming. But, given the rapid aging of the world’s population [e.g., Ref. (68)], the problem will rapidly grow much worse unless existing efforts to improve vestibular screening, vestibular diagnoses, vestibular treatments, balance treatments, fall prediction, and fall prevention are accelerated.
Brief Summary
We measured vestibular perceptual thresholds in 105 healthy humans (54F/51M) ranging from 18 to 80 years of age. We found that thresholds significantly increased above the age of 40 for all five motion directions investigated. Even taking age and other factors into consideration, we found a significant correlation of balance test failures with increasing roll-tilt thresholds.
Author Contributions
MB, TC, and DM designed the study and assisted in statistical analyses and interpretation and manuscript preparation. WW, YB, and TL also assisted in manuscript preparation, and statistical analyses and interpretation.
Conflict of Interest Statement
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Acknowledgments
This research was supported by NIH/NIDCD R01-DC01458 and R01-DC014924. We also thank Raquel Galvan-Garza, Wangsong Gong, Bob Grimes, Csilla Haburcakova, Faisal Karmali, Kristen Kirk, Rick Lewis, Koeun Lim, and Yongwoo Yi.
Footnotes
1. ^Prior to multiple comparison correction, only the normalized Z-translation bias for subjects who passed the balance test suggested a statistically significant effect (t-test, p = 0.0441).
2. ^A reviewer helpfully suggested that the paper might be better off without the appendix. After dialog engendered by the Frontier’s process, this footnote has been added to specifically note that we all agree that (a) the estimated range is large because available data do not allow solid estimates, (b) the issue was too important to gloss over by ignoring it, (c) the only way to resolve the matter is to obtain better data, and (d) including these broad estimates is likely to encourage the acquisition and analysis of better data.
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Appendix
A. Estimating Annual Fatalities Related to Vestibular Dysfunction
According to the CDC online web-based injury statistics query and reporting (69), 26,734 persons over 40 years of age died in the US in 2011 as a direct result of unintentional falls. This is consistent with a National Vital Statistics Report (70) that stated that 26,009 persons died in the US in 2010 as a direct result of unintentional falls. Of course, only some of the 26,734 fall-related deaths were due to vestibular dysfunction. To provide this estimate of deaths related to vestibular dysfunction, some simple calculations are required. Such calculations require that we know (a) the prevalence of vestibular dysfunction and (b) the increased risk of fall due to vestibular dysfunction, both of which were discussed earlier. Specifically, we will use (a) the 35.4% estimate of prevalence provided by Agrawal et al. (25), because it is the most comprehensive broad assessment based on objective measures, and (b) the reported odds ratio of 6.3 for those individuals over the age of 40 defined as having vestibular dysfunction using the balance metric (25), because it arises from the same comprehensive data set. We note that using these estimates yield a smaller (i.e., more conservative) estimated death rate than if we used the 27% prevalence rate for vestibular dysfunction with clinical symptomology with the 12.3 odds ratio for falls in this population.
If the total pertinent population at a point in time is x, then 35.4% (0.354x) have vestibular dysfunction and 64.6% (0.646x) do not. Let us represent the risk of falling without vestibular dysfunction as w. Then, the risk of falling with vestibular dysfunction [as defined by Agrawal et al. (25)] is 6.3 times higher (6.3w). While it can be argued that the risk of a bad fall for those with vestibular dysfunction is likely higher than for those with normal function, we conservatively assume that the risk of death due to a fall is independent of vestibular status (y). The total number of US deaths directly due to falls (26734) equals the sum of deaths in those with vestibular dysfunction (0.354 × 6.3 w x y = 2.23z) and those without vestibular dysfunction (0.646 w x y = 0.646z), where z = w x y, so 26,734 = 2.23z + 0.646z. This can be solved for z, which equals 9296; therefore, 26,734 = 2.23(9296) + 0.646(9296); thus, we can estimate that 20,729 (2.23 × 9296) equals the number of fall deaths in those individuals with vestibular dysfunction. Of course, these individuals had a chance of falling independent of their vestibular status. By definition, this risk is the same as for individuals without vestibular dysfunction, so 3,291 (0.354 × 9296) of these would have fallen independent of their vestibular dysfunction, leaving an estimated 17,438 deaths directly attributable to falls due to vestibular dysfunction. These calculations suggest that 65% of deaths directly attributable to falls are related to vestibular dysfunction (We note that death due to falling is relatively rare; so, risk and odds here would be nearly equivalent).
But falls also indirectly lead to death. For example, falls cause hip fractures, among other injuries, and hip fracture has a high mortality rate following fracture. There were 306,000 hospital admissions for hip fractures in 2010 (71), and it has been estimated that more than 95% are due to falls (72). One study reported that the overall 1-year post-fracture mortality rate was 27.3% and further reported that mortality after hip fracture at the end of the follow-up was 79.0% (73). If we conservatively use the 1-year mortality rate of 27.3%, this suggests that more than 79,361 patients die each year following hospitalization for a hip fracture. Repeating the exact same calculations outlined in the previous paragraph, we estimate that there may be 51,767 deaths correlated with falls (i.e., following hip fracture) that are related to vestibular dysfunction. As for the calculations in the previous paragraph, some fraction of these deaths is unrelated to the fall and hip fracture. The same study reported an average death risk ratio of 3.26 in this hip fracture population relative to an age-matched population. Analogous to the above calculations, the total number of deaths equals those related to the hip fracture and those that would have occurred anyway (51,767 = 3.26v + v), yielding the estimated number of deaths related to the hip fracture as 39,615. Simply summing these two death estimate numbers (i.e., the number of fall deaths directly and indirectly related to vestibular dysfunction) yields an estimate that vestibular dysfunction contributes to 57,053 deaths each year.
Given the conservative nature of these estimates (using only 1-year hip fracture mortality, not including traffic and other non-fall accidents, using the lower odds ratio, etc.), these estimates suggest that vestibular dysfunction likely contributes to more than 57,000 deaths each year. If categorized this way, according to a national vital statistics report (74), this would rank number 10 on the list of leading causes of death in 2010 behind heart disease (598,000), cancer (575,000), chronic respiratory diseases (138,000), stroke (129,000), accidents (121,000), Alzheimer’s (83,000), and diabetes (69,000). Table A1 in Appendix provides a range of estimates – some more conservative and some less so. The annual death estimates correlated with vestibular dysfunction range from 48,000 to 152,000.
TABLE A1
www.frontiersin.org
Table A1. Deaths due to vestibular dysfunction under different assumptions.
Keywords: vestibular, perception, thresholds, aging
Citation: Bermúdez Rey MC, Clark TK, Wang W, Leeder T, Bian Y and Merfeld DM (2016) Vestibular Perceptual Thresholds Increase above the Age of 40. Front. Neurol. 7:162. doi: 10.3389/fneur.2016.00162
Received: 24 May 2016; Accepted: 14 September 2016;
Published: 03 October 2016
Edited by:
Yuri Agrawal, Johns Hopkins University, USA
Reviewed by:
Paul MacNeilage, Ludwig Maximilian University of Munich, Germany
Benjamin Thomas Crane, University of Rochester, USA
Copyright: © 2016 Bermúdez Rey, Clark, Wang, Leeder, Bian and Merfeld. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Daniel M. Merfeld, [email protected]
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Huntington's Disease Youth Organization
Can you modify the gene to have a baby without HD?
HDYO has more information about HD available for young people, parents and professionals on our site:
www.hdyo.org
Q. Hi, my mother-in-law has HD, is 60, her late father too, my husband had symptoms and is in his 30’s. We decided not to have a baby for this reason. Now someone told my husband is possible kind of “modify the gene” in the embryo/fetus to have a baby without HD, but this procedure is very expensive and not so common….is it true???
BA, Young Adult, USA
Ask a question
A. Dear BA
Many thanks for your question. I think what they are referring to is a process called ‘preimplantation genetic diagnosis’ (PGD), which is a way of trying to avoid passing on a known genetic change (in this case the gene expansion that causes HD) to a child.
PGD is a process that aims to select embryos that do not carry the gene expansion (it does not modify the gene itself). The process initially works in a similar way to standard in vitro fertilisation (IVF), where embryos are created outside the body using sperm and egg cells collected from each member of the couple. The extra step for PGD involves testing the embryos before they are replaced to the womb (they do this by removing one cell from each developing embryo when it is still very small, usually around 16 cells in size) to see if the gene change is present or not. They would then plan to only replace embryos to the womb that do not carry the gene change.
Unfortunately, due to the drugs and specialised techniques involved, and the fact that it involves multiple clinic appointments, PGD is expensive. A cycle costs around $15000, and it is not usually covered by health insurance. Also, sadly not all cycles of PGD result in a successful pregnancy (the success rates are usually an average of around 1 pregnancy for every 3 or 4 cycles) and this means that as well as the financial costs, it can often be quite physically and emotionally demanding. If you would like to know more about PGD, as well as other prenatal options, I would recommend that you see a Genetic Counselor who could provide further information and support. If you wish, this website may help you to find your local Genetics service.
There is also some useful information about prenatal options including PGD in this HDYO article
I hope you find this answer useful, and please do not hesitate to get back in touch of you have any further questions, or if you have any difficulty accessing your local Genetics service.
Bill
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3,515,201,951,594,778,000
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What is POSTERIOR COMMISSURE?
Written by Pam MS, NCSP | Fact checked by Psychology Dictionary staff
a big group of nerve fibers within the brain which passes over the midline of the epithalamus just dorsal to the place where the cerebral aqueduct opens into the fourth ventricle. It is made up mainly of myelinated fibers linking oculomotor and corresponding cells of the midbrain.
POSTERIOR COMMISSURE: "The posterior commissure was partially severed during the accident."
More On This Topic
Link to This Definition
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-2,880,602,850,112,177,000
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All About Cortisol
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What is cortisol?
Cortisol is a hormone that belongs to a family of steroid hormones known as glucocorticoids. It’s secreted by the adrenal cortex, which is located in your adrenal glands that sit atop your kidneys. Cortisol is the main glucocorticoid in humans.
Glucocorticoids affect every cell in the body so needless to say, they’re pretty important.
In particular, glucocorticoids released in the body send feedback to the brain and influence the release of CRH (corticotropin-releasing hormone) and ACTH (adrenocorticotropic hormone). ACTH stimulates the adrenal glands to secrete cortisol. The rise in cortisol secretion follows ACTH release after a 15-minute to 30-minute delay.
Why is cortisol so important?
Cortisol accelerates the breakdown of proteins into amino acids (except in liver cells). These amino acids move out of the tissues into the blood and to liver cells, where they are changed to glucose in a process called gluconeogenesis. A prolonged high blood concentration of cortisol in the blood results in a net loss of tissue proteins and higher levels of blood glucose.
Isn’t this bad?
Well, not exactly. By raising plasma glucose levels, cortisol provides the body with the energy it requires to combat stress from trauma, illness, fright, infection, bleeding, etc.
Obviously, this is bad from a muscle breakdown perspective; however, the body is simply trying to preserve carbohydrate stores and deliver energy when it’s needed most. Acutely, cortisol also mobilizes fatty acids from fat cells and even helps to maintain blood pressure.
As it’s part of the inflammatory response, cortisol is necessary for recovery from injury. However, chronically high levels of cortisol in the blood can decrease white blood cells and antibody formation, which can lower immunity. This is the most important therapeutic property of glucocorticoids, since they can reduce the inflammatory response and this, in itself, suppresses immunity.
Thus, cortisol is:
• Protein-mobilizing
• Gluconeogenic
• Hyperglycemic
Whether these effects are “good” or “bad” depends on whether cortisol’s release is acute (ie brief and infrequent) or chronic (ie ongoing).
Cortisol_production_PI
What you should know
Here are the cortisol reference ranges. Notice that they depend on the mode of measurement (urine vs serum) and time of day.
• Cortisol, free (urine) 20-90 mcg/day
• Cortisol (serum) 4-22 mcg/dL (morning specimen)
• Cortisol (serum) 3-17 mcg/dL (afternoon specimen)
Cortisol has a close relationship to exercise and training status.
For example, cortisol levels can be a sign of overtraining. To be indicative of overtraining, cortisol increases may need to be higher than 800 nmol/L.
Exercise type
The type of exercise regimen performed can dictate hormonal response.
Acute high intensity resistance exercise is associated with increased plasma cortisol concentration. In other words, after something like a sprint or a high-intensity conditioning or bodybuilding-style workout, plasma cortisol concentration increases. The response is similar to that seen of growth hormone. The most dramatic increases occur when rest periods are short and total volume is high.
Cortisol responses to increased training volume are variable. Response depends on specific training protocols and diurnal variations (variations over the course of the day).
Again, it is important to distinguish between acute and chronic cortisol release. When muscle glycogen concentrations are low, cortisol is released and fuel use shifts toward protein or fat so that judicious use is made of the little glucose that remains. However, in the long-term, excessive cortisol will encourage fat synthesis and storage, along with provoking appetite.
On the other hand, aerobic endurance training, particularly running, is linked with protein loss from muscle (partially induced by cortisol). Endurance trained individuals typically have a higher cortisol response, while resistance trained individuals have a higher testosterone response. Secretion of cortisol is elicited at exercise intensities between 80% and 90% of VO2 max, which means that in this case, we’re not necessarily describing recreational exercise — we’re referring to endurance training.
Time of day and time of eating
The degree of cortisol release during high intensity exercise depends in part on the time of day and the timing of meals. When exercise is performed during a time of already high cortisol levels (for example, in the morning), it doesn’t increase above already elevated levels.
Cortisol secretion displays 7 to 15 spontaneous or meal-associated “pulses” throughout the day.
Cortisol circadian rhythms are closely coupled to the sleep-wake cycle. Peak cortisol release occurs between 7 and 9 in the morning, the time of dark-light transition.
Changes in cortisol over a 24-hour period
Changes in cortisol over a 24-hour period
The physiological environment
Cortisol causes atrophy in muscle (mainly fast twitch type 2) and bone. The anabolic effects of testosterone and insulin oppose cortisol’s catabolic effects.
The acute increases in cortisol following exercise also stimulate acute inflammatory response mechanisms involved with tissue remodeling. In the short term, this is a necessary response that helps with repairing damage produced by training. Only long-term cortisol elevations seem to be responsible for adverse catabolic effects.
Stress (both psychological and physical) can result in the “alarm reaction.” If stress is ongoing, this can cause enlarged adrenal glands and atrophied lymphatic organs. When adrenals enlarge, they can produce excessive cortisol; when lymphatic organs shrink, they create fewer white blood cells. The immunosuppressive effects of intense exercise have been attributed to high plasma cortisol concentrations that prevail after prolonged intense exercise.
For extra credit
• Excessive secretion of glucocorticoids produces a collection of symptoms called Cushing’s syndrome. One of the symptoms is a redistribution of body fat, known as lipodystrophy.
• Protein and carbohydrate consumption after exercise can offset the cortisol response.
• High blood levels of glucocorticoids can stimulate gastric acid and pepsin production and may exacerbate ulcers.
• Cortisol levels can be up to 50% higher in animals under stress if alone (ie socially isolated).
• Estradiol increases the binding protein for cortisol so that circumstances associated with increased (pregnancy) or decreased (exercise induced amenorrhea and menopause) estradiol alters the amount of circulating free cortisol and its actions.
• Exercising in a depleted state can result in high levels of gluconeogenesis (protein breakdown).
Summary and recommendations
• Take regular, planned breaks from intense training
• Consume enough calories from non-processed foods to prevent depletion
• Get 7-9 hours of sleep per night to decrease stress and cortisol release
• Consume carbohydrates and protein after exercise sessions
• Don’t isolate yourself – spend time with friends and family
• Regularly participate in a stress-relieving activity like mild yoga or meditation
• Avoid excessive amounts of intense aerobic endurance training (unless training for endurance event)
References
Click here to view the information sources referenced in this article.
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3,353,919,710,446,689,300
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Top
10
Doctor insights on: Will Losing Weight Make Your Nose Slimmer
Share
1
1
Does the skin of your nose get thinner when losing weight?
Does the skin of your nose get thinner when losing weight?
Skin on nose: Not really. You may lose the fat that is under your skin, but there isn't much on your nose anyway. So i wouldn't worry about it. ...Read more
Dr. Heidi Fowler
1,932 doctors shared insights
Losing Weight (Definition)
Many people resolve to lose weight in the New Year for different reasons. For those who are overweight or obese, there are many health benefits to losing weight. It can help decrease your chances of developing diseases including diabetes, heart disease, high blood pressure, osteoarthritis, and even certain types of cancer. Low-calorie diets combined with increased physical activity are thought to be most effective long term. The healthiest weight loss regimen, therefore, is one that consists of making lifestyle changes that incorporate a balanced diet ...Read more
5
5
I'm loosing weight, finding dried up blood in my nose, and I have a cough, which is getting better. I don't smoke, so it can't be lung cancer, can it?
I'm loosing weight, finding dried up blood in my nose, and I have a cough, which is getting better. I don't smoke, so it can't be lung cancer, can it?
Very unlikely: From the information you provided the risk of lung cancer is minimal. You may try applying a small amount of an emollient in the nares. Do apply only small amount as you do not want the emollient to be inhaled. For good health - Have a diet rich in fresh vegetables, fruits, whole grains, milk and milk products, nuts, beans, legumes, lentils and small amounts of lean meats. Avoid saturated fats. Exercise at least 150 minutes/week and increase the intensity of exercise gradually. Do not use tobacco, alcohol, weed or street drugs in any form. Practice safe sex. ...Read more
9
9
I want to make my nose look slim but naturally?
I want to make my nose look slim but naturally?
Hmmm: There is no way to alter the shape of your nose significantly without surgery. We have adopted a variety of beauty standards in our culture that are arbitrary and in many cases unhealthy. My advice is to focus your attention on things that matter more than superficial external appearances. After all, do you really want someone to like you for the shape of your nose? ...Read more
See 1 more doctor answer
Dr. Jack Mutnick
1,167 doctors shared insights
Nasal (Definition)
NaSal is a nasal preparation which is a kind of ...Read more
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Molecular Vision 2012; 18:1361-1378 <http://www.molvis.org/molvis/v18/a142>
Received 24 July 2011 | Accepted 28 May 2012 | Published 31 May 2012
A novel in vitro three-dimensional retinoblastoma model for evaluating chemotherapeutic drugs
Moutushy Mitra,1 Chandana Mohanty,2 Anju Harilal,1 Uma K. Maheswari,3 Sanjeeb Kumar Sahoo,2 Subramanian Krishnakumar1
1Department of Ocular Pathology, Vision Research Foundation, Sankara Nethralaya, Tamil Nadu, India; 2Laboratory of Nanomedicine, Institute of Life Sciences, Chandrasekharpur, Bhubaneswar, India; 3CeNTAB, SASTRA University, Tanjore, India
Correspondence to: Subramanian Krishnakumar, Department of Ocular Pathology, Vision Research Foundation, Sankara Nethralaya, No. 18 college Road, Nungambakkam, Chennai – 600006, India; Phone: 91-44-28271616, ext 1302; FAX: 91-44-28254180; email: [email protected]
Abstract
Purpose: Novel strategies are being applied for creating better in vitro models that simulate in vivo conditions for testing the efficacy of anticancer drugs. In the present study we developed surface-engineered, large and porous, biodegradable, polymeric microparticles as a scaffold for three dimensional (3-D) growth of a Y79 retinoblastoma (RB) cell line. We evaluated the effect of three anticancer drugs in naïve and nanoparticle-loaded forms on a 3-D versus a two-dimensional (2-D) model. We also studied the influence of microparticles on extracellular matrix (ECM) synthesis and whole genome miRNA-gene expression profiling to identify 3D-responsive genes that are implicated in oncogenesis in RB cells.
Methods: Poly(D,L)-lactide-co-glycolide (PLGA) microparticles were prepared by the solvent evaporation method. RB cell line Y79 was grown alone or with PLGA–gelatin microparticles. Antiproliferative activity, drug diffusion, and cellular uptake were studied by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, a yellow tetrazole (MTT) assay, fluorescent microscope, and flow cytometry. Extra cellular matrix (ECM) synthesis was observed by collagenase assay and whole genome miRNA-microarray profiling by using an Agilent chip.
Results: With optimized composition of microparticles and cell culture conditions, an eightfold increase from the seeding density was achieved in 5 days of culture. The antiproliferative effect of the drugs in the 3-D model was significantly lower than in the 2-D suspension, which was evident from the 4.5 to 21.8 fold differences in their IC50 values. Using doxorubicin, the flow cytometry data demonstrated a 4.4 fold lower drug accumulation in the cells grown in the 3-D model at 4 h. The collagen content of the cells grown in the 3-D model was 2.3 fold greater than that of the cells grown in the 2-D model, suggesting greater synthesis of the extracellular matrix in the 3-D model as the extracellular matrix acted as a barrier to drug diffusion. The microarray and miRNA analysis showed changes in several genes and miRNA expression in cells grown in the 3-D model, which could also influence the environment and drug effects.
Conclusions: Our 3-D retinoblastoma model could be used in developing effective drugs based on a better understanding of the role of chemical, biologic, and physical parameters in the process of drug diffusion through the tumor mass, drug retention, and therapeutic outcome.
Introduction
A suitable three dimensional (3-D) culture system provides a more physiologically relevant approach to the analysis of gene function, regulation, and cell phenotype ex vivo [1]. It has previously been shown that engineering the cell culture micro-environment to create growth conditions that more accurately mimic the in vivo behavior of cells is an essential step for improving the predictive accuracy of the drug discovery process [2]. Evidence suggests that modification of cell growth conditions can radically influence the behavior of cells in response to chemical reagents [3]. Many important studies have been done on cell proliferation, differentiation, and function in vitro; however, experience with cells in a flat tissue culture flask is different from the complexities of tissues within the body. In tissues, cells connect to each other as well as to the extracellular matrix (ECM), which is a key regulator of normal homeostasis and tissue phenotype [1]. Receptor complexes on the surface of cells facilitate interactions with their neighbors, with the ECM, and with other exogenous factors to enable cells to interpret the multitude of biochemical and physical cues from the immediate environment. The metastatic potential of tumor cells is believed to be regulated by interactions between the tumor cells and their extracellular environment (i.e., ECM). These interactions can be modified by the accumulation of genetic changes and by the transient alterations in gene expression induced by the local tumor microenvironment [4]. Given this intricate mechanical and biochemical interplay; important biologic properties may be missed if cells are studied within an in vitro culture system [5]. It has also been suggested that many important signals, key regulators, and tissue phenotypes are lost when cells are cultured on substrates such as culture plates [6]. Therefore, developing an in vitro model of a tumor that in many aspects would resemble an actual tumor to obtain a realistic assessment of drug efficacy before their testing in animal models or patients is important [7]. Based on previous reports [7] we hypothesized that the cells grown with poly(D,L)-lactide-co-glycolide (PLGA)–gelatin microparticles behave differently than cells grown without PLGA–gelatin microparticles because of the structural, molecular, and genetic variations in cells grown in two different structural configurations. We selected three model anticancer drugs (doxorubicin, carboplatin, and etoposide), which are currently used in clinical practice for the treatment of retinoblastoma, and drug-loaded nanoparticles to determine the drug efficacy in both models. We studied drug diffusion and cellular uptake to understand the discrepancy in drug efficacy in cells grown with or without PLGA–gelatin microparticles. In addition we studied the influence of microparticles on ECM synthesis and whole genome miRNA-microarray profiling to identify 3-D-responsive genes that have been implicated in oncogenesis, survival, and growth of in vivo tumor.
Methods
Materials
PLGA (copolymer ratio 50:50, molecular weight [MW]=34,000 Da, inherent viscosity=0.41) was purchased from Birmingham polymers, Inc. (Birmingham, AL). Carboplatin, doxorubicin hydrochloride (DOXHCL), etoposide, polyvinyl alcohol (PVA; average MW 30,000–70,000 Da), BSA (fraction V), sucrose, chitosan from crab shells (85% deacetylated), and gelatin were purchased from Sigma-Aldrich (St. Louis, MO). All other chemicals used were of analytical grade obtained from Sigma-Aldrich. Media and fetal bovine serum (FBS) were purchased from Gibco-BRL (Rockville, MD). Y79 cells were cultured in RPMI 1640 medium (Biocolor Ltd, County Antrim, UK). The Sircol Soluble Collagen Assay kit was purchased from Biocolor Ltd. TRIZOL reagent was purchased from Invitrogen (Carlsbad, CA). TURBO DNase was purchased from Ambion (Genetix Biotech Asia Pvt. Ltd., New Delhi, India).
Preparation of different drug-loaded nanoparticles
Carboplatin-loaded nanoparticles-- Nanoparticles containing carboplatin (CNPs) were prepared as decribed by Parveen et al. [8]. Briefly, an aqueous solution of 2 ml sodium alginate (0.625 mg/ml) was added dropwise into 8 ml of chitosan solution (0.5 mg/ml dilute solution of HCl, with pH adjusted to approximately 5.5 with 0.1 M NaOH) containing carboplatin (1.25 mg). After overnight stirring of the emulsion, the CNPs were recovered by ultracentrifugation (Sorvall Ultraspeed Centrifuge; Kendro, Asheville, NC) at 30,000× g for 30 min at 4 °C. The nanoparticles were formed as a result of the interaction between negative groups of alginate and positively charged amino groups of chitosan. The pellets were dispersed in double-distilled water and lyophilized (LYPHLOCK 12; Labconco, Kansas City, MO) for 48 h and then stored at 4 °C for further studies.
Etoposide-loaded nanoparticles-- Etoposide-loaded nanoparticles (ENP) were formulated by using the single emulsion–solvent evaporation technique. In this method, etoposide (equivalent to 10% weight [w]/w dry weight of polymer) was dissolved in 3 ml organic solvent (chloroform) containing 90 mg of polymer (PLGA) to form a primary emulsion. The emulsion was further emulsified in an aqueous PVA solution (12 ml, 5% w/volume [v]) to form an oil-in-water emulsion. The emulsification was performed using a microtip probe sonicator (VC 505; Vibracell Sonics, Newton, CT) at 39 W of energy for 2 min in an ice bath. The emulsion was stirred using a magnetic stirrer overnight to evaporate the organic solvent. The resultant nanoparticles were ultracentrifuged at 125,000× g for 20 min at 4 °C with twice washing with double-distilled water to remove the excess amount of PVA and unencapsulated etoposide. The obtained particles were resuspended in double-distilled water and lyophilized for 48 h to obtain the powder form and then stored at 4 °C for further use.
Doxorubicin-loaded nanoparticles-- Doxorubicine-loaded nanoparticles (DNP) were prepared by using the single emulsion–solvent evaporation technique. In brief, a solution of 100 mg of PLGA polymer and 10 mg of doxorubicin (DOX) in 3 ml of 12.5% (v/v) methanol in chloroform solution was emulsified in 12 ml of 2% w/v aqueous solution of PVA to form an oil-in-water emulsion. The emulsification was performed using a microtip probe sonicator set at 55 W of energy output for 2 min over an ice bath. The emulsion was stirred overnight at room temperature on a magnetic stirring plate to allow evaporation of the organic solvent and formation of DNPs. DNPs were recovered by ultracentrifugation at 125,000× g for 20 min at 4 °C, washed twice with double-distilled water to remove unbound PVA and unencapsulated drug, and then lyophilized for 2 days to obtain the powdered DNPs. The lyophilized DNPs were stored at 4 °C until further use.
Formulation of gelatin microparticles
PLGA microparticles were prepared by the solvent evaporation method with slight modifications [9]. In brief, 800 μl of an aqueous phase (W1) was prepared with BSA (2.5% w/v), sucrose (10% w/v), chitosan (1.25% w/v), gelatin (5% w/ v), and PVA (5% w/v) and emulsified with polymer solution (O; 200 mg PLGA in 4 ml of dichloromethane), using an homogenizer (Biospec Product Inc., Bartlesville, OK) at 80× g to form an oil-in-water primary emulsion. The resultant primary emulsion was added dropwise into a 1% w/v aqueous solution of PVA containing 10% w/v sucrose (W2) under constant magnetic stirring on a stirring plate to form a multiple emulsion (W1/O/W2). The emulsion was stirred overnight on a magnetic stir plate to evaporate the organic solvent. The resultant microparticles were recovered by centrifugation at 15,000× g, washed three times with distilled water, and then lyophilized for 48 h the lyophilized microparticles were stored at 4 °C until further use.
Characterization of different drug-loaded nanoparticles
Mean particle size and size distribution of the different drug-loaded nanoparticles were determined by using a Malvern Zeta-sizer Nano ZS (Malvern Instrument, Malvern, Worcestershire, UK) based on quasi-elastic light scattering. Briefly, approximately 1 mg/ml of different formulations of the nanoparticle solutions were prepared in double-distilled water and sonicated for 30 s in an ice bath. Size measurements were performed in triplicate following the dilution (100 ml diluted to 1 ml) of the NP suspensions in MilliQ water at 25 °C. The Zeta potential was measured in the same instrument at 25 °C using the above protocol. All measurements were performed in triplicate.
Characterization of gelatin microparticles
The shape and surface morphology of gelatin microparticles were characterized by scanning electron microscopy (SEM, Hitachi S-3400N; Hitachi High-Technologies, Krefeld, Germany). The powdered microparticles were attached to a brass stub through double adhesive tape and were gold coated using a sputter gold coater at 20 KV (Hitachi, E-1010, Ion Sputter; Hitachi High-Technologies). The stub was fixed in a sample holder and placed in the vacuum chamber of the SEM (Hitachi S-3400N; Hitachi High-Technologies) and observed under low vacuum. The average particle diameters of microparticles were determined from the SEM picture.
Cell culture and cell seeding for gelatin microparticle composition optimization
Y79 cells RCB1645 were obtained from the RIKEN cell bank (Ibaraki, Japan) and maintained in RPMI-1640 media supplemented with 10% FBS and 1% penicillin streptomycin in T-75 cm2 flasks in an incubator (Thermo Electron Corporation, Asheville, NC) at 37 °C and 5% CO2. Fresh retinoblastoma tumor cells were isolated from RB-enucleated eyeballs (Vision Research Foundation, Sankara Nethralaya, Chennai, India) and cultured as described above. All samples were collected with the approval of the institutional review board at VRF (Vision Research Foundation) and in accordance with the Declaration of Helsinki. Each formulation of PLGA microparticles was weighed (approximately 2 mg/ml) and soaked for 3 h at 37 °C in 70% alcohol. Microparticles were centrifuged to remove alcohol and washed twice with media. Fifty percent FBS was added, and the solution was kept in a CO2 incubator for 3 h.
For studying the effects of microparticle composition on cell growth, 1 ml of the microparticle suspension prepared as above was transferred to separate wells of 6-well plates. The medium from each well was aspirated carefully, leaving microparticles in the wells before cell seeding. A 500-μl aliquot of Y79 cell suspension (1×106 cells/ml)/fresh RB cell suspension in RPMI 1640 medium was added directly onto microparticles in each well. After 3 h of incubation at 37 °C in a CO2 incubator, an additional 1.5 ml of medium was added to each well and cells were allowed to grow in the incubator. The medium was changed on alternate days, and cells were counted at 7 days post seeding to determine the effect of microparticle composition on Y79 cell growth. To study the total number of cells grown in gelatin microparticles, the adherence cells from a microparticle clump was recovered after 10 days of post seeding. Cell detachment was done by treating the microparticles with 1 ml of 0.1 M citrate buffer containing 0.1% crystal violet for 1 h at 37 °C. After detachment, the total number of cells grown with a different formulation of microparticles was counted separately using a hemocytometer. Photomicrographs of selected plates with cells attached to microparticles were taken with a phase-contrast inverted microscope fitted with a digital camera. The fluorescent images of Y79/RB cells labeled with CellTracker™ CM-DiI reagent (Molecular probes, Invitrogen, Bangalore, India) grown with the scaffold were captured.
Antiproliferative effects of anticancer drugs and drug-loaded nanoparticles
The antiproliferative effects of drugs, both in the native form and encapsulated inside nanoparticles, were analyzed using the methodology of Horning et al. [7]. For this study the Y79/RB cells were allowed to grow in a 2-D suspension (tissue culture-treated Petri dishes) and a 3-D model (in microparticles). The tissue culture-treated Petri dishes (100 mm×20 mm; #353003; Becton Dickson, Franklin Lakes, NJ) taken for the 2-D study provided more surface area for cells to grow without reaching confluency. For the 3-D model, nontissue culture Petri dishes (100 mm×15 mm; #08–757–13; Fisher Scientific, Mumbai, India) were used; these enabled better cellular attachment and growth onto microparticles compared to the surface of a Petri dish. Cell seeding in the case of the 2-D monolayer was performed the second day post seeding on microparticles at a cell density of 0.5×106 cells/ml. This protocol for cell seeding and growth was optimized to obtain approximately the same cell count in both sets of experiments at the time of drug treatment for a better comparison of drug efficacy. Three model anticancer drugs, i.e., doxorubicin, carboplatin and etoposide, were selected to determine their IC50 values in Y79/RB cells grown on 2-D as well as 3-D models. The chosen drugs are currently being used in the treatment of retinoblastoma and are well known DNA intercalating anticancer agent. For the cell toxicity study the stock solutions of drugs were prepared in DMSO and diluted appropriately in tissue culture medium to obtain the desired concentration [8]. Similarly, equivalent concentrations of drug encapsulated in nanoparticles (doxorubicin and etoposide in PLGA nanoparticles, carboplatin in chitosan nanoparticles) were prepared with RPMI medium. On day 5 of post seeding, media was carefully removed and replaced with 5 ml of media containing different concentrations of drugs and drug-loaded nanoparticles. After 48 h the treated cells (2-D and 3-D culture) were collected and filtered through 35 µm nylon mesh to separate cells from microparticles. The detached cells were stained using 0.4% (w/v) trypan blue in deionized water, and viable cells (unstained) were counted using a hemocytometer.
Collagen assay
Collagen content was assayed using the manufacturer’s protocol. Cells with/without PLGA–gelatin microparticles were suspended in PBS (137 mM NaCl, 2.7 mM KCl, 10 mM sodium phosphate dibasic, 2 mM potassium phosphate monobasic and a pH of 7.4). The preparations were centrifuged at 80× g using an Eppendorf microcentrifuge (5417R; Eppendorf-Netheler-Hinz-GmbH, Hamburg, Germany), and the sediment was treated with 1 ml of 0.5 M acetic acid for 18 h at 4 °C. One milliliter of the dye reagent supplied with the assay kit was added to 100 μl of the acid extract in 1.5 ml Eppendorf tubes and mixed gently for 30 min at room temperature. The collagen-bound dye complex was recovered after centrifugation at 7,800 ×g for 10 min as above. The complex was solubilized in 1 ml of the alkali reagent provided with the assay kit. The absorbance of the samples was measured at 550 nm using a microwell plate reader (Fisher Biotech, Pittsburgh, PA). A standard plot of collagen was prepared under similar conditions. Either microparticles without cells or PBS was used as controls. The amount of collagen present in the native microparticles was deduced from the actual collagen amounts obtained in 2-D and 3-D culture experiments. Therefore the there was no interference of the polymer used in microparticles in the assay.
Recovery of cells from poly(D,L)-lactide-co-glycolide–gelatin microparticles following freezing
To determine whether the cells grown in the 3-D model could be rescued after freezing, microparticles were seeded (seeding density) 0.5×106 cells/mg of microparticles) and cultured as above in noncell culture Petri dishes for 5 days. Cells with PLGA–gelatin microparticles were washed with RPMI-1640 medium, resuspended in 1 ml of cryopreservation media (DMSO, 10%; FBS, 90%), transferred into cryovials, and then frozen in liquid nitrogen. After 24 h of freezing, cells were thawed and the entire content of each cryovial was transferred into Petri dishes and recultured for 48 h in RPMI medium. Cells with PLGA–gelatin microparticles cultured as above for the same time period but not subjected to the freezing step, were used as the control. Cells cultured without PLGA–gelatin microparticles (0.5×106 cells/ml of cryopreservation media) were also frozen and recultured as above. Cell viability for each sample was determined using trypan blue as above. The percentages of cells with or without PLGA–gelatin microparticles rescued were calculated from the cell numbers with and without the freezing step.
Flow cytometry
Doxorubicin was used for this study because of its inherent fluorescent property. Fluorescent intensity as a measure of drug uptake by cells with or without PLGA–gelatin microparticles was determined using a FACSCalibur flow cytometer (Becton Dickson) at 488 nm excitation and a 585/42 filter (564–606 nm) to match the emission spectra of doxorubicin. On day 5 post seeding, media were carefully removed and 5 ml of doxorubicin solution (2,500 ng/ml) was added to each Petri dish and placed at 37 °C for 4 and 8 h each with triplicates. Cells were trypsinized from microparticles and monolayered as described above, centrifuged, and resuspended into a single cell suspension in DPBS + 2% FBS at concentrations of either 2×106 cells/ml or 1×106 cells/ml. The cell suspensions containing microparticles were filtered twice through a 35-μm nylon mesh tube cap into a 12×75 mm round-bottom tube (#352235; Becton Dickson) to remove microparticles from the cell suspension.
Oligonucleotide arrays
Total RNA used for the microarray analysis was isolated from cultured cells using TRIZOL reagent and treated with TURBO DNase to remove the DNA contamination. The RNA samples (10 μg each) in a 50-μl reaction were treated with 1 μl of TURBO DNase (2 U) in 1× TURBO DNase buffer at 37 °C for 30 min. After incubation, the RNA sample was extracted with phenol–chloroform to inactivate the TURBO DNase. Agilent's Low RNA Input Linear Amplification Kit PLUS (Agilent Technologies Genotypic, Bangalore, India) was used to generate fluorescent complementary RNA (cRNA). This method uses T7 RNA polymerase, which simultaneously amplifies the target material and incorporates cyanine 3-labeled cytidine tri-phosphate. Qiagen’s RNeasy mini spin columns (Qiagen, New Delhi, India) were used for purification of the amplified cRNA samples, and the samples were then hybridized to the Human Whole Genome 44K Oligo Microarray for 17 h at 65 °C, as recommended by the manufacturer (Agilent Technologies). Data analysis was done using Genespring GX version 10 (Agilent Technologies). Agilent Feature Extraction software (G25677AA; Agilent Technologies) was used to analyze the microarray data. Two biologic replicates were used for gene expression microarray analysis.
MicroRNA isolation and expression analysis
RNA extraction-- Total RNA was isolated using TRI-Reagent (Ambion, Austin, TX). RNA concentration and purity were quantified using a Nanodrop (Nanodrop, Santa Clara, CA) spectrophotometer with the nanodrop ribogreen assay, and the quality of the total RNA was determined on an Agilent bioanalyzer (Agilent, Santa Clara, CA).
MicroRNA array hybridization and detection-- Two biologic replicate samples were used for the miRNA microarray analysis. Human miRNA V2 8×15k Agilent arrays, which represent 723 human and 76 human viral miRNAs, were used for the miRNA analysis. Total RNA underwent phosphatase treatment. The 3′ end of the dephosphorylated RNA was ligated with one molecule of cyanine 3-cytidine bisphosphate (3-pCp), as this reagent selectively labels and hybridizes mature miRNAs with greater than 30% efficiency. A hybridization cocktail was added to the arrays, and hybridization was performed in the hybridization oven set at 55 °C for 20 h. The microarrays were washed using Agilent wash buffer. Scanning and extraction was performed using Agilent feature extraction software. The study was done in three biologic replicates. Data analysis was done using Genespring GX version 10. Agilent Feature Extraction software (G25677AA) was used to analyze the microarray data. The sum of background-subtracted signals for each repeated miRNA was calculated and log transformed to log base 2. The cut off was greater than 1 (log-transformed value) and less than 1 (log-transformed value).
Real-time quantitative reverse-transcriptase (RT)-PCR-- RNA was extracted by the guanidine isothiocyanate and chloroform method (TRI Reagent; Sigma-Aldrich, Bangalore, India). All RNA samples were treated with DNase (Turbo; Ambion, Genetix Biotech Asia Pvt. Ltd). For all samples, 1 μg of total RNA was used to synthesize first-strand cDNA with reverse transcriptase (SuperScript II; Invitrogen, Joyvel, Chennai, India) and random primers. The cDNA synthesis was performed at 37 °C for 60 min after heat inactivation at 95 °C for 10 min. The primer sequences of the selected genes from the microarray are listed in Table 1. PCR was performed using 1× SYBR Green PCR Master Mix (Applied Biosystems, Lab India, Chennai, India) on a real-time PCR system (Prism 7300; Applied Biosystems). Cycling conditions were as follows: 2 min at 50 °C, 10 min at 95 °C, and 40 cycles of 15 s at 95 °C, plus 1 min at 60 °C. Commercial software (SDS ver.2.3; Applied Biosystems) was used to calculate ΔΔCt relative expression values for all the genes studied, normalized to the GAPDH endogenous control.
Statistical analysis
The statistical analysis included the independent Student t test. Statistical analysis was performed using SPSS version 12.0 software (Chicago, IL). P values less than 0.05 were considered significant.
Results
Characterization of different drug-loaded nanoparticles
The size distribution and surface charge of different drug-loaded nanoparticles were measured by dynamic light scattering analysis. This study revealed that ENPs, CNPs, and DNPs have an average diameter of 256 nm, 507 nm, and 249 nm, respectively, as shown in Figure 1 and have an average Zeta potential of −13 mV, –36 mV, and −5.56 mV, respectively.
Formulation and characterization of poly(D,L)-lactide-co-glycolide microparticles
In the current study, we prepared a 3-D tumor model with PLGA–gelatin microparticles for in vitro evaluation of different anticancer drugs (native and loaded in nanoparticles). It was previously well documented that gelatin is a suitable candidate for scaffold materials because of its biocompatibility, low immunogenicity, and biodegradability. Gelatin contains Arg–Gly–Asp (RGD)-like sequences that promote cell adhesion and migration by forming a polyelectrolyte complex. Furthermore, the anionic cell surface provided by the gelatin–chitosan-blended microparticles provide better cell adhesion and cellular bioactivity for proliferating cells. A successful microparticle formulation was achieved with a highly porous matrix to facilitate the infiltration of proliferating cells. As evidenced from the SEM image, the formulated microparticle showed a porous infrastructure with interconnected void structures and had a spherical shape covered with a thin film of polymer (Figure 2). This rough surface could be due to deposition of cationic chitosan on the anionic microparticle surface, which is apparent from the surface characteristics [7]. Similarly, particle size is an important parameter that could affect the degradation of the polymer matrix [10]. To achieve a microparticle of a desired diameter, the conditions for emulsification and formulation composition were optimized. The average diameter of the formulated microparticle in this study ranged from 145 μm to 162 μm.
Effect of composition of the scaffold and influence of cell seeding density on Y79 cell growth
We studied the effect of gelatin concentration (used in microparticle composition) on the proliferation of Y79 cells. The Y79 growth kinetic results on the gelatin microparticle demonstrated that the composition of the formulated microparticle facilitated profound Y79 cell proliferation (Figure 3). It was further seen that the microparticles formulated with a higher gelatin content (5% w/v) demonstrated better cell growth than those formulated with a lower gelatin content (3% w/v; Figure 4). Therefore, PLGA microparticles fabricated with 5% gelatin were chosen as a suitable formulation for further studies.
The optimized composition of microparticles, which consisted of 5% gelatin and 1.25% chitosan, demonstrated cell growth from an initial seeding cell density of 0.05×106 to a cell density of 0.4×106 cells/mg of microparticles, which is an eightfold increase in cell density after 6 days of culture. Cells attached more to the microparticles rather than to the surface of the nontissue culture Petri dish. Initially, cells were seen attached to the microparticle surface, and with time cells engulfed the microparticles completely, forming a 3-D tumor-like structure (Figure 5A-C phase contrast and Figure 5D fluorescence-labeled Y79 cells). Either a single microparticle or a cluster of two to three microparticles were witnessed to form the 3-D tumor-like structure.
Extracellular matrix synthesis and retrieval of cells from a three-dimensional model following freezing
After 5 days of growth, cells in the 3-D model synthesized 59.8±1.2 µg of collagen per 1×106 cells, which was significantly higher than the 25.29±0.7 µg of collagen synthesized for the same number of cells in the 2-D monolayer (p<0.05, n=5). Following the freezing step, cell viability was slightly higher in the 3-D model compared to that in the 2-D monolayer (41% versus 35%; Figure 6).
Antiproliferative activity of drugs and drug-loaded nanoparticles on Y79 cells grown with or without a scaffold
Cytotoxicity of model anticancer drugs was determined in Y79/RB cells grown with or without PLGA–gelatin microparticles following 48 h of drug treatment. Cell numbers were similar in both models at the time of treatment, and the inhibition in cell growth was calculated according to the respective untreated controls. IC50 values of drugs and drug-loaded nanoparticles were significantly higher in Y79 cells with PLGA–gelatin microparticles than in cells grown without PLGA–gelatin microparticles (Figure 7). The differences in the IC50 values observed were 4.5 to 21.8 fold depending upon the drug and drug-loaded nanoparticles (Table 2). Similarly, we observed significantly higher IC50 values of native drugs in RB tumor cells with PLGA–gelatin microparticles compared to RB cells grown without PLGA–gelatin microparticles (Figure 7G-I). The differences in the IC50 values of native drugs in RB tumor cells observed were 2.4 to 13.4 fold (Table 2).
Drug uptake by cells with or without poly(D,L)-lactide-co-glycolide-gelatin microparticles
After treatment with doxorubicin (2,500 ng/ml), significantly fewer (p<0.05) cells with PLGA–gelatin microparticles exhibited drug uptake compared to cells grown without microparticles. The difference in fluorescence intensity was 4.4 fold at 4 h (Figure 8A), which increased to 15.9 fold at 24 h (Figure 8B).
Microarray analysis
Results of the cDNA microarray revealed changes in the expression of 4,490 genes (overexpression of 2,490 genes; downregulation of 2,000 genes) in cells grown with PLGA–gelatin microparticles compared to those grown without microparticles (Figure 9A). Only genes with p≤0.05 and a log ratio of at least 2.0 for upregulation (≥1 fold) and a log ratio of 0.5 for downregulation (≤0.5 fold), keeping a median log ratio of 1 in both biologic replicates, were considered for expression analysis [11]. The important upregulated (Table 3 and Table 4) and downregulated (Table 5) genes are provided. We classified the altered transcripts based on their biologic roles. The data also identified several candidate genes that are found to be highly overexpressed in retinoblastoma tumors and that keep tumors in a proliferation state, such as Homo sapiens v-myc myelocytomatosis viral-related oncogene (MYCN) [12,13], H. sapiens jun oncogene (Jun) [11], H. sapiens v-erb-b2 (ERBB3) [14], and H. sapiens insulin-like growth factor binding protein 5 (IGFBP5) [15]. We also found enhanced expression of collagen, integrins, fibronectin, and laminin, which crosslink and stiffen the tissue stroma to promote transformation, tumor growth, motility, and invasion and enhance cancer cell survival [16].
MicroRNA analysis
Results of the microRNA analysis revealed changes in the expression of 52 miRNAs (overexpression of 6 miRNAs; downregulation of 46 miRNAs) in cells grown with PLGA–gelatin microparticles compared to those grown without microparticles (Figure 9B). The important differentially regulated miRNAs are provided in Table 6. We classified the altered miRNAs based on their biologic roles (oncomirs and tumor suppressors). Our data has identified downregulated tumor suppressor miRNAs in cells with PLGA–gelatin microparticles, such as let-7 miRNAs (let-7 family) and miR-34a (which may enhance retinoblastoma tumor proliferation) [17,18] and miR-15a and miR-16, which have been implicated in cell-cycle control and apoptosis [19]. We also identified upregulated miRNAs, such as miR-198, which may play significant roles in regulating retinoblastoma tumor genesis [20]; miR-18a and miR-19b, which are upregulated in various carcinomas and increased expression of this cluster contributes to cancer formation [21]; and miR-106a, which is a potential biomarker in the diagnosis of gastric carcinoma [22].
Real-time quantitative RT–PCR
Seven upregulated genes-erythroblastic leukemia viral oncogene homolog 3(ERBB-3), B-cell leukemia/lymphoma 2 (BCL-2), v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (MYCN), ATP-binding cassette, sub-family C-member 6 (ABCC6), High mobility group AT-hook 2 (HMGA-2), Matrix metallopeptidase 9 (MMP-9), ATP-binding cassette, sub-family A-member 3 (ABCA-3) and four down-regulated genes- Cyclin-dependent kinase inhibitor 2A (CDKN-2), Cyclin-dependent kinase inhibitor 1A (CDKN-1A), Programmed cell death 2 (PDCD-2) and apoptotic peptidase activating factor 1 (APAF-1)-from the microarray data have been confirmed by real-time quantitative RT–PCR. The results are consistent with the microarray data. The fold changes of all the genes studied was only slightly higher when measured using quantitative RT–PCR compared to the microarray fold changes, reflecting the better dynamic range of quantitative RT–PCR (Figure 10).
Discussion
Owing to excellent biocompatibility and high mechanical strength, the biodegradable polyester PLGA has been frequently used (as biomaterial) for drug delivery systems as well as for tissue engineering applications. However, due to its hydrophobic properties it is difficult to wet the microparticles (constituent of PLGA) in cell culture medium and hence this limits the adhesion of proliferating cells [7,23]. To circumvent this problem, our formulated microparticles were coated with a hydrophilic polymer of natural origin, i.e., gelatin. Further, with a view to promoting better cell adhesion, we incorporated PVA in the internal phase of the primary emulsion. Here, the amphiphilic PVA could anchor at the interface of the microparticle with its hydrophobic portion embedded in the PLGA matrix structure and its hydrophilic portion available for hydration in the cell culture media [7,24]. Furthermore, the anchored PVA can provide functional OH groups, which have been reported as being helpful in cell attachment [25]. Beside PVA, another polymer—chitosan—was incorporated in the internal matrix structure for better cell growth of cultured cells in our formulated microparticles. Here, chitosan can support cell attachment owing to its chemical structure resembling glycosaminoglycans, which is abundant in extracellular matrix components [26]. Similarly, sucrose was added (in the internal phase of the primary emulsion sucrose) to increase the surface tension of water [27]. Formation of larger water droplets upon leaching out can generate more porous microparticles, which in turn provided more surface area to promote cell adhesion, proliferation, and growth, as found in our study.
Tumor progression ensues within a 3-D microenvironment, and the metastatic potential of tumor cells is believed to be regulated by interactions between the tumor cells and their extracellular environment (i.e., ECM). These interactions can be modified by the accumulation of genetic changes and by the transient alterations in gene expression induced by the local tumor microenvironment, which consists of cellular and noncellular components. Noncellular aspects of the tumor microenvironment, such as ECM, have been shown to influence tumor progression either directly by destabilizing tissue integrity and promoting tumor cell motility, invasion, and survival [28] or indirectly by inducing tumor angiogenesis and enhancing tumor cell survival and selection [29,30]. 3-D tumor models using different substrates, such as Matrigel [31], laminin-rich extracellular matrix [1], irradiated HeLa cells [32], or teflon membrane [33,34], have been developed to study the various aspects of, for example, tumor biology, phenotypic alterations, and invasive and migratory behavior of cells. Y79 cells when grown on porous microparticles tend to synthesize extracellular matrix proteins, such as collagens (including type I and III) and fibronectin, which together contribute to the mechanical strength of the tissue. Collagenase assay analysis also showed significantly higher collagen synthesis by Y79 cells grown on microparticles. It is known that in tumor masses not all cancer cells are exposed to the same concentration of drugs because of poor drug diffusion through the extracellular matrix of the tumor [35]; this causes the tumor to relapse or develop drug resistance [8]. Our study also demonstrated significantly slow diffusion and heterogeneous distribution of drugs and drugs encapsulated in nanoparticles in the cells grown on PLGA–gelatin microparticles compared to cells grown without. The important application of our study will be to predict the efficacy of drugs in vivo. Our study also reports significant genomic variations in the cells when grown with porous microparticles. Enhanced expression of the collagen family members laminin and fibronectin were observed in our study, which strongly supports our initial findings. In response to collagen synthesis, we observed increased expression of matrix metalloproteinases (MMPs), such as MMP-13 [36] and MMP-9 [37,38], the latter facilitates the tumor cells to invade the extracellular matrix. Several candidate genes, such as MYCN, ERBB3, JUN, and IGFBP5, were also significantly upregulated, which keeps the tumor in a proliferative state [11-15].
Changes in the upregulation of genes were coupled with downregulation of a few genes that function as tumor suppressor/apoptotic inducers. Homo sapiens APAF-1, transcript variant 3, mRNA (Apaf-1) is a central component of the intrinsic pathway of apoptosis and is important for cellular responses to DNA damage [39]. When DNA is damaged by chemotherapeutic agents, oncogenic stimuli, ultraviolet and ionizing radiation, and hypoxia, cytochrome c is released from the mitochondria, binds to Apaf-1 in the cytosol, and in association with dATP/ATP facilitates a conformational change of Apaf-1 to expose its CARD domain [40]. It has been shown that inactivation of Apaf-1 substantially reduces the number of cells required to form tumors in nude mice transplanted with Myc/Ras-transformed fibroblasts, implying that Apaf-1 actually acts as a tumor suppressor [41]. Homo sapiens cyclin-dependent kinase inhibitor 2A (CDKN2A; melanoma, p16, inhibits CDK4), a major CDK inhibitor, is the product of a tumor-suppressor gene that has been found inactivated in different cancer types. CDK inhibitor p21 (CDKN1A) is induced by both p53-dependent and p53-independent mechanisms following stress, and induction of p21 may cause cell-cycle arrest; as a proliferation inhibitor, p21 is poised to play an important role in preventing tumor development [42]. This notion is supported by data indicating that p21 null mice are more prone to spontaneous and induced tumorigenesis and that p21 synergizes with other tumor suppressors to protect against tumor progression in mice. Homo sapiens programmed cell death 2 (PDCD2), transcript variant 1, mRNA promotes apoptosis in several human lymphomas. Repression of PDCD2 expression by BCL6, which in turn leads to downregulation of apoptosis, is one mechanism involved in BCL6-associated lymphomatous transformation [43].
MicroRNAs are short (20–23 nucleotides in length) noncoding RNAs that mediate coordinated cellular programs by posttranscriptional mRNA silencing and protein translation inhibition [44]. A growing number of miRNAs have been implicated in promoting or suppressing tumorigenesis in a variety of tissues [45,46], suggesting that they may play a role as a novel class of oncogenes or tumor suppressor genes. Our study revealed alterations in miRNA expression when a Y79 cell line is grown with microparticles.
We observed enhanced expression of oncogenic microRNAs, such as miR-18a, miR-19b [47], miR-106a [22], and miR-198 [20], which subsequently promote proliferation, inhibit apoptosis, and promote tumor angiogenesis. There was also decreased expression in miRNAs, such as let-7 family [48], miR 15a and miR16–1 [49], and miR 34a [50] which act as tumor suppressors in various carcinomas, including retinoblastoma. Let-7 downregulates oncogenes, such as Ras, Myc, and HMGA2, and inhibits proliferation and tumorigenesis when ectopically expressed [51].
In this study, we fabricated porous microparticles with a composite interface containing PLGA and chitosan, which causes cancer cells to develop into a tumor-like structure in vitro. The drug efficacy was significantly lower in cells grown with microparticles than in cells grown without microparticles, suggesting a role of cellular architecture on drug uptake, distribution, and efficacy. Our tumor model could potentially be applicable in developing effective drugs based on a better understanding of the role of chemical, biologic, and physical parameters in the process of drug diffusion through the tumor mass, drug retention, and therapeutic outcome. A correlation between the drug effects seen in the tumor model to the in vivo efficacy would further establish the usefulness of our model in drug discovery. In conclusion, we developed a novel, retinoblastoma, in vitro, 3-D model that could be used for evaluating chemotherapeutic drugs in the future.
Acknowledgments
We thank Department of Biotechnology (DBT), Govt. of India (grant No. BT/PR7968/MED/14/1206/2006), for the financial support and the core laboratory technical staff, Vision Research Foundation for the flow cytometry technical help.
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Skip to main content
Feasibility and adherence to moderate intensity cardiovascular fitness training following stroke: a pilot randomized controlled trial
Abstract
Background
Stroke is a leading cause of disability worldwide and the cardiovascular fitness levels of stroke survivors are diminished to an extent that impairs functioning and activities of daily living performance. While cardiovascular training seems an empirically appropriate intervention, the optimal dosage and intensity of cardiovascular training in stroke survivors remains unclear. The aim was to determine the safety and feasibility of moderate-intensity cardiovascular training following stroke, including measurement of adherence to training.
Methods
A pilot, prospective, patient- and assessor-blinded randomised controlled trial conducted in a tertiary, metropolitan hospital-based community rehabilitation centre. Eligibility criteria included ambulant (> 100 m), 6 weeks-12 months post stroke. Moderate-intensity fitness training or control (low-intensity) exercise was offered biweekly for 12 weeks. Outcome measures included adverse events, peak oxygen uptake (VO2), functional exercise capacity (6-Minute Walk Test, 10-m Walk Test) and health-related quality of life (Short Form-36) and mood (Patient Health Questionnaire, PHQ9).
Results
Feasibility: Seventy-one (50%) of 141 screened participants were eligible (29% did not agree to participate). Twenty participants (10 intervention, 10 control) were recruited. The median (%; IQR) supervised sessions was 19.5 (81%; 12, 20); and 20 (83%; 19, 22) in the intervention and control groups, respectively. Progression of duration and intensity was limited; mean of 10 sessions to achieve target duration (30 min). There were no adverse events. Baseline peak oxygen uptake (VO2) levels were low (15.94 ml/kg/min). Significant improvements in VO2 peak in both groups were observed (p < 0.05). Although there were no significant between-group differences, this feasibility trial was not powered to detect change.
Conclusions
Moderate-intensity fitness training was safe but achievement of target duration and intensity was challenging for stroke survivors. A definitive adequately-powered randomised trial is required. Alternative fitness training protocols may need to be explored.
Trial registration
The trial protocol was prospectively registered on the Australian New Zealand Clinical Trials Registry (ACTRN 12613000822785) on 25/07/2013.
Peer Review reports
Background
Stroke is a leading cause of disability [1, 2] with more than half of stroke survivors requiring assistance with daily living activities [3] and one-third affected by post-stroke depression [4]. Sedentary behaviour is highly prevalent (> 77%) in people after stroke [1]. While physical inactivity is an independent risk factor for stroke [5], moderate-intensity exercise may have a protective effect against subsequent stroke and vascular events [6].
Cardiorespiratory fitness, measured as peak oxygen uptake (VO2 peak), has been estimated at 8 to 22 ml.kg.min following stroke; between 26 and 87% of age and gender-matched normative levels [7,8,9]. Such values fall below or just surpass the minimum aerobic capacity required for independent living (15 and 18 mL.kg.min for women, and men, respectively) [8, 10]. The presence of very low cardiorespiratory fitness following stroke is likely to contribute to disability and dependence.
Meta-analyses demonstrate cardiorespiratory training improves fitness, walking speed and endurance in stroke survivors [7, 11, 12], whilst efficacy on mood and quality of life (QOL) has not been established [12]. International guidelines for the general and post-stroke population recommend 30 min of moderate-intensity aerobic activity (40–59% heart rate reserve) on most days of the week [13,14,15]. However, a recent Cochrane review found an ‘optimal dosage for the content of training for people with stroke has yet to be established’ [12]. Actual dosages achieved by stroke survivors (rather than dosage prescribed) has been under-reported in previous studies [7, 12] which may limit analysis of dose-response [16].
This pilot study aimed to inform the design of a future adequately-powered randomized controlled trial (RCT), with the following specific objectives: 1) evaluate the feasibility of recruitment and trial procedures; 2) evaluate the safety and feasibility of implementation of the recommended CV training dosage, including actual achievement of target dosage in clinical practice, in addition to usual care, and 3) estimate preliminary effect of moderate-intensity CV training, compared to a low intensity, on CV fitness (defined as VO2 peak), walking speed and endurance, QOL and depression.
Methods
Trial design, setting and location
This study was an investigator-initiated, pragmatic, patient- and assessor-blinded, parallel group pilot randomised controlled trial. The study was conducted in a community-based rehabilitation (CBR) service of a tertiary, metropolitan hospital (Sunshine Hospital, Melbourne, Australia), during the period October 2013 to May 2016, with follow-up completed in August 2016.
Ethics and consent statement
The institutional review board approved the study (Melbourne Health HREC Project number: 2013.105). The trial protocol was prospectively registered on the Australian New Zealand Clinical Trials Registry (ACTRN 12613000822785) and reported according to the Consolidated Standards of Reporting Trials (CONSORT) statement and extensions for a pragmatic non-pharmacological intervention trial [17, 18], and the TIDieR checklist [19], with pilot study design guidance obtained from previous publications [20, 21].
Written informed consent was provided by all participants. Informed consent was sought using accredited interpreters for participants with a non-English speaking background.
Participants
A convenience sample of 20 participants was recruited. Eligible participants were aged 18 years and over; diagnosed with stroke (ischaemic or haemorrhagic) within the past 6 weeks (minimum) to 12 months (maximum) and able to walk at least 100 m (with or without aids or standby supervision). Key exclusion criteria (for full list, see Supplemental File 1) included pregnancy; documented medical restrictions to CV training; unstable cardiovascular, metabolic and renal co-morbidities and inability to physically participate in a cycle ergometry test (safely mount and cycle stationary exercise bike at 50 rpm (RPM)).
Procedure
Physiotherapists screened all people with stroke attending CBR for eligibility. Potential participants underwent medical screening against the inclusion/exclusion criteria with a neurology physician prior to inclusion and randomisation. Patients underwent a battery of initial outcome measures in the week following recruitment (prior to randomization), and then attended the relevant 12-week protocol at CBR depending on randomization. Outcome measures were repeated after the 12-week training program.
Interventions
Table 1 outlines the intervention and control protocols.
Table 1 Description of intervention and usual care groups
The intervention was a 12-week progressive fitness training program designed according to ACSM guidelines [13, 22], with participants aiming to progress to a total of five 30-min sessions per week of moderate-intensity (40–59% heart rate reserve) CV exercise. Individualised target heart rate (THR) was calculated each session using the Karvonen method, reflecting the rate of energy expenditure during physical activity more accurately than other prescription methods [13]. See Supplemental File 2 for additional intervention progression detail. Physiotherapists with at least 2 years’ experience with a neurology population were trained to deliver the standardised CV fitness training intervention. Attendance (or reason for non-attendance), duration achieved, adherence to target heart rate/intensity and adverse events were recorded.
The control protocol was a low-intensity ‘conventional exercise program’; designed to mimic standard stroke rehabilitation, previously shown to be conducted at low intensity (< 40% heart rate reserve (HRR)) [23, 24], and aimed to match total contact time in both groups with duration progressed from weeks 1–12. Five minutes (maximum) of low intensity exercise on a stationary bike was included to limit a cycle familiarisation effect on testing for the intervention group. Exercise selection was based on individual patient’s functional capacity. Heart rate and BORG-RPE were monitored every 5 min to ensure participants maintained low intensity exercise (calculated each session with Karvonen method). If HR exceeded low intensity, a seated rest was taken for heart rate to return below 40% HRR. Physiotherapists or allied health assistants delivered the control protocol.
Both groups were prescribed a home exercise program (HEP, see Supplemental File 3), incorporated to reduce reliance on clinical resources, where two centre-based sessions were deemed to be clinically feasible based on usual capacity of community rehabilitation service resources. Participants in both groups continued usual care rehabilitation (i.e. physiotherapy, excluding fitness training, and multidisciplinary allied health) at the discretion of the treating clinicians. No modification of interventions occurred during course of study.
Randomisation
The randomisation sequence was computer generated by a research team member (who did not participate in group assignment of enrolled participants), using a random numbers table in Microsoft Excel with a 1:1 allocation ratio, to the intervention or standard care (control) group. The participant allocation sequence was sealed in individual, consecutively numbered opaque envelopes. The investigators randomised participants following baseline assessment by opening the envelopes in sequential order according to recruitment date. Randomisation was stratified by beta blocker use (Yes/No), to ensure equal numbers of patients in both groups, to avoid skewing results based on beta-blocker status.
Blinding
Participants were informed that they would receive one of two different exercise interventions with the intent to blind participants to group allocation. Intervention and control group participants were not present in the gym at the same time. The neurology medical team (who assessed for medical suitability and stroke severity), outcome assessors and statisticians were blinded to group assignment. It was not possible to blind therapists who provided the intervention or control protocol.
Demographic descriptive data
Baseline demographic data were collected including age, gender, time since stroke, type of stroke (ischaemic or haemorrhagic), and beta-blocker usage. Stroke severity was assessed by a blinded neurology physician using the National Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS). Both scales are reliable and valid measures in stroke survivors [25, 26]. Accredited interpreters were used for participants with a non-English speaking background to conduct outcome measurement and intervention.
Feasibility, safety & adverse events
Feasibility was assessed by reporting eligibility and consent rates; the proportion of outcome measure completion, attendance, retention, and adherence to training protocols. Safety during outcome measurement or intervention/control protocols was assessed by the occurrence of any adverse events, which included falls, cardiac, respiratory, or new neurological abnormalities, and new musculoskeletal pain.
Clinical outcome measurement
The following outcomes were measured at baseline and following completion of the 12-week intervention:
Cardiorespiratory Fitness (VO2 Peak) - Graded Exercise Test (GXT)
Measurement of maximum oxygen uptake (VO2max) is the gold standard for determining cardiorespiratory fitness [13]. However, in clinical populations (including stroke), peak oxygen update (VO2 peak, the highest VO2 attained during incremental exercise before symptoms or safety criteria result in termination of testing) is preferred [8, 27].
A graded exercise test (GXT) was conducted to determine VO2 peak, according to ACSM guidelines [13], on an electronically braked upright cycle (Monark) ergometer with a 12 lead electrocardiogram (ECG; Mortara) continuously monitoring heart rate (see Supplemental File 4).
Functional exercise capacity (6MWT, 10MWT)
The Six-Minute Walk Test (6MWT) is a reliable and valid measure of functional exercise capacity and walking ability following stroke, with a minimum detectable change of 54.1 m [28]. Testing was conducted with standardised instructions [29]. The distance walked (metres) within 6-min was recorded. The 10-m walk test (10MWT) has excellent test-retest reliability (ICC =0.95 to 0.99) and validity in the stroke population [30] and was used to assess fast and self-selected walking speed. Testing was conducted with standardised instructions and time taken to walk the middle 10 m of a 14 m walkway was recorded. The best result of three tests was taken and converted to velocity (metres per second).
Health-related quality of life and mood
Health-related quality of life was assessed with the Short Form-36 (SF-36), Australian version, Version 2 [31, 32], and mood was assessed using the English-language version of the Patient Health Questionnaire (PHQ-9), a 9-item scale (total scores range from 0 to 27), recommended as a screening tool for post stroke depression [4], see Supplemental File 5.
Statistical analysis
Feasibility, adverse events and outcome measure completion rates were calculated using simple count and proportion data. Statistical analysis was performed by a statistician blinded to group assignment using SPSS Statistics™ Version 22.0.0.0 (IBM Corporation, Armonk, NY, USA). All data are presented as median (IQR) or mean (SD) unless otherwise specified. Normality of distributions was assessed using the Kolmogorov-Smirnov statistic. Missing data were ignored and no data were imputed. As this was a pilot trial, no interim analyses were planned, and no stopping guidelines were implemented based on prior existence of safety data.
Where appropriate according to distribution, independent and paired t-tests were used to analyze parametric differences over time between and within group respectively and non-normally distributed data were analyzed using the Mann-Whitney U for independent samples and Wilcoxon-signed ranks tests for dependent group data. p < 0.05 was accepted as statistical significance. Cohen’s effect size was calculated and interpreted within-group from baseline to follow-up; and between-group on change scores (interpreted as 0.4 or less = small; 0.5 = moderate and 0.8 = large) [33]. Estimated sample sizes for a future adequately powered RCT design were estimated using G*Power (Version 3.1.9.2, Universität Düsseldorf, Düsseldorf, Germany) [34].
Results
Screening, eligibility and recruitment rates
One-hundred and forty-one patients were screened to recruit 20 participants (Fig. 1). Sixty-nine (49%) were excluded on criteria, and 41 (29%) did not consent to participation.
Fig. 1
figure 1
CONSORT Diagram
Five patients who consented were excluded: two were not medically cleared, and three withdrew prior to randomisation (see Table 2 for full list of reasons for exclusion).
Table 2 List of reasons for exclusion
Participant demographics
Demographic and other characteristic data are summarized in Table 3. Eighteen (90%) of recruited participants were male, and all four patients with haemorrhagic stroke who were recruited were randomised only to the intervention group. Baseline stroke severity assessed using the NIHSS showed six participants with moderately severe impairment (NIHSS 5–14) and 13 with mild impairment (NIHSS < 5) [n = 1 missed]. Most participants were in the sub-acute phase post stroke, with 16 (80%) recruited within 6 months; nine (45%) of these within 3 months following stroke. The intervention group were recruited significantly earlier (p = 0.02) and had a higher proportion of left sided lesions (p = 0.03). There were no other statistically significant differences in baseline demographics between groups.
Table 3 Demographic and clinical details of the cohort. Data are mean (SD) unless otherwise specified
There were no statistically significant differences in baseline performance measures (Table 4), although the intervention group had a trend to higher, but non-significant, baseline VO2 peak (17.5 ml/kg/min (2.9)) compared with control (14.4 ml/kg/min (3.7), p = 0.06) (Table 4). Using the cut-off score of ≥10 on the PHQ-9, three (30%) participants in each group had a score suggestive of depressive illness at baseline.
Table 4 Pre and post data, mean (SD) unless otherwise specified
Outcome measure completion rates
Outcome measure completion rates were high (Table 4). VO2 peak was calculated for 18 participants: one participant’s baseline gas exchange data was not included due to calibration issues resulting in physiologically impossible values; one participant became claustrophobic during the warm-up and was unable to tolerate the spirometry mouthpiece at baseline; follow up was not attempted. The most common reason for test termination was reaching a BORG-RPE > 17, achieved in 11 participants at baseline and eight post intervention. Other reasons for termination included inability to maintain adequate pedaling cadence and requesting to stop. Fifteen (83%) participants at baseline, and 17 (94%) post, recorded peak RER greater than 1.10. One participant was lost to follow up for walking measures and questionnaires.
Retention and attendance
Nineteen participants completed the 12-week program (9 intervention, 10 control). One intervention group participant withdrew after seven sessions due to self-reported worsening of lower limb dystonia. The median (%; IQR) number of attended sessions was 19.5 (81%; 12, 20); and 20 (83%; 19, 22) in the intervention and control groups, respectively. Illness, including inpatient admission for co-morbid conditions, was the primary reason for non-attendance.
Intervention delivery
Intervention group training parameters are detailed in Supplemental File 6. All intervention participants could undertake moderate-intensity (40–59% HRR) CV training. The primary mode of fitness training was upright stationary bike, followed by treadmill, recumbent bike, stepper, cross trainer, repetitive step ups or stair climbing, and arm ergometer.
Progression to the target training duration (30 min) was gradual, requiring a mean of 10 (range 6–19) sessions. The mean (SD) duration at target heart rate was 21.5 (7.9) minutes across the 12-week trial. This increased to a mean 27.8 (4.4) minutes in the final 4 weeks of the trial. The protocol required 30-min training duration before increasing intensity and as such, peak intensities achieved were relatively modest: two participants achieved 55% HRR, three 50% HRR, one 45% HRR and three remained at 40% HRR. The one participant who withdrew did not progress beyond 40% HRR.
Weekly home exercise data collection sheets, including a tick box section for participants to indicate adherence, were inadequately completed and returned. This limited accurate recording or analysis of home exercise adherence.
Adverse events and safety
No adverse events were reported during testing or training sessions in either group. One participant presented with tachycardia before training and did not commence the session; subsequent medical clearance from their cardiologist was sought and granted to continue trial participation. One VO2 peak testing session was postponed (and successfully rescheduled for 1 week later) as the participant recorded a low blood sugar level on the day of testing.
Usual care
Both groups were comparable in usual care physiotherapy attendance (median (IQR): intervention 10.5 (5, 22); control 10.5 (3, 22)). All participants were involved with at least one other allied health discipline (median 2.5, range 1, 8); with 10 participants (50%) involved with at least four disciplines including physiotherapy (Supplemental File 7).
Cohort outcomes and effect sizes
Both groups recorded statistically significant improvements in mean VO2 peak (intervention 2.6 ml/kg/min, p < 0.02; control 3.0 ml/kg/min, p < 0.01) from baseline to follow-up, but there were no differences between groups. Both groups also experienced statistically significant improvements in peak watts across the study period (p < 0.05, Supplemental File 8). Mood and SF-36 mental component summary (MCS) score improved significantly in the control group (Table 4). See Supplemental File 9 for all SF-36 domain results. The proportion of participants with PHQ9 scores ≥10 (depressive illness) at follow-up was 1/10 (10%) and 0/9 (0%) in the intervention and control group respectively.
There were no statistically significant differences between the groups for mean change in any outcome measure (Table 5). There were no between-group differences in peak watts (control 14.0 (12.6), intervention 21.2 (12.5); mean difference [95% CI] 7.2 [− 4.6, 19.0], p = 0.22). Effect sizes were generally small, though the estimates were imprecise with large confidence intervals (Tables 4 and 5). The largest between-group effect size point estimates in change scores were seen for the SF-36 MCS and PHQ-9, in favour of the control group; and the 6MWT in favour of the intervention group (Table 5). Estimated sample sizes per group for a future RCT are included in Supplemental File 10.
Table 5 Change scores and effect sizes, mean (SD) unless otherwise specified
Discussion
This pilot study demonstrated the implementation of moderate-intensity CV fitness training following stroke was safe in addition to usual care, in our sample, in a hospital-outpatient rehabilitation setting. Supervised-session attendance was good and comparable to previous studies (72% (7) and 65–100% (12)), demonstrating most enrolled participants were willing to engage in fitness training. Outcome measurement was feasible, including aerobic graded exercise testing. Whilst it has been suggested that exercise testing is often terminated for non-cardiopulmonary reasons following stroke [35], the achievement of RER > 1.10 in 84% of tests shows near maximal effort was attained by most participants, with 1.0 previously suggested as reasonable criterion for maximum effort in the stroke population [27]. However, challenges were identified: lower than expected recruitment rates, and achievement of the recommended CV training dosage (30 min, 5 days/week) across the 12-week trial.
Eligibility and consent rates were low. This could be partly attributed to the usual prevalence of co-morbidities, and contraindications to peak aerobic testing, in the post-stroke population [13, 36]. With appropriate medical supervision, future pilot studies could test the safety of relaxing the inclusion criteria to peak aerobic testing, given the paradox in the prohibition of those who potentially have most to benefit from participating in cardiovascular training either in research or practice. Frequently, reasons cited for non-consent were consistent with previously identified barriers to post-stroke exercise participation: access factors (transport and inability to drive); health problems; and, stroke-related impairments [37]. Although funding of transport costs may be beneficial to facilitate recruitment, such low consent rates raise concern about patient and family perceptions of fitness training following stroke, which warrants further qualitative investigation [37]. It is noteworthy that the enrolled sample comprised a high proportion of male participants (90%), compared with the Australian stroke population (55%) [38] and our screened sample (65%). Alternative trial designs (adaptive clinical trials [39, 40], stepped wedge [41, 42]) could be considered to facilitate the feasibility of trial conduct and acquittal, as well as strategies to ensure appropriate representation of women.
This trial demonstrates a gap between guideline recommendations and actual intervention delivery. Progression of training duration was slow (mean 10 sessions/5 weeks to reach 30 min) in the recruited cohort of stroke survivors, who had very poor baseline fitness levels [13], below those previously recorded in community ambulatory stroke survivors [43]. This limited training volumes achieved (21 min mean duration at target HR) across the 12-week training period. Similarly, previous studies reporting actual dosage achieved by stroke survivors, as opposed to prescribed dose, found mean durations limited to 15 to 25 min at THR over 4 to 19-weeks [44, 45]. Of note, 88% of participants in this trial reached 30 min and the actual dosage achieved in the final 4 weeks was a mean duration (at THR) of 27.8 (4.4) minutes. This demonstrates most of the stroke survivor cohort did reach the target duration parameters but required a lengthy adaptation period.
Furthermore, intensity progression was modest (only 50% reached or exceeded 50% HRR). Following the ACSM guidelines, which recommend achievement of target duration prior to intensity progression [13], meant participants could not maintain previously achieved durations if intensity was increased. Variable intensity achievement (peak THR) has been previously reported: mean of 48–54% HRR [44]; 80% exceeded 50% HRR [45]; 30% of participants unable to progress beyond 40% HRR, whilst 70% achieved over 50% HRR [35]; however, it is unclear if these protocols required the achievement of requisite duration prior to progressing intensity. Improved reporting of adherence to aerobic training programs is needed in future trials [12, 16].
It is logical that stroke-related impairments and low cardiovascular fitness impair stroke survivors’ ability to physically achieve target training parameters. Our results suggest adherence to training frequency may also play a role: the three participants unable to progress intensity (> 40%HRR) attended less than 70% of centre-based sessions, two of which did not achieve the target 30-min session duration. The primary reason for non-attendance (illness) reflects a cohort of patients where co-morbidities and stroke sequelae limit consistent participation in fitness training, which may subsequently hinder training progression. It is unknown if poor compliance with recording the home exercise sessions corresponded to poor home exercise adherence, and thus training frequency, but this is likely. In this study, both groups received similar encouragement and training to complete their HEP, as typically done in clinical practice, and it would be useful for further research to evaluate methods of improving home exercise program adherence.
Since the commencement of this trial, exercise recommendations in stroke survivors have been revised, maintaining the aim of 20–60 min’ duration, but acknowledging that multiple short bouts of moderate intensity exercise repeated throughout the day may be better tolerated than aiming to achieve duration targets in a single session (as evidenced by our trial) [46, 47]. Interval training, including high intensity, is feasible in stroke survivors [44, 48, 49], and warrants further investigation as a method of enabling duration and intensity achievements in the post-stroke population [16].
Both groups experienced statistically significant improvements in VO2 peak, which were comparable to meta-analyses [7, 12, 50]. VO2 peak at follow-up exceeded the requirement for independent living [10] in the intervention group only, although the control group baseline VO2 peak was lower (non-significant). Improvements in the control group suggest aerobic benefit may be derived from lower volumes or intensities than predicted (fitness gains with intensities as low as 30% HRR have been demonstrated in the deconditioned cardiac population [51]). However, this is not supported by pooled meta-analyses which identified higher training intensity and higher baseline VO2 peak as the only factors significantly associated with greater improvements in aerobic capacity following stroke [16, 50].
Further research is required to understand both the minimum volume of training for effect in stroke survivors, particularly in those with very low baseline fitness; and to determine dose-response-intensity relationships, to elicit the most effective methods of restoring cardiovascular fitness in the post-stroke population, to benefit function, and reduce risk of further events [46]. Furthermore, to accurately test the target training dosage, the inclusion of an adaptation/conditioning period should be considered in future trials to meet minimum dosage requirements before proceeding to efficacy evaluation. However, the feasibility of sustained implementation of prolonged, supervised training programs in routine clinical practice is limited and highlights the need to further explore strategies to optimise adherence to the recommended frequency (5 days/week), including regular home or community-based fitness training [52]. Funding wearable activity-tracking technology devices or smartphone apps for accurate recording and analysis of home exercise adherence (including intensity and duration) could be considered in future trials [53].
The small sample size limited the estimate of intervention effect; usual in a pilot trial where the primary aim is to ascertain feasibility [21]. There were no statistically-significant between group differences and effect sizes were generally small, however it is likely the theoretical effect of moderate-intensity fitness training was underestimated as most participants were only able to reach the recommended training volume for the latter part of the trial [12]. Whilst our active control group minimized bias by providing equal exposure time, the regular extra exercise duration, albeit of a low intensity, may have elicited an improvement in fitness in these participants with low baseline fitness levels [12]. The ‘active’ control protocol was designed to mimic the prevailing model of care, however, given the modest progression of intensity in the intervention group, there was unexpectedly little separation in training intensity between groups, and this is an important issue that must be considered in the design of future adequately-powered RCTs, although as acknowledged recently by Saunders and colleagues, it is possible that engagement in exercise which is regular and progressive is the more important intervention, than prescription of precise intensity [12].
The control group did experience significant improvements in mood. However, half of the control group received clinical psychology during their rehabilitation (compared to 30% of the intervention group). Given the dynamic natural history of post-stroke depression [4], future trials should consider relevant covariates and co-interventions in adjustment of results in the primary outcome.
Limitations
As this is a pilot study, data of effect should be considered as demonstration of feasibility only, and not indicative of true effect, for which an adequately-powered RCT would be required. Use of age-predicted maximum heart rate to calculate exercise intensity as a percent of heart rate reserve, rather than actual maximum heart rate, may contribute to challenges in intensity achievement, although no intervention participants were taking beta-blockers, which can result in lower than expected maximum heart rates, heart rate response to exercise, or both [54].
Budget limitations prevented funding for transport, dedicated staffing for enrollment and sophisticated data collection methods for home exercise adherence. This study did not aim to test feasibility of CV training in patients who were aphasic, non-ambulant or within six-weekspost-stroke. Recent research has shown early aerobic exercise (commencing at 6 days after stroke) is feasible [9]. Future studies could consider earlier implementation of intervention, particularly indicated given training adaptation periods demonstrated in this trial; however, the AVERT trial suggests that high-dose intervention in the first 24 h following stroke may not be beneficial [55].
Conclusions
A protocolised moderate-intensity cardiovascular fitness training program was safe in stroke survivors, in addition to usual care. VO2 peak significantly improved in both groups, who had very low baseline fitness. There were no between group differences, however progression of training parameters was slow, subsequently limiting the overall dosage provided. A large RCT with power to make significant conclusions about the impact of moderate-intensity CV training program on the defined outcomes is now required; alternative protocols and dose-response relationships could also be trialled for feasibility to determine the most effective training method to improve functional capacity and limit the risk of stroke recurrence.
Availability of data and materials
All data and materials (including Participant Information and Consent Forms) available from corresponding or senior author (on reasonable request).
All authors, external and internal, had full access to all data (including statistical reports and tables) in the study and can take responsibility for the integrity of the data and the accuracy of the data analysis.
Abbreviations
6MWT:
Six minute walk test
10MWT:
Ten metre walk test
ACSM:
American College of Sports Medicine
CBR:
Community-based rehabilitation
CONSORT:
Consolidated Standards of Reporting Trials
CV:
Cardiovascular
ECG:
Electrocardiogram
GXT:
Graded exercise test
HEP:
Home exercise program
HREC:
Human Research Ethics Committee
HRR:
Heart rate reserve
ICC:
Intraclass correlation coefficient
IQR:
Inter-quartile range
MCS:
Mental Component Summary score (of the SF 36)
mRS:
Modified Rankin scale
NIHSS:
National Institutes of Health Stroke Scale
PCS:
Physical Component Summary score (of the SF 36)
PHQ-9:
Patient Health Questionnaire
QOL:
Quality of life
RCT:
Randomized controlled trial
RER:
Respiratory exchange ratio
RPE:
Rating of perceived exertion
SD:
Standard deviation
SF36:
Short Form 36
THR:
Target heart rate
VO2 :
Peak oxygen uptake
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Acknowledgements
The authors would like to acknowledge Professor Andrew Stewart, Associate Professor Itamar Levinger, Professor Remco Polman and Dr. Toby Cumming for their assistance in study design. The authors also acknowledge the following physiotherapy staff for their contribution to data collection and intervention delivery (alphabetical order): Katharine Bennett, Erin Bicknell, Mia Carrick, Apoorva Charukonda, Tammy Dinh, Dannielle Grioli, Avetta Malcolm, Vanessa Mayes, Rohan McBean, Diana Myers and Jake Whitford. The authors acknowledge Associate Professor Cathy Said for manuscript review.
Funding
This work was funded by the Australian Institute of Musculoskeletal Science (AIMSS) and supported in-kind by the Community-Based Rehabilitation and Physiotherapy Departments of Western Health. The funding body had no role in the conception/design of the study, data collection, analysis or interpretation, or the writing/approval of the manuscript.
Author information
Authors and Affiliations
Authors
Contributions
All authors approved the final manuscript. HR was involved in the conception and design of the study, recruitment, data collection, data analysis and interpretation, completed the initial draft of the manuscript and reviewed the manuscript for intellectual content. SS was involved in the conception and design of the study, recruitment, data collection, data analysis and interpretation, and reviewed the manuscript for intellectual content. JT was involved in the conception and design of the study, recruitment, data analysis and interpretation, and reviewed the manuscript for intellectual content. SE was involved in recruitment, data collection, data analysis and interpretation, and reviewed the manuscript for intellectual content. EH was involved in study design, data collection and interpretation and reviewed the manuscript for intellectual content. AH was involved in study design, data collection and interpretation and reviewed the manuscript for intellectual content. TW was involved in study design, recruitment and data collection and reviewed the manuscript for intellectual content. ES was involved in study design, recruitment, data analysis and interpretation and reviewed the manuscript for intellectual content.
Corresponding author
Correspondence to Elizabeth H. Skinner.
Ethics declarations
Ethics approval and consent to participate
The institutional ethical review board approved the study (Melbourne Health HREC Project number: 2013.105). Written informed consent for participation including dissemination of findings (publication, presentation) was provided by all participants. Informed consent was sought using accredited interpreters for participants with a non-English speaking background.
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Not applicable.
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The authors have no competing interests to declare.
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Supplementary Information
Additional file 1: Supplemental File 1.
Full list of inclusion and exclusion criteria. Supplemental File 2. Additional Intervention (Exercise) Progression Details. Supplemental File 3. Home Exercise Program Details. Supplemental File 4. VO2 Peak Graded Exercise Testing Procedure. Supplemental File 5. Additional detail on SF-36 and PHQ-9.Supplemental File 6. Training parameters achieved in centre-based sessions. Supplemental File 7. Other allied health intervention by group (n, %). Supplemental File 8. Peak Wattage Pre-Post.Supplemental File 9.SF-36 domains pre-post within groups for both intervention and control groups. Supplemental File 10. Estimated sample size calculation for future RCT.
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Reynolds, H., Steinfort, S., Tillyard, J. et al. Feasibility and adherence to moderate intensity cardiovascular fitness training following stroke: a pilot randomized controlled trial. BMC Neurol 21, 132 (2021). https://doi.org/10.1186/s12883-021-02052-8
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• DOI: https://doi.org/10.1186/s12883-021-02052-8
Keywords
• Stroke
• Aerobic exercise
• Physical fitness
• Mood
• Randomized controlled trial
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5eff3d1f6f98e57329caed0ceb9053d3
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629,361,700,566,412,300
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grant
Novel, high-throutyput platform for rapid identification, quantintation, differential diagnosis, and resistance testing [ 2006 - 2008 ]
Also known as: Rapid quantified differential diagnosis and resistance for influenza
Research Grant
[Cite as http://purl.org/au-research/grants/nhmrc/402870]
Researchers: Prof Jonathan Iredell (Principal investigator) , Dr Belinda Herring Mr Bruce Harrison Prof Alison Kesson Prof Dominic Dwyer
View all 7 related researchers
Brief description This proposal utilizes a newly invented process (multiplex tandem polymerase chain reaction, MT-PCR) to measure multiple (up to 100) genetic targets (eg RNA or DNA) in one sample. A range of different virus and bacterial genes can be detected, including those which make the influenza virus different (eg H1N1 or H5N1) and allow it to bypass vaccine immunity or resist drug therapy (due to neuraminidase inhibitor resistance). We will simultaneously target infections which are influenza-like (ILI) or which might make influenza infection worse (eg staphylococcal pneumonia) as well as their resistance genes (eg MRSA). The test is rapid and automated and includes a specimen processing (DNA and RNA extraction) function that is being developed in parallel. We expect to be able to conduct high-throughput screening of multiple samples for a limited number of targets or conduct multiple tests on fewer specimens, simply by adjusting assay configuration. Measurement of the rise and fall in concentrations of influenza virus in infected persons will allow us to understand when they are no longer infectious to others, to predict when they are getting better or worse, and allow us to better understand the pattern of illness in people who are immunized against influenza or on drug therapy, or are in some other special category (eg immune compromise due to organ transplantation). While this will be able to be rolled out by our industry partners in the event of an influenza pandemic, it does not require an outbreak for successful development, and has value well beyond influenza diagnosis.
Funding Amount $AUD 333,362.07
Funding Scheme NHMRC Strategic Awards
Notes Urgent Research - Pandemic Influenza - H5N1
Click to explore relationships graph
Identifiers
Viewed: [[ro.stat.viewed]]
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5eff3d1f6f98e57329caed0ceb9053d3
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2,889,503,324,308,451,000
|
A Closer Look At Orthotic Technologies And Modifications
Author(s):
Guest Clinical Editor: Lawrence Huppin, DPM
Dr. Volpe does heat molding for prominences and also performs occasional gluing or top cover modifications. However, he does few modifications in the office aside from quick, minor adjustments. He also feels there is better quality control if an orthotic lab makes the modification.
Q: What materials and equipment do you keep in the office for orthotic modifications?
A: In his office, Dr. Kirby uses 1/8- and 1/4-inch of adhesive felt, 1/4-inch of Korex and neoprene insole material for foot orthosis modifications. Drs. Kirby and Volpe use grinders, barge cement and several sizes of metatarsal pads. In addition, Dr. Volpe keeps a heat gun, some top covers and soft tissue supplements, basic add-ons and metatarsal pads in his office.
Dr. Huppin uses 1/8-inch of soft ethylene vinyl acetate (EVA), a long-lasting cover material which he says is easy to work with, conforms to the deepest heel cups and cuts cleanly to provide a professional look to the orthosis. He also uses the FumeBuster fume filtration system (Purex), which he says vacuums fumes into a charcoal filter, eliminating barge odors.
Q: When writing an orthotic prescription, what are the most important concepts to consider to achieve the best clinical outcomes?
A: Dr. Huppin says the most important factor is the patient’s presenting pathology. First, one should determine the etiology of the pathology and base the orthotic prescription on those findings. For example, if the patient has plantar fasciitis, Dr. Huppin says the goal with functional orthotic therapy is decreasing tension in the plantar fascia. Plantar fascial tension increases when the foot lengthens, whether it is due to an everted heel or an everted forefoot, according to Dr. Huppin. If the plantar fasciitis appears to be caused by an everted heel, Dr. Huppin says he might use a deep heel cup and a medial skive. If it is due to an everted forefoot, he may prescribe a reverse Morton’s extension.
Likewise, Dr. Kirby emphasizes the importance of tailoring orthotics to individual foot types, taking into account differing structure and function.
“Far too many podiatrists are lazy in their orthosis prescribing habits. They basically order the same orthosis design for each patient, somehow expecting that the arch support they are creating for their patient will ‘magically’ have an effect on their patient’s foot so his or her symptoms will improve,” says Dr. Kirby.
Dr. Volpe initially performs a static biomechanical evaluation and follows this with a dynamic gait assessment. After making a diagnosis, he suggests DPMs should weigh the diagnosis, the existence of biomechanical and other comorbidities, consider what they want the orthotic to accomplish, and then write a prescription that will best meet that patient’s goals. Dr. Volpe emphasizes considering the patient’s shoe gear as well.
Q: What is the role of computerized foot pressure analysis systems in prescribing foot orthoses?
A: Dr. Huppin cautions DPMs to take a critical look at pressure analysis products and carefully evaluate the claims of the companies that sell them. He says pressure analysis can play a vital role in prescribing orthotics. Systems like the F-Scan (Tekscan) provide information on pressure distribution and force/time curves that can help an experienced practitioner write orthotic prescriptions and adjust orthoses, according to Dr. Huppin.
Dr. Kirby cites the best pressure analysis devices as the F-Scan, RSscan (RSscan) and Emed (Novel) systems. He says each system has advantages and disadvantages as far as sensor accuracy, software for computer analysis, ease of setup and price. Although he does not use those particular systems, he has followed technological advances in the pressure analysis area and believes those devices improve every year. Dr. Kirby says those who use such products can utilize the devices’ objective data to enhance their outcomes with orthotics.
Add new comment
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1.
PLoS Pathog ; 16(12): e1008893, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33326490
RESUMO
Bacterial bloodstream infections (BSI) are a major health concern and can cause up to 40% mortality. Pseudomonas aeruginosa BSI is often of nosocomial origin and is associated with a particularly poor prognosis. The mechanism of bacterial persistence in blood is still largely unknown. Here, we analyzed the behavior of a cohort of clinical and laboratory Pseudomonas aeruginosa strains in human blood. In this specific environment, complement was the main defensive mechanism, acting either by direct bacterial lysis or by opsonophagocytosis, which required recognition by immune cells. We found highly variable survival rates for different strains in blood, whatever their origin, serotype, or the nature of their secreted toxins (ExoS, ExoU or ExlA) and despite their detection by immune cells. We identified and characterized a complement-tolerant subpopulation of bacterial cells that we named "evaders". Evaders shared some features with bacterial persisters, which tolerate antibiotic treatment. Notably, in bi-phasic killing curves, the evaders represented 0.1-0.001% of the initial bacterial load and displayed transient tolerance. However, the evaders are not dormant and require active metabolism to persist in blood. We detected the evaders for five other major human pathogens: Acinetobacter baumannii, Burkholderia multivorans, enteroaggregative Escherichia coli, Klebsiella pneumoniae, and Yersinia enterocolitica. Thus, the evaders could allow the pathogen to persist within the bloodstream, and may be the cause of fatal bacteremia or dissemination, in particular in the absence of effective antibiotic treatments.
Assuntos
Infecções Bacterianas/sangue , Infecções Bacterianas/imunologia , Ativação do Complemento/imunologia , Acinetobacter baumannii/crescimento & desenvolvimento , Acinetobacter baumannii/patogenicidade , Bacteriemia/sangue , Bacteriemia/imunologia , Bacteriemia/microbiologia , Bactérias , Burkholderia/crescimento & desenvolvimento , Burkholderia/patogenicidade , Proteínas do Sistema Complemento/imunologia , Escherichia coli/crescimento & desenvolvimento , Escherichia coli/patogenicidade , Humanos , Klebsiella pneumoniae/crescimento & desenvolvimento , Klebsiella pneumoniae/patogenicidade , Testes de Sensibilidade Microbiana , Infecções por Pseudomonas/sangue , Infecções por Pseudomonas/imunologia , Infecções por Pseudomonas/microbiologia , Pseudomonas aeruginosa/crescimento & desenvolvimento , Pseudomonas aeruginosa/patogenicidade , Yersinia enterocolitica/crescimento & desenvolvimento , Yersinia enterocolitica/patogenicidade
2.
Nat Rev Rheumatol ; 16(10): 581-589, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32733003
RESUMO
Reports of widespread thromboses and disseminated intravascular coagulation (DIC) in patients with coronavirus disease 19 (COVID-19) have been rapidly increasing in number. Key features of this disorder include a lack of bleeding risk, only mildly low platelet counts, elevated plasma fibrinogen levels, and detection of both severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and complement components in regions of thrombotic microangiopathy (TMA). This disorder is not typical DIC. Rather, it might be more similar to complement-mediated TMA syndromes, which are well known to rheumatologists who care for patients with severe systemic lupus erythematosus or catastrophic antiphospholipid syndrome. This perspective has critical implications for treatment. Anticoagulation and antiviral agents are standard treatments for DIC but are gravely insufficient for any of the TMA disorders that involve disorders of complement. Mediators of TMA syndromes overlap with those released in cytokine storm, suggesting close connections between ineffective immune responses to SARS-CoV-2, severe pneumonia and life-threatening microangiopathy.
Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/complicações , Pneumonia Viral/complicações , Trombose/imunologia , Anticoagulantes/uso terapêutico , Antivirais/uso terapêutico , Proteínas do Sistema Complemento/imunologia , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/virologia , Citocinas/imunologia , Coagulação Intravascular Disseminada/tratamento farmacológico , Coagulação Intravascular Disseminada/imunologia , Coagulação Intravascular Disseminada/patologia , Coagulação Intravascular Disseminada/virologia , Fibrinogênio/análise , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Imunossupressores/uso terapêutico , Pandemias , Troca Plasmática/métodos , Contagem de Plaquetas/métodos , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Pneumonia Viral/virologia , Fatores de Risco , Trombose/tratamento farmacológico , Trombose/patologia , Trombose/virologia , Microangiopatias Trombóticas/tratamento farmacológico , Microangiopatias Trombóticas/imunologia , Microangiopatias Trombóticas/patologia , Microangiopatias Trombóticas/virologia
4.
PLoS Pathog ; 16(8): e1008754, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32776975
RESUMO
Arbovirus infection of Aedes aegypti salivary glands (SGs) determines transmission. However, there is a dearth of knowledge on SG immunity. Here, we characterized SG immune response to dengue, Zika and chikungunya viruses using high-throughput transcriptomics. We also describe a transcriptomic response associated to apoptosis, blood-feeding and lipid metabolism. The three viruses differentially regulate components of Toll, Immune deficiency (IMD) and c-Jun N- terminal Kinase (JNK) pathways. However, silencing of the Toll and IMD pathway components showed variable effects on SG infection by each virus. In contrast, regulation of the JNK pathway produced consistent responses in both SGs and midgut. Infection by the three viruses increased with depletion of the activator Kayak and decreased with depletion of the negative regulator Puckered. Virus-induced JNK pathway regulates the complement factor, Thioester containing protein-20 (TEP20), and the apoptosis activator, Dronc, in SGs. Individual and co-silencing of these genes demonstrate their antiviral effects and that both may function together. Co-silencing either TEP20 or Dronc with Puckered annihilates JNK pathway antiviral effect. Upon infection in SGs, TEP20 induces antimicrobial peptides (AMPs), while Dronc is required for apoptosis independently of TEP20. In conclusion, we revealed the broad antiviral function of JNK pathway in SGs and showed that it is mediated by a TEP20 complement and Dronc-induced apoptosis response. These results expand our understanding of the immune arsenal that blocks arbovirus transmission.
Assuntos
Aedes/imunologia , Apoptose , Febre de Chikungunya/imunologia , Proteínas do Sistema Complemento/imunologia , Dengue/imunologia , Sistema de Sinalização das MAP Quinases , Glândulas Salivares/imunologia , Infecção por Zika virus/imunologia , Aedes/virologia , Animais , Febre de Chikungunya/metabolismo , Febre de Chikungunya/prevenção & controle , Febre de Chikungunya/virologia , Vírus Chikungunya/imunologia , Proteínas do Sistema Complemento/metabolismo , Dengue/metabolismo , Dengue/prevenção & controle , Dengue/virologia , Vírus da Dengue/imunologia , Feminino , Interações Hospedeiro-Patógeno , Proteínas de Insetos/genética , Proteínas de Insetos/metabolismo , Insetos Vetores/imunologia , Insetos Vetores/virologia , Glândulas Salivares/virologia , Transcriptoma , Replicação Viral , Zika virus/imunologia , Infecção por Zika virus/metabolismo , Infecção por Zika virus/prevenção & controle , Infecção por Zika virus/virologia
6.
Molecules ; 25(12)2020 Jun 26.
Artigo em Inglês | MEDLINE | ID: mdl-32604797
RESUMO
Viruses can be spread from one person to another; therefore, they may cause disorders in many people, sometimes leading to epidemics and even pandemics. New, previously unstudied viruses and some specific mutant or recombinant variants of known viruses constantly appear. An example is a variant of coronaviruses (CoV) causing severe acute respiratory syndrome (SARS), named SARS-CoV-2. Some antiviral drugs, such as remdesivir as well as antiretroviral drugs including darunavir, lopinavir, and ritonavir are suggested to be effective in treating disorders caused by SARS-CoV-2. There are data on the utilization of antiretroviral drugs against SARS-CoV-2. Since there are many studies aimed at the identification of the molecular mechanisms of human immunodeficiency virus type 1 (HIV-1) infection and the development of novel therapeutic approaches against HIV-1, we used HIV-1 for our case study to identify possible molecular pathways shared by SARS-CoV-2 and HIV-1. We applied a text and data mining workflow and identified a list of 46 targets, which can be essential for the development of infections caused by SARS-CoV-2 and HIV-1. We show that SARS-CoV-2 and HIV-1 share some molecular pathways involved in inflammation, immune response, cell cycle regulation.
Assuntos
Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/metabolismo , Mineração de Dados/métodos , Infecções por HIV/epidemiologia , Infecções por HIV/metabolismo , Interações Hospedeiro-Patógeno/imunologia , Pandemias , Pneumonia Viral/epidemiologia , Pneumonia Viral/metabolismo , Anti-Inflamatórios/uso terapêutico , Antígenos de Diferenciação/genética , Antígenos de Diferenciação/imunologia , Antivirais/uso terapêutico , Betacoronavirus/efeitos dos fármacos , Betacoronavirus/imunologia , Betacoronavirus/patogenicidade , Proteínas do Sistema Complemento/genética , Proteínas do Sistema Complemento/imunologia , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/imunologia , Bases de Dados Genéticas , Regulação da Expressão Gênica , Infecções por HIV/tratamento farmacológico , Infecções por HIV/imunologia , HIV-1/efeitos dos fármacos , HIV-1/imunologia , HIV-1/patogenicidade , Interações Hospedeiro-Patógeno/efeitos dos fármacos , Interações Hospedeiro-Patógeno/genética , Humanos , Imunidade Inata/efeitos dos fármacos , Fatores Imunológicos/uso terapêutico , Inflamação , Interferons/genética , Interferons/imunologia , Interleucinas/genética , Interleucinas/imunologia , Redes e Vias Metabólicas/efeitos dos fármacos , Redes e Vias Metabólicas/genética , Redes e Vias Metabólicas/imunologia , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/imunologia , Proteínas Repressoras/genética , Proteínas Repressoras/imunologia , Transdução de Sinais , Receptores Toll-Like/genética , Receptores Toll-Like/imunologia , Ubiquitina-Proteína Ligases/genética , Ubiquitina-Proteína Ligases/imunologia
7.
PLoS One ; 15(6): e0234934, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32569286
RESUMO
BACKGROUND: Studies on adriamycin mice model suggest complement system is activated and together with IgM contributes to the glomerular injury of primary focal segmental glomerulosclerosis (FSGS). We recently reported primary FSGS patients with IgM and C3 deposition showed unfavorable therapeutic responses and worse renal outcomes. Here we examined the plasma and urinary complement profile of patients with primary FSGS, aiming to investigate the complement participation in FSGS pathogenesis. METHODS: Seventy patients with biopsy-proven primary FSGS were enrolled. The plasma and urinary levels of C3a, C5a, soluble C5b-9, C4d, C1q, MBL, and Bb were determined by commercial ELISA kits. RESULTS: The levels of C3a, C5a and C5b-9 in plasma and urine of FSGS patients were significantly higher than those in normal controls. The plasma and urinary levels of C5b-9 were positively correlated with urinary protein, renal dysfunction and interstitial fibrosis. The plasma C5a levels were positively correlated with the proportion of segmental sclerotic glomeruli. The urinary levels of Bb were elevated, positively correlated with C3a and C5b-9 levels, renal dysfunction, and interstitial fibrosis. The plasma C1q level was significantly decreased, and negatively correlated with urinary protein excretion. Urinary Bb level was a risk factor for no remission (HR = 3.348, 95% CI 1.264-8.870, P = 0.015) and ESRD (HR = 2.323, 95% CI 1.222-4.418, P = 0.010). CONCLUSION: In conclusion, our results identified the systemic activation of complement in human primary FSGS, possibly via the classical and alternative pathway. The activation of complement system was partly associated with the clinical manifestations, kidney pathological damage, and renal outcomes.
Assuntos
Ativação do Complemento/imunologia , Proteínas do Sistema Complemento , Glomerulosclerose Segmentar e Focal/imunologia , Glomérulos Renais , Adulto , Biomarcadores/sangue , Biomarcadores/urina , Proteínas do Sistema Complemento/imunologia , Proteínas do Sistema Complemento/urina , Feminino , Humanos , Glomérulos Renais/imunologia , Glomérulos Renais/lesões , Masculino , Pessoa de Meia-Idade , Adulto Jovem
9.
Sci Rep ; 10(1): 7787, 2020 05 08.
Artigo em Inglês | MEDLINE | ID: mdl-32385381
RESUMO
Idiopathic pulmonary fibrosis (IPF) is a lung parenchymal disease of unknown cause usually occurring in older adults. It is a chronic and progressive condition with poor prognosis and diagnosis is largely clinical. Currently, there exist few biomarkers that can predict patient outcome or response to therapies. Together with lack of markers, the need for novel markers for the detection and monitoring of IPF, is paramount. We have performed label-free plasma proteomics of thirty six individuals, 17 of which had confirmed IPF. Proteomics data was analyzed by volcano plot, hierarchical clustering, Partial-least square discriminant analysis (PLS-DA) and Ingenuity pathway analysis. Univariate and multivariate statistical analysis overlap identified haptoglobin-related protein as a possible marker of IPF when compared to control samples (Area under the curve 0.851, ROC-analysis). LXR/RXR activation and complement activation pathways were enriched in t-test significant proteins and oxidative regulators, complement proteins and protease inhibitors were enriched in PLS-DA significant proteins. Our pilot study points towards aberrations in complement activation and oxidative damage in IPF patients and provides haptoglobin-related protein as a new candidate biomarker of IPF.
Assuntos
Proteínas Sanguíneas , Proteínas do Sistema Complemento/imunologia , Haptoglobinas/metabolismo , Fibrose Pulmonar Idiopática/imunologia , Fibrose Pulmonar Idiopática/metabolismo , Estresse Oxidativo , Proteômica , Transdução de Sinais , Idoso , Biomarcadores , Estudos de Casos e Controles , Proteínas do Sistema Complemento/metabolismo , Biologia Computacional/métodos , Feminino , Humanos , Fibrose Pulmonar Idiopática/patologia , Masculino , Proteoma , Proteômica/métodos , Curva ROC
10.
Cell Host Microbe ; 27(6): 863-869, 2020 06 10.
Artigo em Inglês | MEDLINE | ID: mdl-32464098
RESUMO
The coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 has had devastating global impacts and will continue to have dramatic effects on public health for years to come. A better understanding of the immune response to SARS-CoV-2 will be critical for the application and development of therapeutics. The degree to which the innate immune response confers protection or induces pathogenesis through a dysregulated immune response remains unclear. In this review, we discuss what is known about the role of the innate immune system during SARS-CoV-2 infection, suggest directions for future studies, and evaluate proposed COVID-19 immunomodulating therapeutics.
Assuntos
Infecções por Coronavirus/imunologia , Imunidade Inata , Pneumonia Viral/imunologia , Proteínas do Sistema Complemento/imunologia , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/patologia , Citocinas/imunologia , Humanos , Células Matadoras Naturais/imunologia , Células Mieloides/imunologia , Pandemias , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/patologia
12.
PLoS One ; 15(4): e0231655, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32325480
RESUMO
Despite the potential for the chemokine class as therapeutic targets in immune mediated disease, success has been limited. Many chemokines can bind to multiple receptors and many receptors have multiple ligands, with few exceptions. One of those exceptions is CCL20, which exclusively pairs to CCR6 and is associated with several immunologic conditions, thus providing a promising therapeutic target. Following successful evaluation in a single dose, first time in human clinical study, GSK3050002-a humanized IgG1 monoclonal antibody against human CCL20-was evaluated in a 26-week cynomolgus monkey toxicology study. A high incidence of unexpected vascular and organ inflammation was observed microscopically, leading to the decision to halt clinical development. Here we report a dose-responsive increase in the incidence and severity of inflammation in multiple organs from monkeys receiving 30 and 300 mg/kg/week by either subcutaneous or intravenous injection. Histomorphological changes resembled an immune complex-mediated pathology, which is often due to formation of anti-drug antibodies in monkeys receiving a human protein therapeutic and thus not predictive of clinical outcome. However, the presentation was atypical in that there was a clear dose response with a very high incidence of inflammation with a low incidence of ADA that did not correlate well individually. Additionally, the immunohistologic presentation was atypical in that the severity and distribution of tissue inflammation was greater than the numbers of associated immune complexes (i.e., granular deposits). An extensive ex vivo analysis of large molecular weight protein complexes in monkey serum from this study and in human serum samples demonstrated a time-dependent aggregation of GSK3050002, that was not predicted by in vitro assays. The aggregates also contained complement components. These findings support the hypothesis that immune complexes of drug aggregates, not necessarily including anti-drug antibodies, can fix complement, accumulate over time, and trigger immune complex disease. A situation which may have increased clinical relevance than typical anti-drug antibody-associated immune complex disease in monkeys administered human antibody proteins.
Assuntos
Anticorpos Monoclonais Humanizados/uso terapêutico , Anticorpos Monoclonais/uso terapêutico , Quimiocina CCL20/imunologia , Proteínas do Sistema Complemento/imunologia , Doenças do Complexo Imune/tratamento farmacológico , Doenças do Complexo Imune/imunologia , Imunoconjugados/uso terapêutico , Animais , Anticorpos Monoclonais/toxicidade , Doença Crônica , Cristalização , Determinação de Ponto Final , Feminino , Humanos , Inflamação/imunologia , Inflamação/patologia , Macaca fascicularis
13.
Pathologe ; 41(3): 238-247, 2020 May.
Artigo em Alemão | MEDLINE | ID: mdl-32240352
RESUMO
Increasing interest in the role of the complement system in systemic and renal disease is based on new pathophysiological and therapeutic insights of the recent past and particularly in genetic analyses in children with atypical hemolytic uremic syndrome (aHUS). aHUS is the prototypical systemic disease associated with excessive activation of the alternative complement pathway and manifests in the kidney, but also in other organs as thrombotic microangiopathy (TMA). Pathomechanisms discovered to induce the overactivation of the alternative complement pathway in aHUS led to the first successful therapeutic application of a C5b9 inhibitor. This suppression of the terminal complement cascade succeeded in inhibiting local tissue damage. Thereafter, thanks to advanced modern technologies, further systemic and renal diseases associated with mutations or auto-antibodies targeting the complement pathway were identified. Hereby, disease onset is frequently associated with an additional trigger, e.g. infection or hormonal alterations/imbalances, against the background of a pre-existing predisposition of the patient.Due to the growing understanding of the regulation, and thus the possibility of therapeutic modulation of the different complement pathways, and due to the increasing availability of a variety of drugs inhibiting the complement system, interest in complement-mediated systemic and renal disease has been steadily increasing, making it a "hot-topic" in medicine in recent years.
Assuntos
Síndrome Hemolítico-Urêmica Atípica/imunologia , Ativação do Complemento , Proteínas do Sistema Complemento/imunologia , Nefropatias/imunologia , Criança , Humanos , Microangiopatias Trombóticas/imunologia
15.
Immunol Cell Biol ; 98(4): 305-317, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32142167
RESUMO
Antibody-dependent complement activity is associated not only with autoimmune morbidity, but also with antitumor efficacy. In infectious disease, both recombinant monoclonal antibodies and polyclonal antibodies generated in natural adaptive responses can mediate complement activity to protective, therapeutic or disease-enhancing effect. Recent advances have contributed to the structural resolution of molecular complexes involved in antibody-mediated complement activation, defining the avid nature of participating interactions and pointing to how antibody isotype, subclass, hinge flexibility, glycosylation state, amino acid sequence and the contextual nature of the cognate antigen/epitope are all factors that can determine complement activity through impact on antibody multimerization and subsequent recruitment of complement component 1q. Beyond the efficiency of activation, complement activation products interact with various cell types that mediate immune adherence, trafficking, immune education and innate functions. Similarly, depending on the anatomical location and extent of activation, complement can support homeostatic restoration or be leveraged by pathogens or neoplasms to enhance infection or promote tumorigenic microenvironments, respectively. Advances in means to suppress complement activation by intravenous immunoglobulin (IVIG), IVIG mimetics and complement-intervening antibodies represent proven and promising exploratory therapeutic strategies, while antibody engineering has likewise offered frameworks to enhance, eliminate or isolate complement activation to interrogate in vivo mechanisms of action. Such strategies promise to support the optimization of antibody-based drugs that are able to tackle emerging and difficult-to-treat diseases by improving our understanding of the synergistic and antagonistic relationships between antibody mechanisms mediated by Fc receptors, direct binding and the products of complement activation.
Assuntos
Anticorpos Monoclonais/imunologia , Doenças Transmissíveis/imunologia , Ativação do Complemento/imunologia , Proteínas do Sistema Complemento/imunologia , Neoplasias/imunologia , Animais , Anticorpos Monoclonais/efeitos adversos , Anticorpos Monoclonais/metabolismo , Antígenos/imunologia , Antígenos/metabolismo , Autoanticorpos/efeitos adversos , Autoanticorpos/imunologia , Engenharia Biomédica , Doenças Transmissíveis/microbiologia , Doenças Transmissíveis/patologia , Doenças Transmissíveis/virologia , Complemento C1q/química , Complemento C1q/imunologia , Complemento C1q/metabolismo , Proteínas do Sistema Complemento/química , Proteínas do Sistema Complemento/metabolismo , Humanos , Fragmentos Fc das Imunoglobulinas/imunologia , Imunoglobulina G/química , Imunoglobulina G/imunologia , Imunoglobulina G/ultraestrutura , Neoplasias/patologia , Receptores Fc/imunologia , Receptores Fc/metabolismo
16.
Mol Immunol ; 121: 99-110, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32199212
RESUMO
The complement cascade consists of cell bound and serum proteins acting together to protect the host from pathogens, remove cancerous cells and effectively links innate and adaptive immune responses. Despite its usefulness in microbial neutralization and clearance of cancerous cells, excessive complement activation causes an immune imbalance and tissue damage in the host. Hence, a series of complement regulatory proteins present at a higher concentration in blood plasma and on cell surfaces tightly regulate the cascade. The complement cascade can be initiated by B-1 B cell production of natural antibodies. Natural antibodies arise spontaneously without any known exogenous antigenic or microbial stimulus and protect against invading pathogens, clear apoptotic cells, provide tissue homeostasis, and modulate adaptive immune functions. Natural IgM antibodies recognize microbial and cancer antigens and serve as an activator of complement mediated lysis. This review will discuss advances in complement activation and regulation in bacterial and viral infections, and cancer. We will also explore the crosstalk of natural antibodies with bacterial populations and cancer.
Assuntos
Infecções Bacterianas/imunologia , Imunidade Humoral , Imunidade Inata , Neoplasias/imunologia , Viroses/imunologia , Antígenos de Bactérias/imunologia , Antígenos de Bactérias/metabolismo , Antígenos de Neoplasias/imunologia , Antígenos de Neoplasias/metabolismo , Antígenos Virais/imunologia , Antígenos Virais/metabolismo , Apoptose/imunologia , Linfócitos B/imunologia , Linfócitos B/metabolismo , Ativação do Complemento , Proteínas do Sistema Complemento/imunologia , Proteínas do Sistema Complemento/metabolismo , Humanos , Imunoglobulina M/imunologia , Imunoglobulina M/metabolismo , Receptores de Complemento/imunologia , Receptores de Complemento/metabolismo , Evasão Tumoral
17.
J Leukoc Biol ; 108(1): 339-351, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32182389
RESUMO
The complement system is a collection of soluble and membrane-bound proteins that together act as a powerful amplifier of the innate and adaptive immune systems. Although its role in infection is well established, complement is becoming increasingly recognized as a key contributor to sterile inflammation, a chronic inflammatory process often associated with noncommunicable diseases. In this context, damaged tissues release danger signals and trigger complement, which acts on a range of leukocytes to augment and bridge the innate and adaptive immune systems. Given the detrimental effect of chronic inflammation, the complement system is therefore well placed as an anti-inflammatory drug target. In this review, we provide a general outline of the sterile activators, effectors, and targets of the complement system and a series of examples (i.e., hypertension, cancer, allograft transplant rejection, and neuroinflammation) that highlight complement's ability to bridge the 2 arms of the immune system.
Assuntos
Imunidade Adaptativa , Proteínas do Sistema Complemento/imunologia , Sistema Imunitário/imunologia , Sistema Imunitário/patologia , Imunidade Inata , Inflamação/imunologia , Animais , Rejeição de Enxerto/imunologia , Humanos
18.
Infect Immun ; 88(5)2020 04 20.
Artigo em Inglês | MEDLINE | ID: mdl-32122944
RESUMO
The spirochete Borrelia burgdorferi sensu lato is the causative agent of Lyme disease (LD). The spirochetes produce the CspZ protein that binds to a complement regulator, factor H (FH). Such binding downregulates activation of host complement to facilitate spirochete evasion of complement killing. However, vaccination with CspZ does not protect against LD infection. In this study, we demonstrated that immunization with CspZ-YA, a CspZ mutant protein with no FH-binding activity, protected mice from infection by several spirochete genotypes introduced via tick feeding. We found that the sera from CspZ-YA-vaccinated mice more efficiently eliminated spirochetes and blocked CspZ FH-binding activity than sera from CspZ-immunized mice. We also found that vaccination with CspZ, but not CspZ-YA, triggered the production of anti-FH antibodies, justifying CspZ-YA as an LD vaccine candidate. The mechanistic and efficacy information derived from this study provides insights into the development of a CspZ-based LD vaccine.
Assuntos
Proteínas de Bactérias/imunologia , Borrelia burgdorferi/imunologia , Fator H do Complemento/imunologia , Doença de Lyme/imunologia , Carrapatos/microbiologia , Animais , Anticorpos/imunologia , Sítios de Ligação/imunologia , Proteínas do Sistema Complemento/imunologia , Feminino , Humanos , Vacinas contra Doença de Lyme/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C3H
19.
Postgrad Med ; 132(2): 184-191, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32124678
RESUMO
Invasive meningococcal disease (IMD) is a potentially devastating infection associated with high mortality and long-term sequelae; however, vaccines are available to protect against the five common disease-causing serogroups (A, B, C, W, and Y). Because traditional field efficacy clinical trials were not feasible due to low IMD incidence that necessitates a very large number of participants, serum bactericidal antibody (SBA) assays using rabbit (rSBA) or human (hSBA) complement were established as in vitro surrogates of meningococcal vaccine efficacy and are now routinely used to support vaccine licensure. Specifically, rSBA assays have been used to evaluate responses to meningococcal capsular polysaccharide-protein conjugate vaccines against serogroups A, C, W, and Y; the accepted correlate of protection for rSBA assays is a titer ≥1:8. Importantly, because the bacterial capsular polysaccharide antigen is conserved across strains, only one test strain that expresses an invariant polysaccharide capsule for each serogroup is required to assess coverage. rSBA assays are unsuitable for subcapsular protein-based serogroup B (MenB) vaccines, and therefore, hSBA assays have been used for licensure; titers ≥1:4 are considered the correlate of protection against IMD for hSBA. In contrast to MenACWY vaccines, because bacterial surface proteins are antigenically variable, MenB vaccines must be tested with hSBA assays using multiple test strains that represent the antigenic diversity of disease-causing isolates. As this complexity regarding SBA assessment methods can make data interpretation difficult, herein we describe the use of hSBA assays to evaluate MenB vaccine efficacy and to support licensure. In addition, we highlight how the two recently approved MenB vaccines differ in their use of hSBA assays in clinical studies to demonstrate broad protection against MenB IMD.
Assuntos
Infecções Meningocócicas/imunologia , Vacinas Meningocócicas/imunologia , Neisseria meningitidis Sorogrupo B/imunologia , Animais , Anticorpos Antibacterianos/imunologia , Antígenos de Bactérias/imunologia , Proteínas do Sistema Complemento/imunologia , Humanos , Infecções Meningocócicas/prevenção & controle , Vacinas Meningocócicas/administração & dosagem , Coelhos
20.
Molecules ; 25(3)2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-32012928
RESUMO
PEGylated nanomedicines are known to induce infusion reactions (IRs) that in some cases can be life-threatening. Herein, we report a case study in which a patient with rare mediastinal and intracardiac IgG4-related sclerosing disease received 8 treatments of intravenously administered PEGylated liposomal methylprednisolone-succinate (NSSL-MPS). Due to the ethical requirements to reduce IRs, the patient received a cocktail of premedication including low dose of steroids, acetaminophen and H2 blockers before each infusion. The treatment was well-tolerated in that IRs, complement activation, anti-PEG antibodies and accelerated blood clearance of the PEGylated drug were not detected. Prior to the clinical study, an in vitro panel of assays utilizing blood of healthy donors was used to determine the potential of a PEGylated drug to activate complement system, elicit pro-inflammatory cytokines, damage erythrocytes and affect various components of the blood coagulation system. The overall findings of the in vitro panel were negative and correlated with the results observed in the clinical phase.
Assuntos
Fatores Imunológicos/administração & dosagem , Lipossomos , Hemissuccinato de Metilprednisolona/administração & dosagem , Biomarcadores , Ativação do Complemento/efeitos dos fármacos , Ativação do Complemento/imunologia , Proteínas do Sistema Complemento/imunologia , Suscetibilidade a Doenças , Feminino , Humanos , Inflamação/etiologia , Inflamação/metabolismo , Lipossomos/química , Masculino , Hemissuccinato de Metilprednisolona/farmacocinética , Polietilenoglicóis/química
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1,114,307,622,127,492,100
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Inflammatory and transcriptional roles of poly (ADP-ribose) polymerase in ventilator-induced lung injury
Je Hyeong Kim, Min Hyun Suk, Dae Wui Yoon, Hye Young Kim, Ki Hwan Jung, Eun Hae Kang, Sung Yong Lee, Sang Yeub Lee, In Bum Suh, Chol Shin, Jae Jeong Shim, Kwang Ho In, Se Hwa Yoo, Kyung Ho Kang
Research output: Contribution to journalArticlepeer-review
35 Citations (Scopus)
Abstract
Introduction: Poly (ADP-ribose) polymerase (PARP) participates in inflammation by cellular necrosis and the nuclear factor-kappa-B (NF-κB)-dependent transcription. The purpose of this study was to examine the roles of PARP in ventilator-induced lung injury (VILI) in normal mice lung. Methods: Male C57BL/6 mice were divided into four groups: sham tracheostomized (sham), lung-protective ventilation (LPV), VILI, and VILI with PARP inhibitor PJ34 pretreatment (PJ34+VILI) groups. Mechanical ventilation (MV) settings were peak inspiratory pressure (PIP) 15 cm H2O + positive end-expiratory pressure (PEEP) 3 cm H2O + 90 breaths per minute for the LPV group and PIP 40 cm H2O + PEEP 0 cm H2O + 90 breaths per minute for the VILI and PJ34+VILI groups. After 2 hours of MV, acute lung injury (ALI) score, wet-to-dry (W/D) weight ratio, PARP activity, and dynamic compliance (CD) were recorded. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), myeloperoxidase (MPO) activity, and nitrite/nitrate (NOX) in the bronchoalveolar lavage fluid and NF-κB DNA-binding activity in tissue homogenates were measured. Results: The VILI group showed higher ALI score, W/D weight ratio, MPO activity, NOX, and concentrations of TNF-α and IL-6 along with lower CD than the sham and LPV groups (P < 0.05). In the PJ34+VILI group, PJ34 pretreatment improved all histopathologic ALI, inflammatory profiles, and pulmonary dynamics (P < 0.05). NF-κB activity was increased in the VILI group as compared with the sham and LPV groups (P < 0.05) and was decreased in the PJ34+VILI group as compared with the VILI group (P = 0.009). Changes in all parameters were closely correlated with the PARP activity (P < 0.05). Conclusion: Overactivation of PARP plays an important role in the inflammatory and transcriptional pathogenesis of VILI, and PARP inhibition has potentially beneficial effects on the prevention and treatment of VILI.
Original languageEnglish
Article numberR108
JournalCritical Care
Volume12
Issue number4
DOIs
Publication statusPublished - 2008 Aug 22
ASJC Scopus subject areas
• Critical Care and Intensive Care Medicine
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Asthma and Lung Cancer
Published: 2017-12-04 18:06:50
370 words
2 pages
4 min to read
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Categories:
Type of paper:
Essay
Cancer and Asthma
Introduction
If this sample essay on
"Asthma and Lung Cancer" doesn’t help,
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• There are several risk factors that can predispose an individual to being affected with cancer and asthma. Among those, this presentation will focus on one risk factor together with the ways to improve the patient lives and outcomes Risk factor for Asthma-family history
•The family gene that one inherits predispose an offspring to asthma if the parents were had it.
•It is considered that three fifths of all the cases of asthma to be genetic.
•If a person has a parent with asthma the chances are that the individual will develop it in the future.
Risk factor for cancer-family history
•In this context the risk factor of cancer can be found through the history of the family in life modification and the lifestyle factors.
•Some of these include the behavioral factors like drinking alcohol and smoking alcohol.
•If a family has got a history of indulging in those type of behaviors, then the siblings might follow suit thus the spread of cancer.
•Poverty history in a family can lead to poor lifestyle which can predispose the generation to poor sanitation and lack of proper diet that can lead to poor choices of food and lack of exercise
Asthma Recommendations
Teaching to improve the patient life and outcomes
•Dietary improvements- some diets like fruits and vegetables contain healthy components like water, minerals and fiber which can improve the outcomes of the patient indefinitely.
•The patient should limit themselves to alcohol use so as to reduce other complications and moderate the rate of cholesterol.
•Alcohol is carcinogenic and may increase the rate of cancer.
•Focus on screening so that some malignant conditions can be identified and detected early enough.
•The patient of asthma should keep track of their asthma symptoms so that it can be easier to track the combination of symptoms that causes the attack.
•The patient should be a regular visitor to the specialist so as to be guided on how to deal with exposures
•Regular exercise while following the doctor’s advice.
References
Adams, R. (2010). Improving health outcomes with better patient understanding and education. RMHP, 61. doi:10.2147/rmhp.s7500
Richard Beasley, A. S. (2015). Risk factors for asthma: is prevention possible? The Lancet, 386(9998), 1075-1085. doi:10.1016/s01406736(15)00156-7
Cite this page
Asthma and Lung Cancer. (2017, Dec 04). Retrieved from https://speedypaper.com/essays/asthma-and-lung-cancer
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seal
(redirected from put the seal on)
Also found in: Dictionary, Thesaurus, Legal, Financial, Idioms, Encyclopedia.
seal
(sēl),
1. A tight closure.
2. To effect a tight closure.
SEAL
Heart surgery A clinical trial–Simple & Effective Arterial Closure Study which evaluated the safety and efficacy of the Duett vascular sealing device
seal
Public health Any air- and/or water-tight closure on a product–blood components, medications intended to maintain a product sterilely until used by a consumer; products with broken seals should be discarded
staining, fluorescein
The artificial coloration of tissue by fluorescein. Under ultraviolet illumination, it stains dead or degenerated corneal epithelial cells due to abrasions, old age or following inadequate contact lens fit, a yellowish-green colour. It also stains the tears, thus facilitating the evaluation of tear drainage or the blood flow through the retina and choroid when injected intravenously. Corneal staining resulting from contact lens wear may present in various shapes, locations, depths or severity. A very common form is punctate staining as appears in punctate epithelial keratitis. There may be arcuate stains located in different parts of the cornea, some inferiorly (called inferior epithelial arcuate lesions) or superiorly (called superior epithelial arcuate lesions, acronym: SEAL, or epithelial splitting), which usually do not give rise to symptoms and appear mainly with soft or silicone hydrogel lenses. A very severe form of staining is called epithelial plug. It is typically round in shape and represents a loss of the full thickness of the epithelium. Corneal staining resulting from contact lens wear typically disappears after cessation of contact lens wear. See fluorescein angiography; dye dilution test; fluorescein test.
seal
(sēl)
1. Tight closure.
2. To effect a tight closure.
seal,
n 1. something that firmly closes or secures.
2. a tight and perfect closure.
v 3. to keep shut, enclosed, or confined.
seal, border,
seal, double,
n a seal consisting of gutta-percha underneath another material such as temporary cement; used to close the coronal opening in a tooth during endodontic treatment.
seal, hermetic,
n perfect and absolute obliteration of all space within a tooth.
seal, peripheral,
seal, posterior palatal,
n the seal at the posterior border of a denture produced by displacing some of the soft tissue covering the palate by extra pressure developed in the impression or by scraping a groove along the posterior seal area in the cast on which the denture is to be processed.
seal, postpalatal,
n See seal, posterior palatal.
seal
1. a marine mammal; member of the suborder Pinnipedia. There are two major groups, the earless seals (family Phocidae) including many species, and the eared seals (family Otariidae) including sealions and fur seals. They are carnivorous and have four paddles which enable them to move on land and to swim.
2. a very dark brown coat color of cats, seen in brown (or sable) Burmese and on the extremities of seal-point Siamese and Colorpoint cats.
seal pox
see sealpox.
Patient discussion about seal
Q. HONEY Use honey to seal MRSA (METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS) wound.
A. honey has an antimicrobial activity due to it's acidity, osmotic power and hydrogen peroxide. about MRSA - there is a New Zealandic research about a type of honey that is effective against infections of MRSA. but it's only one research and another investigation is required.
More discussions about seal
Full browser ?
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Updated review of resistance to neuromuscular blocking agents
Anesth Pain Med 2018;13(2):122-7
Published online April 30, 2018
© 2018 The Korean Society of Anesthesiologists.
Ki Tae Jung, and Tae Hun An
Department of Anesthesiology and Pain Medicine, Chosun University Hospital, Chosun University School of Medicine, Gwangju, Korea
Correspondence to: Tae Hun An, M.D. Department of Anesthesiology and Pain Medicine, Chosun University Hospital, Chosun University School of Medicine, 365 Pilmun-daero, Dong-gu, Gwangju 61453, Korea Tel: 82-62-220-3223 Fax: 82-62-223-2333 E-mail: [email protected]
Received October 24, 2017; Revised November 21, 2017; Accepted November 21, 2017.
cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Since neuromuscular blocking agents (NMBAs) were introduced to the surgical field, they have become almost mandatory for the induction and maintenance of anesthesia. However, resistance to NMBAs can develop in certain pathological states, such as central nerve injury, burns, and critical illnesses. During such pathological processes, quantitative and qualitative changes occur in the physiology of acetylcholine and the acetylcholine receptor (AChR) at the neuromuscular junction. Up-regulation of AChR leads to changes in the pharmacokinetics and pharmacodynamics of NMBA. As NMBA resistance may result in problems during anesthesia, it is of utmost importance to understand the mechanisms of NMBA resistance and their associations with pathological status to maintain adequate neuromuscular relaxation. This review presents the current knowledge of pharmacokinetic and pharmacodynamic changes and pathological status associated with NMBA resistance.
Key Words : Cholinergic receptors, Drug resistance, Neuromuscular blocking agents, Up-regulation
INTRODUCTION
Since neuromuscular blocking agents (NMBAs) were introduced into the surgical field, they have become indispensable for surgery. However, there are many reports of resistance to NMBAs, which are commonly referred to as tachyphylaxis or hyposensitivity [1,2]. Resistance to NMBAs is identified based on increases in the NMBA dosage required to inhibit the muscular twitch response, the time to maximum response, and decreases in the degree of twitch depression or the duration of neuromuscular blockade after a bolus [1].
Approximately 1% of all patients administered general anesthesia exhibit inadequate relaxation, interrupting the procedure [3]. Thus, it is of great importance to understand the mechanisms of NMBA resistance associated with different pathological states to maintain adequate neuromuscular relaxation.
Certain pathological states, such as central nerve injury [4], burns [5], and critical illnesses [6], are associated with resistance to NMBAs. This resistance can be explained by up-regulation of acetylcholine receptors (AChRs) in skeletal muscle [2]. In addition, quantitative and qualitative changes in the physiology of acetylcholine (ACh) and AChR at the neuromuscular junction (NMJ) develop during pathological processes, which lead to changes in the pharmacokinetics and pharmacodynamics of NMBAs [1,2].
PHARMACOKINETIC CHANGES IN NMBA RESISTANCE
Pharmacokinetic changes in NMBA resistance are associated with changes in the volume of distribution (VD), protein binding, and clearance of NMBAs (Table 1). These changes result in a decrease in the effective NMBA concentration at the receptor site (Fig. 1), and are observed in patients with hepatic dysfunction, thermal injury, oncological diseases, and acid-base disturbances.
Pharmacokinetic Changes in NMBA Resistance
Changes Disease/conditionMechanism
Volume of distribution Liver diseaseIncreased volume of distribution
Thermal injury
Critical illness
Protein bindingThermal injuryIncreased AAG, decreased albumin
TumorsIncreased AAG
Multiple myelomasIncreased paraproteins, lgG, and so forth
AnticonvulsantPhenytoin increased AAG
Acid-base statusConformational changes in ammonium group and ionization degree of NMBA
ClearanceThermal injury burnsIncreased hepatic blood flow and GFR
PhenytoinHepatic enzyme induction
CarbamazepineDoubled clearance
Hyperthermia and alkalosis Altered Hofmann elimination
NMBA: neuromuscular blocking agent, AAG: α1-acid glycoprotein, IgG: immunoglobulin G, GFR: glomerular filtration rate.
Fig. 1.
Schematic drawing of the neuromuscular junction (NMJ) and the mechanism of resistance to neuromuscular blocking agents (NMBAs). (A) A normal NMJ and normal interaction between the acetylcholine (ACh) receptor and NMBA. NMBA resistance resulting from pharmacokinetic changes, such as increased volume of distribution (VD), increased protein binding, and increased clearance, is associated with a decrease in NMBA concentration at the receptor site. (B) NMBA resistance associated with increased volume of distribution. (C) NMBA resistance associated with increased protein binding. (D) NMBA resistance associated with increased clearance. Pharmacodynamic changes in NMBA resistance are mostly associated with changes in ACh receptor physiology, such as upregulation, which results in a change in the availability or reactivity of receptors. (E) NMBA resistance associated with upregulation.
Increased VD
An increase in VD may increase resistance to NMBAs, which leads to delayed onset or a shorter duration of action (Fig. 1B). These changes can occur in patients with liver disease, thermal injury, or critical illness. In patients with liver disease, the VD of NMBAs increases [7]; the changes in distribution are multifactorial and depend on the severity of liver dysfunction [1].
Increased protein binding
Diseases, thermal injury, drugs, and acid-base disturbances can increase protein binding of NMBAs and lead to resistance to these agents (Fig. 1C). Usually, acidic drugs bind to albumin and basic drugs bind to α1-acid glycoprotein (AAG) [1]. AAG increases in response to inflammation, surgery, malignancy, myocardial infarction, and thermal injury. An increase in AAG may be responsible for NMBA resistance because the effective NMBA concentration at the receptor site may decrease due to an increase in NMBA protein binding. However, this is only clinically significant when protein binding is >85%. After thermal injury, the plasma concentration of AAG increases and plasma protein binding of NMBAs increases [5,8].
Proteins released from certain tumors are also related to resistance to NMBAs. Patients with adenocarcinoma of the stomach and Wegener’s granulomatosis show a marked increase in AAG and resistance to atracurium because of increased binding to AAG [9,10]. Although, resistance to vecuronium and atracurium has been reported in a patient with multiple myeloma despite a normal AAG concentration [11], paraproteins, immunoglobulin G, and β2-microglobulin increase in these patients, and these proteins bind more NMBA molecules. Thus, availability of NMBA at the receptor site is thought to decrease.
Phenytoin, carbamazepine, and other anticonvulsants may cause resistance to NMBAs [1,2]. Chronic phenytoin therapy decreases recovery time and the recovery index of rocuronium through release of acute-phase reactant proteins such as AAG [12]. However, the mechanisms of phenytoin-induced resistance to NMBAs are complex and include increased hepatic metabolism and clearance through the induction of specific enzymes in the cytochrome P450 system and up-regulation of AChR.
Increased clearance
Increased clearance is also associated with pharmacokinetic changes in NMBA resistance (Fig. 1C). The hyperdynamic state in burn patients, which occurs approximately 48 hours after thermal injury, may increase hepatic blood flow and the glomerular filtration rate, resulting in increased drug clearance [1]. However, pharmacokinetic changes after thermal injury may contribute only partly to NMBA resistance because resistance may continue after recovery from burns [13].
As mentioned above, phenytoin is associated with NMBA resistance through the induction of enzymes in the cytochrome P450 system [12]. Carbamazepine affects NMBA resistance to rocuronium by inducing pharmacokinetic changes, including a two-fold increase in clearance [14].
Resistance to atracurium is related to characteristic metabolism, such as Hofmann elimination and ester hydrolysis. In particular, Hofmann elimination, which accounts for approximately 40% of clearance, is affected by temperature and pH [15]. An increase in body temperature reduces atracurium-induced neuromuscular blockade, and respiratory or metabolic alkalosis also significantly reduce the effects of atracurium and recovery time. However, hyperthermia and alkalosis only appear to contribute minimally to atracurium resistance [1,2].
PHARMACODYNAMIC CHANGES IN NMBA RESISTANCE
Pharmacodynamic changes in NMBA resistance include up-regulation of AChR physiology, enhanced release of ACh at the NMJ, and the inhibition of cholinesterase activity in serum. These changes are seen in patients with denervation injury, thermal injury, immobilization, prolonged use of NMBAs, chronic use of anticonvulsants, and infections (Table 2).
Pharmacodynamic Changes in NMBA Resistance
Causes Disease and etiology
Denervation injury Lower motor neuron and upper motor neuron injury
Thermal injuryDenervation-like syndrome
ImmobilizationDisuse atrophy
AnticonvulsantsPhenytoin, carbamazepine, and so forth
InflammationRelease of APR proteins
Infection–toxinsInhibit the release of acetylcholine
NMBA: neuromuscular blocking agent, APR: acute phase-reactant.
The up-regulation theory refers to a change in the availability or reactivity of receptors (Fig. 1E). In the normal state, AChR consists of five proteins (α, β, ε, and δ in a 2:1:1:1 ratio) only in the junctional area of the NMJ, and the number of extrajunctional AChRs is insignificant [2]. During the absence of neural stimulation or denervation, immature AChRs, with a newly immature glycoprotein γ, instead of ε, develop and proliferate in the junctional and extrajunctional areas of the NMJ [2]. This leads to an increase in the number of remaining unblocked AChRs [16]. In this situation, the effects of a typical dose of an NMBA are weaker, leading to increased sensitivity to agonists and decreased sensitivity to antagonists.
However, not all mechanisms can be explained with these theories, and the pharmacodynamic changes in NMBA resistance are also complex. Other mechanisms have been proposed, such as increased susceptibility of the muscle membrane to depolarization by ACh [17], the effects of NMBAs as partial agonists on immature AChR via altered pharmacological activity [18], and decreased acetylcholinesterase activity after nerve injury [19]. However, the contribution of these components to NMBA resistance is small [2]. The up-regulation and decreased affinity of AChR could be an important component of NMBA resistance.
Denervation injury
NMBA resistance after lower motor neuron injury may be associated with the proliferation of immature AChRs. After such an injury, the number of AChRs increases and resistance to NMBAs occurs only on the injured side [2]. In an animal study in which denervation of the left gastrocnemius was done by creating a 75%–80% lesion of the sciatic nerve, the effective dose of d-tubocurarine increased and the number of AChRs significantly increased in the denervated leg compared to the contralateral leg and uninjured control legs [20]. The effective dose of d-tubocurarine and the number of AChRs were positively correlated.
NMBA resistance develops in patients with an upper motor neuron injury, such as those observed in stroke, cerebral palsy, multiple sclerosis, and hemiparesis secondary to a cerebrovascular accident or cerebral tumor [1,2]. NMBA resistance after a stroke occurs on the paretic side [4] and can start as early as 4–8 hours after the stroke [21]; it is observed most frequently in the distal arm and hand muscles [22]. After an injury, the deprivation of trophic factors or normal input from descending motor pathways lead to central denervation and the transsynaptic degeneration of motor neurons [23]. Furthermore, the number of extrajunctional AChRs increases by collateral reinnervation or axonal nerve sprouting from the surviving lower motor neurons [21].
Thermal injury
NMBA resistance after thermal injury can also explained by denervation-like changes. These changes include fibrillation potentials and positive sharp waves, polyneuropathies and axonal neuropathy, reduced motor nerve conduction, prolonged motor and sensory distal latencies, and reduced amplitude of sensory nerve action potentials [24]. Denervation-like syndrome is associated with increased nicotinic AChR occurrence at the NMJ [25]. In general, 2- to 3-fold higher dosages of NMBAs and 3- to 5-fold higher serum concentrations are required to obtain a general degree of neuromuscular blockage in burn patients [5,26]. A burn with an area greater than 25%–30% of the body surface area that lasts at least 7 days is associated with the development of NMBA resistance [27].
However, the other possible mechanisms of NMBA resistance after thermal injury are complex and associated with other factors, such as immobilization, disuse atrophy, increased protein binding, increase in evoked end plate potentials, altered receptor binding affinity, burn wound-induced contracture, and decreased cholinesterase activity in serum [1,2].
Immobilization and muscle atrophy
NMBA resistance resulting from immobilization and muscle atrophy is also associated with the proliferation of AChR, but it is of a lesser magnitude than denervation syndrome [1,2]. Immobilization does not directly damage the cord or nerves, as muscle fibers are innervated and function normally [19]. The proliferation of extrajunctional AChR, increased ACh sensitivity, terminal nerve sprouting, decreased cholinesterase activity, decreased muscle volume, and decreases in muscle contractile proteins, mitochondria, and sarcoplasmic reticulum have been proposed as etiologies of NMBA resistance based on immobilization and muscle atrophy [2,16]. As has been shown in animal studies, NMBA resistance occurs approximately 4 days after immobilization, whereas an unaffected extremity can show resistance after 1–4 weeks [1,2]. However, the diaphragm is not affected [28].
Prolonged use of NMBAs
The prolonged use of NMBAs may result in resistance through up-regulation of AChR-like immobilization. The chronic use of NMBAs, even in the absence of immobilization or paralysis, causes an up-regulation in the number of receptors and leads to drug tolerance. Chronic administration of d-tubocurarine results in NMBA resistance associated with increased extrajunctional AChR [29]. However, diaphragmatic AChR does not change.
Chronic use of anticonvulsants
Anticonvulsants also cause pharmacodynamic changes in NMBA resistance through antagonism of ACh in pre- and postsynaptic areas [1,2]. The effects of anticonvulsants on NMJ are similar to those of small nonparalytic doses of NMBA. Carbamazepine and phenytoin acutely suppress post-tetanic repetition through their presynaptic inhibitory action on ACh release at the nerve terminal [30]. Therefore, chronic administration of anticonvulsants results in chronic chemical denervation and the subsequent proliferation of AChR.
Infections
Inflammation and infection alters the number of AChRs or the response to NMBAs at the NMJ. The infection-mediated inflammatory response is associated with the release of acute phase-reactant (APR) proteins [8]. NMBAs bind to the APR proteins and then a higher dose is required for neuromuscular block. Toxins from bacteria of the Clostridium genus inhibit the release of ACh at the NMJ; if this state is prolonged, the number of AChRs may increase [31]. Botulinum toxin binds strongly to motor nerve terminals and becomes internalized, which ultimately reduces the release of ACh [31]. Blocking the release of ACh leads to a functionally denervated state in which the muscles became atrophic and extrajunctional AChR dominates.
CONCLUSION
Patients with numerous pathological states are treated with surgery. Some of these patients may be resistant to NMBAs, leading to inadequate neuromuscular blockade, which results in patient movement and interruption of the procedure. Numerous pharmacodynamic and pharmacokinetic changes in VD, protein binding, clearance, and upregulated AChR physiology are associated with the etiology of NMBA resistance. An understanding of the association between the mechanisms of NMBA resistance and the pathological state of the patient would be helpful to maintain adequate neuromuscular relaxation and avoid problems that result from resistance to NMBAs during surgical procedures.
ACKNOWLEDGMENTS
This study was supported by research funds from Chosun University, 2015.
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Treating Vitreous Eye Floaters Treatment using a YAG laser by an Eye Doctor http://www.thefloaterdoctor.com Everything About Treating Eye Vitreous Floaters - moving shadows & spots in your vision Thu, 08 Nov 2018 22:11:47 +0000 en hourly 1 https://wordpress.org/?v=4.6.1 WEISS RING FLOATERS – EVERYTHING THAT MAKES THEM SPECIAL http://www.thefloaterdoctor.com/weiss-ring-floaters/ Mon, 30 Jul 2018 02:44:55 +0000 http://www.thefloaterdoctor.com/?p=1957 For much of my practice I assumed that Weiss Ring floaters should be capitalized as if they were eponymously named after the first doctor to describe them, probably some Austrian, German, or Swiss eye doctor in the 19th century. I am probably wrong. The German word ‘weiss’ simply translates to “white” in English. Weiss ring may simply be descriptive.
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For much of my practice I assumed that Weiss Ring floaters should be capitalized as if they were eponymously named after the first doctor to describe them, probably some Austrian, German, or Swiss eye doctor in the 19th century. I am probably wrong. The German word ‘weiss’ simply translates to “white” in English. Weiss ring may simply be descriptive. When you illuminate these floaters in the eye, they appear as white or light cream colored, dense, hyaline (from Greek, glass-like) densities.
Weiss ring floaters do not need to be a complete ring. They may be a partial ring, a dense clump, a semi-transparent sheet, or other, but they do still have some characteristic identifying features that distinguish them from other cloudy (synersesis type), or cob-web strand types of floaters.
Floaters are not formed over time, but instead they pre-exist. They are a particular density of the vitreous cortex that originates at or surrounding the optic nerve as the optic nerve enters the eye. Until they separate from the retina, they are not seen by the examining eye doctor and they are without any symptoms.
Normal eye without floaters
NORMAL EYE WITH CLEAR VITREOUS. The clear vitreous fluid takes up most of the volume of the eye. The vitreous is mostly (99% water with about 1% collagen proteins dispersed evenly and homogeneously throughout. These proteins make the vitreous a bit like dilute Jello: watery and ‘jiggly”.
Very early separation of the vitreous from the retina.
EARLY POSTERIOR VITREOUS DETACHMENT: The vitreous also has an outer layer, the vitreous cortex. It also consists of collagen proteins, but it is more organized. The main vitreous fluid is like Jello, whereas the vitreous cortex is more like a sheet of transparent plastic. Here, the vitreous cortex is just beginning to separate from the retina. At the optic nerve area, there is a particular thickening of the vitreous cortex ‘sheet’. This ring-like thickening is the weiss ring.
The vitreous has completely separated, There is both a Weiss ring and some separate cloudy floater (syneresis) formation.
Here, the vitreous has mostly separated from the retina. It is a mostly ring-like structure that is integrally part of the (in fact, just a thickened part of) vitreous cortex ‘sheet’. Given a little more time (days to a few weeks) the weiss ring will move more anterior (in this illustration, to the left) and will typically settle and stabilize in the mid-portion of the vitreous. In this illustration, there is also a hazy, cloudy and less-distinct, syneresis-type floater just to show that weiss rings are not necessarily all by themselves.
So here is the good news:
• There can only be one posterior vitreous detachment (PVD) per eye. In addition, there can only be one weiss ring per eye.
• Weiss rings typically settle into the middle portion of the vitreous chamber quite safely away from the retina and lens.
• I have never seen a patient respond to the treatment of a weiss ring with an elevated eye pressure. I do not believe it is a potential complication of treatment – assuming that the weiss ring is the only entity being treated.
• Weiss ring floaters are the most responsive to the YAG laser and the most efficiently treated ultimately yielding the best results, and…
• Unlike the diffuse and cloudy syneresis floaters, weiss ring floaters do not have the tendency to reform and re-aggregate after treatment.
The downside:
• Weiss ring floaters are rarely seen in younger patient, and younger patients rarely experience posterior vitreous detachments
• Even if you have been told you have a PVD, or weiss ring, you may not. I have found that some doctors will describe the floaters as such, but they are not.
Since these dense, hyaline eye floaters are tethered and suspended as part of the vitreous cortex sheet, there is no expectation that they will just move out of the way regardless of what your well-qualified, and well-intentioned local eye care provider has suggested. The good news is that if you have had you eyes examined and they have reassured you that there is no retinal involvement (retinal hole, tear, or detachment), then there is no urgency or medical necessity to rush in and treat the eye floater. If you doctor has suggested waiting 6 months, then I will have no problem with that. Wait as long as you feel comfortable. There is NO loss of treatment advantage or loss of benefit by waiting. I will be ready when you are.
-Dr. Johnson
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RESPONDING TO YOUR DOCTOR’S WARNINGS OF LASER RISKS http://www.thefloaterdoctor.com/responding-to-your-doctors-warnings/ Mon, 30 Jul 2018 00:11:30 +0000 http://www.thefloaterdoctor.com/?p=1948 I recently received a follow-up email message from a floater sufferer trying to do his research and due diligence prior to any treatment with me or anyone else. The message was full questions and concerns which are common especially after the floater sufferer has spoken to their local eye care provider, be it general ophthalmologist or retina specialist.
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I recently received a follow-up email message from a floater sufferer trying to do his research and due diligence prior to any treatment with me or anyone else. The message was full questions and concerns which are common especially after the floater sufferer has spoken to their local eye care provider, be it general ophthalmologist or retina specialist. Here is the bulk of the message and following it I will deconstruct it and answer and address the main concerns:
“…I need further verification that indeed this will not cause further issues. Dr. A. at the XYZ eye clinic (which I understand is the Mayo Clinic of eye care) even was implying that this was more just a money-making thing, stating that they usually don’t do anything for them there, and the (weiss) rings normally much reduce after ~6 months. He said the treatment is not quite as simple as implied, and may take multiple rounds of treatment. How many of your patients have needed multiple sessions? Dr. A also stated that putting that much energy into the vitreous jelly, it can ricochet off the jelly if it is located in the back and may cause a tear/detachment of the retina, whereas if it is towards the front of the eye, it can cause instantaneous cataracts that are difficult to treat. I know you address the cataract issue, so I am ok there, but what about detachments? Dr. A said he didn’t know of anyone he worked with who did this right now, and it is not commonplace. He also said he would recommend vitrectomy surgery if I really insisted, which they do for retinal detachment and the like. He said none of his retina colleagues were doing it either, and none recommended it. So… the question is what percent of procedures have resulted in retinal detachments…?
“…implying that this was more just a money-making thing”
I am not ashamed to admit that my medical practice is a business that exchanges medical services for money. This is the model for most medical practices, I imagine, unless there is some other source of subsidization either via a government program or other benefactors. Even the highly esteemed XYZ clicic referred to in the original message must pay their overhead which I imagine to be quite substantial. Many American medical practices are contracted with medical insurers to provide care for the insured. For the exchange of services, whether it is the doctor’s time and expertise, or for procedures, such as diagnostic imaging, labs, as well as invasive surgical procedures, the medical practice submits a claim to the insurer, and the insurance carrier pays the medical practice. Understand that the insurance claim only states that an effort was made. The claim codes have no modifiers that reflect success with treatment. In fact the patient could die on the operating room table, and the hospital will still submit a claim to the insurer for supplies, the room, and the professional services.
“…stating that they usually don’t do anything for them”
This is true. I have addressed this at length elsewhere in my web site here.
“…and the (weiss) rings normally much reduce after ~6 months”
A weiss ring floaters is a very thickened part of the vitreous cortex membrane that has peeled away from the posterior (back part) of the retina. Normally it is very loosely attached to the retina, and the weiss ring peels away from the retina along with the transparent ‘plastic-sheet-like” membrane. The weiss ring type floaters do not just fall out of the way unless the whole membrane collapses which it rarely does. If your doctor has suggested waiting 6 months, you are welcome to wait. For typical floaters of all types, there is no harm in waiting 6 months or longer if you wish to test that recommendation.
“…He said the treatment is not quite as simple as implied, and may take multiple rounds of treatment.”
My web site has about 30 individual pages and about 29 blog posts all describing the difficulty and complexity of this procedure. My fee structure is such that the first ( and presumed necessary second procedure ) are bundled together to help set the expectation that it does take more than one procedure. Much of my effort (this web site, emails communication, and phone calls) is spent managing the expectations of potential patient floater-sufferers.
“…How many of your patients have needed multiple sessions?”
Virtually all of them.
“…Dr. A also stated that putting that much energy into the vitreous jelly, it can ricochet off the jelly if it is located in the back and may cause a tear/detachment of the retina, whereas if it is towards the front of the eye, it can cause instantaneous cataracts that are difficult to treat.”
Dr. A does not have experience in treating eye floaters with the YAG laser. This statement reveals it. Laser energy does not ‘ricochet’ around in the back of the eye. From a more practical measure, I have been exclusively treating floaters since 2007, with thousands of procedures of all kinds of complexity. There has never been a retinal detachment in any of my patients. Injury to retina is of course possible, but quite comfortably avoidable with experience and good decision making – which includes NOT offering treatment to those that are not good candidates for treatment. As of 2018, my total laser shot count (that is, the cumulative number of individually aimed and fired laser shots) is over 11 million. None of those 11 million shots of the laser has caused a cataract. The risks exist and I describe it (and the others) in my web site as part of my effort towards transparency and education, but again, I think the numbers show that Dr. A’s warnings are out of proportion to the real risk.
“He also said he would recommend vitrectomy surgery if I really insisted…”
Floater-only vitrectomy (FOV) is an invasive surgical procedure requiring placing three holes in the whites of the eyes, and cutting and removing all (or most) of the vitreous fluid and replacing it with a modified saline solution. Many retina specialists will advise their patients that there is a 100% risk of developing cataracts within a year of the procedure. In addition, there are risks of chronic macular edema, retinal detachment, and infection. The last three risks are low likelihood, but could result in devastating vision loss.
There is risk with everything we do. Drive a car? Risk. Start a business? Risk. Enter a relationship? Risk. And with medical procedures, because health and function are potentially at risk, there are special considerations. Ultimately it comes down to weighing the potential risk of a procedure vs. the potential benefit. The good news is that eye floaters are not a condition that HAS to be treated to save the eye health and visual function. But that is not how my medical practice is promoted. I am trying to improve the quality of vision and quality of life for those suffering significantly bothersome and distracting, and sometimes intermittently obstructive eye floaters – and doing so with a procedure that is acceptable low risk in the hands of an experienced laser surgeon.
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CATARACTS & FLOATERS: TIMING OF TREATMENT(S) http://www.thefloaterdoctor.com/cataracts-and-floaters/ Tue, 17 Apr 2018 19:57:09 +0000 http://www.thefloaterdoctor.com/?p=1932 I have commented elsewhere on some of the challenges of treatment on patients who have already had cataract surgery with artificial lenses: The artificial lenses have a smaller aperture which can sometimes limit my view, and more importantly limit the amount of energy from the laser that can be delivered. Increased difficulty does not equate with increased risk to the eye,
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I have commented elsewhere on some of the challenges of treatment on patients who have already had cataract surgery with artificial lenses: The artificial lenses have a smaller aperture which can sometimes limit my view, and more importantly limit the amount of energy from the laser that can be delivered. Increased difficulty does not equate with increased risk to the eye, it generally will mean that it may be less efficient and require more treatment overall.
My preference is to treat a virgin (no prior surgery) eye with a natural lens with a big, dilated pupil. That is my preference, but I rarely get my preference. Often a patient will inquire as to the preferred order of treatment when they have some cataract changes and floaters.
So let’s start with the basics. A cataract is ANY yellowing, clouding, opacity, or optical irregularity to the crystalline lens of the eye. It is NOT an ‘all or none’ phenomenon. It occurs along a spectrum of involvement and degree. A person may have very mild cataract changes and still have 20/20 or better vision and not even be aware of the lens changes. Another person may have cataracts so advanced that they can not see at all out of the eye.
Cataract surgery involves removing the natural lens and replacing it with a perfectly clear artificial lens. It is one of the most common surgeries performed in the world. Generally, the usually tipping point for the doctors to recommend cataract surgery is when the ‘best corrected’ (best spectacle corrected) vision drops to 20/40 or worse and it is believed due to the cataract.
The laser used to treat eye floaters must pass through the lens to deliver its energy to the eye floaters in the vitreous cavity. The more advanced the cataract, the less organized and less energy can be delivered. Although it was seem a ‘no brainer’ for me to prefer working through an artificial lens (it is perfectly clear AND it eliminated one of the risks of treatment – that of the laser causing a cataract if it is grossly misdirected), the problem with the artificial lenses is that 1. they have a smaller aperture to work through which may limit my view and decrease the delivered energy, and 2. some of the multi-focal lenses intended to give you both near and distance vision will direct my laser’s energy to two focal points in stead on one and also diminish the delivered energy.
I treat patients with natural lenses and artificial lenses. I get whatever walks through the door and I will adapt my technique and effort appropriately. Both groups may benefit from treatment with very acceptable low risk.
So what about when a prospective patient has both floaters and cataract and asks me for my recommendation as to the timing and order of both procedures?
1. If the cataract is mild, that is, best corrected vision is still 20/30 or better, then it may be awhile before cataract surgery will be indicated, and the lens changes are probably mild enough to go ahead and do floater treatment first.
2. If your local doctor is suggesting surgery and vision is now 20/40 or worse (diminished due to cataracts), then go ahead and have your cataract surgery first. Wait a couple months (assuming it is uncomplicated) and then we can treat the floaters.
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YOUNG PATIENTS: WHAT CAUSED THIS? WILL IT GET BETTER? WILL IT GET WORSE? http://www.thefloaterdoctor.com/young-patient-questions/ Tue, 23 Jan 2018 20:19:16 +0000 http://www.thefloaterdoctor.com/?p=1916 I receive many, many email messages through this web site from eye floater-sufferers from all walk and from ages and from allover the world. As they are doing their research they may have stumbled onto this and other web sites – some of which are purely educational, and some, like my medical practice that may actually offer some relief from the unrelenting annoyance and distraction caused by these vitreous eye floaters.
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I receive many, many email messages through this web site from eye floater-sufferers from all walk and from ages and from allover the world. As they are doing their research they may have stumbled onto this and other web sites – some of which are purely educational, and some, like my medical practice that may actually offer some relief from the unrelenting annoyance and distraction caused by these vitreous eye floaters.
Here is a typical inquiry from a younger patient:
Hello, I am XX and I am (20-39) years old. I have eye floaters that are driving me crazy and making me depressed. I have been to (2-3) eye doctors and they have told me that my eyes are very healthy and that it is nothing to worry about. I am (studying/working) at XX and I can not concentrate and do my tasks. I want:
a. you to tell me if this is going to get worse with time. I don’t think I will be able to stand it.
and/or
b. you to tell me what I can do to make it better
and/or
c. to come out for treatment
First, a disclaimer. We do not have a doctor-patient relationship and I can not give specific medical advice based on a few sentences in an email. Any response is for educational purposes only and more general in nature. With that aid, I will also state that not much is known about floaters in younger people. It is not well researched, and I do not see that changing in the near future.
Here are some general positions that I take of the etiology of your floaters:
• I do not think that using your eyes, e.g. extensive studying and computer/mobile phone use contributes to the formation of eye floaters.
• You looked toward the sun at the last eclipse? I don’t think that did it either.
• You work near lasers? Laser energy may affect the retina, but it would pass right through the vitreous and not affect it.
• You had LASIK and noticed floaters soon afterwards? That is possible. There is some distortion of the eye and possibly some inflammation afterwards.
• You took an elbow or racquetball to the eye? Possible. Blunt injury can distort the eye momentarily and may cause some changes.
• You are taking some new or different medication? Possible, but I haven’t seen or heard of any strong clusters of patients to come up with a list of possible culprits.
• You masturbate a lot? (yes, I am talking to you Mr. Young Guy from India). No, that didn’t cause your floaters. If that were the case, my practice would be flooded with young men and their floaters. The old victorian-era admonition that masturbation caused blindness is ‘probably’ a myth and unrelated to eye floaters.
Many younger patients will often suggest a possible explanation for their floaters, and I may not necessarily agree, but I can not necessarily refute their theories. Here’s the deal: I don’t necessarily really need to know the “why’s”, I need to be more certain of the “how’s”. That is, I don’t need to know why you have floaters, I NEED TO KNOW IF YOU CAN BE TREATED SAFELY AND WITH A HIGH EXPECTATION FOR SUCCESS. When you write to me and tell me your age, I will quickly place you into an age category based on my extensive experience in evaluating and treating patients of all ages. Younger patients, regardless of the putative or assumed etiology, are not usually candidates for treatment with the laser as their floaters are usually located too close to the retina. As such, I am generally pretty pessimistic in response to their inquiries to my practice. Every initial consultation to my office is money collected, but out of respect to the need for travel to Southern California, lodging, etc., I believe that it is out of respect to the patient and their low likelihood of treatment success that I am not very encouraging to them. But, in spite of all this, I do not refuse appointments to younger patients with floaters. If you want to make an appointment for an evaluation and consultation, I will be glad to accommodate you.
-Dr. Johnson
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WHAT CAUSES FLOATERS? http://www.thefloaterdoctor.com/what-causes-floaters/ Fri, 11 Aug 2017 16:10:26 +0000 http://www.thefloaterdoctor.com/?p=1903 Mostly it is aging. Aging doesn’t explain all circumstances as I do have many younger patients also suffering from eye floaters.
The reality is that it is not a well-studied topic as mostly the standard-of-care expectation for doctors is simply to check the retina and reassure the floater-sufferer that everything is OK. The vast majority of my patients are over the age of 45-50 and are otherwise healthy.
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Mostly it is aging. Aging doesn’t explain all circumstances as I do have many younger patients also suffering from eye floaters.
The reality is that it is not a well-studied topic as mostly the standard-of-care expectation for doctors is simply to check the retina and reassure the floater-sufferer that everything is OK. The vast majority of my patients are over the age of 45-50 and are otherwise healthy. Some have had previous eye procedures such as refractive surgery or cataract surgery, but many have not. I have not made the connection or have correlated any previous or concurrent behaviours, diets, activities, medications, family history, or diets that might be associated with the onset of floaters.
My personal and professional opinion is that floaters just happen. They may be more likely to happen if you are very nearsighted, or suffered some injury or trauma to the eye, but again, many if not most of my patients do not have any remarkable eye history or extreme behaviors that may explain the floaters.
OK, I know what you’re thinking. You were doing something different or unusual and that ‘must’ have caused your floaters. Some of my patients swear it was being at high altitude, another says it was scuba diving, and a young guy from Algeria absolutely believes it was excessive masturbation. I can’t really prove you wrong if you believe that, but a single anecdote doesn’t make the case. In science and medicine we say ‘correlation does not prove causation’. Unless I see a bunch or scuba divers in my office, or many people on a certain medication or extreme diet or lifestyle, these theories will remain correlations.
Really it may just be nature trying to break us back down to dust. There are no strong evolutionary pressures to keep perfectly clear vitreous. Fortunately, I don’t really need to have all the answers to these interesting and esoteric floater questions. I don’t need to answer all the ‘whys’, I need to be able to responsibly answer ‘how’.
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HOW LONG DOES TREATMENT EFFECT LAST? http://www.thefloaterdoctor.com/how-long-does-treatment-effect-last/ Tue, 25 Jul 2017 16:13:41 +0000 http://www.thefloaterdoctor.com/?p=1899 Occasionally I am asked about how long a treatment lasts or some similar sentiment. As with any fair answer to a medical question, it should begin with “It depends…”
Everyone who has sat in the exam chair in my office comes to me with a unique sets of variables: Different types of floasters,
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Occasionally I am asked about how long a treatment lasts or some similar sentiment. As with any fair answer to a medical question, it should begin with “It depends…”
Everyone who has sat in the exam chair in my office comes to me with a unique sets of variables: Different types of floasters, amounts, distribution and location, amount of movement of floaters due to liquifaction, as well as important variables in the optics of the eye (previous refractive surgery, cataract surgery, pupil size, etc.).
There is a limited amount of protein available in the eye to aggregate and form the protein densities that are the floaters in your eye. You do not replenish or replace them. It is a fixed amount. That said, there is a wide variety in how it presents to me. Simply, some types of floaters are more desireable to treat than others, in part, because they are more efficient to treat requiring less overall laser energy and/or treatment sessions.
Ultimately, my goal with the laser is to vaporize the proteins and convert them to microscopic gas bubbles where they will dissolve and go away forever. Other, less desireable types of floaters, the diffuse and cloudy types are much less efficiently treated, and have the pesky tendency to reform, although reforming to a smaller floater. That reformed floater will then require treatment. Treating these cloudy floaters feels like taking a journey of “3-4 stpes forward, and 1-2 steps backwards”. It can be frustrating, but as they say in software programming, “it is not a bug, but a feature”.
It is not unusual to still have pretty good initial treatment results with these difficult-to-treat floaters (e.g. 60-75% improved) and then see the same patient back in 3-12 months for some continued clean up attempts. This introduces my version of the Pareto Principle wherein it feels like I spend 80% of my time at the laser trying to clean up that last 20% of the floater problem.
This is not a simple answer to the question “How long does treatment last”, but it is a more complex explanation to a complex and HIGHLY VARIABLE problem where it is difficult to make concrete predictions. There are some types of floaters (e.g. Weiss Ring types) that are by definition a one-time event. After using the laser to obliterate that material it can not return and there are no more Weiss rings in the eye. These are my favorite to treat.
What do you have? I don’t know. Ultimately it takes an in-person evaluation to determine that with more confidence. Also, I have not found the chart notes from your local eye care provider to be very helpful in this regard.
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MY RESPONSE TO A CONSUMER AFFAIRS ARTICLE http://www.thefloaterdoctor.com/consumer-affairs-article/ Wed, 07 Jun 2017 23:54:41 +0000 http://www.thefloaterdoctor.com/?p=1896 A patient recently sent me a link to an old (2007) piece from consumeraffairs.com written by Mark Huffman, who from his bio usually reports on matters of real estate, gas prices and the economy. From the article ( https://www.consumeraffairs.com/news04/2007/09/floaters.html ):
The AP enthusiastically reported on a controversial laser procedure practiced by a Northern Virginia eye surgeon,
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A patient recently sent me a link to an old (2007) piece from consumeraffairs.com written by Mark Huffman, who from his bio usually reports on matters of real estate, gas prices and the economy. From the article ( https://www.consumeraffairs.com/news04/2007/09/floaters.html ):
The AP enthusiastically reported on a controversial laser procedure practiced by a Northern Virginia eye surgeon, John Karickhoff, quoting Karickhoff as claiming a “success rate of better than 90%.”Of course, if the 90% claim is accurate, that would mean the procedure has a 10% failure rate — way too high for the not insubstantial risk it involves, other eye surgeons say.
My comments: The lead in paragraph is already problematic. Success is not defined here or elsewhere. In fact, when it come to an entirely subjective phenomenon not related to eye health or pathology, performing any kind of pre- and post-treatment measurements of the culprit floaters is impossible, and even if you could, it would not necessarily correlate with the patient’s symptoms. Logically this first paragraph does not make sense either. What if there was a non-invasive, non-surgical, fast recovery, non-scarring, non-addictive method of treating chronic pain. Pain that was interfering with the patient’s quality of life and activities of daily living. But what if this theoretical treatment was 90% successful and had a 10% failure rate. Now understand… failure is not the same as complications or damage to the body’s normal functions or health of the organs, it just meant that 10% could not be helped to a significant degree. That’s actually an excellent success rate.
I will say that the 90% success rate may be optimistic and it all depends on how you define it. If you include ALL patients suffering floaters, then the success rate is probably lower as that would include the younger patients who are generally not goof candidates for treatment. If instead your are ‘cherry-picking’ a bit and include only those over 50 years with a true posterior vitreous detachment, then the success rate may even be higher. If you define it as ANY improvement and the absence of complications or damage to critical eye structure, then that would approach nearly 100% – But in my practice I don’t consider ANY improvement to be ‘good-enough-better. In other world, 10-20% percent improvement is not a success as I define it. The article continues:
“Don’t you even think of having that,” a Northern Virginia ophthalmologist advised a patient who had asked about Karickhoff’s procedure. “I have floaters myself,” the surgeon said. “I wouldn’t think of subjecting myself to that procedure and I beg my patients not to do it.”You’re risking catastrophic harm to fix a condition that isn’t even a problem for the vast majority of patients,” the surgeon, who asked not to be publicly identified, said.
My Comments: Any procedure to the eye including the very common cataract surgery and LASIK risks catastrophic injury to the eye. Fortunately these events are rare, but they do occasionally happen. Collectively, our profession has decided that the overall improvement in quality of vision and quality of life is worth this small but potentially devastating risk. There is a certain prejudice against floaters by the eye care community. They are not thought to be important or bothersome enough to justify treatment. The general consensus is just to live with them as evidenced by professor of ophthalmology and cell biology Dr. Robert Frank’s quote:
“The floaters, though disturbing, usually do not interfere with vision, Frank said, and over time, usually settle out. The vast majority of patients can learn to live with floaters, said Richard Bensinger of the American Academy of Ophthalmology. Those patients who demand treatment, he said, “are mostly obsessive-compulsive types” who allow the floaters to drive them to distraction.”
This is pretty much the company line professed by the American Academy of Ophthalmology as well many, many statements conveyed to me by my frustrated patients seeking my help. You are expected to suffer them, and if you can’t, then you must be psychologically maladaptive. This is an embarrassment for my profession. They should know that there is no intrinsic mechanism within the eye to clear that junk out. These recommendations are something they must have heard in their training,and mindlessly repeat without actually thinking about it, or actually listening to the patient’s frustrations.
And that, people is part of the problem, they just don’t think about floaters as a problem, so why would they be bothered to look for a solution to a non-problem.
]]> I HAVE SOME RETINA ISSUES. CAN I BE TREATED? http://www.thefloaterdoctor.com/retina-issues-can-i-be-treated/ Thu, 01 Jun 2017 04:16:12 +0000 http://www.thefloaterdoctor.com/?p=1892 I’ve had a few recent email queries from floater-sufferings with some concurrent retinal issues: peripheral degenerations, peripheral retinal holes (possibly lasered and treated or left to ‘probably’ heal on its own, retinal edema or swelling, macular hole, macular degeneration, etc.)
In addition to recent or active conditions, there may be a history of now healed and generally stable retinal issues like previously lasered retinal holes and tears,
]]> I’ve had a few recent email queries from floater-sufferings with some concurrent retinal issues: peripheral degenerations, peripheral retinal holes (possibly lasered and treated or left to ‘probably’ heal on its own, retinal edema or swelling, macular hole, macular degeneration, etc.)
In addition to recent or active conditions, there may be a history of now healed and generally stable retinal issues like previously lasered retinal holes and tears, retinal detachment repairs of various types, previous vitreous hemorrhage, etc.
I thought it might be worth explaining some of my thoughts, concerns, and recommendations in a lengthier blog post here, rather than recreating a more abbreviated response every time someone emails me.
I have less concern about my YAG laser causing or aggravating retinal problems than I am in being temporally associated with any potential for their natural progression and worsening. I’ll explain. The use of the YAG laser to treat floaters has been in existence for more than 20 years, but it still is not mainstream, and many eye care providers still know very little about the procedure, it’s safety record in the hands of an experienced floater-treating doctor. Their default mode is generally to recommend against treatment with the laser and to do nothing at all. I get it. I understand that position. Why would they recommend a procedure they are not comfortable with?
My concern with treating someone with new, recent-onset, or not fully healed or stable retinal issues is that they may naturally progress to a worsened condition. For instance, someone may experience a sudden shower of floaters and flashes of light. It may simply be a common posterior vitreous detachment (PVD), but while that is occurring, the peripheral retina may be at its greatest risk of developing a retinal hole or tear. If we rush into treatment of the very bothersome eye floaters with the laser, and the patient then goes on to develop a retinal detachment, it may be a not-entirely-illogical conclusion that the retinal detachment was caused by the floater treatment even if it was not.
Medico-legally, I have to look at the possible accusations and conclusions that other professionals may direct towards me. If you have your floaters treated, you then develop a retinal detachment, and if your local and trusted eye care provider states that is probably caused by the YAG laser treatment, it may create distrust and doubt at the minimum, and potentially a malpractice lawsuit.
Since floaters are not emergencies, and there is no ‘treatment disadvantage’ to waiting for treatment, I recommend waiting until unstable conditions become stable before pursuing treatment.
Here are a few unstable retinal conditions that warrant waiting until treatment:
• New or recent-onset posterior vitreous detachment with continued peripheral ‘flashes’ (the vitreous is still ‘tugging’ on the retina placing it at risk for a retinal hole or tear)
• Recently lasered peripheral retinal tear or hole. The argon laser is used to create local inflammation and eventually, better adhesion of the retina to the underlying sclera. It takes a few weeks for this to occur. It is not instant ‘spot-welding’ as it is sometimes described.
• Recent retinal detachment repair
• Macular hole, macular pucker deemed unstable possibly requiring surgery
• Recent vitreous hemorrhage, sometime associated with new onset (larger) floaters as well as ‘thousands’ of tiny dark specks. These are the individual red blood cells. Red blood cells remain dark with pigment for up to 4 months, so even with an uncomplicated vitreous hemorrhage, it is worth waiting longer before seeking treatment. I’ll recommend at least 3-4 months to allow any chance of spontaneous improvement to occur.
If it has been months since some type of interventional repair or laser and your ophthalmologist has deemed the eye(s) to be stable, it is probably safe to proceed with lasering of eye floaters. If you have a particular situation that is not addressed here, please contact me via the form at the bottom of this page with your details. I’ll do my best to make sense of it.
-Dr. Johnson
]]>
MY DOCTOR SAID THE LASER IS TOO RISKY – WHAT’S THE WORST CASE SCENARIO? http://www.thefloaterdoctor.com/worst-case-scenario/ Tue, 25 Apr 2017 21:49:09 +0000 http://www.thefloaterdoctor.com/?p=1884 Occasionally I am asked the above question. I have already addressed the risks of laser vitreolysis elsewhere in the web site which answer most of the questions people will have about risks. What appears to be a simple question: “What’s the worst thing that can happen?” is a reasonable one, but not simply answered.
]]>
Occasionally I am asked the above question. I have already addressed the risks of laser vitreolysis elsewhere in the web site which answer most of the questions people will have about risks. What appears to be a simple question: “What’s the worst thing that can happen?” is a reasonable one, but not simply answered. Any and every medical procedure carries some risk, and even an apparently simple procedure like removing a skin mole or wart could conceivable end poorly (even death?!) if the patient is allergic to the anesthetic or antibiotics.
I think this question has a two part answer: 1). The worst conceivable outcome or complication, and 2). The LIKELIHOOD of that event occurring. Ask your eye doctor about their most commonly performed eye surgery – probably cataract surgery. Then ask them to convey the list of possible complications. It should list infection, retinal detachment, dropped lens material into the posterior part of the eye requiring a vitrectomy, chronic macular edema affecting central vision, and the worst possible outcome, blindness.
I find it interesting the double standard applied here. Admonishing eye floater sufferers seeking relief for their distracting-to-obscuring opacities in the vitreous, yet they are champing at the bit to perform cataract surgery for increasing distortion and opacity of the lens of the eye.
So what is the worst possible outcome(s) of laser vitreolysis? First, it would be a direct laser shot to the fovea of the macula of the retina. Second, would be a direct hit to the natural crystalline lens causing a traumatic cataract. Third, an intractably elevated eye pressure unresponsive to medications or time.
What is the likelihood of any of these event happening? First, I believe the answer depends on the laser operator’s experience. Like any complex skill, it takes a lot of practice and experience to get good, and well as a few lessons along the way to better understand what can be treated as well as what should not be treated. I have been treating floaters exclusively since 2007 with thousands of procedures of experience and several million laser bursts in treating these floaters.. As of the date this is written, no patient of mine has lost vision due to any devastating, traumatic injury such as those listed here. Even so, I am obligated to list these potential negative outcomes in my informed consent form.
One laser manufacturer is promoting their YAG laser as a ‘floater treatment laser’ and any doctor purchasing that laser is promoted by the laser manufacturer web site as a floater treatment ‘specialist’. Remember, it is not the laser that treats floaters, it is the doctor. In order to mitigate any risk of the procedure, it is imperative to choose someone with experience. The more experience, the better.
The majority of my patients have variously complex vitreous problems. I don’t get the simpler isolated Weiss Ring nearly as much as I’d like. The decision-to-treat and/or the decision-how-to-treat is difficult and humbling at times for me, even with my experience. But complexity does not necessarily correlate to risk.
Ultimately, I have found that the pat, reflexive, dismissive warnings and admonitions by your well-meaning local eye care providers are unfounded and not based on the reality and statistical likelihood of these ‘worst case scenarios’ assuming that the doctor is very experienced and places safety first.
]]>
HD VIDEO: TREATING A CLASSIC WEISS RING TYPE FLOATER http://www.thefloaterdoctor.com/treating-a-classic-weiss-ring-type-of-eye-floater-now-in-hd-video/ Mon, 17 Apr 2017 18:25:39 +0000 http://www.thefloaterdoctor.com/?p=1881
]]>
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Building muscle through strength-training will not only increase your strength and tone, but will also increase your metabolism, as muscular people have been shown to burn more calories even when they’re at rest. You could work with weights, do squats, push ups, or crunches, among many other exercises.[5] If going to the gym isn’t for you, try strength-training at home.
Try a diet in which you consume 2200 calories (men) or 2000 calories (women) per day. This should cause a deficit sufficient for you to lose one or two pounds per week, depending on your activity level. Some women may require lower daily calorie intake, such as 1800 or 1500 a day. Start by limiting yourself to a 2000 calorie limit per day, and lower the limit if you do not see progress.
The mistake that many people make with their resolutions, though, is that they don't give themselves specific ways to actually achieve these goals. But if you're looking to get fit and feel strong next year, you're in luck. Ridge Davis, personal trainer in West Hollywood, CA, has designed a plan for you to shape up and feel amazing in the gym, no matter what your fitness level may be!
This is ratio of weight in kilograms to the square of height in meters. This parameter helps doctors judge whether the person will suffer from heart disease or strokes. Those having a BMI of 25-29.9 are considered overweight and those with a BMI of 30 are considered obese. However, this parameter is not always accurate in measuring belly fat. In fact, you can measure your belly fat with a measuring tape in front of the mirror, and set your own targets to reduce belly fat. Looking at the mirror and checking regularly will motivate you to lose the unhealthy fat lining your abdomen.
getfit is great in that it is pretty satisfying to see how my physical activity measures up. It also prompts me to kick myself when the goals are not met. The different elements that allow the community to get to know MIT better (e.g., the tunnel walks) are pretty cool. It provides another avenue for me to connect with my friends, and I think getfit is a great program to enhance wellness at MIT.
×
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Ectopic Pregnancy: a complication of IVF treatment with a simple prevention
Earlier this year, a comprehensive review of advanced fertility treatments demonstrated that the risk of serious complications as a result of advanced reproductive techniques (ART) was relatively low. Still, there is always an effort to try to reduce any adverse outcomes even further. One of the rare but more serious complications associated with successful IVF treatments is the risk of developing an ectopic pregnancy; a situation that results when the embryo migrates from where it had been placed within the patient’s uterus to another site, most commonly the fallopian tube. The frequency of ectopic pregnancy in patients that conceive through IVF is between 2% and 5%. Ironically, this is higher than the 2% to 3% incidence seen with naturally conceived pregnancies. New insights suggest what may be contributing to the elevated risk associated with ART and what steps that we can take to prevent it from happening
In order to better understand why IVF has a higher risk of ectopic pregnancy, let’s consider what we now know about implantation. The process whereby an embryo successfully establishes contact with the uterine lining is actually a coordinated event that depends upon the timing of several important factors. One major factor is development. The embryo must be develop to the blastocyst stage—where it appears as a fluid filled ball with a clump of cells concentrated at one location. It then must break out of its protective coating in a process called hatching. Another important factor is the hormonal milieu. The uterine lining must be hormonally prepared for the initial contact with the hatched blastocyst; there is typically a limited time period of about 36 hours during which the conditions are ideal for attachment (the first step towards implantation) to occur. A recent analysis compared several variables associated with different embryo transfer strategies.
For their study, they reviewed over 3,300 embryo transfers. They compared the developmental stage of the embryos as well as whether the embryo transfers were done during the same cycle as the egg retrieval (Fresh) or whether they had been cryopreserved and transferred later (Frozen). The difference between a Fresh transfer and a Frozen transfer is two-fold. Not all embryos develop at precisely the same rate. So with Fresh transfers, some embryos are more developed than others. In fact, they separated their analysis based upon whether it was 3, 5 or 6 days after the egg retrieval. In a natural cycle, an embryo typically enters the uterus 5 or 6 days after it is released from the ovaries. With Frozen embryos, they are actually preserved when they have reached a specific stage of development chosen by the IVF center. As a result most frozen embryos are at the morula stage (day 3) of development or the blastocyst stage where they are ready to hatch. Some embryos reach this preimplantation stage on the 5th day of development and others take until the 6th. If they do not make it by day 6 it is considered an unhealthy embryo. The other distinction is that Fresh transfers tend to be associated with higher than normal hormone levels as a result of the ovaries producing multiple mature eggs instead of just one or two. By contrast, the goal of a Frozen transfer is to create a hormonally balanced environment within the uterus that more closely represents what happens in a natural physiologic conception.
In order to try to differentiate both of these factors, this study compared Day 3-Fresh and Day 5-Fresh to Day 3-Frozen, Day 5-Frozen and Day 6-Frozen, The finding in this analysis was that risk of ectopic pregnancy was lowest for Day 5-Frozen embryo transfers. In fact, the calculated risk for those patients was far less than 1% suggesting that the ideal transfer strategy is to split the ART cycle to optimize the healthy pregnancy rate while minimizing the risk of ectopic pregnancy. A previous study also found that embryos that were judged to be of poorer quality—based upon their appearance under the microscope—also pose an elevated risk of ectopic pregnancy making the embryo grade a potential third factor to consider. There have also been two other studies that have also found that frozen embryo transfers (FET) have lower ectopic pregnancy rates than fresh embryo transfers.
Since many centers now have advanced freezing techniques to safely preserve embryos it makes sense for more patients to separate the process of ART into two parts; the first month to create the embryos and the second month to transfer them. Although this split cycle strategy lengthens the time from start to pregnancy, there is compelling evidence that for many patients it will improve their chance of having the highest pregnancy rate with the fewest possible complications and the lowest possible risk.
Link to http://jama.jamanetwork.com/article.aspx?articleid=2088842#Discussion
Link to http://www.fertstert.org/article/S0015-0282(14)02379-6/abstract
Link to http://journals.lww.com/greenjournal/Fulltext/2006/03000/Ectopic_Pregnancy_Risk_With_Assisted_Reproductive.11.aspx
Link to http://www.fertstert.org/article/S0015-0282(12)01889-4/abstract and http://www.fertstert.org/article/S0015-0282(11)00267-6/abstract
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Weight Loss Medication Garcinia
, , Comments Off on Weight Loss Medication Garcinia
Accelerate Your Weight-loss With Herbs And Also Seasonings
I wonder just how much it is typically recognized that the advantages of making use of herbs and also spices can accelerate your weight reduction initiatives, by quite a substantial quantity in fact.Weight Loss Medication Garcinia
Most of us recognize that herbs as well as flavors are utilized with food preparation to varying levels, and also of course the primary factor for doing so is making food far more delicious and fascinating.
I suspect nonetheless that you may be shocked at the substantial health advantages that could also be gained by using them. In stating this I am referring to those day-to-day things that could be found in
most food supplies, as well as not necessarily those unique and also possibly not so well known varieties.
I occurred to uncover the numerous advantages of herbs and also flavors and also that they could be most advantageous to a weight reduction program, when I was doing incredibly thorough research for my most current book.
The results of that research were so extensive, that it could be the basis in itself for a total magazine, and a lot more in-depth for that reason, than I might perhaps include in this brief article.
However I have actually been able to consist of a reasonable amount of information below concerning various natural herbs and spices which are understood to especially assist to accelerate fat burning, which is also along with their superb total health and wellness benefits by the method.
You ought to locate that you will be able to buy these herbs from any kind of good Herbalist distributor.Weight Loss Medication Garcinia
Garcinia Cambogia: (Garcinia cambogia) is an herb which is offered largely for enhancing weight-loss as well as increasing the quantity of lean muscle. This is additionally called hila or brindell berry. One of the major benfits of Garcinia is that it acts as a cravings suppressant and also quits the body from storing fat.
Pysillium: (Plantago spp.) This saucy little herb has several health and wellness advantages. Physillium is understood to assist reduced cholesterol, and one more significant benefit is that it additionally aids to
stop irregularity. If you use it as component of your fat burning program, it can aid you to consume less calories but still feel really full.
This is due to the quantity of fiber that it contains.
I mentioned earlier that it does assist in preventing constipation, but in order to accomplish this you must ensure that you drink a lot of water.
Siberian Gingsing: (Eleutherococcus senticosus) If you are mosting likely to begin normal exercise as component of your health and wellness and weight reduction routine, which is generally to be very advised, after that this is an actually beneficial natural herb.
It could aid your body adjust to the stress of unfamiliar modifications, and it will certainly aid to make you feel much less exhausted also when you are doing straightforward exercises like strolling for instance.
So in turn therefore you are more probable to adhere to your workout regimen.
Little Understood Keys In Your Food supply
Cayenne: (also called Capsicum, warm pepper, chilli pepper, tabasco pepper). The majority of us have cayenne in our groceries, and also it is very generally used in numerous food dishes. Cayenne can be located in numerous forms such as ground flavors, teas, and would certainly you think it, topical creams.
It is popular for its antitoxidant activity, and also substantially helps with osteoathritis and rhumatoid athritis, shingles, as well as diabetic neuropathy. Pure Garcinia Cambogia Ultra Bogota
A note of care nonetheless: Cayenne might act with anticoagulant medicines so make sure to consult with your doctor. Extreme use may likewise irritate the intestinal system.
Made topical capsacin creams could trigger a burning sensation, so test initially on a tiny area of the skin, bearing in mind to clean hands extensively after applying the cream. This will certainly prevent it infecting the eyes nose or other delicate areas.
Fennel: is belonging to the Mediterranean and also is commonly made use of throughout the globe. You will certainly discover it in teas, pills, casts and also lozenges. Fennel can be used to assist with bloating, windiness, moderate digestion spasms, catarrh, as well as coughs. It also has antimicrobal, antispadmodic, and also anti inflammatory residential or commercial properties.
A note of care below: Fennel can in some cases trigger unusual sensitive skin as well as respiratory tract reactions. Fennel is likewise a prospective source of artificial oestrogens and also need to be prevented if you are pregnant.
Garlic: you can acquire this fresh, or the one you will most likely have in your food supply will be dried out. The downside of garlic is the smell which it leaves on your breath, yet chewing some
parsley after eating will quickly figure out that problem.
Garlic is also understood in order to help boost the body immune system, as well as to help in dealing with cancer. Well recorded wellness benefits consist of lowering cholesterol, battling infections, and decreasing blood
pressure.
Once again a note of care: garlic may also engage with anticoaglant drugs, so do make certain to contact your doctor if in any type of doubt. Rare instances of allergies are known, and some people could potentially experience heartburn and even windiness.
These are simply a few of the natural herbs you could use in food preparation, yet do remember that there are numerous many more, and the benefits being used them frequently can be fairly impressive.
You will realize naturally that when utilizing them as component of any type of meal to use them sparingly, regarding add too much would certainly just spoil the dish.
Similar to everything in life one ought to try and also strike an equilibrium, after all you understand just what they claim “all points in moderation”.Weight Loss Medication Garcinia
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Call : (817) 923-9000
4750 Bryant Irvin Rd N
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» What Do I Do About This Bulging Disc?
What Do I Do About This Bulging Disc?
One of the most common expressions that we hear from our patients is that they are having back pain because of a bulging disc. This is one of the most common pathologies to show up on imaging with an MRI. While it is true that you might have a bulging disc, it is not always the cause of your symptoms. Here’s some information about bulging discs, more commonly known as disc herniations so hopefully you can have a better understanding of what these are and how they are usually not as scary as they sound.
Whenever you hear your physician tell you that you have a herniated disc, they are referencing one of the small cushions that sits in between each level of vertebra in the spine. An easy way to think of the structure of the disc is to compare it to a water balloon that has a rubber casing.
Essentially if you have a dysfunctional movement taking place anywhere in your spine it can cause a shift in the position of the disc over time. This is how your spine typically adapts to the load being placed on it with whatever activities you are doing. If enough stress is placed on the disc, the nucleus of the disc can push through the outer coating.
If this is taking place it can irritate the nerve structure near the involved level of the spine. When the nerve becomes irritated you can have numbness, burning, weakness, or shooting pain into the arm or leg. However, we don’t frequently see a pattern of symptoms that indicate a true disc dysfunction and symptoms. Most of the time there are several different factors involved with what you may be feeling so the bulging disc is just one small part of the issue.
As I just mentioned it is pretty rare to actually have symptoms strictly because of the disc dysfunction. The most important thing that needs to happen is to identify which movements are causing the symptoms you may be experiencing. One of the best ways to do this would be to do a quick 15 minute screen. Then based on different patterns that we see; we can tell you if you are experiencing a significant nerve dysfunction due to a disc bulge and what we should do to address it. It is rare for the disc bulge to be the main issue but, if it is we will quickly identify if conservative treatment will be the most effective option for you at this time.
One of the most common concerns that we hear in the clinic is that patients believe that they need surgery for their symptoms. The MAJORITY of the time we can get a positive response in your symptoms with conservative treatment. This means that most of the time we can avoid surgery entirely! We can also identify if there are other structures influencing what you may be feeling such as the joint or muscle tissue around the area.
Here are some symptoms that you may experience if a nerve is being impacted by either a disc or joint dysfunction in the spine:
Arm or leg pain: Depending on which segment of the spine is affected
Weakness: Because of the potential nerve irritation, certain muscle groups may be inhibited.
Burning, numbness, or tingling in the extremities: These are all classic signs and symptoms consistent with nerve irritation and pain.
Something else we get asked frequently is if the actual disc herniation will go away. There have been studies that show that it CAN change over time with the right treatment progression. As I mentioned earlier a significant amount of the disc composition is water, so it is very adept to changing with movement. We typically like to see significant changes in patient symptoms relatively quickly with what we do. Again, usually these are asymptomatic, so the priority is to address the muscle imbalance and movement impairments to relieve stress on the spine. The emphasis isn’t necessarily on changing the position of the disc as it may just be an adaptation to the activities you perform in your daily life.
If you happen to be going to a visit to your doctor for back pain, here are a couple of things to know. It is extremely common to see disc herniations, disc bulges, or prolapsed discs on MRI results. Sometimes it is scary to hear the results without knowing what it truly is. You may get told you have something called “degenerative disc disease.” As concerning as this may sound it is actually a normal process that our disc tissue goes through over time. If you are not experiencing any “red flags” then there is a good chance your symptoms can be resolved with the appropriate treatment interventions.
If you do happen to get these results, there is a good chance that it can be relieved with conservative treatment that we do here at Curnyn Physical Therapy. If the symptoms are relatively recent, we like to see a quick turnaround for most of our patients and their back or neck pain.
Here are a couple of symptoms that may indicate you do need to seek medical attention immediately (red flags):
• Bowel or bladder changes
• Sensation loss in the inner thighs or groin area
If you happen to be experiencing these symptoms it may indicate a severe compression of the nerve by either the joint or disc tissue at a specific level of your spine.
On our Facebook page we have a video discussing a couple of straight forward exercises you can do to address nerve irritation due to a disc herniation. We will also have an in-depth video discussing what we can do for you and what to look out for. Thanks for reading and please let us know if there is anything, we can do for you. If you happen to be suffering from back or neck pain, please give us a call at (817) 923-9000 and we will get you set up with a FREE 15 minute screen to see if PT is the right choice for you. You would be surprised how often it is!
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Long-term effects of an underweight baby
Written by cina coren | 13/05/2017
Long-term effects of an underweight baby
Weight gain in babies is based on many factors (Siri Stafford/Photodisc/Getty Images)
Parents are always concerned about the weight gain of their new baby. A doctor may conclude that a baby is not gaining enough and is considered "underweight." What that means differs from doctor to doctor, but most physicians use various charts and comparisons to determine a baby's status and try to work with the parent to alleviate the condition and bring the baby to an acceptable weight for its age.
Why Are Some Babies Underweight?
There are many reasons why a baby would not be gaining properly, and the side effects of being underweight can sometimes be long lasting and dangerous. When a doctor is taking the history of the baby and its parents, he is usually looking for some behavioural or genetic causes for the baby's inability to put on weight. A careful review of the family's medical history as well as the actual birth process may provide information that explains the baby's condition. A physical examination will usually reveal any metabolic, neurological or gastronomical problems, but these are rarely the cause of slow weight gain. Vitamin D deficiency, sometimes referred to as rickets, is sometimes cited as a cause for being underweight, but is most often not the case.
Underweight Babies May be Slower to Develop
A baby who continues to lose weight or does not gain weight according to his age and body structure can suffer from many physical and mental health implications. Low caloric intake can result in below-normal brain development, slower motor skills and biological difficulties. Often the baby is colicky and uncomfortable. He may be hyperactive and have difficulty quieting down or relaxing. Low weight babies are subject to additional problems. Often they have difficulty sucking and will be unable to breast feed, missing out on the vitamins, minerals and other nutrients found in breast milk. These will have to be supplemented. Underweight babies have less immunity and therefore are more susceptible to viruses and other bacteria.
Problems in Childhood and Adulthood
Singapore researchers reported in a 2002 issue of the British Medical Journal that underweight babies have more than 20 per cent more psychological problems as adults than babies whose weight falls in the acceptable percentiles. In addition, children who were underweight as babies reach their developmental milestones later than babies who were of normal weight. As children, they have more difficulty paying attention in school and may lack certain social skills.
Underweight Babies Should be Treated Seriously
If a child is not gaining sufficient weight over a period of a few months, or if she has lost weight over this time, extreme measures must be taken, as being underweight can have long-term effects into childhood and adulthood. Working side by side with a psychologist, who can work on reducing the baby's stress, a nutritionist can provide the necessary guidelines to resolve the problem. The appropriate formulas and food supplements can make quite a difference in a baby's weight gain. Conditioning the infant in the best ways of eating is important for immediate gains as well as for her future.
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Search For a Provider Facebook Twitter Instagram YouTube ES Contact Us
Did You Know?
Nocturnal Penile Tumescence
Nocturnal Penile TumescenceMen have several erections while they sleep at night.
The clinical name for these erections is nocturnal penile tumescence (NPT). They happen to males of all ages, even babies, but they have nothing to do with sexual stimulation.
So why do they happen? Scientists aren’t completely sure, but NPT seems to be affected by sleep cycles.
==================================================
Who knew? There's a science of "morning wood." Click here to tweet.
==================================================
Humans go back and forth between deep sleep and rapid eye movement (REM) sleep several times during the night. REM sleep is lighter sleep and is the cycle when dreams occur.
Continued...
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Medication Guide App
Radiopharmaceuticals
Radiopharmaceuticals are radioactive chemicals or pharmaceutic preparations, labeled with a radionuclide in tracer or therapeutic concentration. Radiopharmaceuticals are agents used to diagnose certain medical problems or treat certain diseases. They may be given to the patient in several different ways. For example, they may be given by mouth, given by injection, or placed into the eye or into the bladder.
Please refer to the drug classes listed below for further information.
Hide
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High blood pressure (hypertension) may be an autoimmune disease
By: Dr. Victor Marchione | Blood Pressure | Friday, September 11, 2015 - 09:30 AM
High blood pressure (hypertension) may be an autoimmune diseaseMedical experts have known for a long time that there are about 80 different types of autoimmune disease, and new evidence suggests that we might be able to consider high blood pressure or hypertension as another autoimmune disease.
High blood pressure or hypertension is a common cause of heart attacks, strokes and kidney failure, making it the biggest risk factor for disability and death around the globe. While a lot of investigation has pointed to obesity, high stress and diet as contributing to the disease, an exact cause has never really been established. Living with it gives sufferers an uneasy feeling. This latest research sheds more light on the condition.
Scientists at Monash University in Melbourne, Australia discovered that when they stimulated the immune system of mice, they could cause hypertension. When they cut down the immune response it could restore blood pressure back to normal.
Associate Professor, Grant Drummond, was involved in the experiment and has said that the results could open up a new way of treating high blood pressure or hypertension. Following the study he described how stimuli that can cause hypertension can in fact lead to an increase in B cells and the production of antibodies. These antibodies get stuck within artery walls and seem to promote inflammation. Inflammation causes the arteries to become stiff and scarred. Stiff arteries are what can cause hypertension.
The research team discovered that mice raised without mature B cells didn’t develop hypertension; while at the same time, blocking cells in normal mice led to a return to normal blood pressure. In other words, it cured the mice of their hypertension.
About 70 million Americans have high blood pressure and 4 million Australians struggle with it. Blood pressure is a force of blood that pushes against our artery walls as it circulates throughout our bodies. It usually rises and falls throughout the day; however, when it stays high for a long period of time, it can cause serious health complications.
Causes and risk factors of high blood pressureCauses and risk factors of high blood pressure
High blood pressure or hypertension is essentially the same ailment. For some people high blood pressure happens over several years. This is referred to as “primary hypertension.” Others experience high blood pressure when they also have kidney problems, thyroid issues, defects in their blood vessels, are on certain medications, suffer from obstructive sleep apnea or are abusing alcohol or drugs. This type of high blood pressure is called “secondary hypertension.” There is also a class of high blood pressure known as “pulmonary hypertension.” It is high blood pressure that takes place in the arteries of the lungs.
Although high blood pressure causes can be hard to define, there are a number of risk factors. Some are listed and described below:
• Age – high blood pressure or hypertension is more common in men and more likely over the age of 65.
• Genetics – high blood pressure tends to run in families.
• Race – statistics show high blood pressure is more common among black people.
• Overweight – you need more blood to supply oxygen to your tissues if you are overweight. This puts pressure on your artery walls.
• Tobacco use – chemicals in tobacco can damage artery walls, increasing blood pressure.
• Physically inactive – the more inactive you are, the harder your heart has to work, thus putting pressure on your arteries.
• Too much salt – consuming too much salt leads to fluid retention, and that can increase blood pressure.
• Too little potassium – if you don’t get enough potassium in your diet, you may accumulate too much sodium in your blood, which can lead to high blood pressure.
Stress is another one of the high blood pressure causes that we should pay close attention to. Stress often leads to a temporary increase in high blood pressure. Unfortunately, many people try to fight stress by relaxing with alcohol or cigarettes, which only adds to the problem.
Pregnancy can also lead to high blood pressure. In fact, high blood pressure occurs in up to eight percent of all pregnancies. Many pregnant women with high blood pressure have perfectly healthy babies, but some develop what is referred to as “gestational hypertension,” so they must be monitored closely. High blood pressure can harm the mother’s organs, cause low birth weight or lead to premature delivery.
Symptoms of high blood pressure
With most diseases we receive a warning through the presence of symptoms. So what are the symptoms of high blood pressure? Actually, most people with high blood pressure don’t have any. This is why the condition is called “the silent killer.” Sometimes high blood pressure can be dangerously high, and the person has no idea. On rare occasions a person can experience headaches and nosebleeds, but these symptoms don’t happen until the blood pressure is so high that it is life threatening.
Most people have their blood pressure taken as part of a regular doctor’s appointment. Those who don’t have their blood pressure checked on a regular basis can discover it is high after damage has been caused to their kidney, their heart, or after they have had a stroke.
There are a number of complications linked to high blood pressure or hypertension, aside from heart and stroke. High blood pressure can lead to aneurysms forming in the blood vessels. An aneurysm is a bulge in the wall of an artery. If it bursts it can be fatal. Blood vessels in the eyes can also be affected by high pressure. They can burst causing vision problems, including blindness.
High blood pressure prevention
High blood pressure preventionLeading a healthy life that includes exercise and a nutritious diet is the best high blood pressure prevention. The National Heart and Blood Institute developed the DASH diet based on studies showing that certain foods could improve the level of fats in our bloodstream, which can reduce the risk of cardiovascular disease.
Here are the basics of the DASH diet:
• Vegetables, fruits, and fat-free or low-fat dairy products
• Whole grains, poultry, fish, beans, seeds, nuts, vegetable oils
• Limited sodium, sweets, red meats, sugary drinks
• Low in saturated fats and trans fats
• Rich in potassium, calcium, magnesium, fiber, and protein
Being active is an important part of maintaining good overall health, but research shows it is an excellent stabilizer when it comes to blood pressure. Recent studies also suggest that exercise can benefit people who suffer from pulmonary hypertension. In the past pulmonary hypertension patients were discouraged from exercising due to fear it would add extra stress to their hearts, but a study conducted by cardiologists at UT Southwestern Medical Centre showed low levels of exercise had a positive impact on the heart and overall health of those with pulmonary hypertension. The authors of the study do suggest that if you have pulmonary hypertension, you consult with your doctor before starting an exercise program.
It is never good to take matters into your own hands when it comes to your health; however, as an added precaution, you can monitor your own blood pressure in addition to having your doctor check it on a regular basis. Home blood pressure monitoring kits can be purchased at some pharmacies and medical supply outlets (some pharmacies also have blood pressure machines free for customer use). This can help you keep a closer eye on your blood pressure and help alert you to potential problems. Home monitoring kits do have limitations, and some kits are more accurate than others. It is important if you are taking medications for high blood pressure to continue with that medication even if you suddenly get a normal pressure reading. Talk to your doctor first before taking any drastic steps.
Monitoring and treating blood pressure can be tricky. For some people the slightest amount of stress can give a false reading. In certain cases, the body will reject hypertension medications, making it very difficult to lower blood pressure. The Australian study that suggests blood pressure or hypertension is an autoimmune disease could help reform the way many people who are resistant to traditional drug therapies are treated in the future.
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Related Reading:
A daily nap could reduce blood pressure, prevent heart attack
Pulmonary hypertension patients can benefit from exercise training: Study
Sources:
http://www.abc.net.au/n,ws/2015-09-09/scientists-make-breakthrough-in-fight-against-hypertension
http://www.cdc.gov/bloodpressure/faqs
http://www.nhlbi.nih.gov/health/resources/heart/hbp-pregnancy
http://www.nhlbi.nih.gov/health/health-topics/topics/hbp/signs
http://www.nhlbi.nih.gov/health/health-topics/topics/hbp/prevention
http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/AboutHighBloodPressure/What-is-Pulmonary-Hypertension
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Wormwood & parasites, cancer, inflammation and more benefits
By: Cat Ebeling
Co-author of the best-sellers: The Fat Burning KitchenThe Top 101 Foods that Fight Aging & The Diabetes Fix
Wonders of Wormwood
Wormwood. To those who are unfamiliar with this herb, it doesn’t conjure up a pretty picture does it? Either you think of some of rotting hunk of wood full of worms, or you just get the heebie-jeebies from anything you might put in your body with the word “worm” attached to it. However, wormwood is a valued herb, and you may find it to be one of your biggest allies, especially if you travel or have been exposed to parasites—and like it or not, most all of us have been exposed to parasites, at one point or another.
Yikes! Parasites?
A parasite is a general term for any organism that can live off another living organism. Parasites can be anything from pin worms or tapeworms, to something so small it takes a microscope to view, like any type of fungal infection, protozoa or amoeba. So even things like food poisoning can often result in an intestinal parasite taking up residence in your body. And, if you’ve ever traveled (especially to Latin American or South America), you may have had to deal with a bout of ‘intestinal distress’ which is often caused from a giardia infection—a protozoan parasite that often gets into water and food supplies. Giardia is actually very common in the United States as well, especially in our rivers and streams. Other common parasites can come from undercooked meat, sushi, soil or unclean water, and even spread from person to person. If you’ve ever had food poisoning, you know what parasites are.
General symptoms of a parasitic infection often include fever, aches, nausea, fatigue, stomach pains, bloating, and diarrhea. While our bodies can sometimes fight off an intestinal parasitic infection, it can take up to 6-8 weeks of being entirely miserable, and never straying far from the bathroom. And some can take up residence in our bodies indefinitely! Conventional medicine has several medications for different types of parasitic infections that often include some type of antibiotic, which also kill off all the helpful, protective bacteria in our guts.
How Can Wormwood Help?
Wormwood, or Artemisia absinthium as it is officially called, is of the same plant family as daisies and ragweed. Wormwood is an herb that has been around since Biblical times, and is best known as the primary ingredient in Absinthe, an alcoholic beverage. Absinthe was outlawed for many years in the U.S. because it is considered toxic, addictive, and can cause hallucinations, but wormwood is still allowed as an herbal supplement. Wormwood contains a volatile chemical compound called, “thujone” which is concentrated in the alcoholic liquor, absinthe, and is responsible for the toxic reactions to it. When using wormwood for therapeutic uses, it contains little if any, thujone, so is not toxic, but only take as directed, and in smaller doses.
Eliminates Parasites
Wormwood, as it is aptly named, is extremely effective for intestinal parasites. It works especially well on intestinal worms like the common pinworm and roundworms. Pinworms are a very common infection, especially in small children (but check with your physician before giving wormwood to children). Wormwood also works well to eliminate bacterial infections such as E.coli, salmonella, and even fungi like candida albicans. Wormwood often comes in combination with black walnut, and clove extract, which all work together to be highly effective against all parts of the parasite life cycle. Since wormwood is so effective at killing pathogenic bacteria such as salmonella, E.coli, as well as parasitic organisms such as giardia, it is no surprise that wormwood is an effective treatment for SIBO, or small intestine bacterial overgrowth as well.
Stops Malaria
Malaria is a very serious disease also caused by a parasite that gets into our bloodstream from the bite of an infected mosquito. People who contract malaria from a mosquito bite can be seriously ill. And unfortunately, anti-malarial drugs have a lot of side effects, both on the preventative side and the therapeutic side.
Artemisinin is one of the extracts that is taken from the Artemesia or wormwood plant that is highly effective against malaria. This substance is known as one of the most powerful antimalarials there is. It is even acknowledged by the World Health Organization as being a powerful antimalarial for P.falciparum malaria, and recommends it as a first line of defense.
Artemesinin turns deadly when in the presence of iron. Recent experiments show artemisinin is effective against the malaria parasite because it reacts with higher levels of iron in the parasite to produce free radicals. The free radicals then destroy the cell walls of the malaria parasite.
Cancer Killer
Wormwood’s active ingredient, Artemisinin, has also been shown in studies to actually be effective on certain types of cancer, including breast cancer and prostate cancer. Artemesinin works in a similar way with cancer cells and iron. Cancer cells often feed on iron present in the body, and the greater the iron content, the more Artemesisin interacts with the cell to kill it.
Certain cancer cells can be loaded with iron, and Artemisinin interacts with the iron to break down the cancer cells and kill them. In a 2012 study on breast cancer cells and normal breast cells using Artemisinin, the breast cancer cells all died, leaving behind healthy normal cells.
Anti-Inflammatory
Wormwood is also highly effective at decreasing the inflammation and discomfort associated with Crohn’s disease, to the point where the patients did not need to take their normal dosage of steroids. Researchers also found a steady improvement in symptoms and 65% went into complete remission over the placebo group. Wormwood also showed to have positive effects on mood and quality of life, and none of the side effects of steroids.
Wormwood is also valuable as relaxation agent as a calming agent and to promote restful sleep. It also reduces inflammation, swelling, and pain, as well as being extremely useful for autoimmune disease. It also functions as a highly effective antibacterial agent, for internal intestinal issues, as well as external wounds, ulcers, and rashes. And unlike conventional antibiotic agents and medications, bacteria and parasites do not usually develop resistance to this powerful natural healing substance.
Wormwood is generally found fresh or dried, essential oil, tablets, and capsules from most health food stores. It can also be used in fresh or dry form to make an infusion or tea. It’s best in its dried form as it contains very little of the toxic substance, thujone. Wormwood tea is especially help for digestion and bloating. You can also make a homemade bitters recipe, like this one. Wormwood is often found in combinations with black walnut extract and cloves as a parasitic cleansing agent. To rid oneself of parasites, its best in a pill or capsule form.
Since wormwood is a relative of the daisy and ragweed family, caution if you are allergic or sensitive to ragweed pollen—you may be sensitive to wormwood as well. Wormwood should be taken under the supervision of a professional, and not taken for more than four weeks at a time. It is not meant for long term usage. Do not take if pregnant or nursing, or if you have epilepsy or seizures. And avoid using it as an essential oil in aromatherapy as it contains high amounts of the toxic ingredient thujone which can act as a neurotoxin.
300handsanitizer1jpg
References:
https://draxe.com/wormwood/
http://www.sciencemag.org/news/2001/11/wormwood-extract-kills-cancer-cells
https://www.earthclinic.com/herbs/artemisinin.html
About The Watchdog
Mike Geary has been a Certified Nutrition Specialist and Certified Personal Trainer for over 15 years now. He has been studying nutrition and exercise for almost 25 years, ever since being a young teenager. Mike is originally from Pennsylvania, but has fallen in love with mountain life and now resides in the picturesque mountains of Utah. Mike is an avid adventurist and when he’s not spending his time skiing, mountain biking, hiking, or paddleboarding on the lake, he has enjoyed skydiving, whitewater rafting, piloting an Italian fighter plane (seriously), scuba diving, heli-skiing, and traveling all around the world, enjoying learning about different cultures. At the age of 40, Mike now feels healthier, stronger, and more energetic than when he was 20... All because of a healthy lifestyle and great nutrition!
Check Also
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By: Cat Ebeling, RN, MSN-PHN, co-author of the best-sellers: The Fat Burning Kitchen, The Top 101 Foods …
6 comments
1. Thank you for informative facts about this plant. I will look for it in the pasture and try to use it carefully : )
2. I love this info. I have been studying Alternative since my daddy died of Radiation poisoning in 1978.
I had a cyst taken out of my breast. they said for prevention I needed 6 1/2 weeks of Radiation.
I refused and my family insisted I do as I was told. I did. and now I am paying for it. I have scars on my lungs.
I have a breathing machine at night and a Nebulizer during the day. I like to make my own breathing solution for the Nebulizer. Activz Silver, a few drops of Peppermint Oil and Distilled Water. I also take” Terry Talks Nutrition products.” When I did this I coughed up a lot of mucus.
I have cyst all over the Thyroid Gland. Dr. Terry said I needed a lot of the right kind of Iodine to dissolve the cysts. I am taking his recommendation and feeling much better.
oil and deionaved
• Hello Mary Smith,
What kind of iodine your taking to dissolve the cysts?
• You might want to consider systemic enzymes. I am not a doc but have seen amazing results from simple enzymes to heal the scar tissue created from radiation as well as dissolving cysts. The product you need to look at IMO is Vitalzyme Xe, but you want the Xe which is the professional strength…
• Mary, I am sorry you went through this. Most don’t understand the outcome of the treatments. I know your family felt it was best.
I don’t do mammograms, I do sono grams. My body doesn’t like radiation.
I am interested in knowing what Iodine your doctor suggested.
Keep doing the natural as best you can. Great work.
SB
3. Is wormwood contraindicated with medication like beta blockers, in particular Metoprolol succinate ER? I took Parasid Forte, containing wormwood and black walnut, under my physician’s supervision and was on it for shy of a month (I was supposed to take it for 2 months) when I had a stress-induced heart episode for which I took 50 mg of Metoprolol. While my heart calmed down on its own later that day (the Metoprolol didn’t do anything), I got very ill with nausea and vomiting beginning the next day, ultimately discovering my liver had been damaged. It took weeks of careful diet and healing foods and supplements for the liver for me to heal it, but I am left wondering what caused the liver damage. A contraindication with the Metoprolol remains suspect but I can find no information on it.
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Quit Smoking and Live a Healthy Life
Smoking has numerous side effects. It affects the smoker as well as the ones around him/her. A smoker inhales only 15% of the cigarette smoke while the rest is let out in the atmosphere and poses a serious danger to his family. More than 50% of the smokers die of a smoking related cause.
Smoking is recognized as the single most common preventable cause of death. Cigarette smoke contains more than 4000 chemicals out of which around 23 are recognized as carcinogens. Needless to say, cigarette smoke is very dangerous to the body.
Quit smoking
Cigarette smoke kills millions of people each year and still men continue to smoke. If you are really concerned about your health and of the ones around you, it is advisable to quit smoking. Once you stop smoking, the blood circulation in your body improves and your blood pressure returns to normal levels. You can avoid the risk of cancer in the long term by quitting smoking, and live a happy and healthy life.
Addiction to cigarettes causes mental problems such as anxiety and depression.
A person who is trying to quit smoking faces numerous withdrawal symptoms, such as loss of appetite, anxiety, and sleeplessness. Depression can become a serious condition and it can affect the individual adversely, if it is not treated on time. You can follow these tips to quit smoking.
Believe in yourself. Lack of self belief will scare you from many problems. If you believe that you can quit, one day you will. Determination is the first thing you should have.
After you complete reading this list, make your own list. Create a personal plan for quitting.
Write down why you wish to stop smoking. Is it to feel better, live longer or become closer to your family? Read it daily so that you can stick your goal.
Ask your friends and family to support this decision of yours and be non-judgmental about it. Tell them to support you even if you are a little irrational at times in this endeavour.
Set a quit date and stick to it. Extinguish your cigarettes and cigarette related problems forever on this date.
Exercise daily and eat a balanced diet. Drink a lot of water.
Keep yourself occupied in some work or the other.
Talk with your doctor if you need additional support for quitting. Your doctor may prescribe you certain medications such as Champix, so that you can quit smoking easily.
Champix
Varenicline, marketed as Champix is an is an FDA approved oral prescription drug use by smokers to quit smoking. It works in two ways; first, by reducing the nicotine cravings by binding the receptors in the brain that respond to use of nicotine and by reducing the withdrawal symptoms. Secondly, it reduces the pleasure received by the smokers on smoking a cigarette.
Whatever your decision, you must always consider the risks. Start smoking or even stop smoking, you have to enjoy it and you have to do it wholeheartedly. USB lighter gives you comfort in smoking, besides being easy to carry and elegant, this lighter does not need any ingredients, because it is an efficient way of charging by means of a USB charge. if you make a decision to smoke, then be an elegant smoker.
A dose of 0.5 mg is to be taken daily for the first 3 days. The similar dose is taken twice a day from the fourth to the seventh day and after that, a dose of 1mg is taken everyday.
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Norvasc side effects
Alternatively, the norvasc starting dose effects is 900 mg/day given as three equally divided doses. These doses are side lower than the side therapeutic doses for effects both drugs. Dosage is determined by the side treating norvasc physician according to side individual tolerance and side efficacy. As effects with other anti-epileptics, attempts side to effects withdraw concomitant anti-epileptics in treatment refractive patients on more than one anti-epileptic, in order to side reach gabapentin monotherapy have a low success rate. Analysis of norvasc 10 mg norvasc responder rate using combined data from all three studies and effects all doses (N162, neurontin; N89, placebo) also showed a significant advantage for neurontin over placebo in reducing the frequency of effects secondarily generalized tonic-clonic seizures. Their synthetic analogs are primarily used norvasc for their potent anti-inflammatory effects in disorders of side many organ systems. This antibiotic can treat many different types of bacterial infections, and is only available with a prescription from a veterinarian. It is recommended that latent amebiasis or active amebiasis be ruled out before initiating corticosteroid therapy in any patient who has spent norvasc 10 mg time in the tropics or any patient with unexplained diarrhea. Who should NOT take this medication? Discontinuation of corticosteroids may norvasc norvasc result in clinical improvement. This is, in addition, to effects poorly digested carbohydrates and other harmful substances, which in the future can lead to obesity. That was a really scary experience for someone who depends on hearing to be able to do live radio. Dogs with liver or kidney problems should also refrain norvasc 5mg from using doxycycline, as continued use norvasc of antibiotics will impact on the overall health of these vital organs and potentially lead to a premature death. Prednisone can be a life saving drug. Side effects of Prednisone might affect a wide variety of human systems norvasc and organs. The ear, nose and throat specialist diagnosed my deafness as idiopathic sudden effects sensorineural hearing loss. My doctor never warned me about any of this. Peak plasma concentrations were similar across the entire age group and occurred side 2 to 3 hours postdose. Table 2 dosage OF gabapentin IN adults based ON renal function Creatinine Clearance (mL/min) Total Daily Dosea (mg/day) b-600 15c 150b-300 a Total daily effects dose should be administered as three divided doses. If your side veterinarian has prescribed doxycycline for your side dog, it norvasc is important that you follow their guidelines carefully and give your dog the medication for the full regimen that your vet advises. Gabapentin pharmacokinetic parameters without and with probenecid were comparable. Similarly, corticosteroids should be used with great care in patients with known or suspected Strongyloides (threadworm) infestation. Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa such as: allergic corneal marginal ulcers, herpes zoster ophthalmicus, anterior segment inflammation, diffuse posterior uveitis and choroiditis, sympathetic ophthalmia, allergic conjunctivitis, keratitis, chorioretinitis, optic norvasc neuritis, iritis and iridocyclitis. Irritability, panic attacks, extreme worry, restlessness, acting without thinking. Corticosteroids should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Ophthalmic blurred vision, cataracts (including posterior subcapsular cataracts central effects serous chorioretinopathy, establishment of secondary bacterial, fungal and viral infections, exophthalmos, glaucoma, increased intraocular pressure (see norvasc side effects precautions : Ophthalmic optic nerve damage, papilledema. The doctor can prescribe 15-100 mg per day of the initial dose or 5-15 mg per day as a supporting hormone therapy. Pregnancy: This medication should not be used during pregnancy unless the benefits outweigh the risks. References and Further Reading Boothe, Dawn. Table 4: Adverse Reactions in Pooled Placebo-Controlled Add-On Trials In Epilepsy Patients 12 years of age neurontin* norvasc side effects N543 Placebo* N378 Body As A Whole Fatigue 11 5 Increased Weight 3 2 Back Pain 2 1 Peripheral Edema 2 1 Cardiovascular. Convulsions have been reported with this concurrent use. Tell your doctor right away if you notice symptoms such as persistent nausea / side vomiting, severe diarrhea, or weakness in your newborn. Phenytoin In post-marketing experience, there have been reports of both increases and decreases in phenytoin levels with dexamethasone co-administration, leading to alterations in seizure control. As with other antiepileptic medicinal products, some patients may experience an increase in seizure frequency or the onset of new types of seizures with gabapentin. Has your dog ever used doxycycline? Disclaimer: Our goal is to provide you with the most relevant and current information. When suggestions are available use up and down arrows to review and enter to select. This medication should not be administered to animals younger than seven months of age, as Doxycycline may bind to calcium in the teeth, causing discoloration. Clinical improvement or recovery after stopping corticosteroids may require weeks to years. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids. Prednisone comes as an immediate-release effects tablet, a delayed-release tablet, and a liquid solution. Drug/Laboratory Test Interactions Because false positive readings were reported with the Ames N-Multistix SG dipstick test for urinary protein when gabapentin was added to other antiepileptic drugs, the more specific sulfosalicylic acid precipitation procedure is recommended to determine the presence of urine protein. You side should know norvasc what the drug is and why you are taking. Travel When traveling with your medication: Always carry your medication with you. Neurontin side effects Get emergency medical help if you have signs of an allergic reaction to Neurontin : hives; difficult breathing; swelling of your face, lips, tongue, or throat. For people with heart or kidney disease: Prednisone may make you retain salt and water, which can raise your blood pressure. Do not stop taking this medication without first talking with your doctor. Gastrointestinal Diseases, to tide the patient over a critical period of the disease in: ulcerative colitis, regional enteritis. Possible Side Effects of Doxycycline, doxycycline is generally safe and effective for use in animals when administered according to the prescription and in most cases, it does not produce negative side effects. Side effects of doxycycline in dogs are fairly rare. Avoid contact with people who have infections that may spread to others (such as chickenpox, measles, flu ). Elevation of creatinine kinase may occur. Gabapentin also displays efficacy in several pre-clinical animal pain models. Dosage and Administration, as a general guideline, dogs should be given 2mg to 5mg of the drug, per pound of body weight every 12 hours or 24 hours. Dosage for Epilepsy with Partial Onset effects Seizures. Do not stop taking neurontin without first talking to your healthcare provider. Encourage patients to enroll in the naaed Pregnancy Registry if they become pregnant. They really are the best people to trust when it comes to treating and preventing medical conditions in your pooch. As well, some forms of this medication may not be used for all of the conditions discussed here. Bupropion, taking bupropion with prednisone may cause seizures. Before taking prednisone, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. These effects occurred when pregnant mice received oral doses of 1000 or 3000 mg/kg/day during organogenesis and in rats given 2000 mg/kg prior to and during mating and throughout gestation. Let your doctor know if you have osteoporosis or are at increased risk for the condition. Use in patients undergoing haemodialysis For anuric patients undergoing haemodialysis who have never received gabapentin, a loading dose of 300 to 400 mg, then 200 to 300 mg of gabapentin following each 4 hours of haemodialysis, is recommended. 4.5 Interaction with other medicinal products and other forms of interaction There are spontaneous and literature case reports of respiratory depression and/or sedation associated with gabapentin and opioid use. Table 4 lists adverse reactions that occurred in at least 1 of neurontin-treated patients 12 years of age with epilepsy participating in placebo-controlled trials and were numerically more common in the neurontin group. Hot side Flashes (Causes, Symptoms Medication Treatment in Men and Women) Hot flashes norvasc (or side flushing) is the most common symptom experienced by a woman prior to and during the early stages of menopause. Like with most medications, you should give your dog doxycycline with food. Indications and Usage for Prednisone, prednisone tablets and solutions are indicated in the following conditions: Endocrine Disorders, primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the first choice: synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy. The oral volume of distribution normalized per body weight was constant across the age range. In vitro studies have shown that gabapentin binds with high- affinity to the 2 subunit of voltage-activated calcium channels; however, the relationship of this binding to the therapeutic effects of gabapentin is unknown. Gender Although no formal study has been conducted to compare the pharmacokinetics of gabapentin in men and women, it appears side that the pharmacokinetic parameters for males and females are similar and there are no significant gender differences. Pay attention to any changes, especially sudden changes, in mood, behaviors, thoughts, side norvasc or feelings. Your diet Steroids such as prednisone change the amount of water and salts in your body. Stay rigidly on the course prescribed by the vet. 4.2 Posology and method of administration. Usually, however, this side effect is so minor that it does not require treatment. I didnt sleep for three days, even with sleeping pills. Infection General Patients who are on corticosteroids are more susceptible to infections than are healthy effects individuals. Contraindications, prednisone tablets and oral solutions are contraindicated in systemic fungal infections and known hypersensitivity to components. A typical dose prescribed will be from two to five milligrams per pound of body weight for your pet, and this dose may be ordered once or twice per day. While it's legal for a doctor to prescribe drugs for off-label purposes, it's illegal for a drug manufacturer effects effects to actively promote off-label uses. But the way I was and am feeling, Im not daring to drive even one block. Precautions for Doxycycline Use. It may be helpful to triple or even quadruple the daily maintenance dose and administer this every other day rather than just doubling the daily dose if difficulty is encountered. The purpose of this registry is to collect information about the safety of antiepileptic drugs during pregnancy. A small number of postmarketing cases report gabapentin misuse and abuse. If this medication is used for an extended time, laboratory and/or medical tests (such as blood mineral levels, blood glucose, complete blood count, height/weight measurements, bone density tests, blood pressure, eye exams) should be performed periodically to monitor your progress or check for side effects. Killed or inactivated vaccines may be administered. Prednisone for oral use is quickly and fully norvasc absorbed from the digestive tract. Clinical experience during gabapentin's premarketing development provides effects no direct means to assess its potential for inducing tumors in humans. I pray I do not ever have to take prednisone again ever. Drug-seeking behaviour, dose escalation, development of tolerance. Among the gabapentintreated patients, most of the reactions were mild to moderate in intensity. There are various factors that influence withdrawal from any medication and/or powerful drug like Gabapentin. If after long-term therapy the drug is to be stopped, it recommended that it be withdrawn gradually rather than abruptly. Always speak with your healthcare provider about possible interactions with all prescription drugs, vitamins, herbs and supplements, norvasc and over-the-counter drugs that youre taking. Your doctor will determine the best dosage for your child. If youre a senior, you may need a lower dose or a different dosing schedule. Since complications of treatment with glucocorticoids are dependent on the size of the dose and the duration of treatment, a risk/benefit decision must be made in each individual case as to dose and duration of treatment and as to whether. Clomid, a woman would be increasing her chances of having twins dramatically, but that is not true. Grapefruit and grapefruit juice may interact with buspirone and lead to unwanted side effects.
Norvasc 5mg
Lek Amlodipine Aurobindo moe wpywa na zdolno prowadzenia pojazdw i obsugiwania maszyn. Other medicines : You can use nitroglycerin and norvasc together. The mean duration of follow-up was 19 months. What norvasc should I tell my doctor before taking norvasc? Nazwa preparatu, posta; dawka; norvasc opakowanie, producent, cena norvasc 100. Problem, dziaanie/waciwoci, ukady narzdowe, sposb aplikacji, producent. What to norvasc do if you norvasc miss a dose: If you miss a dose, take it as soon as you remember. If youre taking amlodipine for chest pain, this drug reduces your risk of hospitalization and surgeries due to chest pain. Always discuss possible side effects with a healthcare provider who knows your medical history. To lower your risk of dizziness and lightheadedness, get up slowly when rising norvasc from a sitting or lying position. Zaleca si stosowanie norvasc leku o tej samej porze kadego dnia, popijajc wod. Children: The safety and effectiveness of amlodipine have not been established for children less than 6 years of age. If you take nitroglycerin for angina, don't stop taking it while you are taking norvasc. Disclaimer: Our goal is to provide you with the most relevant and current information. Bardzo rzadko: zmniejszenie liczby norvasc 10 mg biaych krwinek, zmniejszenie liczby pytek krwi, nadmiar glukozy we krwi (hiperglikemia zaburzenia nerww, kaszel, obrzk dzise, wzdcia brzucha (nieyt odka nieprawidowa czynno wtroby, zapalenie wtroby, zacenie skry (taczka zwikszenie aktywnoci enzymw wtrobowych, zwikszenie napicia miniowego, zapalenie. U pacjentw z chorob niedokrwienn serca, lek Amlodipine Aurobindo uatwia dopyw krwi do minia sercowego zwikszajc norvasc ilo dostarczanego tlenu, co w rezultacie zapobiega blowi w klatce piersiowej. Szczegln ostrono naley zachowa w pocztkowym okresie leczenia. Kiedy zachowa szczegln ostrono stosujc Norvasc? Are there any other precautions or warnings for this medication? Liver function: norvasc Liver disease or reduced liver function may cause this medication to build up in the body, causing side effects. It works to control blood pressure and reduces the number of angina attacks by widening and relaxing blood vessels. Poinformuj lekarza: norvasc Jeli masz uczulenie na amlodypin lub ktrykolwiek z pozostaych skadnikw leku lub na jakiegokolwiek norvasc innego antagonist wapnia. In general, wait 7 to 14 days between titration steps. Preparat wywiera niewielki lub umiarkowany wpyw na zdolno prowadzenia pojazdw i obsugiwania urzdze i maszyn. If massive overdose should occur, initiate active cardiac and respiratory monitoring. With norvasc there were norvasc more reports of pulmonary edema. If your doctor has recommended a dose different from the ones above, do not change the way that you are taking the medication without consulting norvasc your doctor.
Norvasc dosage
Effects of norvasc doxycycline on heartworm embryogenesis, transmission, circulating microfilaria, and adult worms in microfilaremic dogs. The dosage and duration of treatment depend upon the type of infection your dog is suffering from. The no-effect dose for embryo-fetal developmental toxicity in mice was 500 mg/kg/day or approximately of the maximum recommended human dose (mrhd) of 3600 mg/kg on a body surface area (mg/m) basis. Continue Find out more dosage here. Gabapentin is a prescription drug, marketed as Neurontin and Horizant, that's used to dosage treat norvasc epilepsy. This disorder is variable in its expression, and other organ systems not noted here may be involved. Gabapentin has been shown in vitro to interfere with activity of the 2 subunit of voltageactivated calcium channels, dosage a receptor involved in neuronal synaptogenesis. Nursing Mothers Gabapentin is secreted into human milk following oral administration. Using leftover dosage prescriptions is a bad idea because you may be giving the dog too high a milligram tablet. Reduction of these factors reduce the pain and inflammation your pet experiences. Further information Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances. Neuropathic Pain norvasc Neuropathic pain is a chronic condition that leads to ongoing pain symptoms. Advise patients of the need to be alert for the emergence or worsening dosage of symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts, behavior, or thoughts about self-harm. Doxycycline Clearance of Experimentally Induced Chronic Ehrlichia canis Infection in Dogs. Avoid intramuscular or subcutaneous injection. If you see signs of an allergic reaction, contact your veterinarian immediately. Gabapentin is not a narcotic (opioid however, it does share signs and symptoms associated with drug abuse and addiction. Pooled analyses of 199 placebo-controlled clinical trials (mono- and adjunctive therapy) of 11 different AEDs showed that patients randomized to one of the AEDs had approximately twice the risk (adjusted Relative Risk.8, 95 CI:1.2,.7) of suicidal thinking. An additional neurontin 1200 mg/day dosage group (N52) provided dose-response data. Symptoms of the overdoses included dizziness, double vision, slurred speech, drowsiness, loss of consciousness, lethargy and mild diarrhoea. Precautions for Doxycycline Use. Author: Giano Panzarella help desk software. This medicine may impair your thinking or reactions. Use In Pregnancy Instruct patients to notify their physician norvasc if they become pregnant or intend to become pregnant during therapy, and to notify their physician if they are breast feeding or intend to breast feed during therapy see Use In Specific Populations. Studies in animals have shown reproductive toxicity (see section.3). Doxycycline can be administered to a pregnant patient in the second half of the pregnancy, but typically only when the benefits outweigh the risks. So its better to mix the medicine, liquid or tablet form, in with their food as this will dramatically decrease the likelihood of them vomiting or feeling nauseous from the bitterness. If you notice side effects, inform your veterinarian so they can create a treatment plan and make your dog more comfortable. Antibiotics are routinely given to dogs whose immune system isnt strong enough norvasc to fight off a particular infection. This reaction may occur several weeks after norvasc you began using Neurontin. In other words, doxycycline for dogs works by causing norvasc the dangerous cells to lose the ability to create energy and makes them more susceptible to outside forces, such as your dogs immune system. Administration Information Administer neurontin orally with or without food. Conclusion, coming back to the initial question, yes you can give doxycycline to your dog. Neurontin should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. The shorter the duration of time that you were on this medication, the easier it should be for you to come off. Maalox (Aluminum Hydroxide, Magnesium Hydroxide) norvasc The mean bioavailability of gabapentin was reduced by about 20 with concomitant use of an antacid (Maalox) containing magnesium and aluminum hydroxides. Journal of Veterinary dosage Internal Medicine. The most common infections that doxycycline is used to fight against in dogs are Ehrlichiosis, Rocky Mountain spotted fever, norvasc Toxoplasmosis, Mycoplasma, Psittacosis, Lyme dosage disease, and Leptospirosis, many of which come from ticks. Risk related to gabapentin Gabapentin crosses the human placenta. Nausea can be reduced if the medication is given to the dog with food.
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Does winstrol shut you down
Winstrol will also drastically reduce HDL cholesterol levels and increase LDL levels which will bump up your blood pressure. Testosterone levels won’t shut down completely from taking winny, but some bodybuilder like to combine it with testosterone because your natty production of test will be low after your cycle. To prevent yourself from experiencing low T, it’d be ideal to run testosterone as your coming off winstrol to keep this muscle-building hormone high. This will also help cement your gains, helping you hang on to the muscle you’ve gained on winny.
Winstrol (Stanozolol) is an Anabolic Steroid that was derived from Testosterone in 1962 by Winthrop Labs . The original purpose of this steroid was to help treat people suffering from anemia, it is also often used for veterinary purposes. This high anabolic, low androgenic steroid does not bind to the androgen receptor. For this reason Winstrol is considered a weak steroid in terms of its muscle building properties, it does however cause great increases in strength. Stanozolol is also a popular steroid for females due to its low androgenic properties it makes it a safer choice as side effects such as voice deepening and facial hair are a lower risk when compared to steroids such as Dianabol . This doesn’t mean females should use Winstrol as irreversible masculine side effects are still a risk.
Does winstrol shut you down
does winstrol shut you down
Media:
does winstrol shut you down
http://buy-steroids.org
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Healthy life
Your abdominals and back are command central when it comes to toning. Every move you make involves those two parts of the body, says Anderson. When you strengthen them, you'll have more stamina to do more activities with less likelihood of injury. The best exercises for your abdominals are crunches. Do as many as you can every day. An exercise called "superman" is a great strengthener for your back. Lie on your stomach, lift one leg and the opposite arm straight up, then lower. Repeat with the other leg and arm. Do 12 to 15 on each side every day.
When you're exercising regularly, you need protein—along with your carbs such as fruit and veggies—throughout the day. The reason: protein helps repair the microscopic tears in your muscles after a workout to build better muscle mass. Women tend to eat all their protein at lunch and dinner, and skip it at breakfast, says Anderson. An active woman should get 0.8 to 1.2 grams of protein per kilo of body weight. So if you weigh 150 pounds (68 kilos), you need between 54 and 82 grams of protein a day. (One ounce equals 28 grams.) Here are some protein-rich ideas to help you start your day off right: spread a thin layer of ricotta cheese or light peanut butter on rye toast; scramble some egg whites with green and red pepper; add a small handful of slivered almonds to your low-fat plain yogurt.
Why we love it Canola boasts even more heart-healthy omega-3 fatty acids than olive oil and it's packed with vitamin E, which has been linked to a lower risk of heart disease. Drizzle it into your salad dressings or substitute it for butter or shortening in baked goods.
Why we love them Usually fresh is best, but with these veggies, canned may be better. Cornell University researchers recently reported that the heat used during the canning process increases the antioxidants in sweet corn by 550 per cent. These ant
...
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Healthy life. (1969, December 31). In MegaEssays.com. Retrieved 07:53, February 28, 2017, from https://www.megaessays.com/viewpaper/21683.html
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Volume 25, Issue 2 (July 2021) Physiol Pharmacol 2021, 25(2): 178-188 | Back to browse issues page
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Ouahhoud S, Touiss I, Khoulati A, Lahmass I, Mamri S, Meziane M, et al . Hepatoprotective effects of hydroethanolic extracts of Crocus sativus tepals, stigmas and leaves on carbon tetrachloride induced acute liver injury in rats. Physiol Pharmacol 2021; 25 (2) :178-188
URL: http://ppj.phypha.ir/article-1-1584-en.html
Abstract: (995 Views)
Introduction: The present study investigated the hepatoprotective effects of stigmas, tepals and leaves of Crocus sativus on carbon tetrachloride (CCL4) induced liver injury in rats. Methods: Hydroethanolic extracts of Crocus sativus (stigmas, tepals and leaves) were administrated daily for 14 days by oral gavage. In the present study, 30 male rats divided into five groups were treated as 1: normal rats gavaged with distilled water; 2: intoxicated rats gavaged with distilled water and injected with CCL4; 3: rats treated with stigmas extract and injected with CCL4; 4: rats treated with tepal extract and injected with CCL4; 5: rats treated with leaf extract and injected with CCL4. Bodyweight and the relative liver weight were determined. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), total cholesterol, triglycerides, bilirubin direct and total, total protein, albumin, urea and creatinine measured in plasma. Malondialdehyde (MDA) was quantified in liver homogenate. Results: The experimental data showed that the stigmas and tepals extracts significantly prevented weight body loss and improved the relative liver weight. They significantly protected against elevation of ALT, AST, direct bilirubin, total bilirubin, LDH, ALP, creatinine and MDA. Also, they enhanced significantly total proteins and albumin compared to the CCL4 control group. Moreover, leaves reduced ALT, AST, total bilirubin, LDH and MDA significantly. Conclusion: In conclusion, these results suggest that tepals, stigmas, and leaves extracts of Crocus sativus have hepatoprotective effects on CCL4 induced liver injury in rats.
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Treatments for stage 0 esophageal cancer
The following are treatment options for stage 0 esophageal cancer. Your healthcare team will suggest treatments based on your needs and work with you to develop a treatment plan. They will usually do a nutritional assessment before treatment begins. You may need a feeding tube to make sure you get enough nutrition during treatment.
You may be offered one or more of the following treatments.
Surgery
You may be offered esophagectomy for stage 0 esophageal cancer. This surgery removes part or all of the esophagus and nearby lymph nodes. Sometimes part of the stomach is also removed.
Endoscopic treatments
You may be offered endoscopic treatments for stage 0 esophageal cancer.
Endoscopic mucosal resection (EMR) is sometimes used to treat a small tumour that is only in the inner layer, or mucosa, and has not spread to the other underlying layers of the esophagus. During EMR, the doctor injects a liquid or uses suction to first lift a tumour away from the submucosa and then removes it. If you have EMR, your healthcare team will do close follow-up to check that the cancer has not come back. They will use an endoscope to check your esophagus every 3 months for the first year, and then once a year after that.
Photodynamic therapy (PDT) destroys cancer cells using a photosensitizing drug, which makes cells sensitive to light.
Radiofrequency ablation (RFA) uses a high-frequency electrical current to destroy cancer cells.
Clinical trials
You may be asked if you want to join a clinical trial for esophageal cancer. Find out more about clinical trials.
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Importance of amino acid composition to improve skin collagen protein synthesis rates in UV-irradiated mice
Abstract
Skin collagen metabolism abnormalities induced by ultraviolet (UV) radiation are the major causes of skin photoaging. It has been shown that the one-time exposure of UV irradiation decreases procollagen mRNA expression in dermis and that chronic UV irradiation decreases collagen amounts and induces wrinkle formation. Amino acids are generally known to regulate protein metabolism. Therefore, we investigated the effects of UV irradiation and various orally administered amino acids on skin collagen synthesis rates. Groups of 4–5 male, 8-week-old HR-1 hairless mice were irradiated with UVB (66 mJ/cm2) twice every other day, then fasted for 16 h. The fractional synthesis rate (FSR; %/h) of skin tropocollagen was evaluated by incorporating l-[ring-2H5]-phenylalanine. We confirmed that the FSR of dermal tropocollagen decreased after UVB irradiation. The FSR of dermal tropocollagen was measured 30 min after a single oral administration of amino acids (1 g/kg) to groups of 5–16 UVB-irradiated mice. Branched-chain amino acids (BCAA, 1.34 ± 0.32), arginine (Arg, 1.66 ± 0.39), glutamine (Gln, 1.75 ± 0.60), and proline (Pro, 1.48 ± 0.26) did not increase the FSR of skin tropocollagen compared with distilled water, which was used as a control (1.56 ± 0.30). However, essential amino acids mixtures (BCAA + Arg + Gln, BCAA + Gln, and BCAA + Pro) significantly increased the FSR (2.07 ± 0.58, 2.04 ± 0.54, 2.01 ± 0.50 and 2.07 ± 0.59, respectively). This result suggests that combinations of BCAA and glutamine or proline are important for restoring dermal collagen protein synthesis impaired by UV irradiation.
Introduction
Skin aging, especially wrinkling and sagging, is induced by several factors, including ultraviolet (UV) irradiation, dryness, chemical stimulation, malnutrition, and exposure to activated oxygen species (Rittie and Fisher 2002). In particular, UV radiation is a potent agent of skin aging, and many reports suggest that chronic UV irradiation damages the skin protein and induces wrinkle formation in humans and animals (Boyer et al. 1992; Fisher et al. 2000, 2001; Rittie and Fisher 2002; Takema et al. 1996). Dermal collagen is a major component of skin dermis and is necessary to maintain skin structure. UV irradiation stimulates several factors, such as AP-1, TGF-β, EGF, IL1, and TNF-α, that affect collagen metabolism. Fischer has reported that in humans, procollagen mRNA levels are decreased and matrix metalloprotease mRNA levels are increased by single UV irradiation (Fisher 2005; Fisher et al. 2000, 2001). Takema found that in mice, chronic UV irradiation decreases the dermal collagen protein, resulting in wrinkle formation (Takema et al. 1996). These articles indicated that the decrease in dermal collagen protein resulting from chronic UV stimulation is one of the main causes of skin aging (Rittie and Fisher 2002). Cellular protein levels are regulated by protein turnover processes, such as protein synthesis and breakdown. However, there has been little study of the impact of UV irradiation on dermal collagen protein synthesis rates. To maintain steady dermal collagen levels, it is important to correct changes in the protein turnover rate induced by UV irradiation.
Amino acids are protein substrates and regulators of protein metabolism and are highly safe for humans. In an in vitro study, Bellon et al. (1995, 1987) found that glutamine increases procollagen mRNA levels and collagen content, and suggested that de novo proline synthesis from glutamine is important for collagen synthesis. Proline and its precursors, glutamate and pyrroline-5-carboxylate, increase collagen synthesis in human fibroblast cells (Karna et al. 2001). Some amino acids, such as arginine (Shi et al. 2003; Stechmiller et al. 2005) and ornithine (Shi et al. 2002), and amino acid mixtures (Badiu et al. 2010; Corsetti et al. 2010) enhance wound healing in rats. Zhang also indicated that leucine supplementation has an anabolic effect on protein metabolism in skin wounds in rabbits (Zhang et al. 2004). However, few studies have focused on amino acids’ ability to restore dermal collagen synthesis after UV irradiation. UV irradiation and wounds provoke different healing responses (Fisher 2005; Johnstone and Farley 2005).
Consequently, the present study was performed to investigate the effects of UVB irradiation on the FSR of mouse skin collagen and to investigate which amino acids can correct these FSR changes.
Methods
Animals
This study was approved by the Institutional Animal Care and Use Committee of Ajinomoto Co., INC. Nine-week-old male HR-1 hairless mice (Sankyo lab service Co. Japan) were housed in a temperature-controlled room with a 12-hour light and dark cycle. The animals were given standard commercial chow (CR-F1, Charles River, Japan) and water ad libitum.
UV irradiation
UVB radiation was generated with a bank of six sun lamps (FL20S-E-30/DMR, 20W, peak emission near 305 nm; Toshiba Medical Supply, Tokyo, Japan). The minimal erythema dose (MED) determined 24 h after UV irradiation was 66 mJ/cm2.
Experimental design
The first experiment investigated the effect of UVB irradiation on the FSR of skin tropocollagen. Mice (four or five in each group) were irradiated with UVB (66 mJ/cm2) on the dorsal skin one, two, three, or four times at a one-day intervals. The FSR was evaluated using the flooding dose method described by Garlick and McNurlan (1998). After 16 h of fasting after the last UV irradiation, the mice were injected in the tail veins with flooding doses of phenylalanine (1.5 mmol/kg body weight) containing l-[ring-2H5]-phenylalanine (50 mol percent excess, Cambridge isotope, Cambridge, MA). The mice were killed by decapitation 5 min after the phenylalanine injection. Blood was then collected from the necks, and the dorsal skins were removed. Subcutaneous skin fat was immediately removed, and the dermis was frozen in liquid nitrogen and stored at −80°C. Blood was separated from plasma by centrifugation at 3,000g for 15 min at 4°C, and the plasma was stored at −80°C.
The second experiment investigated the effect of orally administered amino acids on the skin tropocollagen FSR of UV-irradiated mice. The mice’s dorsal skins were irradiated with UVB (66 mJ/cm2) twice every other day. After 16 h of fasting, different amino acid solutions (1 g/ml/kg body weight) were orally administered by gastric tube to groups of 5–16 mice. The amino acid amount in the solutions was an amount commonly used in animal experiments to investigate acute amino acid effects (Farges et al. 1999; Smriga and Torii 2003). The compositions of the solutions are shown in Table 1 (all amino acids were manufactured by Ajinomoto Co., Inc.). Twenty-five minutes after the solutions were administered, the mice were injected with flooding doses of phenylalanine, and skin and blood were collected as described above.
Table 1 Compositions of amino acid solution
Sample preparation
Tropocollagen was extracted using a modification of Volpi’s method (Volpi et al. 2000). Briefly, approximately 0.5 g of dorsal skin was homogenized on ice in Buffer A (10 ml/g of skin), a pH 7.4 buffer containing 150 mM NaCl, 50 mM Tris–HCl, 2 mM EDTA, 1 mM phenylmethylsulfonyl fluoride, 2 mM N-ethylmaleimide, and 0.2 mM 2-aminopropionitrile. The homogenized sample was shaken overnight at 4°C, and then centrifuged at 7,500g for 10 min at 4°C. The supernatant was filtered with a 75-mm mesh, brought to 4.5 M with NaCl, and shaken for 5 h. The solution was centrifuged at 70,000g for 30 min at 4°C. The precipitate was dissolved in Buffer B, a pH 7.6 buffer containing 200 mM NaCl, 50 mM Tris–HCl, and 2 mM EDTA, and the solution was dialyzed in Buffer B for 2 h. This dialyzed sample, which included large amounts of skin tropocollagen, was hydrolyzed with hydrochloric acid for 16 h at 90°C, and the hydrolysate was used to measure isotope incorporation rates in the tropocollagen. To confirm the purity of the extracted tropocollagen, the dialyzed sample was subjected to SDS-PAGE (E-pagell, gradient gel 5–20%, ATTO, Japan) using a molecular mass standard (Bio-Rad, USA). Two wells were loaded with same amounts of the same samples. One was stained with Coomassie Brilliant Blue to detect proteins, and the other was blotted on nitrocellulose to identify collagen proteins using Western blotting with a mixture of antibody anti-collagen types I, III, and VII (Calbiochem, USA).
Approximately 0.04 g of dermal skin was homogenized with 15% sulfosalicylic acid, and the homogenate was centrifuged at 10,000g for 10 min at 4°C. The supernatant was used as skin tissue fluid. The precipitate was hydrolyzed in 2 ml of 6 N HCl at 90°C for 16 h and was used as mixed skin protein.
Amino acids that included hydrolysates and tissue fluid were purified by cation exchange chromatography (Dowex 50W 8X; Bio-Rad Laboratories, USA) and dried in a rotary evaporator (Nakajima corp., Japan).
Analysis
Phenylalanine enrichment (E (skin free)) in the tissue fluid was determined by its tert-butyldimethylsilyl (t-BDMS, Pierce, USA) derivatization. Gas chromatography–mass spectrometry was used to monitor Ions 336 and 341 in the electron impact mode (GC–MS; 6890 GC system and 5473 Network mass selective detector, Agilent, USA). Phenylalanine enrichment in the tropocollagen and mixed skin protein samples (E (tropocollagen), E (mixed skin)) was determined by measuring their AQC-detergent (Waters, USA) derivatization using liquid chromatography–mass spectrometry to monitor ions 336 and 341 in the first MS and 171 in the second MS (LC–MS/MS; Prominence HPLC system, Shimazu, Japan and API 3200, Applied Biosystems, USA). Plasma insulin concentrations were measured using a commercial ELISA-kit (Morinaga Institute Biological Science, Japan), and amino acid concentrations were measured with an automatic amino acid analyzer (L-8500, Hitachi, Japan).
Calculation and statistics
The FSR of the skin tropocollagen and mixed skin protein was calculated with the precursor-product model. The precursor represented the free phenylalanine enrichment in the skin tissue fluid, and the product represented the enrichment of the phenylalanine-incorporated skin tropocollagen or mixed skin protein. The FSR was calculated as FSR (%/h) = E (tropocollagen or mixed skin)/(E (skin free) × t) × 100, where t represents the time interval between phenylalanine injection and sampling.
Values are presented as means ± SD. Comparisons with the control group (given distilled water, DW) were made via Dunnett’s test after ANOVA for multiple comparison (JMP, SAS Institute, Cary, NC, USA). Values of P < 0.05 were considered significant.
Results
Skin tropocollagen extracted from the dorsal skin was assayed with Western blotting to confirm its purity. The protein bands of extracted skin tropocollagen separated by SDS-PAGE corresponded to Type I, III, and VII collagen bands (Fig. 1). The purity of the extraction was confirmed as described in a previous article (Volpi et al. 2000).
Fig. 1
figure1
SDS-PAGE and Western blot analysis of isolated skin tropocollagen fractions. Type I, III and VII collagen were identified using Western blot, and the purity of extracted collagen was confirmed. sd Standard protein, and TP tropocollagen
The FSR of skin tropocollagen tended to decrease after UVB irradiation, especially for mice that were irradiated twice with a one-day interval between irradiations (Fig. 2). The effect of orally administered amino acid on the FSR in the dermal tropocollagen of UVB-irradiated mice is shown in Fig. 3. Thirty minutes after oral amino acid administration, BCAA + Arg + Gln, BCAA + Gln, BCAA + Pro, and essential amino acids (EAA) significantly increased the FSR of skin tropocollagen compared with the control group (2.04 ± 0.54, 2.01 ± 0.50, 2.07 ± 0.59 and 2.07 ± 0.58%/h, respectively, in amino acid groups compared with DW, 1.47 ± 0.21%/h). However, single amino acids (Arg, Gln or Pro: 1.66 ± 0.39, 1.73 ± 0.67 or 1.45 ± 0.26%/h, respectively) and amino acid mixtures (BCAA, Arg + Gln or BCAA + Glu: 1.30 ± 0.32, 1.72 ± 0.26 or 1.74 ± 0.34, respectively) did not increase the FSR.
Fig. 2
figure2
Effect of UVB irradiation on the FSR of skin tropocollagen. Samples were irradiated with UVB one, two, three, or four times at one-day intervals. The FSR of tropocollagen decreased to its minimum value after two UVB irradiations. Values are means ± SD
Fig. 3
figure3
Effect of orally administered amino acids on the FSR of skin tropocollagen in UVB-irradiated mice. BCAA + Arg + Gln (BCAARQ), BCAA + Gln (BCAAQ), BCAA + Pro (BCAAP) and an essential amino acid mixture (EAA) significantly increased the FSR of skin tropocollagen 30 min after oral administration, but single amino acids did not increase the FSR. It is necessary to include BCAA in amino acid mixtures to increase the FSR of skin tropocollagen. Values are presented as means ± SD. Comparisons with the control group (DW distilled water) were carried out with a Dunnett’s test after ANOVA for multiple comparison (*P < 0.05)
The effect of oral amino acid administration on the FSRs of mixed skin protein is shown in Fig. 4. The FSRs of mixed skin protein were increased by UVB irradiation. However, oral amino acid administration did not affect the FSRs.
Fig. 4
figure4
Effect of orally administered amino acids on the FSR of mixed skin protein in UVB-irradiated mice. The FSR of mixed skin protein, including dermis and epidermis, was increased by UVB irradiation. This suggests that the synthesis rate of keratin, the most abundant protein in epidermis, increases with UVB irradiation. Amino acids did not further increase the FSR of mixed skin protein. Values are presented as means ± SD. Statistical comparisons with the control group (DW, distilled water) was carried out with a Dunnett’s test after ANOVA for multiple comparisons (# P < 0.05)
Plasma insulin concentrations 30 min after oral amino acid administration are shown in Fig. 5. Arg + Gln significantly increased plasma insulin concentrations compared to the DW group (1.14 ± 0.61 vs. 0.56 ± 0.6 nag/ml). However, there was no correlation between plasma insulin concentration and the FSR of skin tropocollagen (r 2 = 0.0049; Fig. 6).
Fig. 5
figure5
Plasma insulin concentrations 30 min after oral amino acids administration to UVB-irradiated mice. Arg + Gln (RQ) significantly increased plasma insulin concentrations 30 min after oral administration. However, there was no correlation between plasma insulin concentration and the FSR of skin tropocollagen. We postulate that BCAA + Arg + Gln (BCAARQ), BCAA + Gln (BCAAQ), BCAA + Pro (BCAAP), and the essential amino acids mixture (EAA) increased the FSR of skin tropocollagen independently of insulin. Values are presented as means ± SD. Comparisons with the control group (DW distilled water) were conducted with a Dunnett’s test after ANOVA for multiple comparison (*P < 0.05)
Fig. 6
figure6
Correlation between the FSR of tropocollagen and plasma insulin. Multivariate correlation was evaluated between the FSR of tropocollagen and plasma insulin concentration. There was no significant correlation between groups (r 2 = 0.004)
Plasma amino acid concentrations are shown in Table 2. Plasma branched-chain amino acid concentrations increased by approximately five times in the BCAA + Arg + Gln, BCAA + Arg, BCAA + Gln, BCAA + Pro, BCAA + Glu and EAA groups compared with the DW group. Plasma tryptophan, histidine, tyrosine, threonine, serine and especially, glycine concentrations decreased in the groups that received solutions containing BCAA. Plasma proline concentrations increased in the groups that received solutions containing proline and slightly increased in Arg and Arg + Gln groups.
Table 2 Plasma amino acids concentration 30 min after oral amino acids administration in UV-irradiated mice
Discussion
The object of this study was to investigate the effects of UV irradiation on the rate of skin tropocollagen protein synthesis and to determine which amino acid increases dermal tropocollagen protein synthesis in UV-irradiated mice. It was observed that the tropocollagen FSR generally decreased after UVB irradiation and that some amino acid mixtures, such as BCAA + Arg + Gln, BCAA + Gln, BCAA + Gln + Pro, and a mixture of essential amino acids significantly increased the tropocollagen FSR in UV-irradiated mice. This is the first paper to indicate which single amino acids or amino acid mixtures can correct UV irradiation-induced changes in collagen protein synthesis.
Decreasing amounts of collagen result in skin aging, such as formation of wrinkles and sagging skin, and the main cause of skin aging is UV irradiation (Takema et al. 1996). However, few studies have examined collagen protein metabolism. To help prevent skin aging, it is important to understand how UV irradiation induces changes in dermal collagen metabolism and how these changes can be reversed. A long-term study of changes in the amount dermal collagen is necessary because collagen protein turnover is very slow. Thus, we focused on measuring the FSR of tropocollagen, a soluble collagen that includes intracellular and extracellular procollagen. In many reports, 13C or 14C-labeled proline is used as a tracer to measure the FSR of collagen, and hydroxyproline enrichment is measured because hydroxyproline is specifically modified from the proline within collagen protein (McAnulty and Laurent 1987). However, it is thought that proline is not a suitable tracer for measuring collagen protein metabolism, especially in investigating the effect of amino acid supplementation on collagen protein metabolism because proline stimulates collagen synthesis in human fibroblast cells (Bellon et al. 1987). For this reason, we used l-[ring-2H5]-phenylalanine as a tracer and a method involving extraction of tropocollagen to measure the collagen FSR. Phenylalanine is commonly used to investigate the effects of amino acid supplementation on protein metabolism. The FSR of tropocollagen tended to decrease after one-time UV irradiation, and a similar decrease was observed after additional UV irradiation (Fig. 2). This result corresponded to that obtained by Fisher et al. (2000), who found that human skin procollagen mRNA levels decreased with UV irradiation. Thus, it was confirmed that UVB irradiation also decreases the collagen protein synthesis rate.
Several amino acids used in the present study, such as EAA, BCAA, Gln, Glu, and Arg, have been reported to stimulate protein synthesis in several tissues in in vivo and in vitro studies (Anthony et al. 2000; Bellon et al. 1987, 1995; Kimball and Jefferson 2004; Krause et al. 2002a; Oehler and Roth 2003; Proud 2004; Stechmiller et al. 2005; Stoll et al. 1992; Tipton et al. 1999; Xu et al. 2001). In particular, Arg, Gln, and their metabolites increased collagen synthesis in vitro or in wound healing in rats (Bellon et al. 1987, 1995; Shi et al. 2002, 2003; Stechmiller et al. 2005). However, there is little information on the effect of amino acid on dermal collagen protein synthesis after UV irradiation. It is important to investigate UV irradiation’s effect in mice because the process of collagen deposition differs between UV irradiation and wounds (Fisher 2005; Johnstone and Farley 2005). Some amino acid mixtures containing BCAA, such as EAA, BCAA + Arg + Gln, BCAA + Gln, and BCAA + Pro, significantly increased the FSR of tropocollagen (Fig. 3). BCAA in particular, but also leucine and its metabolites, modulate mammalian targets of rapamycin (mTOR) and stimulate phosphorylation of the 70-kDa ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor-binding protein-1 (4E-BP1), initiating translation and transcription in protein synthesis (Anthony et al. 2000; Kimball and Jefferson 2004; Meijer 2003; Proud 2004; Xu et al. 2001). However, BCAA and BCAA + Glu did not increase the FSR of dermal tropocollagen (Fig. 3). In addition, other amino acids, such as Arg, Gln, Pro, Arg + Gln, also did not increase the FSR (Fig. 3). This result indicates that while BCAA is important for skin tropocollagen synthesis, other specific amino acids, such as Gln or Pro, are also necessary to stimulate dermal tropocollagen synthesis.
In an in vitro study, Bellon and Karna showed that Gln and its metabolites (glutamate, pyrroline-5-carboxylate, arginine) increase collagen synthesis and suggested that de novo synthesized proline is important for collagen synthesis (Bellon et al. 1995, 1987; Karna et al. 2001). In the present study, the FSR of tropocollagen did not increase when amino acids containing precursors of proline (Gln, Arg, BCAA + Glu and Arg + Gln) were administered, but did increase with an amino acid mixture containing exogenous proline (BCAA + Pro). In addition, plasma proline concentrations were not increased by collagen synthesis-stimulating amino acid mixtures containing proline precursors (BCAA + Gln, BCAA + Gln + Arg), but were slightly increased by Arg + Gln and Arg, neither of which stimulated the tropocollagen FSR. These results indicate that de novo proline synthesis is not the main cause of increased collagen protein synthesis. Proline constitutes one-third of collagen protein’s amino acid residues. However, there is little information proline supplementation’s effect on dermal skin collagen synthesis. Further study is needed to understand the mechanism underlying the effect of BCAA + Pro on the FSR of tropocollagen.
Xu found that the combination of leucine and glutamine synergistically stimulates the activity of S6K in pancreatic beta cells. Some reports indicate that glutamine regulates protein synthesis (Xu et al. 2001). For example, glutamine restores energy metabolism into cells (Krause et al. 2002b), increases cell swelling (Oehler and Roth 2003), and activates GAPP (glutamate dependent protein phosphatase, which correlates with mTOR activation) (Krause et al. 2002a; Stoll et al. 1992). Arginine also improves wound healing by increasing collagen synthesis; the mechanism of this effect is thought to be the stimulation of growth hormone secretion and nitric oxide synthesis (Stechmiller et al. 2005). Williams reported that an orally administered amino acid mixture consisting of metabolites of leucine (b-hydroxy-b-methylbutyrate), arginine, and glutamine increased the collagen content in subcutaneously implanted tubes in healthy volunteers (Williams et al. 2002). In addition, Corsetti reported that amino acid mixtures that included leucine, proline, lysine, and glycine improved wound healing associated with the modulation of nitric oxidate synthase and transforming growth factor-β1 (Corsetti et al. 2010). Dioguardi (2008) also reported that collagen synthesis is efficiently maintained only when specific amino acids are continuously available and present in a specific ratio. Therefore, a possible explanation of our findings is that BCAA + Gln and BCAA + Gln + Arg synergistically stimulate dermal tropocollagen protein synthesis using each amino acid’s individual effects on protein synthesis. In addition, insulin is a powerful protein synthesis stimulator, and leucine and arginine stimulate insulin secretion. However, insulin was not the main cause of the increase of the dermal tropocollagen FSR by the amino acid mixtures, because there was no correlation between insulin and the tropocollagen FSR in any group (r 2 = 0.034; Fig. 6). EAA is known to increase the FSR of skeletal muscle protein (Tipton et al. 1999). In the present study, EAA was the only amino acid observed to increase the FSR of skeletal muscle protein (data not shown). Thus, the tropocollagen FSR improvement resulting from EAA is associated with the improvement of whole-body protein metabolism.
In conclusion, UVB irradiation decreased the FSR of skin tropocollagen, while BCAA + Arg + Gln, BCAA + Gln, BCAA + Pro, and EAA increased the FSR of skin tropocollagen independently of insulin. However, single amino acids and BCAA did not increase the FSR. It should be noted that combinations of specific amino acids, especially BCAA + Gln or BCAA + Pro are vital in stimulating the FSR of skin tropocollagen independently of insulin. However, the dermal collagen protein synthesis stimulation mechanism of these amino acids mixtures is unclear. Further study is necessary to understand the mechanism of the increase tropocollagen FSR by these amino acids.
Abbreviations
UV:
Ultraviolet
FSR:
Fractional synthesis rate
AP-1:
Activator protein 1
TGF-b:
Transforming growth factor-beta
EGF:
Epidermal growth factor
IL1:
Interleukin 1
TNF-a:
Tumor necrosis factor-alpha
mTOR:
Mammalian target of rapamycin
p70S6K:
70 kDa ribosomal protein S6 kinase
4E-BP1:
Eukaryotic initiation factor-binding protein 1
GAPP:
Glutamate-dependent protein phosphatase
BCAA:
Branched-chain amino acids
Leu:
Leucine
Ile:
Isoleucine
Val:
Valine
Gln:
Glutamine
Arg:
Arginine
Pro:
Proline
EAA:
Essential amino acids
Glu:
Glutamate
DW:
Distilled water
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Acknowledgments
We thank Takashi Suzuki, Sayo Inoue, and Shinobu Tanimoto for their assistance with the experimental trial.
Conflict of interest
The authors declare that they have no conflict of interest.
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Correspondence to Hitoshi Murakami.
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Murakami, H., Shimbo, K., Inoue, Y. et al. Importance of amino acid composition to improve skin collagen protein synthesis rates in UV-irradiated mice. Amino Acids 42, 2481–2489 (2012). https://doi.org/10.1007/s00726-011-1059-z
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Keywords
• Amino acids
• Skin collagen
• Protein synthesis rate
• UV-irradiated rat
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Drug Addiction or Drug Dependency; Is There a Cure?
Drug Addiction or Drug Dependency; Is There a Cure
A Holistic Approach
Dependency is not a disease, but a symptom of something that needs your attention. However, addiction is a disease. Dependency and addiction are often confused with one another. Dependency begins with a brain chemistry imbalance and a harmful coping behavior for deep unresolved painful issues. Dependency has biological, emotional, and spiritual components. If all are not addressed, relapse is probable. Curing dependency requires treatment of all the above components, tailoring treatment to each individual.
Cure does not mean having to call a sponsor every day for years to stay sober, fighting cravings indefinitely, that is why traditional group meetings don’t work for some people. They do not help patients discover the unconscious original reason for self-medicating. Healing does not manifest itself through force, humiliation, fear, or dependency. We heal ourselves when we are empowered with the knowledge that we are the masters of our own behaviors. The Universe, or God, is certainly a powerful resource for healing and I use it in my practice, but we are not puppets without any responsibility for our behaviors.
Physiological Causes
Addressing chemical imbalances in the brain that lead to physiological dependency is just as important as counseling. A simple blood test or in-depth questionnaire is all that is required to see which of the four major neurotransmitters, dopamine, acetylcholine, GABA or serotonin, are deficient. These neurotransmitters determine our feelings, thoughts and behaviors. When they are deficient, our emotions and thoughts change, which affects behavior. A knowledgeable holistic doctor prescribes specific supplements and amino acids to help re-build deficient neurotransmitters. An addicted brain is going to be deficient in at least one neurotransmitter.
After time deficiencies in brain chemicals can lead people to self-medicate. Caffeine is a common example of self-medication. Ever feel the need for that morning jump-start? Need a boost from coffee or cola? That “need” can be a deficiency in the neurotransmitter dopamine. People who are depressed often lack sufficient dopamine, so they self medicate with risky behaviors and/or stimulants. Cocaine is an extreme form of self-medication. Cocaine mimics dopamine. Unfortunately, the brain becomes fooled by the cocaine and reduces its own ability to make natural dopamine. With this increased deficiency in dopamine, the brain creates a demand or craving for more and more cocaine. Production of natural dopamine continues to decrease until its production burns out completely. Hallucinogenic mushrooms work similarly on acetylcholine, ecstasy on serotonin.
Smoking cigarettes helps some people think better because it mimics acetylcholine, another excitatory neurotransmitter. People who crave alcohol or carbohydrates are often deficient in serotonin, which is calming, like a tranquilizer. Just because it is legal or a prescription, the outcome is the same; the drug fools the brain. When deficiencies are severe, sometimes a prescribed medication is needed but should only be short term. However, when they are taken over a period of time without correcting the deficiencies, the problem is exacerbated. After a while, the person becomes ill, sometimes chronically. Memory and a sense of well-being are affected, or all sorts of aches and pains begin to manifest or get worse.
Psychological, Emotional, Spiritual Components
The most important path to curing dependency is to understand why you started the addictive behavior. What was it in your life that you did not learn to cope with? That made you feel helpless? What was the original reason? Remember, dependency begins as self-medication, a way in which to cope. The key to cure lies in the answer, which lies deep within the unconscious mind.
Without the answer to why a person started self-medicating, that deep reason continues to lurk beneath the surface with its power of dependency. The drug of choice temporarily relieves the pain when no positive alternative is known. For example, “Jane”, a shy fifteen year old who suffers from deep emotional turmoil she does not know how to relieve, is at a party and drinks some wine. Because the drink calms her, she has another. After a third glass, she is more talkative and having fun. For now, she forgets her pain. Two things happen. First, alcohol fools the brain into thinking it’s GABA, the calming neurotransmitter, so it slows down the production of natural GABA, which was already deficient. Second, Jane becomes “anchored” to, or associated with, alcohol equaling relaxing and feeling better. A pattern of negative behavior begins, psychologically and physiologically. The GABA deficiency she already had becomes worse. The brain, in turn craves alcohol because it has created receptors for it.
To cure dependency one has to discover the true essence of their soul and find their life’s purpose, for which spiritual counseling is valuable. This type of counseling looks within for answers to “why am I here?, who am I?, why did this happen?”
Amazing Treatment Help
There are two medications that are amazing for people who really want to cure dependency. They work by diminishing and even eliminating cravings, which greatly improves therapeutic outcome. Buprenorphin is an opiate-like medication indicated for the treatment of opioid dependence. It is available only by prescription, and must be taken under a doctor’s care as prescribed. Suboxone works on the neurotransmitters. However, even though patients describe the drug as “a miracle,” they only suppress withdrawal symptoms and cravings as long as they are being taken. They in themselves do not cure addiction or dependency. But, without suffering severe withdrawal symptoms, the path to healing is far more realistic. After a time, the doctor in charge will begin helping the patient wean off of Suboxone. Acupuncture is another proven treatment for addiction. Auricular acupuncture, a type of acupuncture where small needles are inserted in the external ear, can be very effective for other addictions. It decreases cravings by stimulating endorphin release.
Healing self-defeating behaviors
There are many helpful therapies and no single one is best for everyone. To help us understand patterns of self-defeating behaviors, Neuro-linguistic programming and hypnosis are great. Connecting to the Higher self and one’s Creator helps a person learn to look within, without fear, for their own answers. We all have the answers inside; we just need to know find them. Some people are afraid to revisit the past, but how do we know what to avoid or change if we fear looking at our past? Once we learn that the painful past is just the past, we are able to heal those events and they lose their power over us.
Meta-physics and healing go hand in hand. It is a philosophy that examines the nature of reality, including the relationship between mind and matter, substance and attribute, fact and value. Thus, we look at the relationship of cause and effect, or taking responsibility for our actions and behaviors. This in turn empowers us! Self-empowerment raises our self-esteem. When we understand all aspect of ourselves we become healthier, in body as well as mind.
Summary
Dependency is a symptom of something that needs attention, usually a combination of a biochemical and emotional imbalances. And because dependency is a combination of biological, emotional and spiritual components, then the best path to curing dependency is by treating the whole person, not just dependency or addiction.
With extensive experience and education, Drs. Ron and Cherie Santasiero have over sixty combined years in medicine. Since 1995, Ron and Cherie have been treating addicted teens, offering integrative care at their practice, The Sedona Holistic Medical Centre.
Their new book, Addicted Kids; Our Lost Generation: An Integrative Approach to Understanding and Treating Addicted Teens is available on Amazon. More information about the Ron and Cherie can be found on www.santasiero.com
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How to make an old drug new again
How to make an old drug new again
Drug repurposing
Summary:
For the past 17 years, Bruce Bloom, MD, CEO of Cures within Reach, has been proselytizing the virtues of drug repurposing while helping to advance treatments for more than a dozen diseases. Here’s why drug repurposing can be a cheaper, faster and often safer way to bring more treatments to market.
Q&A with Bruce Bloom, MD, CEO of Cures within Reach
For the past 17 years, Bruce Bloom, MD has been proselytizing the virtues of drug repurposing, a cheaper, faster and often safer way to bring more treatments to market. As leader of Cures within Reach, he has helped fund more than 75 repurposing projects that have impacted treatments for more than a dozen diseases.
Tell me about Cures within Reach…
Cures within Reach is a global nonprofit headquartered in Chicago with a focus on driving more treatments to more patients more quickly using science and medicine that already exist for human use. We do this through pilot clinical trials that test the repurposing of drugs, devices and nutraceuticals to see if they can bring therapeutic value to patients who have unmet medical needs.
How do you define repurposing?
We use the word repurposing to signify an opportunity where something that’s already available for human use in one disease is tested to validate a new indication in a new human disease. So that could be an already approved drug, nutraceutical or device. What we call repositioning is when you take a compound that’s in the drug pipeline, that’s never been approved for human use, but has already been proven safe for human use, and you find a second or third indication.
And then we also define something as rescue. There are compounds that were in a pharmaceutical development plan that didn’t pan out and have just sort of languished. They’re safe for human use but nobody’s working on them. They can be rejuvenated or rescued and moved into a clinical pathway for a new indication.
Cures Within Reach focuses mostly on repurposing, finding new uses for already approved drugs and devices, or nutraceuticals.
How Old Drugs Are Made New Again
Drug Repurposing vs. Drug Repositioning vs. Drug Rescuing
How does the drug development process look different when you’re repurposing versus developing something from a basic discovery?
For the most part, if your repositioning or rescuing a compound that is in a pharmaceutical pipeline, it just continues from where it was, but you save all the time and money of getting through preclinical and Phase 1 work. That could save you four to seven years and twenty to one-hundred million dollars. If you start with repurposing, where the drug is already approved for human use, you have even bigger potential time and cost savings. Depending on your goal, you might be able to perform a pivotal clinical trial, publish the results and help physicians use the drug off-label in the new indication. If your goal is FDA or other regulatory approval, you may have to complete more clinical research.
Repurposing versus Drug Discovery
If companies can save tens of millions of dollars and it takes half the time, why does repurposing seem like more of an afterthought for industry than a focus?
There’s a couple of reasons why. First, assume you take a drug that’s already available in the marketplace, and it’s a generic drug widely available from a lot of manufacturers at a very low cost.
The problem is – if you spend thirty to sixty million dollars to get it approved for a new indication – how do you charge more money than the generic price? And how do you make sure that physicians don’t just substitute [a different manufacturer’s idential generic drug] for yours? There’s currently not a good incentive system to repurpose low-cost generic drugs. So that’s one reason.
Second, if you test a drug that’s still under patent from a different company, repurpose it and get it approved, you might own the method of use patent and the marketing rights, but you don’t have the right to manufacture it. Unless the other company decides to make it for you, you have to wait until the drug becomes generic before you can market for the new indication. Incentives are not set up to support that kind of drug repurposing.
Third, if you’re a pharmaceutical company and you have a limited amount of resources, does it make sense to spend them over a three to five year period to repurpose a drug that’s going to make forty million dollars a year, or should you spend seven to ten years to do the same thing with a new chemical entity where you might earn six hundred million dollars a year? So there’s also the cost-benefit evaluations that companies look at.
Drug Repurposing Poster Session
One of the missions of Cures within Reach is to figure out how we can create new incentives. The repurposing of generic drugs is shorter, cheaper and in many cases is safer for patients because millions of doses have been taken and we know what drug interactions and side effects to expect. A new chemical entity may only be tested on hundreds of people, and three or four years from now could they cause side effects that we didn’t know about in a two month or six month trial. We saw that with Vioxx. Repurposing a drug usually solves that issue as well.
The repurposing of generic drugs is shorter, cheaper and in many cases is safer for patients because millions of doses have been taken and we know what drug interactions and side effects to expect
How can you create incentives to support repurposing generic drugs?
We just announced a collaboration with a biotech in San Francisco called Notable Labs. Notable Labs is a drug discovery company and they have combined a nutraceutical with a repurposed drug that can help refractory pediatric patients with a rare form of leukemia. By taking this combination, it can move them back in their disease progression to the point where they can take advantage of therapies that are already available. This could create an effective and safe way to save these patients who have no other therapeutic option.
What does the collaboration look like?
Cures within Reach and Notable Labs will work together to secure FDA approval for this combination. One of the compounds in the combination is available for a pediatric priority review voucher. Notable Labs will receive the voucher and use that as their total compensation for bringing this pediatric drug. Notable will gift the license to this combination to Cures within Reach and we will create a way to bring the drug to market at as low a price as we can to cover the costs of manufacturing and distribution and our management of the process.
This is a way for us to establish a new model where the company that discovered the drug combination can get well-compensated through commercialization and the patients can still get the drug at a reasonable cost.
This is a way for us to establish a new model where the company that discovered the drug combination can get well-compensated through commercialization and the patients can still get the drug at a reasonable cost
We’ve also been working in England on a second way of creating new incentives, which is what we call outcome-based financing. There is a rare disease called chronic pancreatitis. On average, each chronic pancreatitis patient costs the UK healthcare system somewhere in the vicinity of ninety thousand pounds each year. o it’s an expensive disease. It’s a chronic disease. The patients typically don’t get better. There’s no therapeutic options for them right now, just palliative care, which is pain management, often with opioids and not a good solution for patients with chronic diseases.
So we’ve gone to the British government and said, ‘If we privately funded repurposing projects, and outcomes showed that chronic pancreatitis patients got significantly better and the cost of their care went down significantly, would you use some of your cost savings to repay those that funded the research and to support more repurposing projects?’ We’ve modeled this and shown that the cost of the research is far below the potential returns. Our goal is to create a cyclical engine for the repurposing of drugs for common and rare diseases that don’t have good therapeutic options right now.
Our goal is to create a cyclical engine for the repurposing of drugs for common and rare diseases that don’t have good therapeutic options right now
There are so many assets at various phases sitting on the shelf, how do you or anyone discover which of them might work for a different indication?
Most of these ideas in the past have come from researchers and clinicians that either have clinical observations or other supportive scientific information.
What we’re seeing now is artificial intelligence and bioinformatics are creating new ways of looking at old compounds. There’s a significant amount of computing speed and power that’s being brought to the repurposing world looking at how we can use artificial intelligence, machine learning and bioinformatics to not only point us to what drugs could be repurposed for what diseases, but also what kinds of side effects and drug interactions they might create, and how we might alter those drugs just slightly to make them easier for patients to tolerate.
What we’re seeing now is artificial intelligence and bioinformatics are creating new ways of looking at old compounds
What can industry do to help facilitate more repurposing opportunities and commercialization of discarded assets?
Over the last seven or eight years, almost every pharmaceutical company we work with has developed its own internal group responsible for taking their own assets and seeing if they can be repositioned or rescued or even repurposed.
The pharmaceutical industry as a whole has also been supporting philanthropic work in the area of repurposing. We have more than a dozen pharmaceutical companies that either currently are helping, or have in the past helped, support some of the work that we do. And most of those companies who support philanthropic repurposing are also looking at ways to both make some money and do some good by out-licensing and in-licensing commercializable repurposing assets.
Cures within Reach Grant
It would be great if we could get new legislation that would somehow favor the repurposing of generic drugs and create some kind of economic incentives. It doesn’t strike me that the pharmaceutical industry is going to be at the forefront of that, but they certainly could make sure that they don’t put up a lot of opposition, especially if there was legislation that was primarily impacting pediatric and rare diseases that they are not pursuing aggressively.
It would be great if we could get new legislation that would somehow favor the repurposing of generic drugs and create some kind of economic incentives
What about specifically in Chicago? Is there anything that the biotech community or the government can do?
We haven’t yet pursued something legislative on a local or state level, but when we think about the idea of outcome-based financing, there are certain diseases in Illinois that cost the state a significant amount of money. For example, asthma has been increasing, it’s very expensive, and lot of state and local medical dollars go towards asthma care. If there was something repurposing that could help, it might make sense for local and state government to be outcome based payers. Also, when you think about local-level economic development, if there are conditions that keep people from being able to work, you might be able to think of repurposing that makes citizens healthier as an economic development or a public aid reduction system, as well.
In terms of supporting your mission, who are you trying to connect with and explain the importance of repurposing?
There are large funders out there who could see the benefits of repurposing as a really economical, effective and efficient way of driving therapies to patients. Healthcare payers, for example, could be interested in repurposing. Payers pay a lot of money for new drugs and if there was a substitute that could be less expensive, it might make sense for them to support that.
As we see health care costs getting unsustainable for governments and other payers, we’re all going to have to pitch in to figure out how we can leverage the untapped therapeutic value that exists in already approved drugs, so we can then afford all of these really marvelous new therapies coming out now.
We’re all going to have to pitch in to figure out how we can leverage the untapped therapeutic value that exists in already approved drugs, so we can then afford all of these really marvelous new therapies coming out now
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Home > Facts > Rosedale Diet
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Rosedale Diet
Definition
The Rosedale diet is a diet that was created by Dr. Ron Rosedale. It limits carbohydrates and proteins and is supposed to be able to help the body stabilize levels of leptin, a hormone believed to trigger the brain to send hunger signals to the body.
Origins
Ron Rosedale, M.D. practices nutritional and metabolic medicine in Denver, Colorado. Metabolic medicine is generally considered an alternative medicine. Practitioners of metabolic medicine believe that a person’s metabolic activity can be altered through diet, stress reduction, and other changes that do not have to include prescription drugs. It is believed that diseases and conditions can be resolved through these types of metabolic changes, and by bringing the metabolic activity of the patient back into a fully functioning state. It is this idea of changing metabolic activity that underlies the Rosedale diet.
Dr. Rosedale attended the Northwestern University School of Medicine, and graduated in 1977. He is the founder of the Rosedale Center in Denver, Colorado, as well as the Carolina Center of Metabolic Medicine in Ashville, North Carolina. He also co-founded of the Colorado Center for Metabolic Medicine in Boulder, Colorado. His book The Rosedale Diet was written with Carol Colman who has co-authored many diet and fitness books. The book first appeared in 2004.
For many years, doctors, researchers, and many others have been trying to decode all of the ways that the body gets signals about food and hunger, and how the body knows when and how much to eat. The process of eating and breaking down food is extremely complex and involves many different glands, hormones, organs, and other body parts. People have been studying leptin for more than a decade to try to determine what role it plays in the body's hunger, eating, and digestion processes. Dr. Rosedale came to the conclusion that leptin problems are responsible for many of the issues that cause people to gain and retain fat. Dr. Rosedale used this information about leptin and his background in metabolic medicine to develop a set of guidelines, called the Rosedale diet, which he believes will help dieters restore the proper functioning of leptin and their metabolic systems and allow them to lose fat and become more healthy.
KEY TERMS
Diabetes mellitus—A condition in which the body either does not make or cannot respond to the hormone insulin. As a result, the body cannot use glucose (sugar). There are two types, type 1 or juvenile onset and type 2 or adult onset.
Dietary supplement—A product, such as a vitamin, mineral, herb, amino acid, or enzyme, that is intended to be consumed in addition to an individual’s diet with the expectation that it will improve health.
Leptin—A hormone produced by fat cells (adipose tissue) that tells the brain that the body has eaten calories and should stop eating.
Mineral—An inorganic substance found in the earth that is necessary in small quantities for the body to maintain a health. Examples: zinc, copper, iron.
Obese—More than 20% over the individual’s ideal weight for their height and age or having a body mass index (BMI) of 30 or greater.
Vitamin—A nutrient that the body needs in small amounts to remain healthybut that the body cannot manufacture for itself and must acquire through diet.
Description
The Rosedale diet is based around the belief that leptin signals the body when to be hungry, when to be full, when to make fat, and when to burn fat. Leptin is a hormone secreted by fat. High leptin levels should tell the brain that there is plenty of stored fat, and that the body doesn't need to store any more. Some stored fat is important, because the body wants to make sure that if food becomes scarce, the body has a back-up store of energy so that it can survive until food becomes more plentiful.
Dr. Rosedale believes that many people with weight problems have become leptin resistant. This means that although their fat continues to produce leptin at normal levels, the brain cannot “hear” those signals correctly any more. Dr. Rosedale compares it to being in an room that smells bad for a long time, and no longer noticing the smell. When a person has a lot of stored fat the leptin signals going to the brain may eventually cause the same kind of phenomenon, beginning a vicious cycle of increased weight gain and increased leptin levels. Because the brain does not hear the leptin correctly, the brain thinks that the body has low levels of leptin. This signals the brain that the body needs to eat more and store more fat. Therefore, a person gets hungry and the body converts much of the food that gets eaten into fat.
The Rosedale diet is designed to get the body's leptin levels back into balance, and allow the brain to know that there is excess fat stored on the body. According to Dr. Rosedale, this will tell the brain to send signals to the dieter that he or she is satiated and not hungry, even if he or she has not eaten recently. Then the body will burn the fat stores, and weight loss will occur. Rosedale claims that this weight loss can occur without the muscle mass loss usually associated with weight loss, if leptin levels are balanced correctly.
The diet begins with a three week period of severe restriction. The only foods allowed during this periodcome from Dr. Rosedale's set of “A list” foods. During this period almost no carbohydrates are consumed, and protein consumption is limited. Saturated fats are restricted, but unsaturated fats are encouraged. Some of the foods suggested during this part of the diet include goat cheese, crab, lobster and other seafoods, olives, avocados, and many types of nuts.
Foods from the “B list” of foods are reintroduced after the initial phase of the diet. Some of the foods eventually allowed include fruit, lamb chops, steak, and beans. The second phase of the diet is intended to be followed for a lifetime to help maintain the body's leptin levels.
Dr. Rosedale suggests that dieters exercise for 15 minutes each day while on this diet. He also makes many recommendations for supplements that he suggests will help dieters lose weight and be more healthy while dieting. At one time, many of these recommended supplements were available from his company Rosedale Metabolics.
Function
The Rosedale diet claims to be able help dieters lose fat mass without losing muscle mass. It is intended to be a lifestyle changing diet that continues after the initial three weeks are over as a changed set of eating habits that continue for a lifetime. It is intended to provide overall better health and well being.
Benefits
There are many benefits associated with weight loss when the weight loss occurs at a moderate pace through healthy eating and regular exercise. There are many diseases and conditions for which obesity is considered a significant risk factor. These include diabetes and cardiovascular disease. People who are the more obese are generally at a higher risk and have more severe symptoms. Losing weight can reduce the severity of symptoms that occur with obesity-related disorders, and in some cases can even help the symptoms resolve completely. Dr. Rosedale believes that his diet can have these positive effects for patients with heart disease, diabetes, hypertension, and other diseases and conditions.
Precautions
Anyone who is thinking about beginning a new diet should consult their physician or another medical practitioner. A physician can help the dieter determine if the diet in question is the right diet to meet their personal health and fitness goals. Requirements of calories, vitamins, and minerals can be very different for different people, and can vary based on age, gender, weight, activity level, the presence of diseases or conditions, and many other factors. A dieter’s physician can help the dieter determine what his or her personal needs are for maintaining good health. This diet limits protein, so it is possible that some people, especially those who are very athletic, or those who are strength training, may not get enough protein for good health. Women who are pregnant or breastfeeding should be especially cautious. When babies are receiving all of their nutrients from their mother, what the mother eats can have a significant impact on the baby's health ! and well-being.
The various merits and risks of a high fat diet, even when the diet is only high in “good” fats are hotly debated. Anyone thinking of beginning this diet who has cardiovascular or any disease for which a high fat diet is considered a risk factor should exercise extreme caution. Before any kind of dietary change is made, especially one that could cause a condition to worsen, a personal physician and any other doctor supervising care (such as a cardiologist) should be consulted and the possible costs and benefits of such a diet should be weighed carefully.
Risks
There are some risks with any diet. Any diet that significantly limits certain types of food may make it
QUESTIONS TO ASK THE DOCTOR
• Is this diet the best diet to meet my goals?
• Would a multivitamin or other dietary supplement be appropriate for me if I were to begin this diet?
• Is this diet appropriate for my entire family?
• Is it safe for me to follow this diet over a long period of time?
• Are there any sign or symptoms that might indicate a problem while on this diet?
hard for a dieter to get enough of all the necessary vitamins and minerals needed for good health. Although this diet recommends a number of vitamins and supplements, a dieter should consult his or her own physician before starting any kind of supplement. Supplements and multivitamins can help reduce the risk of a deficiency occurring during a restricted diet, but taking a supplement or vitamin has its own risks that should be carefully considered.
Research and general acceptance
There has been no significant scientific research on the effectiveness of the Rosedale diet at helping people lose weight or burn fat. It also has not been scientifically shown to allow the body to burn fat without burning any muscle mass. It has not been evaluated to determine its effectiveness at improving the symptoms of or treating any diseases or conditions including type II diabetes, heart disease or hypertension. Studies have shown however that these and other obesity-related diseases and conditions can be improved through weight loss. The Rosedale diet also has not been clinically proven to help people live longer.
Leptin has been studied by many different researchers, but like many things that are engaged in more than one aspect of various reactions within the body, it is not always easy for scientists to come to a definite conclusion. Many of the studies done have been on animals, although some studies have been done on humans as well. It is more difficult for researchers to study reactions in humans because it would be unethical to do something in an experiment that was expected to cause a negative outcome in a person. Because of this, studies of humans often have to rely on evidence that cannot be as carefully controlled as when animal subject are used.
Although not everything is known about the way the leptin acts on the various organs of the body, scientists have linked it to obesity in both mice and humans. Injections of leptin were found to have significant effects on the body weight of mice. Mice with mutated genes that made their body unable to react to leptin were found to have a body mass three times greater than mice that had a normal gene. It is possible that some humans have a similar mutated gene, but evidence suggests that it is more likely that most leptin problems in humans stem from a decreased sensitivity to leptin due to the overproduction over time of the hormone. The presence of high leptin levels has been shown to correlate with obesity and weight gain in humans. In a March 2007 study published in the Journal of Clinical Endocrinology and Metabolism, Abby F. Flesch et al. presented research showing that children with high levels of leptin in the blood were more likely to gain body fat during the follow-up period than children with low leptin levels.
The Rosedale diet suggests that dieters severely restrict carbohydrates in the diet, and eat a large quantity of “good” fats. Although unsaturated fats, like those found in olive oil and many nuts, have been found to be more healthy than saturated fats, such as the fat found in butter and fatty meats, it is not clear that unsaturated fats are good for the body in large quantities. Although some fat is necessary for a healthy diet, most experts recommended a diet low in all types of fats, with unsaturated fats preferable to saturated and trans fats.
The United States Department of Agriculture makes recommendations for the number of servings from each food group that should be eaten each day to get a balanced, healthy diet in its MyPyramid food guide. MyPyramid recommends the equivalent of 3 to 4 ounces of grains each day for healthy adults, of which at least half should be whole grains. Because the Rosedale diet limits carbohydrates so severely, dieters may not eat enough bread and grains to meet this recommendation.
In 2007, the Centers for Disease Control recommended that adults get 30 minutes or more of light to moderate exercise each day for good health. The recommendations that Dr. Rosedale makes for dieters following his diet plan is less than this minimum recommendation. Dieters may wish to consider doing exercise above and beyond the amount recommended by Dr. Rosedale.
BOOKS
Castracane, Daniel V. and Michael C. Henson, eds. Leptin. New York: Springer, 2006.
Rosedale, Ron and Carol Colman. The Rosedale Diet. New York: HarperResource, 2004.
Shannon, Joyce Brennfleck ed. Diet and Nutrition Sourcebook. Detriot, MI: Omnigraphics, 2006.
Willis, Alicia P. ed. Diet Therapy Research Trends. New York: Nova Science, 2007.
ORGANIZATIONS
American Dietetic Association. 120 South Riverside Plaza, Suite 2000, Chicago, Illinois 60606-6995. Telephone: (800) 877-1600. Website: <http://www.eatright.org>
OTHER
Get the Skinny on Diets 2007. <http://www.skinnyondiets.com> (March 26, 2007).
Helen M. Davidson
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Wildlife
Animal Pharm: What Can We Learn From Nature’s Self-Medicators?
Birds do it. Bees do it. Butterflies and chimpanzees do it.
These animals and many others self-medicate, using plants and other surprising materials to improve not only their own health but also the health of their offspring.
Monarch butterflies swarm a tree in Sierra Chincua, Mexico. Photograph by Joel Sartore, National Geographic
video of capuchin monkeys at the Edinburgh Zoo shows them rubbing onions and limes on their skin and into their fur as an antiseptic and insect repellent. Biologists have noticed that parasite-infected female monarch butterflies are more likely to lay their eggs on anti-parasitic milkweed, giving their offspring instant medication, while uninfected females show no preference. And urban birds who incorporate cigarette butts into their nests may be doing so because chemical properties in the smoked cigarettes may repel parasites, according to a 2012 study.
While cigarette-butt wallpaper may not appeal to most of us, other ways that animals self-medicate might be worth watching. Mark Hunter, a University of Michigan ecologist who was involved in the monarch research, says there is plenty to be learned from observing the way animals use the entire outdoors like one big drugstore. It’s something our own species probably once did—and might do well to revisit with modern pharmaceutical engineering and computer modeling techniques.
“It’s not the only way, but it seems to me that a sensible way [to aid in human drug development] would be to watch what animals do in nature to see how they exploit the natural products, the pharmaceuticals that are available to them in the environment, and try to learn from them,” he says.
Earlier this year, Hunter spent time with people of the Shangaan tribe in South Africa.
“If you go for a walk with somebody, every plant you pass has a cultural or medicinal significance, and many of those have been learned from watching animals,” Hunter says. The bark of the black monkey thorn tree, for example, is used as a stomach medication, a choice based on watching how elephants behave.
Diverse “Doctors”
Not long ago primates were thought to be the only animals smart enough to self-medicate. Mark Bowler, the San Diego Zoo Global Institute for Conservation Research postdoctoral fellow who made the capuchin video, says that chimpanzees use a range of medicinal plants, “including some that have a physical, not chemical action: They swallow wads of hairy leaves whole, and the leaf hairs appear to physically ‘brush’ certain parasites out of the gut. I tested some of this with Edinburgh Zoo’s chimps, and they seem to do it spontaneously—no learning process involved.”
The capuchins’ behavior in the video—rubbing the body with a particular chemical or scent—is called “anointing,” and other animals do it, too. Bowler is currently studying whether anointing behavior in some other primates is scent-marking or something else, but says that at least in capuchins, the purpose appears to be self-medication. Anointing can also be a form of self-defense: Ground squirrels chew rattlesnake skins and then lick their fur, a trick likely to deter that particular predator.
Insects have been found to be prolific self-medicators, too. Take the arresting case of the fruit fly Drosophilia melanogaster, which uses alcohol to protect itself against parasitic wasps. The wasps lay their eggs in the fruit fly larvae; the developing wasp grubs will eventually eat the flies from the inside out and burst forth from their dead bodies.
Larvae that consume high doses of alcohol from fermented fruits, however, are less likely to be infected—and if they are, the invading wasp grubs die quite nastily with their internal organs being ejected out of their anus. Moreover, fruit fly mothers who see female parasite wasps nearby will give their young instant protection by laying their eggs in alcohol-soaked environments—which means they see and remember their nemesis. (Related: “Flies Use Alcohol to Protect Their Young From Body Snatchers.”)
“Not a bad defense,” says Hunter, adding that this demonstrates the idea that “the cost we’re willing to pay for a medicine depends on the consequences of not using it.” While the alcohol isn’t necessarily good for the flies (though some species of Drosophilia melanogaster show a resistance to its ill effects), the flies will die if parasitized.
“The alcohol has worse effects on the parasites than it does on them. So it’s worth laying your eggs in a high-alcohol environment if it will save your offspring,” he says.
Bee Benefits
Honey bees self-medicate by protecting their home. The bees traditionally “line their nests with resins that they collect from plants, and those resins contain a wide variety of antimicrobial compounds,” Hunter says. The resulting mix of resins and beeswax is called propolis, and it’s been used as a traditional medication for centuries.
But because beekeepers didn’t want to deal with those sticky resins every time they opened a hive, Hunter says this resin deposition may have been selected out of most commercial bee populations over the years. After the bee genome was sequenced, scientists realized that bees have different immune systems than other insects—“probably because they’ve been relying on this resin,” says Hunter. Disease is one of the many suspected causes of bee die-offs, along with decreased plant diversity (and thus fewer places to get resins from) and pesticides, so encouraging propolis collection is probably a good idea.
Do animals learn to self-medicate, or is it pure instinct? Well, plenty of intelligent animals self-medicate, so it’s not always clear. But in the case of the monarch, Hunter points out, the mothers don’t hang around to see what happens to their babies, so there’s no learning involved. In this case, “the only possibility is that it’s a genetically determined behavior. It’s instinct.”
So the next time you’re on your way to the drugstore and pass a monarch hovering around a milkweed, or a bird who seems to have taken up a smoking habit, consider that they might actually be running an errand, just like you.
Follow Liz Langley on Facebook and Twitter.
Liz Langley is the award-winning author of Crazy Little Thing: Why Love and Sex Drive Us Mad and has written for many publications including Salon, Details and the Huffington Post. Follow her on Twitter @LizLangley and at www.lizlangley.com
• Ima Ryma
The honey bees are in decline,
The reasons varied probably.
It’s now known that honeybees line
Nests with resins protectively.
Antimicrobial compounds
Collected from all kinds of plants.
Beekeepers, in making hive rounds,
Deemed resins sticky disenchants,
And so found ways and means to rid
The hives of resins that well could
Be why honey bees did in did.
Let the resins be for bee good.
Beekeepers, leave bee resins, please,
For more daughters and sons of bees.
• doudou
Realy we human being we are nothing and we have to learn from all animals.Look at this bird who knows about nicotine and other propeties of cigarettes.Thank you mister Hunter and N G
• El Gabilon
Whoever or whatever set this universe in motion is one smart entity. Whether or not the medicinal use of plants etc. by animals other than our own species is genetic or learned it is an indication that IT expected illness to be a problem and provided for it. Is “pot” “grass” “maryjane” a medication provided for medicinal use by humans? Which poses another question…are drugs derived from plants more effective than drugs developed from man made compounds that do not involve natural ingredients?
In the scientific world there is much to learn, we only hope that what we need to learn comes before we destroy ourselves. Some readers of our comments may think we are anti-science which is not the case. Rather, we believe that science must be controlled to prevent mishaps, some scientists should lose their inflated egos, and ideological beliefs not be allowed to interfere with human progress. The clock is ticking and time waits for nothing.
• Bells
I enjoyed this write up. Very interesting.
• Jackie
Since animals are unable to shop in pharmacies for their medicinal needs, they are the ultimate consumers of natural medicines.
• OHTSUKA Tadashi
How smart these animals are!
• Bipul Saha
Very interesting topics, not heard about it earlier. Thanks for the post. Would further follow.
• jacinta cabrera
cut super bella esta foto
• Susan Welsh
Mother nature is the most incredible and smartest thing I know and I will follow her anywhere and everywhere. Great article. I love it.
• KEITH LITTLE
I would like to add that the scientific community needs to get out of the intellectual rut of “door number one “instinct or “door number two “learned behavior.” There has to be another cause or many causes unknown to us that make these fellow Earth inhabitants behave they way they do. I’ve seen spider’s build webs near lights to catch the bugs that are its prey. Since the artificial light was developed by mankind this could not be anything less than reasoning by the spider and had to take place after 1879 when the incandescent light began to become wide spread. So I say to the scientific world to please think out of the deep pit that you’ve dug yourselves in and look for another answer or answers to this magnificent world’s creatures behaviors.
• KEITH LITTLE
I would like to add that the scientific community needs to get out of the academic rut of “door number one “instinct or “door number two “learned behavior.” There has to be another cause or many causes unknown to us that make these fellow Earth inhabitants behave they way they do. I’ve seen spider’s build webs near lights to catch the bugs that are its prey. Since the artificial light was developed by mankind this could not be anything less than reasoning by the spider and had to take place after 1879 when the incandescent light began to become wide spread. So I say to the scientific world to please think out of the deep pit that you’ve dug yourselves in and look for another answer or answers to this magnificent world’s creatures behaviors.
• Ghazaleh
Animal instincts are behaviors that have been naturally included with the animal since its’ birth. Often times these instincts are used for survival. Amazing.
• enkidu
http://www.firstpeople.us/FP-Html-Legends/Origin-Of-Disease-And-Medicine-Cherokee.html
“When the plants, who were friendly to Man, heard what had been done by the animals, they determined to defeat the latter’s evil designs. Each Tree, Shrub and Herb, down to even the Grasses and Mosses, agreed to furnish a cure for each one of the diseases named, and each said: “I shall appear to help Man when he calls upon me in his need.” Thus came medicine; and the plants, every one of which has its use if we only knew it, furnish the remedy to counteract the evil wrought by the revengeful animals. Even weeds were made for some good purpose, which we must find out for ourselves. When the doctor does not know what medicine to use for a sick man the spirit of the plant tells him”
• Leenoh
We could learn something not selfish from any nature things. It is so gentle and nice~^^
• ragini
Truly enjoyed … being a science teacher m looking forward to share it wid my kids tomorrow
thanks
• Mitch Ward
Fantastic if we could just stop and observe nature we could all as humans really learn.
• Ankita Roy
Nice! very interesting
• Dinesh Patel
Necessity is mother of invention is proved here.
• Liz Langley
@ragini thanks for sharing with your class, I hope your students enjoyed it!
• Liz Langley
Very glad so many people connected with this piece – I learned a lot from it and think it’s going to make me take animal activity less for granted, to wonder if there’s more motive behind certain behaviors than I’d have previously thought.
• melissa Larson
Hello there Liz, great article! Im actually in a University class right now called Disease and Behavior, and I am very interested in writing my final paper on animal self-medicating practices. I was wondering if you had additional sources from this article that would be helpful in my research.
Thankyou!
About the Blog
Researchers, conservationists, and others share stories, insights and ideas about Our Changing Planet, Wildlife & Wild Spaces, and The Human Journey. More than 50,000 comments have been added to 10,000 posts. Explore the list alongside to dive deeper into some of the most popular categories of the National Geographic Society’s conversation platform Voices.
Opinions are those of the blogger and/or the blogger’s organization, and not necessarily those of the National Geographic Society. Posters of blogs and comments are required to observe National Geographic’s community rules and other terms of service.
Voices director: David Braun ([email protected])
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But the dark chocolate should be 60 to 70 percent cacao. A review of studies on dark chocolate has found that eating one to two squares of dark chocolate per day may help lower the risk of heart disease by lowering blood pressure and inflammation. The benefits are thought to come from the flavonoids present in chocolate with more cocoa solids. The flavonoids help dilate, or widen, your blood vessels (25).
7. Visit your chiropractor. A special chiropractic adjustment could significantly lower high blood pressure, a placebo-controlled study suggests. “This procedure has the effect of not one, but two blood–pressure medications given in combination,” study leader George Bakris, MD, told WebMD. Your chiropractor can create an effective protocol that helps normalize blood pressure without medication or other invasive procedures.
You didn’t mention that almost all blood pressure meds cause blood sugar to rise which is a real problem if you are pre-diabetic and trying hard to keep your numbers down so that you won’t have to take diabetic meds. My husband’s BP meds make him feel bad and make his blood sugar rise. If he stops the BP meds he feels great but his BP goes up. Happens on each BP med he’s taken.
Meditate or take slow, steady deep breaths to calm the nervous system, relax and your dilate blood vessels. Breathing exercises help calm your sympathetic nervous system and your fight-or-flight response. This technique also encourages blood flow to your body’s tissues and causes your diaphragm to move up and down, which eases blood flow to your heart.
While most Americans with hypertension are treated primarily with drugs, “these drugs do not come close to eliminating all the cardiovascular ills associated with the typical American diet and sedentary lifestyle,” observes Danine Fruge, MD, Medical Director at the Pritikin Longevity Center in Miami. Over the last four decades, the Center has helped thousands worldwide lower blood pressure naturally and significantly reduce many cardiovascular risks.
THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.
According to the American College of Cardiology and the American Heart Association, the goal of blood pressure treatment is to attain a blood pressure reading that's less than 130/80 mmHg systolic and less than 80mmHg diastolic. In general, if you have hypertension, it is likely that you will need to be treated for the duration of your life to maintain this target blood pressure.
CoQ10 is a naturally occurring enzyme. It contains antioxidants that are good for maintaining cardiac health. CoQ10 has been shown to decrease blood pressure and reduces the thickening of the heart muscle (hypertrophy). There are no known side effects of CoQ10 since it naturally occurs in the body. According to the Mayo Clinic, for the treatment of hypertension, take 60-360 milligrams daily for 8-12 weeks.
I would not recommend changing BP medications every 3-4 months just to prevent the onset of potential side-effects, but it certainly makes sense to reassess how you are doing on a BP med after a certain interval (usually after a few weeks, and then every few months or more often if the dose still needs to be refined or if there is concern about potential side-effects).
One of the most important lifestyle changes to adapt when hypertension affects a patient is a more active daily routine. Exercise is reported to be an exceptionally useful method for controlling blood pressure levels and for reducing blood pressure in patients diagnosed with hypertension. Additionally, patients who regularly participate in physical activities are also at a lower risk of developing a complication or complications due to high blood pressure.
Stress hormones constrict your blood vessels and can lead to temporary spikes in blood pressure. In addition, over time, stress can trigger unhealthy habits that put your cardiovascular health at risk. These might include overeating, poor sleep, and misusing drugs and alcohol. For all these reasons, reducing stress should be a priority if you're looking to lower your blood pressure.
Thank you so much for your highly informative article on hypertension for seniors–the best one that I have read. Presently, my wife, age 78, weight 98 lbs., height 4′ 11″, has been on a 4 m Atacand (brand name) per day for close to ten years now. Healthwise, I was concerned about its side effects on her. Pricewise, it is a very, very costly drug and our plan now requires her to pay a newly required deductible of $350 before reaching a new copay that has also become more expensive as well. She does not smoke or drink. Her family doctor has suggested that she switches to a generic brand Atacand but she prefers not to risk with its poorer bioavailability. Is such a preference valid? Are there any benefits in a generic that would outweigh its bioavailability constraint? Is there any alternative brand name drug that would offer her a good transition? Thank you kindly again for sharing the above highly informative, useful, and rare article regarding hypertension for seniors. I’d look forward to your reply with great appreciation–if I may.
Exercise. Doctors recommend at least 150 minutes per week of exercise to help reduce blood pressure. Brisk walking is excellent for reducing blood pressure and improving overall cardiovascular health, but other exercises can work too. Try jogging, riding a bike, swimming, dancing, or interval training to get your aerobic exercise. Strength training is also important to your heart health and can help reduce blood pressure.
Also focus on eating nitrate and nitrite-rich vegetables (not to be confused with the other types of nitrates and nitrites that are found in processed meats) . Nitrates and nitrates from vegetables help to relax and dilate blood vessels throughout your body and increase blood flow. Although it’s a short-term effect, eating more nitrate-rich vegetables like beets, cabbage, leafy greens, and vegetable juices, can reduce blood pressure for a few hours. Recent studies have also shown that those who drank beetroot juice showed an immediate effect on lowering blood pressure. By eating plant-based foods consistently, you’ll see their regular benefits.
This technique is known to surprisingly few health professionals, though it has proved valuable in the treatment of a wide variety of health problems. Recently, this powerful technique has been shown to be an extremely effective method for allowing the body to rapidly normalize high blood pressure more effectively than any other treatment reported in the scientific literature.
Explore the articles below to learn more about blood pressure control and healthy living, and to start developing your own personal guide to lowering blood pressure. Even better, book a health vacation at Pritikin, recently described by The New York Times as the “granddaddy of health-based wellness spas.” Make a personal investment in what matters most – a longer life, a better life.
In a hot tub, as the water comes through the pipes, it has a degree of force. This force is caused by the action of the pump, which puts energy into the circulating system and forces the water through the pipes. When the pump is off, there still may be water in the pipes, but there is no force. The degree of force in the system when the pump is on can be gauged in several ways, such as by putting your hand in front of a “jet.” Another way would be to have a device to measure the amount of force that the water exerts against the walls of the pipes as it circulates. Such a device might yield a numerical measurement of the force, or pressure, of the water within the pipes.
Many leafy greens, including everything arugula and kale to spinach and collard greens, contain potassium and magnesium which are key minerals to control blood pressure, according to Harvard Medical School. These nutrients are an important part of the DASH diet (Dietary Approaches to Stop Hypertension, or high blood pressure), which suggests a variety of foods that lower blood pressure. A potassium-rich diet helps the body become more efficient at flushing out excess sodium, which can raise blood pressure, and magnesium helps promote healthy blood flow, according to nutritionist Joy Bauer.
The acronym FAST can help. F: Face drooping. Can the person smile? Is the smile uneven? A: Arm weakness. Is one arm weak or numb? If the person raises both arms, does one drift down? S: Speech difficulty. Is the person's speech slurred? Can they repeat simple sentences you give them? T: Time to call 911. If the person shows any of these symptoms, even if the symptoms go away, call 911. Check the time so you know when the symptoms began.
Editor’s Note: Considerable controversy exists about whether fat or cholesterol are, per se, drivers of atherosclerosis. They are implicated in some studies, while others indicate that quality of fat, and placement in a wider dietary pattern, may be more significant to ultimate impact. What seems clear, however, is that a diet high in animal products, sugar, and processed foods is often a recipe for high blood pressure and heart disease.
Oatmeal is one of a few semi-processed foods that lower blood pressure. That’s because getting the right amounts of dietary fiber and whole grains is vital to maintaining normal blood pressure, and oatmeal is a tasty source of both. Classic studies have proven that eating oatmeal can lower systolic and diastolic blood pressure. Plus, the fiber can help you maintain a healthy body weight and prevent obesity, a risk factor for high blood pressure. These are the 10 silent signs you could have low blood pressure.
“I always recommend that people find something that they enjoy doing to stay in shape. For example, line dancing, walking outside, and riding a bike are all good ways to get active,” says Scott Parker, a health and fitness trainer and a national spokesperson for #GoRedGetFit — an online fitness challenge for women hosted by the AHA and Macy’s. “It’s also important to find other people you like doing the activity with, because that helps you stick with it.”
Some years ago I was put on medication for elevated blood pressure, as my mother before me. I took my medication and checked my values “religiously”… All of a sudden last October I developed malignant hypertension. I was hospitalized 3 times in 3 days with values over 220, then the hospital sent me to a nephrologist. He started running tests which were all normal. The hospital put me on Clonidine but the nephrologist did not add anything while running tests. In November I had to be hospitalized again. That time the ER doctor said they were not going to release me back to the same situation and added Amlodipine Besylate. My blood pressure has been normal with one brief spike since. Problem now are medication side effects: edema of feet and legs, hearing loss from fluid retention, bloating and constipation and generally not feeling well. I had always worked full time but finally retired this March. I am very disappointed to think that after working so hard for so may years I am going to feel like this in retirement due to side effects. I have talked to my nephrologist, especially a few weeks ago when I developed hearing loss from fluid retention and found that all the side effects are cumulative. He sent me an email saying we will stop the Clonidine and Amlodipine with no adjustments or anything in their place!! My pharmacist has tried to be helpful but can’t change anything. He says Amlodipine is one of the worst meds for side effects and many patients have to stop it for something else. The nephrologist does not seem to have done any research on side effects in order to suggest alternative medications, or to offer adjustments. He seems kind and listens, but offers nothing. In fact all of my medications for this condition were prescribed at the hospital. We have few geriatric doctors in this area, and no geriatric cardiologists. My regular cardiologist who just prescribed my standard meds cancelled my appointment when I developed the spikes. I already knew he was not up to challenges…I see an adult congenital cardiologist every so often even though he tells me I don’t need him as my congenital repair and heart are fine. There are not a lot of nephrologists here, but I think there is a better one in the same group so I doubt he will see me. I am really in a dilemma because I certainly cannot risk spikes, but would hope to feel better and not risk side effects such as fluid retention causing worse problems. It has also elevated my blood glucose which I watch and control through diet and exercise. The medication had my blood pressure running as low as the low 80s over low 50s, obviously too low, which is when the edema developed and I was lethargic. Now values are good. I have found little information on malignant hypertension and had never heard of it. I will greatly appreciate any suggestions. Thank you! PS I do not have a primary care doctor because so many here will not take Medicare and the “good” ones are not taking new patients or retiring. I have been looking for some time. My neurologist even had me send records to his good friend, an internal medicine specialist and they called and said he couldn’t help me….I had endocarditis at age 5 and have some medical PTSD. Sorry to write a novel, but I am thrilled there may be some help for me!
When was the last time you thought about your blood pressure? If you're like most people, it probably hasn't been since your doctor mentioned it during your last checkup. But high blood pressure (hypertension) is a serious condition that can lead to life-threatening problems, like heart attack and stroke. The good news is that you can lower your risk of hypertension with lifestyle changes.
Omega-3 fatty acids, such as those found in fish oil supplements, offer a wide variety of health benefits, including the ability to reduce blood pressure by reducing LDL (or “bad”) cholesterol. It is possible to consume enough Omega-3 fatty acids simply by adding more fatty fish to your diet, but it’s much easier to take it in supplement form. The best forms of Omega-3 oil are krill and calamari oils.
Again, foods that lower blood pressure are usually high in potassium and similar nutrients. Famously rich in blood pressure-lowering potassium, one banana contains about 420 milligrams, or 11 percent of the 4,700 milligrams the American Heart Association recommends people consume daily. Surprisingly, however, many veggies are actually higher in potassium than these popular fruits. A cup of Swiss chard boasts 960 milligrams, a cup of cooked white beans has nearly 1,200 milligrams, and a whole avocado has 975 milligrams.
3. Quit soda. One 12-ounce can of soda contains about 40 grams of fructose, one of the leading high blood pressure risk factors in North America. Consuming 74 or more grams of fructose per day increases your risk of high blood pressure by 77 percent. For people accustomed to drinking a can or two of soda daily, cutting the pop can have a dramatic effect on blood pressure, even eliminating the problem altogether.
Start by eating nuts. Pistachio nuts, singled out among other nuts, seem to have the strongest effect on reducing blood pressure in adults. This is according to a recent review and scientific analysis of 21 clinical trials, all carried out between 1958 and 2013. The review appears online in The American Journal of Clinical Nutrition, a publication of the American Society for Nutrition.
It's time to heed your partner's complaints and get that snoring checked out. Loud, incessant snores are a symptom of obstructive sleep apnea (OSA), a disorder characterized by brief yet potentially life-threatening interruptions in breathing during sleep. And many sleep apnea sufferers also have high levels of aldosterone, a hormone that can boost blood pressure, according to University of Alabama researchers. In fact, it's estimated that sleep apnea affects half of people with high blood pressure.
Common painkillers (so-called non-steroidal anti-inflammatory drugs, NSAID), can increase your blood pressure by inhibiting the production of salt in your kidneys. This includes over-the-counter pills such as Ipren, Ibumetin, Ibuprofen, Diklofenak and Naproxen as well as the prescription drug Celebra. Painkillers with the active substance paracetamol are better for your blood pressure.
Get moving at least a little bit every day, with a standard recommendation of 30-60 minutes a day, 3-5 times a week. Get your heart pumping at a moderate intensity for a few times a week, and mix it up with some strength training. Because life happens, on the days when you can’t fit it in, try to build more activity into your day by parking further away, taking the stairs instead of the elevator, or even just doing a quick sprint or two up and down the block. Every little bit helps.
Common painkillers (so-called non-steroidal anti-inflammatory drugs, NSAID), can increase your blood pressure by inhibiting the production of salt in your kidneys. This includes over-the-counter pills such as Ipren, Ibumetin, Ibuprofen, Diklofenak and Naproxen as well as the prescription drug Celebra. Painkillers with the active substance paracetamol are better for your blood pressure.
In addition to medications your doctor may prescribe, there are several lifestyle changes you can make to help to lower your blood pressure. These include things like eating a healthy diet, maintaining a regular exercise routine, quitting smoking and limiting your alcohol intake. Here are five more blood pressure-reducing techniques that don’t require a prescription:
The calculated difference between the systolic and diastolic pressures is also of interest. If the difference is large (e.g. 170/85), it could be the sign of stiff arteries – often caused by heart disease. This means the blood vessels can’t dilate enough when the heart sends out a pulse, which forces the blood pressure to increase. (The walls can’t expand, so the pressure rises when the heart tries to pump the blood through.)
The main thing that strikes me about your comment is that you are taking three different BP medications. This is necessary for some people, but in other cases, with a little tinkering we are able to provide adequate control with just two medications. The combination of an ACE inhibitor (such as lisinopril) and a calcium channel blocker (such as amlodipine) was shown to be particularly favorable in the ACCOMPLISH trial, so this combination is now recommended by many experts.
The DASH (Dietary Approaches to Stop Hypertension) diet has been proven best for controlling blood pressure, according to the American Heart Association. People who follow the diet eat 2,000 calories a day of fruits, vegetables, low-fat dairy foods and whole grains. The diet is rich in potassium, magnesium and calcium, as well as protein and fiber, and low in sodium. Foods on the diet are low in saturated fat, total fat, and cholesterol.
High blood pressure does not have any noticeable associated symptoms. This is, by far, the most worrisome problem that the healthcare industry and general population is facing when it comes to hypertension today. Chronic high blood pressure can cause damage to arteries and other areas of the body and, in turn, cause several complications to develop. This is why regular screenings for blood pressure levels are vital to help a person identify high blood pressure problems early on. This can help to administer treatment to stabilize blood pressure and avoid further damage to the body.
Eat potassium- and magnesium-rich foods. Potassium can help regulate your heart rate and can reduce the effect that sodium has on your blood pressure. Foods like bananas, melons, oranges, apricots, avocados, dairy, leafy green vegetables, tomatoes, potatoes, sweet potatoes, tuna, salmon, beans, nuts, and seeds have lots of potassium. Magnesium is thought to help blood vessels relax, making it easier for blood to pass through. Foods rich in magnesium include vegetables, dairy, chicken, legumes, and whole grains. It’s better to get vitamins and minerals from food, and a heart-healthy diet like the one we described above is a good way to ensure you get plenty of nutrients. However, you may want to talk to your doctor about whether taking certain supplements might help your blood pressure.
Lowering your blood pressure requires more than just cutting back on sodium, Prevention.com reports. You also need to eat foods high in at least two of these three minerals: calcium, magnesium, and potassium. With white beans, you get the jackpot for all three. Just one cup contains 13 percent of the calcium, 30 percent of the magnesium, and 24 percent of the potassium needed for your daily recommended servings. Here are 7 things your doctor isn’t telling you about your blood pressure.
What is considered low depends a bit on the person, their medical history, and the particular circumstances. It is also important to compare a person’s blood pressure to his or her “usual blood pressure.” A SBP of 102 is different in a young woman who usually has SBP 100-105, compared to an older person who has historically registered SBPs of 130-150.
High blood pressure over an extended period can lead to potentially dangerous complications. This can cause damage to organs, leading to microalbuminuria, cognitive dysfunction, and left-ventricular hypertrophy, as noted by one study. Additionally, the risk of renal failure, dementia and suffering a heart attack also dramatically increases in the population with elevated blood pressure levels.
Again, foods that lower blood pressure are usually high in potassium and similar nutrients. Famously rich in blood pressure-lowering potassium, one banana contains about 420 milligrams, or 11 percent of the 4,700 milligrams the American Heart Association recommends people consume daily. Surprisingly, however, many veggies are actually higher in potassium than these popular fruits. A cup of Swiss chard boasts 960 milligrams, a cup of cooked white beans has nearly 1,200 milligrams, and a whole avocado has 975 milligrams.
Bananas are one great source of potassium, but there are other tasty ways to get your fill. Potatoes actually pack more potassium than the yellow fruit (and you might be surprised to learn there are plenty of other health benefits of potatoes, too). Sweet potatoes, tomatoes, orange juice, kidney beans, peas, cantaloupe, honeydew, and dried fruits like prunes or raisins are other good sources. In all, you should aim to get 2,000 to 4,000 mg of potassium a day, Van Horn recommends.
Yoga is an ancient practice of life science and a way of living that was originated thousands of years ago in India. A great way of reducing high blood pressure, yoga is really effective in treating issues naturally. So practice asanas like Sukhasana, Uttanasana, Adho Mukha Svanasana, Vriasana, Baddha Konasana, Supta Padanugusthasana, Setu Bandhanasna, and Shavasana, for lowering down the blood pressure.
pressure which was averaging 157 in doctors office.I bought Amron blood pressure monitor and check my readings in the morning within 30 minutes of getting up at 4.45 a.m. and the I go for my walk and run or just walk and weight training 5 days a week. My home readings average about 115/67 with heart rate averaging 55.Pl. note that I have been on Amlodopine 2.5 mg. taking it about an hour before going to bed.I also take Flowmax and Avodart for enlarged prostate.
Pickering TG, et al. Recommendations for blood pressure measurement in humans and experimental animals: Part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Hypertension. 2005 Jan;45(1):142-61.
5. Take apple cider vinegar. In addition to lowering blood pressure almost overnight, apple cider vinegar has a myriad of fringe benefits. Apple cider vinegar helps with indigestion, especially if you suffer from diarrhea. It also soothes sore throats, cures hiccups instantly, and lowers cholesterol. Most importantly, it helps with weight loss by improving metabolism and reducing water retention -- and a healthy weight is key to normalizing blood pressure.
A 2013 study published in “Hypertension” concluded that flaxseed lowers blood pressure in hypertensive patients. It is a great home remedy for high blood pressure. More than 100 patients diagnosed with peripheral artery disease, a condition associated with high blood pressure, were assigned to a flaxseed group or a placebo group. The former ate 30 grams of flaxseed every day for 6 months.
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Hypertension can be effectively treated with lifestyle modifications, medications, and natural remedies. Most people with hypertension experience improvement with prescription treatment such as diuretics, ACE inhibitors, beta-blockers, or other options, and some may require more than one prescription medication to reach optimal blood pressure. If your hypertension has a medical cause (secondary hypertension), you may also need treatment for medical issues that are contributing to your high blood pressure.
Oatmeal is one of a few semi-processed foods that lower blood pressure. That’s because getting the right amounts of dietary fiber and whole grains is vital to maintaining normal blood pressure, and oatmeal is a tasty source of both. Classic studies have proven that eating oatmeal can lower systolic and diastolic blood pressure. Plus, the fiber can help you maintain a healthy body weight and prevent obesity, a risk factor for high blood pressure. These are the 10 silent signs you could have low blood pressure.
Diabetics often have lower recommendations for blood pressure, the maximum normal value being seen as 130/80-85. However, it’s questionable whether it’s a good idea to medicate your blood pressure levels down to those values. Diabetics can probably stick to approximately the same upper limit as people with heart disease: 140/90 (according to new studies and expert comments, as well as the latest recommendations from the American Diabetes Association, ADA).
Garlic: Garlic has long been thought to reduce hypertension. Studies show that garlic extract can lower blood pressure, although the optimal dose, frequency, and form are not well established. Garlic may produce this effect by acting directly on the kidneys to eliminate excess salt. It is considered a safe spice to consume, although it can cause some stomach upset.
Common painkillers (so-called non-steroidal anti-inflammatory drugs, NSAID), can increase your blood pressure by inhibiting the production of salt in your kidneys. This includes over-the-counter pills such as Ipren, Ibumetin, Ibuprofen, Diklofenak and Naproxen as well as the prescription drug Celebra. Painkillers with the active substance paracetamol are better for your blood pressure.
Glad to be helpful. If the nephrologist says all the tests were negative, that sounds reassuring and might mean your doctors could try different types of BP medication with you. Generally, three types of medication are considered equally acceptable for first-line treatment of high blood pressure: thiazide-type diuretics, ACE inhibitors or angiotensin receptor blockers (these two are related), or calcium channel blockers such as amlodipine.
Bananas are one great source of potassium, but there are other tasty ways to get your fill. Potatoes actually pack more potassium than the yellow fruit (and you might be surprised to learn there are plenty of other health benefits of potatoes, too). Sweet potatoes, tomatoes, orange juice, kidney beans, peas, cantaloupe, honeydew, and dried fruits like prunes or raisins are other good sources. In all, you should aim to get 2,000 to 4,000 mg of potassium a day, Van Horn recommends.
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Tests During Pregnancy: Abdominal Ultrasound
Written by the Healthline Editorial Team | Published on March 15, 2012
Medically Reviewed by Joan K. Lingen, MD
Prenatal Visits
If you are a healthy woman with a normal pregnancy, your prenatal visits will usually be scheduled every month until 32 to 34 weeks, then every two weeks until 36 weeks, and then weekly until delivery. Obviously, this schedule is flexible. If you experience any complications between your scheduled visits, call your doctor immediately-a month is a long time to worry about something.
Will I Need a First Trimester Ultrasound?
Ultrasound is an essential tool for evaluating your baby during pregnancy. More than one half of all pregnant women in the United States undergo at least one ultrasound examination. Whether or not you receive an ultrasound during your first trimester of pregnancy depends on a number of factors related to your pregnancy, such as your risk for complications.
Common reasons for obtaining an ultrasound examination in the first trimester are to confirm fetal viability (that the fetus is alive) or to determine gestational age. Ultrasound determination of gestational age is helpful if your LMP (last menstrual period) is uncertain, you have a history of irregular periods, conception occurred during oral contraceptive use, or if your initial pelvic examination suggests a gestational age different from that indicated by your LMP.
You may not need an ultrasound if you have no risk factors for pregnancy complications, you have a history of regular periods, you are certain of the date your last menstrual period (LMP) began, and you receive prenatal care during your first trimester.
What Happens During the Ultrasound?
Most ultrasound studies obtain an image by sliding a transducer over the abdomen. The small size of the fetus during the first trimester often necessitates higher resolution than can be achieved from a vaginal approach. Endovaginal ultrasound examination (a probe inserted into the vagina) is another option.
What Will a First Trimester Ultrasound Show?
Typically, a first trimester, endovaginal ultrasound reveals a gestational sac (the sac of water containing the fetus), a fetal pole (arms and legs developed to variable extents, depending on gestational age), and a yolk sac (a structure that provides nourishment to the fetus while the placenta is developing).
By approximately six weeks gestation, a fetal heartbeat is visible through an ultrasound, as well as multiple fetuses (twins, triplets, etc.). Evaluation of fetal anatomy is extremely limited in the first trimester. It is largely limited to assessing the presence or absence of major structures and the assessment of the relative sizes of the present structures.
What if the Ultrasound Shows a Sac Without a Fetal Pole?
The presence of a sac without a fetal pole usually indicates the presence of either an extremely early pregnancy (usually four weeks or less) or a blighted ovum (a fetus that does not develop).
An empty sac in the uterus may occur with an ectopic pregnancy (a pregnancy that implants somewhere other than the uterus). The most common site of an ectopic pregnancy is the fallopian tube. An ectopic pregnancy is a potentially life-threatening situation, due to the risk of hemorrhage. The presence or absence of an ectopic pregnancy can be further determined by checking for an appropriate rise in the amount of the hormone beta-hCG in the blood. A doubling of the level of beta-hCG over a period of approximately 48 hours is considered normal and virtually excludes the diagnosis of ectopic pregnancy.
What if There Is No Heartbeat?
A heartbeat may not be visible during an ultrasound if the examination is performed early in pregnancy-prior to the development of cardiac activity. In this situation, your doctor will repeat the ultrasound later in your pregnancy. Alternatively, the absence of cardiac activity may indicate that the fetus did not survive. Evaluation of surrounding structures, such as the size and shape of the gestational sac relative to the size of the fetus, can provide further clues to help differentiate fetal death from an otherwise normal but early gestation. Furthermore, checking blood levels of beta-hCG can help to distinguish between fetal death in the first trimester and a normally developing, early pregnancy.
How Can Ultrasound Determine Gestational Age?
Usually, determining your baby's gestational age and your due date is calculated from the first day of your last menstrual period (LMP). If your last menstrual period is unknown, an ultrasound evaluation of fetal size can determine gestational age and due date. Ultrasound determination of gestational age is most accurate during the first trimester because there is little biological variability in size from one pregnancy to the next and few factors that significantly affect fetal growth.
Measurement of the fetal pole from one end to the other is called the crown-rump length (CRL). This measurement correlates with actual gestational age within five to seven days. Typically, if the due date suggested by the CRL falls within about five days of menstrual dating, the due date established by the LMP is kept throughout pregnancy. If the due date suggested by the CRL falls outside this range, the due date from the ultrasound is usually kept.
Ultrasound is particularly helpful in establishing gestational age and the due date in women who are uncertain of their last menstrual period, who have a history of irregular menses, or who conceived while taking birth control pills. In the situation of irregular bleeding or conception on birth control pills, the last episode of vaginal bleeding may not be associated with the actual LMP and, hence, may not be a reliable indicator of conception date and of gestational age.
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Can a Bladder Problem be a Back Problem?
Can a Bladder Problem be a Back Problem?
by Dr. Stephen Dobelbower
The nerves to the bladder are located in the lower back. The last five vertebrae of the spine are called the lumbar spine and they house the nerve roots to the bladder. The spinal nerves exit between these vertebrae and the spinal nerve to the bladder, L3, exits between the third and the fourth lumbar vertebrae.
Chiropractors have noticed for many years that if the lower vertebrae are out of alignment the patient often complains of symptoms associated with frequent bladder problems. When lower back vertebrae are out of alignment it can cause irritation or inhibition of the nerve(s) and some of those nerves innervate the bladder. Consequently, the bladder and uterus are more irritated on the right side.
When we need to use the bathroom to void and there isn’t a bathroom around, we use our bladder sphincter muscles to hold our urine. Our sphincter muscles are controlled by voluntary type nerves. When our bladder expands because of the amount of urine stored in it, the traction on our bladder wall elicits a reflex of fullness. This reflex is an involuntary nervous system controlled function. In a state of bladder dysfunction, we may experience a false fullness in the bladder, meaning that there is not enough urine in our bladders to warn the involuntary or reflex response that gives us the urge to use the bathroom.
When the bladder dysfunction is incontinence, there is the inability to control the urine, meaning the voluntary nerve and sphincter muscles are worn out. Kegel exercises are usually recommended to strengthen the sphincter muscles. Kegel exercises can also be practiced preventively to keep the bladder young.
Chiropractic adjustment to the third lumbar (in the low back), for voluntary bladder function, and to the sacrum (the triangular shaped bone at the base of the spine), for the involuntary bladder function can help to balance overall bladder health. Yet, other vertebrae adjustments also help. For example, when the lumbar tree and sacrum cannot be adjusted, because of a malfunctioning of these joints, the chiropractor knows back-up mechanisms, such as to adjust the first vertebra in the neck and dorsal number three, the third vertebra in the middle back. These adjustments will also aid in balancing the bladder.
To learn more or would like to address a bladder or other health concern, schedule a consultation with Dr Dobelbower at 406.222.9373 to see if Chiropractic care can help.
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Peroneal tendonitis
Peroneal tendonitis
Peroneal tendinitis is a condition that involves the muscles on the outside of your leg, called the peroneal muscles. These muscles are also referred to as fibularis longus and fibularis brevis. Tendinitis is a condition where the tendons of these muscle become inflamed. This can cause a painful outer leg, calf and ankle.
Causes of peroneal tendinitis
Peroneal tendonitis is an overuse injury with runners who run along slopes or sand often developing it. This is because running along slopes can cause the foot to roll outwards, which stretches the tendon and causes friction between the bone and the tendon. This continued rubbing of the tendon and ankle bone, called the lateral malleolus, can occur in silence until running ends and the inflammation is given time to build up. In chronic cases we call this peroneal tendinopathy or peroneal tendinosis in some sources. These are technically all a little different but for our purposes when will group them into the same categories.
Symptoms of peroneal tendinitis
The most common symptoms of peroneal tendonitis is pain and swelling on the outside of the ankle. Pain may or may not be felt with pressure to the side of the ankle, but on muscle testing of these muscles a weak and painful responses is usually positive.
Treatments of peroneal tendinitis
Chiropractic and physiotherapy treatments for peroneal tendonitis start with rest, unloading and modifying behaviour. This is to allow the inflammation and injury to heal. This means limited physical activity and no activity if pain if felt or to a plan you chiropractor and physiotherapist come up with. There is evidence that rehabilitation exercises may go into a little pain when treating peroneal tendon injuries however this must be managed by a chiropractor or physiotherapist with sound knowledge and experience in this area. At Sydney Spine & Sports Centre (S3C) our Balmain and Dee Why chiropractors and physiotherapists have advanced clinical training in tendon injuries and their treatment and rehabilitation.
Simple treatments such as applying a cold pack to the area in pain is also recommended straight after an injury is sustained. Typically the recommendations would be to apply the pack every hour for 10 minutes until symptoms improve.Following this heat therapy is showing beneficial effective in the research and should be started, in response to acute injury. To relieve symptoms of pain and inflammation, anti-inflammatory medication may be taken under the advice of your general practitioner. If one of our Balmain or Dee Why chiropractors or physiotherapist think you need extra advice on medications we will send you to one of the general practitioners we typically work with.
Following the acute phase of peroneal tendinitis current tendon guidelines recommended to start a progressive and tailored loading program as this will desensitise the tendon and lead to changes within the tendon and muscular system that reduce pain, improve the tendon’s durability and structural properties and allow the tendon to load better without the risk of injury recurrence.
At Sydney Spine & Sports Centre (S3C) we strive for excellence in all we do, with comprehensive chiropractic and physiotherapy treatments with a personal and individual approach we are passionate about fixing pain and getting you moving again. Give the team a call at the clinic or book directly online.
The chiropractors and physiotherapists at Sydney Spine & Sports Centre (S3C) are passionate about the diagnosis, treatment and management on tendon injuries. For more information, please explore the links below and contact us with any questions or comments. Our Balmain and Dee Why chiropractors and physiotherapists are only too happy to help.
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Is it normal to experience pain during erections after a catheter?
Temporarily. Pain with an erection shortly after a catheter was used/removed is not uncommon. It should only be a cause of concern if it doesn't resolve within a week, or if it is severe pain. It would be useful to know why the catheter was used in the first place as the problem may be due to the underlying issue for which the catheter was placed.
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Top
20
Doctor insights on: How Would You Know If You Have An Infection In A Knee Replacement
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How do you know if you have an infection in your knee after a partial knee replacement?
How do you know if you have an infection in your knee after a partial knee replacement?
Red swollen hot pain: The clinical findings that are concerning for an infected knee are: 1. Redness/pinkness around the incision or knee. 2. Increased swelling around knee 3. Increased pain with bending or weight bearing 4. Fever, chills, lethargy, loss of appetite 5. A knee draining fluid from the incision or a new hole 6. Blood tests with elevated wbc, crp, esr. See your surgeon with any concern asap, don't wait! ...Read more
See 1 more doctor answer
Dr. Mark Ingerman
9 Doctors shared insights
Infection (Definition)
Infections are invasions of some other organism (fungus, bacteria, parasite) or viruses into places where they do not belong. For instance, we have normal gut bacteria that live within us without causing problems; however, when those penetrate the bowel wall and enter the bloodstream, ...Read more
2
2
How can you know if you have an infection in your knee after having a partial knee replacement?
How can you know if you have an infection in your knee after having a partial knee replacement?
Pain and Swelling: Infections in joint replacements can be very hard to diagnose. Generally, doctors with use blood tests, radiographic tests, aspirations (a tap of the fluid in the knee) and some times biopsies to determine if there is an infection. ...Read more
See 2 more doctor answers
3
3
How would you know if you have an infection in your knee after having a partial knee replacement?
How would you know if you have an infection in your knee after having a partial knee replacement?
Red, pain, drainage: The common signs of an infection can include the following: -fever -redness around the incision -swelling with redness -drainage from a red and swollen knee -pain with weight bearing in a red swollen knee -blood test that show an elevated WBC count, elevated c-reactive protein, elevated esr - the gold standard is to drain fluid out of the knee and send it to the lab for gram stain and culture. ...Read more
See 1 more doctor answer
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4
What should I do if I have an infection following a total knee replacement?
See your surgeon: Infection is a serious condition in a total knee replacement and needs urgent treatment. If it is caught early, a surgical washout of the joint with antibiotic therapy may cure the infection. If not, the implants may need to be removed in order to cure the infection. Once accomplished, a total knee may be redone to restore knee function. ...Read more
See 1 more doctor answer
5
5
I had a knee replacement a year ago and the same knee suddenly got hot and swollen, should I be worried about an infection?
I had a knee replacement a year ago and the same knee suddenly got hot and swollen, should I be worried about an infection?
Yes: You definitely need to worry about infection! See your surgeon who will probably order some bloodwork and aspirate your knee to have the fluid aspirated. ...Read more
See 1 more doctor answer
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6
I've been battling an infection after a knee replacement for a little over a year. Is there a natural way to cure Vancomycin resistant Enterococcus?
I've been battling an infection after a knee replacement for a little over a year. Is there a natural way to cure Vancomycin resistant Enterococcus?
Yes and no: Depending on how you look at it, and it may already have been done, the most "natural" way to treat someone with an infected total knee replacement is to remove any foreign bodies in your knee that could potentially harbor infection. Unfortunately, however, this means removing the entire knee replacement itself and then trying to eradicate the infection at that point. ...Read more
See 3 more doctor answers
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7
How to determine if I have an infection in my knee after having a partial knee replacement?
How to determine if I have an infection in my knee after having a partial knee replacement?
Pain, swelling fever: A bacterial infection always produces pain and swelling. A severe one with strep or staph aureus will create a hot knee with fever and constitutional symptoms. Taking fluid out of the knee for analysis is the most definitive test. ...Read more
See 1 more doctor answer
8
8
How do I know that my doctor has chosen the knee replacement of a manufacturer with the fewest problems, i.e. fsilure, infection, etc. Do I have any?
How do I know that my doctor has chosen the knee replacement of a manufacturer with the fewest problems, i.e. fsilure, infection, etc. Do I have any?
Knee arthroplasty: Your orthopedic surgeon should be very open to your valid concerns. She or he should be willing to tell you which manufacturer they prefer and why. Then you can do your own research to "validate" what was stated in your patient encounter. I would hope that they prefer placing hardware that has the best outcome for you. ...Read more
9
9
Can listeriosis infection affect a total knee replacement after 3 months of the surgery?
Can listeriosis infection affect a total knee replacement after 3 months of the surgery?
Unusual pathogen: Risk of prosthetic joint infection is influenced by many modifiers pre/postoperatively. The success of your prosthetic joint in highly dependent of some routine health observation; dental, genitourinary, GI etc. Listeria M. is not a usual pathogen in PJIs. If you are worried about the possibility of infection please contact your surgeon ASAP for proper evaluation. Take care! ...Read more
10
10
Total knee replacement because of mrsa, I may need a revision because of reoccurring cyst, will 2nd time be as hard? No infection now 1st is cemented
Total knee replacement because of mrsa, I may need a revision because of reoccurring cyst, will 2nd time be as hard? No infection now 1st is cemented
Very tough?: If u mean u need a revision because of MRSA infection in the knee now, the process is long. When the implants r removed cultures r taken ; no new implants. Antibiotic impregnated cement is left in ; u r treated with the proper antibiotics. When CRP ; other studies return to normal, the area may b aspirated ; cultured again ; if clean u then can talk 2 ur surgeon about the next step. ...Read more
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11
11
I had a bone scan on knee replacement feb, 2012. My gp said report said could be infection, loosening or trauma. Please help me understand.
Needs correlation: A bone scan looks at the metabolism around the replacement. If there is lots of uptake, that means there is lots of bone turn over. Unfortunately several different things can cause increased turn over. Like infection, a loose prosthesis or even recent trauma and fracture. This must be assessed along with symptoms and possibly blood work. ...Read more
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14
14
How do you know if you have infected knee after having a partial knee replacement?
How do you know if you have infected knee after having a partial knee replacement?
Get to your surgeon: The clinical findings that are concerning for an infected knee are: 1. Redness/pinkness around the incision or knee. 2. Increased swelling around knee 3. Increased pain with bending or weight bearing 4. Fever, chills, lethargy, loss of appetite 5. A knee draining fluid from the incision or a new hole 6. Blood tests with elevated wbc, crp, esr. See your surgeon with any concern asap, don't wait! ...Read more
See 2 more doctor answers
15
15
What do you advise if I had a knee replacement and now my knee dosent ben t?
See Ortho doc: You may need exercises to range your knee, however if there is something wrong with your replacement the orthopedic doc may need to further evaluate you. ...Read more
16
16
On june 10 th I have knee replacement. My knee doesn't respond as well as I expect. It doesn't flex enough. I will have knee manipulation. What is this?
Post surgical knee: Scar tissue that forms following surgery may prevent full range of motion. If physical therapy cannot resolve this, manual manipulation is performed to break the scar tissue ...Read more
17
17
I am having knee replacement in april, 2013. I can't take opium pain medication. What else can I take to relieve the pain? Thanks, dee
Many Choices: It would be very wise to meet with a pain specialist prior to your surgery to set yourself up for success. Alternative investigation too may help: meditation, acupuncture, massage. Possible meds include pain blocker Gabapentin (neurontin) anti inflammatory such as meloxicam, naprosyn, (naproxen) etc opiate alternative tramadol (warning; addictive too) seek specialty advice. ...Read more
See 1 more doctor answer
19
19
I have osteoarthritis in both knees but I am too young for knee replacement how can I manage the pain, I can, t get around very well.
I have osteoarthritis in both knees but I am too young for knee replacement how can I manage the pain, I can, t get around very well.
Arthritis exercise.: Osteoarthritis is best treated with regular exercise and being at your ideal weight. The pain can be treated with acetaminophen, and anti inflammatory medications, such as naproxen, and ibuprofen. Injections to knees with steroids, or the use of Hyaluronate products are effective. ...Read more
See 1 more doctor answer
20
20
How can I avoid knee replacement?
How can I avoid knee replacement?
Exercise stay thin: There are no medicines or nutritional suppliments that proven to stop arthritis, but keeping weight down and exercising cand delay arthritis symptoms. ...Read more
See 5 more doctor answers
Dr. Frederick Buechel, jr. md
439 Doctors shared insights
Knee Replacement (Definition)
It is when a surgeon removes and exchanges some are all of the componets of your knee. The bottom end of the thigh bone (femur), the upper end of the shin bone (tibia) and the undersurface of ...Read more
|
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Depression Therapy
If following any kind of an accident, event or other emotional trigger you suffer a depression, we might help you!
Every once in a while every person has suffered from either an anxiety attack or a minor to major depression.
The most telling sign of it is that no matter what you do, your mind cannot see the world in the positive light anymore… However, even the most severe depression is treatable. So, if your depression is halting you from living the life you want to, never doubt about asking for a professional therapist to give you a proper counseling help.
Getting to understand your depression in a better way will be crucial when you will make a decision to ask for help. From therapy to medication to healthy lifestyle changes, there are many effective treatments that can help you overcome depression and reclaim your life.
Exploring your depression treatment options
Just as no two people are affected the exact same way by depression, there is no completely universal treatment that cures everybody with the exact timing for all… What works for one person might not work for another.
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with No Comments
Post No.: 0329insomnia
Furrywisepuppy says:
Your ‘sleep onset latency’ is the length of time it takes for you to fall asleep from the moment you tuck into bed and switch off the lights. A time of around 15-20 minutes is considered fine. If it’s much shorter then it may indicate that you have been sleep deprived, and if it’s much longer then it may indicate that you have insomnia.
Your ‘sleep efficiency’ is the percentage of time you’re actually asleep compared to the total time you’ve been in bed. An efficiency of 85% or more is considered good.
If you are sleep deprived then you’ll have built up a ‘sleep debt’, which is the cumulative effect of not getting enough sleep. This might either be because of losing a bit of sleep each night for several nights or weeks in a row, or because of not sleeping for over 24 hours (e.g. due to an all-nighter studying… or partying!)
Now we cannot bank sleep in advance, or can only do so slightly and not to the same extent that we can build up a sleep debt. (It’s very loosely similar to the way that eating a large meal can make us feel like we can skip the next meal, but people who bank a lot of food (i.e. who store a lot of fat inside their bodies) can still feel hungry before they’ve spent all of that fat (energy) they’ve previously banked.) If it feels possible to bank some sleep then it’s probably because you’ve been routinely sleep deprived and you think that this sleep-deprived state is normal, hence why that extra sleep feels like a beneficial bonus rather than the healthy or ideal normal way to feel and operate.
Your ‘sleep reactivity’ is the ease in which you manage to fall asleep during a particularly stressful or arousing time, such as the night before you have a crucial meeting, the night before going on an exciting holiday, or the night after a distressing experience. And if you find it hard to fall asleep under these conditions then that’s a strong predictor of whether you’ll suffer from insomnia.
Some people with insomnia have trouble getting to sleep, some struggle to stay asleep, and some both. This insomnia can in turn lead to or exacerbate depression – insomnia can perpetuate a depressive episode long after the original underlying stress event or condition that triggered the depressive episode has been over, removed or cured/solved. For instance, a physical back injury triggered a depressive episode, as well as insomnia because you couldn’t find a comfortable position to sleep in, and now after several months of this, you now associate your bedroom and trying to get to sleep as a stressful experience itself – these types of stresses about struggling to sleep can themselves perpetuate a case of insomnia and/or depression, even though the original physical injury or pain has healed or ceased. This thus results in a vicious cycle of insomnia and/or depression. In short, stressing about sleeping can keep us awake!
Insomnia is often a symptom of some other underlying root cause, such as PTSD, anxiety or chronic stress. The mind is constantly, consciously and/or unconsciously, whirring and ruminating on something like a loss or trauma, perhaps from years ago – and it’s really this that needs to be broached first before the insomnia can be solved. There are different root causes hence there is no ‘one size fits all’ solution to insomnia.
As in most cases that concern one’s health, insomnia involves an interaction between both one’s genes and one’s environment. The stressors or underlying conditions that can affect our sleep can be environmental (e.g. what’s in our bedroom), psychosocial (e.g. a divorce) or medical (e.g. some health conditions or medications). So insomnia sufferers may have a genetic/biological predisposition, they may then face a precipitating factor or stressor, and then they may face a perpetuating factor that perpetuates their insomnia even though the precipitating factor has passed.
Poor ‘sleep hygiene’ includes eating too close to bedtime, or alternatively too far from bedtime (which leaves an uncomfortable rumbling tummy), consuming caffeine too close to bedtime, exercising too close to bedtime, trying to use alcohol to fall asleep, using electronic devices in bed (sometimes for the very reason of not being able to sleep and looking for something to do whilst awake in bed) or doing other sleep incompatible activities such as watching TV in bed. Spending too much time in bed (e.g. being in bed when it’s not bedtime) is also a bad habit – the bed, and ideally entire bedroom, must only be associated with sleeping (and maybe sex) so get out of bed if you cannot sleep or are not tired, and restrict the time you are in or on your bed. One of the worst things is an irregular sleep schedule. Psychological matters might include unrealistic sleep expectations, such as stressing over the notion that you must have 8 hours of sleep if you happen to feel okay with less or better with more, or, again, feeling anxious about not being able to sleep itself. (Post No.: 0219 looked at how much sleep people of different ages need.)
Perpetuating any of these above kinds of habits can also prolong insomnia or a bad relationship with sleep. So one of the best strategies if you have insomnia is to follow those sleep hygiene tips. Go to bed at the same time each night but if you cannot sleep within 15 minutes of tucking into bed then get out of the bedroom and do something that is calm until you’re tired again. And most of all, always get up at the same time each morning (don’t use that snooze alarm!) and immediately open the curtains to get some daylight. Some experts suggest strictly getting up at a consistent time every single day but only going to bed whenever you’re feeling tired, whatever time that may be because no one can be forced to sleep at, say, 11pm every night if they’re not tired at that time. Woof!
Being exposed to enough bright light (preferably sunlight) as soon as you get up, and minimising the amount of light you get before you go to bed, is one of the keys for sleeping well when you want to sleep, and feeling awake when you want to be awake.
The first days you get up at a fixed time even though you need more sleep will feel horrible, but your body should soon learn to adapt to sleeping at that fixed time you should be in bed each night. Some sleep experts allow or even advocate taking naps during the day, but if you are trying to adjust your sleep routine then don’t take any naps during the day – only sleep during the 8-hour or so window you’ve set yourself for sleeping.
If you’re really tired or it’s getting late but you’ve still got some work left to do, you’re highly likely better off going to bed at your usual time and finishing the work the next day if possible. This is because your productivity rate when you’re tired could be half of your normal productivity rate so you’ll take twice as long to complete it in this state, and you’ll feel terrible while doing it too, plus it could get even worse if you make mistakes for being tired. If you do get some sleep and then pick up the work the next day when you’re at normal productivity levels again, you’ll get more work done or you’ll get it done in less time, plus you’ll feel mentally better for the sleep too, and fewer mistakes will likely be made.
All this is true regarding productivity when we work overly long hours – working longer or later doesn’t necessarily mean that people are getting more work done or getting better quality, more creative, work done. Sometimes it’s easier to understand something than to make it happen though, as one might stress about the unfinished work when lying in bed, which might then keep one awake anyway. Well if working beyond expected hours becomes a pattern then it either means the work is unhealthy or one needs to learn to start it earlier.
If you still struggle with insomnia or have other types of sleep problems, such as loud snoring (which could be a sign of sleep apnoea) or night terrors, then it’s best to go see your doctor. He/she might prescribe you cognitive behavioural therapy or something else. Cranial electrotherapy stimulation (CES) might help some people with insomnia, or alternatively any activity that is ultimately calming such as listening to calm music.
Woof. If you have any other tips that have worked for you for getting a good night’s kip then please reply to the tweet linked in the Twitter comment button below. Counting an endless stream of fluffy sheep doesn’t work for most people – but I guess you could give it a try if you want? For me, it keeps me even more awake because all I see are lamb chops(!)
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1. Pharmacokinetic Interaction between Efavirenz and Dual Protease Inhibitors in Healthy Volunteers
The combination of efavirenz with HIV-1 protease inhibitors (PI) results in complex interactions secondary to mixed induction and inhibition of oxidative metabolism. ACTG A5043 was a prospective, open-label, controlled, two-period, multiple-dose study with 55 healthy volunteers. The objective of the present study was to evaluate the potential pharmacokinetic interaction between efavirenz and dual PIs. The subjects received a daily dose of 600 mg efavirenz for 10 days with amprenavir 600 mg twice daily added at day 11 and were randomized to receive nelfinavir, indinavir, ritonavir, saquinavir, or no second PI on days 15–21. Intensive pharmacokinetic studies were conducted on day 14 and 21. Efavirenz plasma concentrations were fit to candidate models using weighted non-linear regression. The disposition of efavirenz was described by a linear two-compartment model with first order absorption following a fitted lag time. Apparent clearance (CLt/F), volume of distribution at steady state (Vss/F), inter-compartmental clearance, and the central and peripheral volume of distribution were estimated. The mean CLt/F and Vss/F of efavirenz were 0.126 l/h/kg and 4.412 l/kg, respectively. Both AUC and CLt/F of efavirenz remained unchanged after 7 days of dual PI dosing. The mean Vss/F of efavirenz increased an average of 89% across arms, ranging from 52% (nelfinavir) to 115% (indinavir) relative to efavirenz with amprenavir alone. Increases were also observed in Vp/F after the addition of nelfinavir, indinavir, ritonavir and saquinavir by 85%, 170%, 162% and 111%, respectively. In conclusion, concomitant administration of dual PIs is unlikely to have any clinically significant effect on the pharmacokinetics of CYP2B6 substrates in general or oral efavirenz specifically.
doi:10.1002/bdd.597
PMCID: PMC4307806 PMID: 18041735
pharmacokinetic modeling; drug interactions; non-nucleoside reverse transcriptase inhibitor; efavirenz; HIV-1 protease inhibitors
2. HIV and asthma, is there an association?
Respiratory medicine 2012;106(4):493-499.
Summary
Objective
To evaluate whether asthma and airway hyper-responsiveness are associated with HIV infection.
Methods
We reviewed the literature on HIV-associated pulmonary diseases, pulmonary symptoms, and immune changes which may play a role in asthma. The information was analyzed comparing the pre-HAART era to the post-HAART era data.
Results
HIV-seropositive individuals commonly experience respiratory complaints yet it is unclear if the frequency of these complaints have changed with the initiation of HAART. Changes in pulmonary function testing and serum IgE are seen with HIV infection even in the post-HAART era. An increased prevalence of asthma among HIV-seropositive children treated with HAART has been reported.
Conclusion
The spectrum of HIV-associated pulmonary disease has changed with the introduction of HAART. Current data is limited to determine if asthma and airway hyper-responsiveness are more common among HIV-seropositive individuals treated with HAART.
doi:10.1016/j.rmed.2011.12.017
PMCID: PMC4235227 PMID: 22285768
Asthma; Airway hyper-responsiveness; HIV; Antiretroviral
3. The Design of Single-Arm Clinical Trials of Combination Antiretroviral Regimens for Treatment-Naive HIV-Infected Patients
Abstract
Single-arm clinical trials are useful to evaluate antiretroviral regimens in certain populations of HIV-infected treatment-naive patients for whom a randomized controlled trial is not feasible or desirable. They can also be useful to establish initial estimates of efficacy and safety/tolerability of novel regimens to inform the design of large phase III trials. In this article, we discuss key design considerations for such single-arm studies.
doi:10.1089/aid.2012.0180
PMCID: PMC3607972 PMID: 23228206
4. Impact of Chemotherapy for HIV-1 Related Lymphoma on Residual Viremia and Cellular HIV-1 DNA in Patients on Suppressive Antiretroviral Therapy
PLoS ONE 2014;9(3):e92118.
The first cure of HIV-1 infection was achieved through complex, multimodal therapy including myeloablative chemotherapy, total body irradiation, anti-thymocyte globulin, and allogeneic stem cell transplantation with a CCR5 delta32 homozygous donor. The contributions of each component of this therapy to HIV-1 eradication are unclear. To assess the impact of cytotoxic chemotherapy alone on HIV-1 persistence, we longitudinally evaluated low-level plasma viremia and HIV-1 DNA in PBMC from patients in the ACTG A5001/ALLRT cohort on suppressive antiretroviral therapy (ART) who underwent chemotherapy for HIV-1 related lymphoma without interrupting ART. Plasma HIV-1 RNA, total HIV-1 DNA and 2-LTR circles (2-LTRs) in PBMC were measured using sensitive qPCR assays. In the 9 patients who received moderately intensive chemotherapy for HIV-1 related lymphoma with uninterrupted ART, low-level plasma HIV-1 RNA did not change significantly with chemotherapy: median HIV-1 RNA was 1 copy/mL (interquartile range: 1.0 to 20) pre-chemotherapy versus 4 copies/mL (interquartile range: 1.0 to 7.0) post-chemotherapy. HIV-1 DNA levels also did not change significantly, with median pre-chemotherapy HIV-1 DNA of 355 copies/106 CD4+ cells versus 228 copies/106 CD4+ cells post-chemotherapy. 2-LTRs were detectable in 2 of 9 patients pre-chemotherapy and in 3 of 9 patients post-chemotherapy. In summary, moderately intensive chemotherapy for HIV-1 related lymphoma in the context of continuous ART did not have a prolonged impact on HIV-1 persistence.
Clinical Trials Registration Unique Identifier:
NCT00001137
doi:10.1371/journal.pone.0092118
PMCID: PMC3956871 PMID: 24638072
5. Phase I/II Trial of the Anti-HIV Activity of Mifepristone in HIV-Infected Subjects ACTG 5200
Background
Mifepristone is a glucocorticoid receptor inhibitor shown in vitro to have anti-HIV activity and anti-simian immunodeficiency virus activity in a macaque model. A phase I/II trial was performed to assess the drug’s safety and anti-HIV activity.
Methods
A 28-day double-blind, placebo-controlled trial of mifepristone at doses of 75 mg, 150 mg, and 225 mg given daily was conducted in HIV+ persons with CD4+ lymphocyte counts ≥350 cells per cubic millimeter who had no recent antiretroviral therapy.
Results
Fifty-six male and 1 female subjects with a median entry CD4+ lymphocyte count of 555 cells per cubic millimeter and plasma HIV-1 RNA of 15,623 copies per milliliter were accrued. Forty-five subjects (78.9%) were available for endpoint analysis. In each arm, changes from baseline to day 28 in plasma HIV-1 RNA and CD4+ lymphocyte count were not significantly different from zero (no change). There was no relationship between mifepristone trough concentrations and plasma HIV-1 RNA. Day 28 morning plasma cortisol levels were significantly higher in the 150 mg and 225 mg arms compared with placebo, confirming biologic activity, and returned to baseline by day 56. Serum lipids did not change during the trial. Fasting blood sugar was 2.5 mg/dL higher on day 28 in the mifepristone arms, but the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) did not change. Three subjects (7.3%) receiving mifepristone developed a grade 2 rash.
Conclusions
Mifepristone at doses of 75–225 mg daily was safe and well-tolerated, but did not show significant anti-HIV activity.
doi:10.1097/QAI.0b013e3181d142cb
PMCID: PMC3477637 PMID: 20130470
antiretroviral; clinical trial; mifepristone
6. Human N-acetyltransferase 1 (NAT1) *10 and *11 alleles increase protein expression via distinct mechanisms and associate with sulfamethoxazole-induced hypersensitivity
Pharmacogenetics and genomics 2011;21(10):652-664.
Objectives
N-acetyltransferase 1 (NAT1) metabolizes drugs and environmental carcinogens. NAT1 alleles *10 and *11 have been proposed to alter protein level or enzyme activity compared to wild-type NAT1 *4 and to confer cancer risk, via uncertain pathways. This study characterizes regulatory polymorphisms and underlying mechanisms of NAT1 expression.
Methods
We measured allelic NAT1 mRNA expression and translation, as a function of multiple transcription start sites, alternative splicing, and three 3′-polyadenylation sites in human livers (one of which discovered in this study), B lymphocytes, and transfected cells. In a clinical study of 469 HIV/AIDS patients treated with the NAT1/NAT2 substrate sulfamethoxazole (SMX), associations were tested between SMX induced hypersensitivity and NAT1 *10 and *11 genotypes, together with known NAT2 polymorphisms.
Results
NAT1*10 and *11 were determined to act as common regulatory alleles accounting for most NAT1 expression variability, both leading to increased translation into active protein. NAT1*11 (2.4% minor allele frequency) affected 3′polyadenylation site usage, thereby increasing formation of NAT1 mRNA with intermediate length 3′UTR (major isoform) at the expense of the short isoform, resulting in more efficient protein translation. NAT1 *10 (19% minor allele frequency) increased translation efficiency without affecting 3′-UTR polyadenylation site usage. Livers and B-lymphocytes with *11/*4 and *10/*10 genotypes displayed higher NAT1 immunoreactivity and NAT1 enzyme activity than the reference genotype *4/*4. Patients who carry *10/*10 and *11/*4 (‘fast NAT1 acetylators’) were less likely to develop hypersensitivity to SMX, but this was observed only in subjects also carrying a slow NAT2 acetylator genotype.
Conclusion
NAT1 *10 and *11 significantly increase NAT1 protein level/enzyme activity, enabling the classification of carriers into reference and rapid acetylators. Rapid NAT1 acetylator status appears to protect against SMX toxicity by compensating for slow NAT2 acetylator status.
doi:10.1097/FPC.0b013e3283498ee9
PMCID: PMC3172334 PMID: 21878835
N-acetyltransferase; NAT1; polyadenylation; allelic expression imbalance; sulfamethoxazole; cotrimoxazole; protein translation; acetylator phenotype; idiosyncratic drug reactions
7. Polymorphism in glutamate cysteine ligase catalytic subunit (GCLC) is associated with sulfamethoxazole-induced hypersensitivity in HIV/AIDS patients
BMC Medical Genomics 2012;5:32.
Background
Sulfamethoxazole (SMX) is a commonly used antibiotic for prevention of infectious diseases associated with HIV/AIDS and immune-compromised states. SMX-induced hypersensitivity is an idiosyncratic cutaneous drug reaction with genetic components. Here, we tested association of candidate genes involved in SMX bioactivation and antioxidant defense with SMX-induced hypersensitivity.
Results
Seventy seven single nucleotide polymorphisms (SNPs) from 14 candidate genes were genotyped and assessed for association with SMX-induced hypersensitivity, in a cohort of 171 HIV/AIDS patients. SNP rs761142 T > G, in glutamate cysteine ligase catalytic subunit (GCLC), was significantly associated with SMX-induced hypersensitivity, with an adjusted p value of 0.045. This result was replicated in a second cohort of 249 patients (p = 0.025). In the combined cohort, heterozygous and homozygous carriers of the minor G allele were at increased risk of developing hypersensitivity (GT vs TT, odds ratio = 2.2, 95% CL 1.4-3.7, p = 0.0014; GG vs TT, odds ratio = 3.3, 95% CL 1.6 – 6.8, p = 0.0010). Each minor allele copy increased risk of developing hypersensitivity 1.9 fold (95% CL 1.4 – 2.6, p = 0.00012). Moreover, in 91 human livers and 84 B-lymphocytes samples, SNP rs761142 homozygous G allele carriers expressed significantly less GCLC mRNA than homozygous TT carriers (p < 0.05).
Conclusions
rs761142 in GCLC was found to be associated with reduced GCLC mRNA expression and with SMX-induced hypersensitivity in HIV/AIDS patients. Catalyzing a critical step in glutathione biosynthesis, GCLC may play a broad role in idiosyncratic drug reactions.
doi:10.1186/1755-8794-5-32
PMCID: PMC3418550 PMID: 22824134
Idiosyncratic drug reaction; Sulfamethoxazole; Hypersensitivity; Glutamate cysteine ligase catalytic subunit (GCLC); Association; HIV/AIDS
8. Antiretroviral drug levels and interactions affect lipid, lipoprotein and glucose metabolism in HIV-1 seronegative subjects: A pharmacokinetic-pharmacodynamic analysis
Background:
HIV-infected patients treated with antiretroviral medications (ARVs) develop undesirable changes in lipid and glucose metabolism that mimic the metabolic syndrome and may be proatherogenic. Antiretroviral drug levels and their interactions may contribute to these metabolic alterations.
Methods:
Fifty-six HIV-seronegative adults were enrolled in an open-label, randomized, pharmacokinetic interaction study, and received a non-nucleoside reverse transcriptase inhibitor (efavirenz on days 1-21) plus a protease inhibitor (PI; amprenavir on days 11-21), with a second PI on days 15-21 (saquinavir, nelfinavir, indinavir, or ritonavir). Fasting triglycerides, total, LDL- and HDL-cholesterol, glucose, insulin and C-peptide levels were measured on days 0, 14, 21, and 2-3 weeks after discontinuing drugs. Regression models were used to estimate changes in these parameters and associations between these changes and circulating levels of study drugs.
Results:
Short-term efavirenz and amprenavir administration significantly increased cholesterol, triglycerides and glucose levels. Addition of a second protease inhibitor further increased triglycerides, total- and LDL-cholesterol levels. Higher amprenavir levels predicted larger increases in triglycerides, total and LDL-cholesterol. Two weeks after all study drugs were stopped, total, LDL- and HDL-cholesterol remained elevated above baseline.
Conclusions:
ARV regimens that include a non-nucleoside reverse transcriptase inhibitor plus single or boosted PIs are becoming more common, but the pharmacodynamic interactions associated with these regimens can result in persistent, undesirable alterations in serum lipid/lipoprotein levels. Additional pharmacodynamic studies are needed to examine the metabolic effects of ritonavir-boosted regimens, with and without efavirenz.
doi:10.1089/met.2006.0034
PMCID: PMC2078603 PMID: 18007962
9. Compartmental Pharmacokinetic Analysis of Oral Amprenavir with Secondary Peaks▿
Amprenavir is a protease inhibitor that has been shown to have secondary peaks postulated to be due to enterohepatic recycling. We propose a model to describe the pharmacokinetics of amprenavir which accommodates the secondary peak(s). A total of 82 healthy human immunodeficiency virus (HIV)-seronegative subjects were administered a single 600-mg dose of amprenavir as part of adult AIDS Clinical Trials Group protocol A5043. Serial blood samples were obtained over 24 h. Samples were analyzed for amprenavir and fit to a compartmental model using ADAPT II software, with all relevant parameters conditional with respect to bioavailability. The model accommodated secondary peaks by incorporating clearance out of the central compartment with delayed instantaneous release back into the gut compartment. The data were weighted by the inverse of the estimated measurement error variance; model discrimination was determined using Akaike's Information Criteria. A total of 76 subjects were evaluable in the study analysis. The data were best fit by a two-compartment model, with 98.7% of the subjects demonstrating a secondary peak. Amprenavir had a mean total clearance of 1.163 liters/h/kg of body weight (0.7), a central volume of distribution of 1.208 liters/kg (0.8), a peripheral volume of distribution of 8.2 liters/kg (0.81), and distributional clearance of 0.04 liters/h/kg (0.81). The time to the secondary peak was 7.86 h (0.17), and clearance into a recycling compartment was 0.111 liters/kg/h (0.74). Amprenavir pharmacokinetics has been well described using a two-compartment model with clearance to a recycling compartment and release back into the gut. The nature of the secondary peaks may be an important consideration for the interpretation of amprenavir plasma concentrations during therapeutic drug monitoring.
doi:10.1128/AAC.00570-06
PMCID: PMC1855557 PMID: 17283195
10. Amprenavir and Efavirenz Pharmacokinetics before and after the Addition of Nelfinavir, Indinavir, Ritonavir, or Saquinavir in Seronegative Individuals
Adult AIDS Clinical Trials Group 5043 examined pharmacokinetic (PK) interactions between amprenavir (APV) and efavirenz (EFV) both by themselves and when nelfinavir (NFV), indinavir (IDV), ritonavir (RTV), or saquinavir (SQV) is added. A PK study was conducted after the administration of single doses of APV (day 0). Subjects (n = 56) received 600 mg of EFV every 24 h (q24h) for 10 days and restarted APV with EFV for days 11 to 13 with a PK study on day 14. A second protease inhibitor (PI) (NFV, 1,250 mg, q12h; IDV, 1,200 mg, q12h; RTV, 100 mg, q12h; or SQV, 1,600 mg, q12h) was added to APV and EFV on day 15, and a PK study was conducted on day 21. Controls continued APV and EFV without a second PI. Among subjects, the APV areas under the curve (AUCs) on days 0, 14, and 21 were compared using the Wilcoxon signed-rank test. Ninety-percent confidence intervals around the geometric mean ratios (GMR) were calculated. APV AUCs were 46% to 61% lower (median percentage of AUC) with EFV (day 14 versus day 0; P values of <0.05). In the NFV, IDV, and RTV groups, day 21 APV AUCs with EFV were higher than AUCs for EFV alone. Ninety-percent confidence intervals around the GMR were 3.5 to 5.3 for NFV (P < 0.001), 2.8 to 4.5 for IDV (P < 0.001), and 7.8 to 11.5 for RTV (P = 0.004). Saquinavir modestly increased the APV AUCs (GMR, 1.0 to 1.4; P = 0.106). Control group AUCs were lower on day 21 compared to those on day 14 (GMR, 0.7 to 1.0; P = 0.042). African-American non-Hispanics had higher day 14 efavirenz AUCs than white non-Hispanics. We conclude that EFV lowered APV AUCs, but nelfinavir, indinavir, or ritonavir compensated for EFV induction.
doi:10.1128/AAC.49.8.3373-3381.2005
PMCID: PMC1196277 PMID: 16048950
11. ACTG 260: a Randomized, Phase I-II, Dose-Ranging Trial of the Anti-Human Immunodeficiency Virus Activity of Delavirdine Monotherapy
ACTG 260 was an open-label, four-arm trial designed to study the safety and anti-human immunodeficiency virus (anti-HIV) activity of delavirdine monotherapy at three ranges of concentrations in plasma compared to those of control therapy with zidovudine or didanosine. Delavirdine doses were adjusted weekly until subjects were within their target trough concentration range (3 to 10, 11 to 30, or 31 to 50 μM). A total of 113 subjects were analyzed. At week 2, the mean HIV type 1 (HIV-1) RNA level declines among the subjects in the three delavirdine arms were similar (0.87, 1.08, and 1.02 log10 for the low, middle, and high target arms, respectively), but by week 8, the subjects in the pooled delavirdine arms showed only a 0.10 log10 reduction. In the subjects in the nucleoside arm, mean HIV-1 RNA level reductions at weeks 2 and 8 were 0.67 and 0.55 log10, respectively. Because viral suppression by delavirdine was not maintained, the trial was stopped early. Rash, which was usually self-limited, developed in 36% of subjects who received delavirdine. Delavirdine monotherapy has potent anti-HIV activity at 2 weeks, but its activity is time limited due to the rapid emergence of drug resistance.
PMCID: PMC89281 PMID: 10348755
12. Use of Monoclonal Antibodies Against Two 75,000-Molecular-Weight Glycoproteins Specified by Herpes Simplex Virus Type 2 in Glycoprotein Identification and Gene Mapping
Journal of Virology 1983;45(3):1223-1227.
We produced two monoclonal antibodies that precipitate different glycoproteins of similar apparent molecular weight (70,000 to 80,000) from extracts of cells infected with herpes simplex virus type 2. Evidence is presented that one of these glycoproteins is the previously characterized glycoprotein gE, whereas the other maps to a region of the herpes simplex virus type 2 genome collinear with the region in herpes simplex virus type 1 DNA that encodes gC.
Images
PMCID: PMC256538 PMID: 6300459
Results 1-12 (12)
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FİLTRE
"memede solid lezyon sebepleri" etiket sonuçları
memede solid lezyon sebepleri ile etiketlenmiş makalelere, videolara ve cevaplara buradan ulaşabilirsiniz.
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Genel Cerrahi
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HÜLYA ŞENDUL tarafından 08.05.2014 tarihinde soruldu.
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Kilo vermekte zorluk çeken, diyet ve egzersize rağmen yetersiz kilo verenlerin aşağıdaki hormonal sebepler yönünden araştırılması gerekiyor. 1-insülin direnci: göbek yağlanması, karaciğer yağlanmasının en sık sebeplerinden biridir. açlık krizleri, doyamama, halsizlik, yorgunluk, sık acıkma gibi ...
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5eff3d1f6f98e57329caed0ceb9053d3
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-6,155,868,227,712,843,000
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Date of Degree
9-2016
Document Type
Dissertation
Degree Name
Ph.D.
Program
Nursing
Advisor(s)
Martha Whetsell
Committee Members
Donna Nickitas
Steven Baumann
William Gallo
Jacqueline Witter
Subject Categories
Other Nursing
Keywords
Fathers, Cancer, Dying, Phenomenology
Abstract
Historically, fathers have been neglected as a research population in the nursing and oncology literature. This was in relation to their role being viewed as a disciplinarian and breadwinner instead of a nurturer. Fast-forward to modern day society, their role has evolved into a more involved parent that is necessary for their child’s development and well-being. The literature has also evolved and in recent years, this population has been gaining recognition and it is of great importance to understand their role, perception, and concerns as it pertains to being involved fathers. Therefore, when considering fathers with advanced cancer when death is imminent, an urgency and importance to continue research in this population is created. Understanding these fathers is of significant value to them and to the nurses who care for them.
The purpose of this qualitative study is to describe and understand the experience of fathers with advanced cancer. Ten fathers were interviewed and shared their experiences. The interviews were analyzed using van Manen’s (1990) phenomenological method and seven themes were uncovered that provided the structure to understand the meaning of their lived experience. Those themes are, live longer, financial security, making memories, fatherhood, maintaining normalcy, finding strength and support and dealing with challenges. From these themes, the essence of a father’s unconditional and eternal love is described and brought to a close this research study of the lived experience of fathers with advanced cancer.
Included in
Other Nursing Commons
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Many women of reproductive age are aware of this diagnosis unfortunately not only from hearsay. In the world, endometriosis is in third place among gynecological diseases, yielding to inflammatory diseases and uterine myoma. The cunning of endometriosis is that for a long time it may not cause any symptoms, being at the same time one of the common causes of infertility. Let's try to figure out what the disease is, what causes it and what so dangerous about it is.
Endometriosis is a gynecological disease characterized by the proliferation of endometrial cells (the inner layer of the uterus) outside this layer. The main role of the endometrium is to create an optimal environment for engraftment of the fertilized gamete in the uterus. During pregnancy, vascular proliferation occurs in the endometrium being a part of the placenta and transferring oxygen and nutrients to the fetus. Endometrium is a hormonally sensitive layer, it grows and thickens in the last phase of the menstrual cycle. If conception does not occur, the upper layer of the endometrium is rejected and naturally leaves the uterus during the menstruation. It is a multicomponent complex system, which includes a variety of different cells, vessels, uterine and tubular glands. This tissue is extremely dependent on the hormonal balance of women. Under the action of estradiol, the endometrium grows in the first phase of the menstrual cycle, and under the action of progesterone it thickens and fills with blood after ovulation.
Naturally, not every cycle of a woman ends in conception. In the process of menstruation, endometrial cells are rejected and naturally excreted from the body through the cervical canal and vagina. If any failure occurs, it is possible to transfer endometrial cells in the cavity, organs and tissues. According to localization, endometriosis is divided into external (cells through the fallopian tubes enter the abdominal cavity and begin to grow) and internal (cells penetrate and expand in the inner layers of the uterus). External and internal endometriosis occur in a ratio of 1: 3. It is also customary to distinguish genital (in the organs and tissues of the reproductive system) and extragenital (outside the genital organs) endometriosis. Once in a favorable environment, the cells take root, grow and begin to form tissues in places completely atypical for them and completely unrelated to them. There have been cases of endometriosis, for example, in the eye or in the navel. Developing, endometrial cells continue to respond to changes in hormonal levels, causing pain and disrupting the functioning of the organs in which they have taken root. With a significant proliferation, compression of the nerves and nerve endings occurs, leading to neurological pathologies, possible bleeding threatening anemia, and the development of endometrial cells into cancer cells.
What is the cause of this disease? Doctors still have not come to a common opinion about the genesis of endometriosis. Some experts believe that endometrial cells are still in the process of fetal development into the organs and tissues, where they later begin to develop; others are inclined to believe that the reason is immune disorders in which the body is unable to cope with atypical cells. It is also commonly believed that the cause of endometriosis can be increased or decreased hormone levels, inflammatory processes, dysfunctional surgery, abortion, genetic predisposition and a number of other factors.
Scientists around the world are looking for methods of treatment and prevention of endometriosis. Unfortunately, today with this disease, the main direction of therapy is to relieve pain symptoms, suppress the activity of foci and restore fertility. Also used drug therapy (immune, hormonal), sometimes in combination with surgery.
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We've got 4 definitions »
What does urinometer mean?
This page provides all possible meanings and translations of the word urinometer.
Wiktionary
1. urinometer(Noun)
A hydrometer used to measure the specific gravity of urine
Webster Dictionary
1. Urinometer(noun)
a small hydrometer for determining the specific gravity of urine
Numerology
1. Chaldean Numerology
The numerical value of urinometer in Chaldean Numerology is: 5
2. Pythagorean Numerology
The numerical value of urinometer in Pythagorean Numerology is: 3
Images & Illustrations of urinometer
Translations for urinometer
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Abstract
Abstract
1. Alport syndrome is a progressive hereditary kidney disease characterized by hematuria, and often associated with extrarenal complications, such as sensorineural hearing loss and ocular abnormalities. By electron microscopy ultrastructural changes, including thinning, thickening, and splitting, can be seen in the glomerular basement membrane (GBM). Alport syndrome is mainly inherited as an X-linked dominant trait (MIM 301050) with mutations in the type IV collagen α5 chain gene (COL4A5), but both autosomal recessive (MIM 203780) and dominant forms also exist. Autosomal Alport syndrome is caused by mutations in the COL4A3 and COL4A4 genes encoding the type IV collagen α3 and α4 chains, respectively. Additionally, numerous deletions involving the 5′ ends of both the COL4A6 gene and the adjacent COL4A5 gene have been reported to cause a rare disorder, diffuse leiomyomatosis, that is associated with Alport syndrome (MIM 308940, 303631). A minority of Alport syndrome patients develop anti-GBM nephritis involving the transplanted allograft.
2. Basement membranes are thin, extracellular, sheet-like structures that separate cells of organized tissues from the interstitial connective tissue. The major complications of Alport syndrome—hematuria and proteinuria—are caused by structural alterations and consequent malfunction of the glomerular filtration barrier, especially glomerular basement membrane, a major component of the glomerular filtration barrier. The molecular structure of the GBM is much the same as that of basement membranes in other tissues. The major structural component is type IV collagen that forms a tightly cross-linked network in which a less dense laminin network is connected via entactin (nidogen) molecules.
3. Different triple-helical type IV collagen molecules are composed of six genetically distinct α-chains, namely α1(IV), α2(IV), α3(IV), α4(IV), α5(IV), or α6(IV). Each type IV collagen α-chain contains a long collagenous domain, a short noncollagenous N-terminus, and a noncollagenous domain (NC1) at the C-terminus. Type IV collagen molecules self-assemble into a complex network structure via C-terminal NC1 domains forming dimers, and at the N-termini forming tetramers. The molecular composition of different type IV collagen networks varies from tissue to tissue.
4. Type IV collagen genes are very large, the smallest one having 46 exons. An interesting feature is that the six genes are located pair-wise in three different chromosomes, sharing a common bidirectional promoter.
5. About 300 mutations have been reported in Alport syndrome patients in the COL4A3, COL4A4, and COL4A5 genes. Different mutations cause different phenotypes, but it is difficult to predict the consequences of a certain mutation, because deletion of a whole gene does not necessarily produce a more severe phenotype than does an amino acid substitution. Immunohistologic studies of tissues from Alport syndrome patients demonstrate the existence of different α-chain networks in different tissues. Thus, differential pattern of staining in skin sections may be used to distinguish between X-linked and autosomal recessive forms of Alport syndrome.
6. Alport syndrome, which primarily affects the renal glomeruli, is an attractive disease target for gene therapy.
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Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
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Protein Page:
EDN3 (human)
Overview
EDN3 Endothelins are endothelium-derived vasoconstrictor peptides. Defects in EDN3 are the cause of Hirschsprung disease type 4 (HSCR4); also known as aganglionic megacolon (MGC). A genetic disorder of neural crest development characterized by the absence of intramural ganglion cells in the hindgut; often resulting in intestinal obstruction. Defects in EDN3 are a cause of congenital central hypoventilation syndrome (CCHS); also known as congenital failure of autonomic control or Ondine curse. CCHS is a rare disorder characterized by abnormal control of respiration in the absence of neuromuscular or lung disease, or an identifiable brain stem lesion. A deficiency in autonomic control of respiration results in inadequate or negligible ventilatory and arousal responses to hypercapnia and hypoxemia. Defects in EDN3 are a cause of Waardenburg syndrome type 4 (WS4B); also known as Waardenburg-Shah syndrome. WS4B is characterized by the association of Waardenburg features (depigmentation and deafness) and the absence of enteric ganglia in the distal part of the intestine (Hirschsprung disease). Belongs to the endothelin/sarafotoxin family. 3 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Secreted; Secreted, signal peptide
Chromosomal Location of Human Ortholog: 20q13.2-q13.3
Cellular Component: extracellular region; extracellular space
Molecular Function: endothelin B receptor binding; hormone activity; receptor binding
Biological Process: artery smooth muscle contraction; blood circulation; cell surface receptor linked signal transduction; cell-cell signaling; inositol phosphate-mediated signaling; multicellular organismal development; neutrophil chemotaxis; peptide hormone secretion; positive regulation of cell differentiation; positive regulation of cell proliferation; positive regulation of heart rate; positive regulation of hormone secretion; positive regulation of leukocyte chemotaxis; positive regulation of MAP kinase activity; positive regulation of mitosis; regulation of gene expression; regulation of systemic arterial blood pressure by endothelin; signal transduction; vasoconstriction; vein smooth muscle contraction
Disease: Central Hypoventilation Syndrome, Congenital; Hirschsprung Disease, Susceptibility To, 4; Waardenburg Syndrome, Type 4b
Reference #: P14138 (UniProtKB)
Alt. Names/Synonyms: EDN3; endothelin 3; Endothelin-3; ET-3; ET3; HSCR4; MGC15067; MGC61498; PPET3; Preproendothelin-3; truncated endothelin 3; WS4B
Gene Symbols: EDN3
Molecular weight: 25,454 Da
Basal Isoelectric point: 6.24 Predict pI for various phosphorylation states
Select Structure to View Below
EDN3
Protein Structure Not Found.
STRING | cBioPortal | Wikipedia | Reactome | neXtProt | Protein Atlas | BioGPS | Scansite | Pfam | Phospho.ELM | NetworKIN | UniProtKB | Entrez-Gene | Ensembl Gene
Modification Sites and Domains
Modification Sites in Parent Protein, Orthologs, and Isoforms
Show Multiple Sequence Alignment
LTP
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.
HTP
HTP: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.
human
0 1 S34‑p DAGRRGVsQAPTAAR
mouse
S34 DSGRASVSQGPPEAG
Home | Curator Login With enhanced literature mining using Linguamatics I2E I2E Logo Produced by 3rd Millennium | Design by Digizyme
©2003-2013 Cell Signaling Technology, Inc.
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Behavior
Wellness Made Easy: The Real Basics of Better Health
The basics of wellness -- eating a balanced diet, exercising regularly and practicing healthful habits -- can help you live a longer, healthier life. Adopting even one of the following components of good health and better self-care can improve your well-being. Embracing all of them will yield significant benefits.
On the Road in Retirement
No matter where you travel, plan ahead for health care when you're on the road.
Baby Blues: Mood Swings or More Serious?
For many women, the "baby blues" pass quickly. For others, the feelings of sadness don't ease and may become worse.
Smoking Adds Another Wrinkle to Aging
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Anger Can Raise Cholesterol Levels
There's evidence that people who respond rigidly to anger-provoking events are likely to wind up with significantly elevated levels of heart-damaging cholesterol.
Alcohol and Your Heart
Alcohol may have some health benefits, including lowering the risk for heart disease, but it may also lead to abusive drinking and other diseases.
Start Some Healthy Holiday Traditions
The Truth About Lying
If the truth be told, most of us lie to some degree, especially when faced with an alternative like hurting someone's feelings. Some of us, however, lie so often that we stop realizing it.
Is Your Teen Abusing Drugs or Alcohol?
Besides having trouble with school and relationships, teenagers taking drugs may display emotional extremes with irritability, anger and changes in sleep patterns.
Q and A: Obsessive-Compulsive Disorder
Rituals such as hand washing, counting, checking or cleaning are often performed in hope of preventing obsessive thoughts or making them go away. Performing these rituals, however, provides only temporary relief, and not performing them markedly increases anxiety. Left untreated, obsessions and the need to perform rituals can take over a person's life. OCD is often a chronic, relapsing illness.
Break Through the Alcoholic's Psychological Defenses
The most important thing that friends and family can do for an alcoholic is to stop enabling the addictive behavior.
Teens and the Self-Esteem Shield
Research shows that adolescents who grow up with high self-esteem are far less likely to abuse drugs or drink, compared with children who grow up without much sense of self-worth.
How to Help Teenagers With Addicted Parents
Growing up is a tough challenge for most adolescents, but when their parents are abusing alcohol or drugs, the obstacles can seem overwhelming.
Sexual Harassment's Emotional Toll
According to researchers at the American Psychological Association, nearly 50 percent of American working women will experience on-the-job sexual harassment at some point in their careers.
Keeping Party Drinking Under Control
The holidays can be enjoyed without drinking alcohol. But if you choose to drink, there are responsible ways to consume alcohol.
Remember This: Many Have Memory Lapses
Unpredictable, frustrating and, at times, embarrassing memory lapses can be common. So if frequent bouts of forgetfulness are causing you stress and worry, take note: there is most likely a simple explanation.
For Seniors: How to Prevent Falls
As you age, your risk for falling increases. More than one-third of people ages 65 and older and half of those ages 75 and older fall each year. And many falls in older adults result in fractures and other severe injuries.
How to Cut Down on Drinking
It helps to understand why and when you drink if you are going to successfully reduce the amount of alcohol you consume.
Social Drinking vs. Problem Drinking
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Breaking Yourself Out of a Rut
A routine isn't necessarily bad; it can be comforting because it adds structure to your life and it isn't stressful. But dissatisfaction may start to gnaw at you and erode your self-esteem if you believe you want something more in your life.
Caregivers Need to Care for Themselves
More than 22 million Americans are involved in some form of helping elderly family members or friends with their daily routines. If you're part of this group, whether you call yourself a caregiver, or simply a good daughter or son, you know that caring for an aging parent or friend has its rewards and its trials.
Cool Tools to Keep Your Kids From Smoking
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Prevent Shaken Baby Syndrome
While being a new Mom brings lots of joy, it also brings stress—something a crying baby can make worse. Better understanding why your baby cries can help you deal with this stress in a healthy way and help you avoid the most common form of child abuse: Shaken baby syndrome.
Performance Anxiety Can Choke Up Athletes
Anxiety can help focus and sharpen performance. For some athletes, however, the pressure of performing well takes its toll in the form of performance anxiety, which causes them to do less than their best.
Depression Not a Normal Part of Aging
In general, only about three percent of the elderly living independently in the community will experience depression. That figure increases to around 20 to 30 percent of persons in nursing homes or with chronic illnesses like emphysema, heart disease or diabetes.
We Can Head Off Teen Tragedies
Preventing teen turmoil starts at birth. Parents set examples in the way they interact, express anger, and treat substance abuse.
Now Is the Time to Get Moving
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Hypothyroidism and Depression
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Keep Your Brain Functioning
If your brain gets too much or too little of what it needs, vital processes are disrupted. When things are out of sync in your brain, it can play havoc with your thoughts and emotions. Depriving your brain of sleep, for example, will impair your ability to concentrate and make decisions.
Binge Drinking Dangers for Young People
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What You Need to Know About Heroin
Until recently, heroin was not considered a problem among children of middle-class parents. But lately, it has been showing up in new places.
Up in Smoke: Cigars and Your Health
Most people realize that cigarettes can cause lung cancer and heart disease. But many people erroneously believe that cigars aren't harmful.
Maintaining Weight Once You've Quit Smoking
Although people generally gain weight when they stop smoking, you can reduce your chances of adding extra pounds by taking steps to prevent it.
Weighing the Benefits and Risks of Alcohol
Excessive drinking can cause potentially fatal conditions, not only high blood pressure, but also damage to the brain, heart or liver; diabetes and stroke.
Important Facts About Amphetamine and Methamphetamine Abuse
Amphetamine abuse is a growing problem in the United States. Each year, the U.S. Drug Enforcement Administration closes down hundreds of illegal laboratories producing these drugs.
How to Develop a 'Can-do' Personality
What's the difference between a can-do and a won't-try person? It's usually a matter of bravery.
Smart Shopping for Women
Nicotine Substitutes Can Help You Quit
For many smokers, nicotine substitutes can ease withdrawal symptoms such as headaches and restlessness.
Quit One Step at a Time
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Focus on Keeping Your Spirits Up
Good mental health is just as important as good physical health. But we all face changes in life that can challenge our emotional well being.
What You Can Do to Prevent Child Abuse
Child abuse can happen in any family and in any neighborhood. Studies have shown that child abuse crosses all boundaries of income, race, ethnic heritage and religious faith.
Many Seniors Go Back to the Books
No matter what you like to do, now is a great time to sign up for a class so that you can explore your interests. Many colleges and other educational organizations offer special discounts to older adults. Here are some ideas about how to get started.
Are You a Compulsive Shopper?
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How You Can Avoid Aggressive Drivers
Where to Turn for Mental Health
It's normal to feel stressed or anxious now and then. But it's time to call for help if emotional issues interfere with your life, your job or your personal relationships.
Teen Suicide: Learning to Recognize the Warning Signs
More than 70 percent of teens who attempt or commit suicide do so in a state of crisis, responding to some acute conflict with peers, parents, or other authorities.
Doing Your Part to Help Prevent Drunken Driving
Just about everybody loves a party. But if your party menu includes alcohol, be a smart host and insist that your guests to play it safe on the way home.
When a Family Grieves
Learning about grief and how it affects your family can help you get through the difficult times together. It may even help your family grow stronger.
An Rx for RV Living
More than a million people have pulled up roots and hit the road full time in recreational vehicles (RVs). If you're thinking of joining them, be sure to consider your health.
Everyday Ways to Activate Your Life
Moderately intense activities such as walking briskly from your parked car to the mall entrance, won't help you train for a sport. But they can help you achieve and maintain a healthful weight and improve your overall fitness level.
Break the Cycle of Repeated Accidents
It’s Never Too Late
Some New Information on Alcoholism (Alcohol Dependence)
Like cancer or heart disease, alcoholism is a primary chronic disease with its own symptoms and causes. The disease is progressive and often fatal if not treated.
Keeping Envy and Jealousy Under Control
When someone gets a raise or a special perk, can you say congratulations and mean it? Or do you seethe inside and think, "That really should have been mine?"
Sunny Self-Talk: Seeing Through the Storm
How you view any situation has a lot to do with how you feel.
Goal Setting for Everyday Success
Setting goals gives direction to your life. Without goals, you can drift and go nowhere.
The Dangers of Binge Drinking
Too many young people are participating in a dangerous practice called binge drinking, or drinking to intoxication. It's defined as having five or more drinks in a row for men; for women, it’s four-plus drinks in a row.
The Facts About Marijuana
Knowing about marijuana can help you recognize its use in children and others and help a user seek treatment.
Could Your Child Have a Drug Problem?
Before assuming your child is taking drugs, find out if something else may be causing him or her to behave unusually.
Should Tattoos Be Taboo?
People who are thinking about getting a tattoo should slow down and think twice.
Caring for the Caregiver
Caregivers come in all shapes and sizes. They can be adult children, spouses, siblings, friends or neighbors, who help with daily activities such as bathing, feeding and clothing.
Adopting a Pet--Cats and Dogs
If you've been thinking about adding a cuddly new cat or dog to your household, take some time to think about what type of pet will best suit you, your family and your lifestyle.
Figure on These Factors When Drinking Alcohol
If you drink, you most likely want to drink reasonably and responsibly. But what are the factors that can help you keep a check on your blood-alcohol content so you don't embarrass yourself or, worse, hurt yourself or others?
Help for the Holiday Blues
The unrealistic expectations of the season, time and financial pressures, missing loved ones and reflecting on past events as the year comes to an end all contribute to the blues.
Thriving After a Heart Attack
Over the long term, your quality of life is tied to how severe your heart attack was and how it was treated. Beyond that, any change will depend largely on you.
Primer: What You Need to Know About Ecstasy
Ecstasy, or MDMA -- also called "Adam," "E," or "XTC" on the street -- is a synthetic, mind-altering drug with hallucinogenic and amphetamine-like properties.
How to Quit Smoking, Again
Fewer than a quarter of those who attempt to quit are able to make it beyond three months before resuming smoking. Women usually find it harder to quit than do men, even though women have a higher risk of smoking-related diseases. The following suggestions can help you kick the habit, again, for good.
Understanding Domestic Abuse
Although the most common form of abuse is males abusing female partners, females can abuse male partners, and abuse also takes place in same-sex relationships.
Understanding Teenage Depression
The medical community once thought depression affected only adults. The risk for the condition begins in the early teens, however, and increases steadily through the mid-20s.
Helping a Friend With an Addiction
When a friend shows signs of abusing alcohol or other drugs, it's hard to know what to do or say.
Don't Swallow Your Emotions
When Kids Want to Buy, Buy, Buy
Don't argue about cost. Do talk with your children about money management and media messages.
For Seniors: Is It More Than the Blues?
Although anyone can suffer from depression, it is particularly common among older adults. Depression affects 15 out of every 100 adults older than 65.
Close the Door on Intimate Partner Violence
The Centers for Disease Control and Prevention defines intimate partner violence as actual or threatened physical or sexual violence, or psychological and emotional abuse, directed at a spouse, former spouse, current or former boyfriend or girlfriend, or dating partner.
Easy Ways to Remember to Take Your Medications
If you have more than two medications to manage, consider getting a pill organizer -- a special container marked with the days of the week. Besides housing multiple medications, a compartmentalized organizer can be useful for keeping track of the medications you've taken.
Keeping Your Anger Under Control
Learning where your anger comes from and how to deal with it can help lead to a happier, more productive life.
The Power of Resilience
When tragedy strikes with the death of a loved one, a serious illness or a job loss, some people fall apart, while others adapt to such life-changing events more easily. Being resilient is what makes the difference.
Women, Alcohol, and Drugs: The Risks Are Higher
As a woman, your body is much more sensitive to the effects of alcohol and more easily damaged than a man’s body. Because women have less water in their body than men, alcohol doesn't dilute as much and more of it gets absorbed into the blood. That’s why women suffer greater physical damage and often become more intoxicated than men when they drink identical amounts of alcohol.
Health Myths and Facts
There are a number health myths where knowing the facts can make a world of difference to your health.
Recognizing Domestic Violence
Domestic violence is behavior someone uses to control a spouse, partner, date or elderly relative through fear and intimidation.
Breaking the Habit: Obsessive-Compulsive Disorder
The symptoms of OCD vary widely from person to person. Without treatment, OCD can last for a lifetime.
Helping an Unwilling Alcoholic
You don't have to wait for someone to hit rock bottom to act. Here are steps to help an alcoholic get treatment.
All About LSD
LSD, also called acid, is one of the most commonly used hallucinogens or psychedelic drugs.
Alternatives to Alcoholics Anonymous
Some treatment programs teach problem drinkers to reduce their drinking, an approach that appeals to people who otherwise might not seek treatment.
Make a Scrapbook for Your Grandkids
If a grandchild is special to you, put your heart into showing it by creating a scrapbook.
How to Lower Your Financial Stress
Whether your credit card balances are soaring, or you and your partner are arguing constantly over nickels and dimes, there are things you can do to relieve financial stress.
Finding Support for Emotional Issues
How do you know when your emotions are of the everyday sort, or when you could benefit from seeing a therapist?
The Word on Talk Therapy
Talk therapy helps people gain insight into and resolve their problems through verbal exchanges with the therapist.
Grow Older in Good Health
Get a jump on the rest of your life by committing yourself to making the following changes in your lifestyle today.
Bullies Go High-Tech
You can now add bullying to the list of things made easier by technology. Bullies use e-mail, instant messaging, and text messaging on cell phones to reach victims.
Techniques for Taming Tantrums
Preventing a tantrum is much easier than stopping one. Here are ideas on how to do that.
Understanding Alcohol's Effects
The extent of alcohol's effect on the central nervous system depends upon how much is in your blood and how much blood you have.
How to Make Love Last Forever
Keeping your primary relationship healthy, positive, supportive and together isn’t easy. But it can be done.
Seniors Can Maximize Happiness by Minimizing Clutter
It's tough to enjoy the golden years among bundles of old newspapers, stacks of store receipts and collections of used margarine tubs. You're also at higher risk for falls and fires.
Working Mom? Aim for Less Stress
In the United States, 78 percent of all mothers with kids ages 6 to 17 work in paid jobs. Most—including married working moms—also are responsible for child care and housework.
For Seniors: Welcome to the World of the Web
The Internet is a great way to stay connected. Older adults can use it to send messages, keep in touch with family, learn new things or be entertained.
Moving Beyond All-or-Nothing Thinking
When you lapse from your goals, remind yourself of all you've learned and how much you've accomplished.
Primer: Smokeless Tobacco
Many people think using smokeless tobacco is safer than smoking. Just because there's no smoke, doesn't mean it's safe.
Understanding the Power of Addiction
When addicted, the drug user will do just about anything to obtain the drug.
Hospices Offer Comfort at Life's End
As medical progress prolongs our lives, the end can linger. So, more and more people are turning to hospice care.
Phobias Are Common, But Treatable
Most of us worry or get nervous every now and then. But, for people with anxiety disorders, these feelings occur all too often, and they may be overwhelming.
Life After Loss: Walking the Path to Wholeness
Whatever the nature of your loss, active grieving can help you get through the following months and years.
Understanding the Teen Brain
Parents need to realize the rational part of a teen’s brain isn’t fully developed and won’t be until he or she is 25 years old or so.
End-of-Life Planning
For many people, end-of-life planning brings peace of mind and a sense of control. It also takes the burden off loved ones, because they don’t have to guess what you would want.
Stages of Substance Abuse
People who become addicted to drugs or alcohol typically go through predictable stages of abuse. Understanding these stages can help you recognize a problem and seek help before substance use becomes an addiction.
The Menace of Methamphetamine
Methamphetamine is related to the legal stimulant amphetamine, but has stronger effects.
Keep Your Noggin Fit with Brain Exercise
Active thinking pumps extra blood into your brain. Getting more blood to the brain is an important way to counteract the effects of aging.
You Can Choose to Have a Healthy Life
Each year, two out of every three deaths in the United States are caused by cancer, diabetes, heart disease, or stroke. That figure could be significantly reduced if Americans made healthier food choices, got more exercise, and stopped smoking.
Understanding Prescription Drug Abuse
Although it’s dangerous to take a prescription medication without a prescription, abusing such medications is the fastest growing type of drug abuse in the United States, outpacing marijuana abuse by a factor of two, according to some studies.
Medications to Treat ADHD in Children
Children who have ADHD are often given medication as part of their treatment plan. The type of medication most often chosen is a psychostimulant.
Getting the Most from a Mental Health Support Group
Mental health support groups offer support, understanding, and helpful information to people struggling with depression, anxiety, post-traumatic stress disorder, and other conditions.
Balancing Work and Home
To keep the scales of work and life balanced, you must be organized. This means you must not only organize your stuff, but also your time.
Alcohol and Older Adults
Many older adults enjoy a glass of wine with dinner or a beer while watching the game on TV. In fact, half of Americans ages 65 and older drink alcohol. Having a drink now and then is fine—as long as you don’t overdo it.
Why Quit Smoking?
You know you should quit smoking. But you just haven't gotten around to it yet. Here are some reasons to help you commit to quitting.
Prescription Drug Addiction
Three kinds of prescription drugs are potentially addictive: opioids, tranquilizers, and stimulants.
Oppositional Defiant Disorder
Children with ODD may refuse to follow commands or requests made by parents, teachers, or other adults.
In Support Groups, You Get (and Give) Help
In a mutual support group, people just like you face similar ordeals and challenges.
Answers to Your Questions About Codependency
Codependency is an emotional and behavioral condition. It affects a person’s ability to have healthy, mutually satisfying relationships.
Understanding Compulsive Overeating
The disorder may develop when others make repeated negative comments about a person's weight.
Coping with Miscarriage
A pregnancy ended by miscarriage can be a traumatic loss. Unfortunately, it’s one that many women experience. Knowing how to deal with your feelings and find support can help you cope during this difficult time.
Quit-Smoking Tools: Help for Kicking Your Habit
As you probably already know, quitting smoking isn't easy. But, millions of other people have done it, and you can, too.
The High Cost of Smoking
When people consider the cost of smoking, they usually focus on the cost of the cigarettes alone. But that's only the first step.
Health Risks of Alcohol and Drug Abuse
It's important to understand how alcohol and drugs can affect your health and well being.
What's the Meaning of Money?
How you deal with money depends a lot on your upbringing and cultural influences, which may leave you unhappy with the way you handle it.
How to Juggle Home Life and Work Life
No matter how energetic you may be, stretching yourself to the limit every day puts your health and happiness at risk.
For Men: Doctors Are Good for Your Health
Men are missing opportunities to detect and address medical problems in their early stages, when many conditions are more treatable and less threatening to overall health.
Putting Disease Risk into Perspective
The way we gauge the peril a given disorder poses is called risk perception.
Generalized Anxiety Disorder
A person with generalized anxiety disorder often worries excessively about health, money, family, or work, and continually anticipates disaster.
Alcohol Use Among Teens Is Epidemic
The leading substance-abuse threat to children may be as close as your refrigerator. About 10 million adolescents drink alcohol. In fact, minors drink 19 percent of the alcohol consumed in the United States.
When Your Child Has a Chronic Health Condition
A chronic, or long-lasting, illness can be difficult for anyone to deal with. But for a young child diagnosed with a chronic health condition, there are challenges for both child and parent.
Bullies: Helping Your Child Cope
Bullying is intentional tormenting that can be physical, social, or psychological. Hitting, shoving, threatening, shunning, and spreading rumors can all be forms of bullying. Kids who experience bullying can become depressed, develop low self-esteem, avoid school, feel physically ill, and even think about killing themselves.
End-of-Life Concerns for Cancer Patients
How you choose to live out and prepare for the end of your life, are choices that you are able to make, to make this time as meaningful as possible.
How to Control Your Temper
At least some anger is necessary for survival. Frequent or intense episodes of anger, however, aren’t good for you or the people around you. If you find yourself boiling mad more often than not, try some of these tips to keep your temper in check.
Finding the Right Rehab Program for Substance Abuse
Drug addiction and alcohol addiction are chronic diseases that can be treated as successfully as many other chronic diseases, including high blood pressure, asthma, and diabetes.
When a Spouse Has Cancer: What to Do and How to Cope
Being a caregiver for a spouse who has cancer may be the toughest job you’ll ever have. It may also be the most vital and the most rewarding. As the spouse, you become part of the cancer treatment team.
Tai Chi: Exercise for Mind and Body
Tai chi is called a mind-body type of exercise because it combines meditation, focused breathing, and physical movement. Because it’s also a low-impact exercise, it may be particularly well suited for older adults, but it’s a beneficial exercise for people of all ages.
Can Optimism Make a Difference in Your Life?
A growing number of scientific studies indicate that optimistic people tend to live longer and have better physical and mental health than pessimistic people.
Sports and Music: Both Good for Kids
Organized sports for children offer obvious benefits such as physical fitness and sportsmanship, but did you know that a musical education program has many of the same benefits? Music education and participation in sports are both great ways to prepare your child for future success.
Older Adults and the Importance of Social Interaction
Research has shown that social interaction offers older adults many benefits. Staying socially active and maintaining interpersonal relationships can help you maintain good physical and emotional health and cognitive function.
When Sadness Is Seasonal
If you feel depressed during fall and winter months, you may have a form of depression called seasonal affective disorder (SAD).
Emotional Eating: How to Cope
Emotional eating affects most everyone from time to time, but regularly letting your feelings guide your food intake can affect your health.
Five Steps to Better Memory
Aging can make it harder to remember some things. But by focusing on your potential and continuing to exercise your mind, you may be able to boost your memory power. Here are some strategies.
Teaching Children Good Sportsmanship
Good sportsmanship is one of the life lessons that children can learn from sports. Its hallmarks include being able to win without gloating, respecting one’s opponents, and being able to lose gracefully.
Stress and Older Adults
Studies show that long-term stress can damage brain cells, leading to depression. Depression is one of the most dangerous effects of stress in older people.
The Benefits of Laughter
Laughter can do more than just put you in a good mood. It may buffer you against depression, reduce your stress, and improve your quality of life.
With Help, You Can Break a Bad Habit
Whether it’s a minor habit like biting your nails or a more serious one, like habitual drinking stopping a troublesome behavior is difficult. With a little hard work and strategy, however, it’s possible to break a bad habit.
Tips for a Successful Quit Smoking Day
Keep this in mind: if you can make it through this first day and this first week when nicotine withdrawal symptoms are at their worst, you will be on your way to success.
Journaling for Mental Health
Teenagers and After-School Jobs
Keep Anxiety from Controlling Your Life
Teaching yourself ways to relax can help settle anxiety before it starts to overwhelm you. Simple lifestyle habits can help you stay calm and in control when you feel the effects of stress.
Overcoming Anti-Gay Harassment
Gay and lesbian teens are often targets of bullying, harassment, and aggression. Anti-gay bullying can range from verbal abuse, such as name-calling, to life-threatening physical assault.
Men and Mental Illness
Mental illness can cause different symptoms in men than in women, so some disorders in men may be harder to recognize. Men who are depressed, for example, may appear angry and irritable rather than sad and withdrawn.
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feeling nauseous after eating candy
feeling nauseous after eating candy
Relief for Feeling Sick after Eating. Adjusting eating practices.Do not require yourself to vomit to rid yourself of the nauseous sensation. This can make your queasiness worse in time and can do damage to the body. Nausea after eating eggs and chicken is a common symptom. Reasons for feeling nauseous after eating include food poisoning, food allergies, intolerances and so on. Why does your tongue feel rough and raw when you eat lots of sour candy? What can cause a person to feel nauseous while eating? Why do I feel nauseous after eating sugar? Why does anaerobic exercise make one feel nauseous sometimes? Feeling nauseous after eating during pregnancy is common and usually happens in the first trimester.Some females get relief from sucking peppermint candies or sipping peppermint tea, especially after eating a meal. Feel bad after eating. Hi everyone, (a little long Im sorry). I was wondering if someone can help me with a few questions. I guess a little first. I was always a very healthy guy until Ive been feeling "sick" since I was around 22 in the mid 80s. Both high insulin waves, high blood sugar and additives in the candy can help make you nauseous, she says If you feel nauseated after eating yogurt or cereal added sugar, this has the same cause. Feeling nauseous before eating - Lately, I have been feeling very bloated after I finish eating and Ive been nauseous.
Ive noticed a decrease in my appetite. Whats happening? A nauseous feeling after eating can be produced by an intestinal virus.To get relief from nausea after eating, chew a piece of peppermint gum or suck a peppermint flavored candy. Acupressure Eating sweets like candy or drinking pop just before you exercise can also cause you to feel nauseous after exercising. Your blood sugar can drop after an insulin rise, and result in fatigue or nausea. FEEL GOOD.Often, the nausea that people experience after eating sweets is not directly caused by sugar, but by other factors that are present at the time.Pregnancy may even trigger nausea after sweets in individuals who previously enjoyed candy with no ill effects. Can too much natural insulin make you feel bad after eating? First of all, eating junk food and candy does not cause diabetes.Does anyone get nauseous AFTER eating - BabyCenter. I feel sick and bloated after I eat lunch and dinner every day! Share. Tweet. Share.
Share. Email. If youre anything like me, you bought a bunch of candy for trick-or-treaters and ate the majority of it yourself. Or maybe you raided your kids stash when you got home. Either way, youre probably feeling pretty sick right now. Heres how to detox after a super binge. I really want to know whats going on because I have dropped down to about 122 lbs, I feel like , and I get serious hunger pains, the second I eat I feel nauseous, and when I stop eating I immediately feel hunger pain again.
What Causes Nausea After Eating? Medically reviewed by Deborah Weatherspoon, PhD, RN, CRNA, COI on September 9, 2016 — Written by Stephanie Watson on September 9, 2016.Try these tips to avoid feeling sick after you eat nausea AFTER eating???? Hey ladies! I think I have evening sickness, not morning sickness. I seem to feel worse 30-60 minutes after I eat and my stomach gets all queezy.YES ME!!!! I feel hungry then eat then feel nauseous. Home Forums > Social > Health and Fitness >. Uncomfortable feeling/slightly nauseous after eating.I have some anxiety issues, and whenever they get particularly bad, its really hard for me to eat (get that nauseous feeling). Feel Sick After Eating Sugar, Scared of Diabetes No More Panic.I feel nauseous, my stomach gets upset, I get really jittery and anxious. Ive been worrying that I have diabetes. Berries and fruits dont seem to affect me too much, but baked goods, chocolate, sweet drinks, or candy makes me feel Lately, even a little bit of sugar can make me feel sick. I feel nauseous, my stomach gets upset, I get really jittery and anxious.Feeling sick after eating sugary things is NOT how diabetes works. When driving home a few hours later felt nauseous, which is unusual for me. Took son to cub scout meeting after work, felt worse.One staffer was skeptical, so we made him eat a bunch and report back to us. Heres what happened. They are an internet-famous candy that causes, uhm Nausea after eating can occur as a result of gastritis, food poisoning, ulcers or bulimia, according to WebMD.People may feel nauseous in response to tasting the regurgitated food that comes back up with acid reflux. A: Not just Ginger ale, but seven up, coke, alka seltzer and any carbonated beverage help. So does candied Ginger and pharmaceuticals like Bonine and Dramamine.What could be wrong if you feel nauseous all the time? feeling lightheaded sexual feelings why do i feel nauseous after i eat Feeling sick or being sick after eating can also have a psychological component. A condition called rumination disorder involves the person regurgitating food soon after eating.A doctor or pharmacist may recommend anti-nausea medication for short-term use. Many people will experience feelings of nausea after eating too much food in one sitting. However, feeling nauseated after eating on a regular basis can be related to a variety of conditions. The conditions that cause nausea after eating range from mild to severe. Nausea is simply the unpleasant feeling that you may potentially vomit. Vomiting, on the other hand, is an automatic response that terminates with the forceful expulsion of gastric contents.What are the causes of nausea after eating? Learn why youre feeling nauseous even though you didnt eat anything bad.Eat something thats high in carbs—like a glass of fruit juice, a piece of fresh or dried fruit, or bread. Candy will also work if healthier options arent available, Dr. Arthur says. Feeling Nauseous after Eating Everytime I Eat I Feel Nauseous, Why? Everytime I eat, I feel nauseous. There may be many causes such as poor eating habits, food intolerance, pregnancy or serious medical conditions such as gallstones or appendicitis. Feeling sick after eating can be due to many different reasons ranging from mild stress or food allergies to serious medical conditions. We need to think of least harmful causes of feeling nauseous after eating first. The couple of times Ive had a little something, it makes me feel sick--usually GI sick, so I stay away from it.I am not diabetic. This is the only time I remember having candy since before my surgery. Or was it the sugarcaffeine combo? Should I be freaked out? After consuming sugary foods or drinks, a person might feel nauseous due to a spike in blood glucose levels.Full Answer. Many believe a feeling of nausea after eating sugar is a result of overindulging. Every time I eat just a little bit of (low cal) candy, I start thinking about how un-healthy it is and get sick.I had no idea the bloating and lethargy was so bad until I ate a small cooked dessert after eating only fruit for a while. Does being sick after eating really help lose weight? When a sick person quits eating? If you want to be thin after eating food how long after to be sick?44 - Why does eating candy make you feel bad? Ive noticed that 99 of the times I feel like total CRAP its after Ive had sugar (cake, cookies, candy, etc). Anyone else have this problem?This whole pregnancy I feel horrible after eating sugar, especially chocolate. Eating and Exercising. Close up of a young woman eating candy.Lack of and too much hydration may increase the chances of feeling nauseous during or after exercise. nausea after eating candy.Becoming sick/nauseous after eating sugar has been happening to Feeling sick after eating sugar | The DIS Disney Oct 06, 2011 Hi guys, I used to be able to eat cakes, cookies, etc and drink pop or juice with no issues. Immediately after I felt sick to my stomach like I wanted to vomit and very full.And for what its worth, my husband experienced a similar feeling when he started eating more vegetables instead of starches. If you are frequently feeling sick or nauseous after eating and/or you are vomiting, it is time to go see your health care practitioner to ensure that something grave is not going on with your health. Home Remedies For Nauseous Feeling After Eating. There is no particular treatment mode for alleviating the feeling of light headedness and nausea after eating. But making change in eating and lifestyle can significantly reduce this discomforting episode. Posted by: | 2015/10/07. Q. Feeling nauseous after eating fruits.Can only eat small amount of fruit high in fructose like bananas and papinos. However if eat a bit of these fruits daily I get sharp pain in the liver area. Feeling sick after eating is typically an indication that you may vomit, though this is not always the case.Certain medical conditions or bad habits can cause you to constantly feel nauseous after you eat, making it difficult to get the nutrition you need. Boca Ciega students felt ill after eating gummies.Four students from Boca Ciega High School were taken to a hospital after eating drug-laced gummy candy. Gulfport Police Department is investigating. Having a feeling of nausea after eating can make mealtimes a worrying event. Of course, its possible to feel nauseous at other times during the day. However, if, after every time you eat, you feel sick and queasy it could take the enjoyment out of eating. Just a few years ago, Ive been feeling nauseous to the point of vomiting whenever I eat my favorite fruits (such as bananas, oranges, watemelons, mango, etc.).I had similar experiences after moving years back and developed what I believed to be a h-pylori infection. 3 reasons you could be feeling sick after eating sugar. If you usually feel sick after eating sugary foods, its probably no coincidence. Discover how sugar could be affecting your body, and what you might do to counter the ill effects of the sweets you consume. Possible symptoms. I ate some trollis candy, it says its sour but it didnt taste sour when I ate it. Then not long after eating it, i feel nauseous and i think it might be acid, I can feel my stomach feels sour or something. So can eating candy make you feel like this? Here we list the 10 most common reasons that can lead to your sick feeling after eating.When this happens, you become nauseous after eating because you are activating your autonomic nervous system in response to a meal. Feeling sick after eating carbs - Duration: 5:31. Tiago Vasconcelos 1,254 views.ASMR: Chocolate Candy Swap | Eating Sounds - Duration: 12:39. Feeling nauseous after eating is typically an indication that you may vomit, though this is not always the case. This is a sign that your intestines or digestive system are suffering from distress. Nausea or feeling nauseous are terms used to describe the unpleasant sensation of wanting to vomit.Nausea after eating typically presents immediately after or within 20 to 30 minutes after eating. Psychology. In some cases the feelings of nausea after eating can be mostly psychological.Another good reason to see a doctor if you feel nauseous after eating is that it could be appendicitis. ber 243 Matching nausea after eating candy Abfrageergebnisse.Feeling nauseated after eating can indicate a variety of underlying conditions. Learn more about the causes of nausea and when to see a doctor.
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bubonic plague
Definition from Wiktionary, the free dictionary
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English[edit]
Wikipedia has an article on:
Wikipedia
Noun[edit]
bubonic plague (uncountable)
1. (pathology) A contagious, often fatal, epidemic disease caused by the bacterium Yersinia pestis, transmitted by the bite of fleas from an infected person or rodent, especially a rat, and characterized by delirium, chills, fever, vomiting, diarrhea, and the formation of buboes.
Translations[edit]
See also[edit]
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Bacitracin zinc-polymyxin b sulfate
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Bacitracin zinc-polymyxin b sulfate
Bacitracin zinc-polymyxin b sulfate
Bacitracin zinc-polymyxin b sulfate is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin zinc; polymyxin b sulfate.
RELATED TERMS
--------------------------------------
Bacitracin
Bacitracin is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Prescription
A prescription, as is well known, is a physician's order for the preparation and administration of a drug or device for a patient.
SIMILAR TERMS
--------------------------------------
Baci-rx
Baci-rx is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Baciguent
Baciguent is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Baciim
Baciim is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Bacillary angiomatosis
A bacterial infection due to a cat scratch most often seen today in people with HIV. The disease characteristically presents with swollen lymph nodes (lymphadenitis), sore throat, fatigue, and fever, chills, sweats, vomiting, loss of appetite, and weight loss. There is usually a little bump (a papule) which may be pus-filled (a pustule) at the site of the scratch. Then more nodules appear on and under the skin. As the number of nodules increases, patients get sicker.
An effective immunization against tuberculosis. Commonly abbreviated BCG, it is an attenuated (weakened) version of a bacterium called Mycobacterium bovis which is closely related to Mycobacterium tuberculosis, the agent responsible for tuberculosis.
Bacillophobia
An abnormal and persistent fear of bacilli (bacteria). A phobia is an unreasonable sort of fear that can cause avoidance and panic. Phobias are a relatively common type of anxiety disorder. Phobias can be treated with cognitive behavioral therapy using exposure and fear reduction techniques. In many cases, anti- anxiety or anti-depressant medication proves helpful, especially during the early stages of therapy. Another term for bacillophobia is bacteriaphobia.
Bacillus
A large family of bacteria that have a rod-like shape. They include the bacteria that cause food to spoil, and also those responsible for some types of diseases. Helpful members of the bacillus family are used to make antibiotics, or colonize the human intestinal tract and aid with digestion.
Bacillus anthracis
The bacterium that causes anthrax. Anthrax differs from most bacteria in that they exist in an inactive (dormant) state called spores. The spores are found in soil, animal carcasses and feces (including sheep, goats, cattle, bison, horses, and deer), and animal products (e.g., hides and wool). Some animals (cats, dogs, rats, and swine) are very resistant to anthrax. Remarkably, anthrax spores can remain dormant in soil for many years, perhaps decades. Likened somewhat to eggs that have the ability to hatch, spores can transform (germinate) into active bacteria under appropriate conditions.
Bacitracin
Bacitracin is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Bacitracin zinc and polymyxin b sulfate
Bacitracin zinc and polymyxin b sulfate is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin zinc; polymyxin b sulfate.
Bacitracin zinc-neomycin sulfate-polymyxin b sulfate
Bacitracin zinc-neomycin sulfate-polymyxin b sulfate is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin zinc; neomycin sulfate; polymyxin b sulfate.
Bacitracin-neomycin-polymyxin
Bacitracin-neomycin-polymyxin is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin zinc; neomycin sulfate; polymyxin b sulfate.
Bacitracin-neomycin-polymyxin with hydrocortisone acetate
Bacitracin-neomycin-polymyxin with hydrocortisone acetate is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin; hydrocortisone acetate; neomycin sulfate; polymyxin b sulfate.
PREVIOUS AND NEXT TERMS
--------------------------------------
Baciguent
Baciguent is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Baciim
Baciim is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Bacitracin
Bacitracin is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin.
Bacitracin zinc and polymyxin b sulfate
Bacitracin zinc and polymyxin b sulfate is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin zinc; polymyxin b sulfate.
Bacitracin zinc-neomycin sulfate-polymyxin b sulfate
Bacitracin zinc-neomycin sulfate-polymyxin b sulfate is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin zinc; neomycin sulfate; polymyxin b sulfate.
Bacitracin zinc-polymyxin b sulfate
Bacitracin-neomycin-polymyxin
Bacitracin-neomycin-polymyxin is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin zinc; neomycin sulfate; polymyxin b sulfate.
Bacitracin-neomycin-polymyxin with hydrocortisone acetate
Bacitracin-neomycin-polymyxin with hydrocortisone acetate is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): bacitracin; hydrocortisone acetate; neomycin sulfate; polymyxin b sulfate.
Baclofen
Baclofen is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): baclofen.
Bacteriostatic sodium chloride 0.9 per cent in plastic container
Bacteriostatic sodium chloride 0.9 per cent in plastic container is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): sodium chloride.
Bacteriostatic water for injection in plastic container
Bacteriostatic water for injection in plastic container is a prescription or over-the-counter drug which is (or once was) legal in the United States and possibly in other countries. Active ingredient(s): water for injection, sterile.
We thank you for using the Health Dictionary to search for Bacitracin zinc-polymyxin b sulfate. If you have a better definition for Bacitracin zinc-polymyxin b sulfate than the one presented here, please let us know by making use of the suggest a term option. This definition of Bacitracin zinc-polymyxin b sulfate may be disputed by other professionals. Our attempt is to provide easy definitions on Bacitracin zinc-polymyxin b sulfate and any other medical topic for the public at large.
This dictionary contains 59020 terms.
© Health Dictionary 2005 - All rights reserved -
bacitracinzinc-polymyxinbsulfate / acitracin zinc-polymyxin b sulfate / bcitracin zinc-polymyxin b sulfate / baitracin zinc-polymyxin b sulfate / bactracin zinc-polymyxin b sulfate / baciracin zinc-polymyxin b sulfate / bacitacin zinc-polymyxin b sulfate / bacitrcin zinc-polymyxin b sulfate / bacitrain zinc-polymyxin b sulfate / bacitracn zinc-polymyxin b sulfate / bacitraci zinc-polymyxin b sulfate / bacitracinzinc-polymyxin b sulfate / bacitracin inc-polymyxin b sulfate / bacitracin znc-polymyxin b sulfate / bacitracin zic-polymyxin b sulfate / bacitracin zin-polymyxin b sulfate / bacitracin zincpolymyxin b sulfate / bacitracin zinc-olymyxin b sulfate / bacitracin zinc-plymyxin b sulfate / bacitracin zinc-poymyxin b sulfate / bacitracin zinc-polmyxin b sulfate / bacitracin zinc-polyyxin b sulfate / bacitracin zinc-polymxin b sulfate / bacitracin zinc-polymyin b sulfate / bacitracin zinc-polymyxn b sulfate / bacitracin zinc-polymyxi b sulfate / bacitracin zinc-polymyxinb sulfate / bacitracin zinc-polymyxin sulfate / bacitracin zinc-polymyxin bsulfate / bacitracin zinc-polymyxin b ulfate / bacitracin zinc-polymyxin b slfate / bacitracin zinc-polymyxin b sufate / bacitracin zinc-polymyxin b sulate / bacitracin zinc-polymyxin b sulfte / bacitracin zinc-polymyxin b sulfae / bacitracin zinc-polymyxin b sulfat / bbacitracin zinc-polymyxin b sulfate / baacitracin zinc-polymyxin b sulfate / baccitracin zinc-polymyxin b sulfate / baciitracin zinc-polymyxin b sulfate / bacittracin zinc-polymyxin b sulfate / bacitrracin zinc-polymyxin b sulfate / bacitraacin zinc-polymyxin b sulfate / bacitraccin zinc-polymyxin b sulfate / bacitraciin zinc-polymyxin b sulfate / bacitracinn zinc-polymyxin b sulfate / bacitracin zinc-polymyxin b sulfate / bacitracin zzinc-polymyxin b sulfate / bacitracin ziinc-polymyxin b sulfate / bacitracin zinnc-polymyxin b sulfate / bacitracin zincc-polymyxin b sulfate / bacitracin zinc--polymyxin b sulfate / bacitracin zinc-ppolymyxin b sulfate / bacitracin zinc-poolymyxin b sulfate / bacitracin zinc-pollymyxin b sulfate / bacitracin zinc-polyymyxin b sulfate / bacitracin zinc-polymmyxin b sulfate / bacitracin zinc-polymyyxin b sulfate / bacitracin zinc-polymyxxin b sulfate / bacitracin zinc-polymyxiin b sulfate / bacitracin zinc-polymyxinn b sulfate / bacitracin zinc-polymyxin b sulfate / bacitracin zinc-polymyxin bb sulfate / bacitracin zinc-polymyxin b sulfate / bacitracin zinc-polymyxin b ssulfate / bacitracin zinc-polymyxin b suulfate / bacitracin zinc-polymyxin b sullfate / bacitracin zinc-polymyxin b sulffate / bacitracin zinc-polymyxin b sulfaate / bacitracin zinc-polymyxin b sulfatte / bacitracin zinc-polymyxin b sulfatee / vacitracin zinc-polymyxin b sulfate / facitracin zinc-polymyxin b sulfate / gacitracin zinc-polymyxin b sulfate / hacitracin zinc-polymyxin b sulfate / nacitracin zinc-polymyxin b sulfate / acitracin zinc-polymyxin b sulfate / bqcitracin zinc-polymyxin b sulfate / bwcitracin zinc-polymyxin b sulfate / bscitracin zinc-polymyxin b sulfate / bxcitracin zinc-polymyxin b sulfate / bzcitracin zinc-polymyxin b sulfate / baxitracin zinc-polymyxin b sulfate / basitracin zinc-polymyxin b sulfate / baditracin zinc-polymyxin b sulfate / bafitracin zinc-polymyxin b sulfate / bavitracin zinc-polymyxin b sulfate / ba itracin zinc-polymyxin b sulfate / bactracin zinc-polymyxin b sulfate / baci5racin zinc-polymyxin b sulfate / baci6racin zinc-polymyxin b sulfate / baciyracin zinc-polymyxin b sulfate / bacihracin zinc-polymyxin b sulfate / bacigracin zinc-polymyxin b sulfate / bacifracin zinc-polymyxin b sulfate / bacirracin zinc-polymyxin b sulfate / baci4racin zinc-polymyxin b sulfate / bacit4acin zinc-polymyxin b sulfate / bacit5acin zinc-polymyxin b sulfate / bacittacin zinc-polymyxin b sulfate / bacitgacin zinc-polymyxin b sulfate / bacitfacin zinc-polymyxin b sulfate / bacitdacin zinc-polymyxin b sulfate / baciteacin zinc-polymyxin b sulfate / bacit3acin zinc-polymyxin b sulfate / bacitrqcin zinc-polymyxin b sulfate / bacitrwcin zinc-polymyxin b sulfate / bacitrscin zinc-polymyxin b sulfate / bacitrxcin zinc-polymyxin b sulfate / bacitrzcin zinc-polymyxin b sulfate / bacitraxin zinc-polymyxin b sulfate / bacitrasin zinc-polymyxin b sulfate / bacitradin zinc-polymyxin b sulfate / bacitrafin zinc-polymyxin b sulfate / bacitravin zinc-polymyxin b sulfate / bacitra in zinc-polymyxin b sulfate / bacitracn zinc-polymyxin b sulfate / bacitracib zinc-polymyxin b sulfate / bacitracih zinc-polymyxin b sulfate / bacitracij zinc-polymyxin b sulfate / bacitracim zinc-polymyxin b sulfate / bacitraci zinc-polymyxin b sulfate / bacitracin ainc-polymyxin b sulfate / bacitracin sinc-polymyxin b sulfate / bacitracin xinc-polymyxin b sulfate / bacitracin inc-polymyxin b sulfate / bacitracin znc-polymyxin b sulfate / bacitracin zibc-polymyxin b sulfate / bacitracin zihc-polymyxin b sulfate / bacitracin zijc-polymyxin b sulfate / bacitracin zimc-polymyxin b sulfate / bacitracin zi c-polymyxin b sulfate / bacitracin zinx-polymyxin b sulfate / bacitracin zins-polymyxin b sulfate / bacitracin zind-polymyxin b sulfate / bacitracin zinf-polymyxin b sulfate / bacitracin zinv-polymyxin b sulfate / bacitracin zin -polymyxin b sulfate / bacitracin zinc=polymyxin b sulfate / bacitracin zinc[polymyxin b sulfate / bacitracin zincppolymyxin b sulfate / bacitracin zinc0polymyxin b sulfate / bacitracin zinc-0olymyxin b sulfate / bacitracin zinc--olymyxin b sulfate / bacitracin zinc-[olymyxin b sulfate / bacitracin zinc-;olymyxin b sulfate / bacitracin zinc-lolymyxin b sulfate / bacitracin zinc-oolymyxin b sulfate / bacitracin zinc-9olymyxin b sulfate / bacitracin zinc-p9lymyxin b sulfate / bacitracin zinc-p0lymyxin b sulfate / bacitracin zinc-pplymyxin b sulfate / bacitracin zinc-pllymyxin b sulfate / bacitracin zinc-pklymyxin b sulfate / bacitracin zinc-pilymyxin b sulfate / bacitracin zinc-p8lymyxin b sulfate / bacitracin zinc-pooymyxin b sulfate / bacitracin zinc-popymyxin b sulfate / bacitracin zinc-po;ymyxin b sulfate / bacitracin zinc-po.ymyxin b sulfate / bacitracin zinc-po,ymyxin b sulfate / bacitracin zinc-pokymyxin b sulfate / bacitracin zinc-poiymyxin b sulfate / bacitracin zinc-pol6myxin b sulfate / bacitracin zinc-pol7myxin b sulfate / bacitracin zinc-polumyxin b sulfate / bacitracin zinc-poljmyxin b sulfate / bacitracin zinc-polhmyxin b sulfate / bacitracin zinc-polgmyxin b sulfate / bacitracin zinc-poltmyxin b sulfate / bacitracin zinc-pol5myxin b sulfate / bacitracin zinc-polynyxin b sulfate / bacitracin zinc-polyjyxin b sulfate / bacitracin zinc-polykyxin b sulfate / bacitracin zinc-poly,yxin b sulfate / bacitracin zinc-poly yxin b sulfate / bacitracin zinc-polym6xin b sulfate / bacitracin zinc-polym7xin b sulfate / bacitracin zinc-polymuxin b sulfate / bacitracin zinc-polymjxin b sulfate / bacitracin zinc-polymhxin b sulfate / bacitracin zinc-polymgxin b sulfate / bacitracin zinc-polymtxin b sulfate / bacitracin zinc-polym5xin b sulfate / bacitracin zinc-polymyzin b sulfate / bacitracin zinc-polymyain b sulfate / bacitracin zinc-polymysin b sulfate / bacitracin zinc-polymydin b sulfate / bacitracin zinc-polymycin b sulfate / bacitracin zinc-polymy in b sulfate / bacitracin zinc-polymyxn b sulfate / bacitracin zinc-polymyxib b sulfate / bacitracin zinc-polymyxih b sulfate / bacitracin zinc-polymyxij b sulfate / bacitracin zinc-polymyxim b sulfate / bacitracin zinc-polymyxi b sulfate / bacitracin zinc-polymyxin v sulfate / bacitracin zinc-polymyxin f sulfate / bacitracin zinc-polymyxin g sulfate / bacitracin zinc-polymyxin h sulfate / bacitracin zinc-polymyxin n sulfate / bacitracin zinc-polymyxin sulfate / bacitracin zinc-polymyxin b wulfate / bacitracin zinc-polymyxin b eulfate / bacitracin zinc-polymyxin b dulfate / bacitracin zinc-polymyxin b xulfate / bacitracin zinc-polymyxin b zulfate / bacitracin zinc-polymyxin b aulfate / bacitracin zinc-polymyxin b qulfate / bacitracin zinc-polymyxin b s7lfate / bacitracin zinc-polymyxin b s8lfate / bacitracin zinc-polymyxin b silfate / bacitracin zinc-polymyxin b sklfate / bacitracin zinc-polymyxin b sjlfate / bacitracin zinc-polymyxin b shlfate / bacitracin zinc-polymyxin b sylfate / bacitracin zinc-polymyxin b s6lfate / bacitracin zinc-polymyxin b suofate / bacitracin zinc-polymyxin b supfate / bacitracin zinc-polymyxin b su;fate / bacitracin zinc-polymyxin b su.fate / bacitracin zinc-polymyxin b su,fate / bacitracin zinc-polymyxin b sukfate / bacitracin zinc-polymyxin b suifate / bacitracin zinc-polymyxin b sulrate / bacitracin zinc-polymyxin b sultate / bacitracin zinc-polymyxin b sulgate / bacitracin zinc-polymyxin b sulbate / bacitracin zinc-polymyxin b sulvate / bacitracin zinc-polymyxin b sulcate / bacitracin zinc-polymyxin b suldate / bacitracin zinc-polymyxin b suleate / bacitracin zinc-polymyxin b sulfqte / bacitracin zinc-polymyxin b sulfwte / bacitracin zinc-polymyxin b sulfste / bacitracin zinc-polymyxin b sulfxte / bacitracin zinc-polymyxin b sulfzte / bacitracin zinc-polymyxin b sulfa5e / bacitracin zinc-polymyxin b sulfa6e / bacitracin zinc-polymyxin b sulfaye / bacitracin zinc-polymyxin b sulfahe / bacitracin zinc-polymyxin b sulfage / bacitracin zinc-polymyxin b sulfafe / bacitracin zinc-polymyxin b sulfare / bacitracin zinc-polymyxin b sulfa4e / bacitracin zinc-polymyxin b sulfat3 / bacitracin zinc-polymyxin b sulfat4 / bacitracin zinc-polymyxin b sulfatr / bacitracin zinc-polymyxin b sulfatf / bacitracin zinc-polymyxin b sulfatd / bacitracin zinc-polymyxin b sulfats / bacitracin zinc-polymyxin b sulfatw /
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5eff3d1f6f98e57329caed0ceb9053d3
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-2,473,721,163,667,187,000
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Noise Stress-Induced Changes in mRNA Levels of Corticotropin-Releasing Hormone Family Molecules and Glucocorticoid Receptors in the Rat Brain.
Folia biologica
PubMedID: 26333123
Eraslan E, Akyazi I, Ergül-Ekiz E, Matur E. Noise Stress-Induced Changes in mRNA Levels of Corticotropin-Releasing Hormone Family Molecules and Glucocorticoid Receptors in the Rat Brain. Folia Biol (Praha). 2015;61(2):66-73.
Noise is a widespread stress resource that may lead to detrimental effects on the health. However, the molecular basis of the stress response caused by noise remains elusive. We have studied the effects of acute and chronic noise stress on stress-related molecules in the hypothalamus and hippocampus and also corticosterone responses. Sprague Dawley rats were randomized into control, acute and chronic noise stress groups. While the chronic noise stress group animals were exposed to 100 dB white noise for 4 h/a day during 30 days, the acute noise stress group of animals was exposed to the same level of stress once for 4 h. The expression profiles of corticotropin releasing hormone (CRH), CRH1, CRH2 receptors and glucocorticoid receptor (GR) mRNAs were analysed by RT-PCR. Chronic noise stress upregulated CRH mRNA levels in the hypothalamus. Both acute and chronic noise increased CRH-R1 mRNA in the hypothalamus but decreased it in the hippocampus. GR mRNA levels were decreased by chronic noise stress in the hippocampus. The present results suggest that while corticosterone responses have habituated to continuous noise stress, the involvement of CRH family molecules and glucocorticoid receptors in the noise stress responses are different and structure specific.
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Chronic pancreatic pancreatitis
Chronic pancreatitisChronic pancreatitis is a disorder in which irreversible damage occurs in the tissues of the pancreas as a result of inflammation.It is a common disease that can develop in people of any age and sex, but is most often observed in adult men between the ages of 40 and 55 years.
In recent decades, the number of people with chronic forms has increased significantly. In addition, the cause of the disease in 75% of cases now is alcohol, whereas earlier alcoholic pancreatitis only occupied 40% of all cases.
The disease develops over several years and is characterized by a change in the periods of exacerbation and remission of the disease. Very often, with chronic pancreatitis, the symptoms of the disease are little or nonexistent. The main stage of treatment is the observance of a special diet and proper nutrition in times of exacerbation and remission.
Causes
What it is? In the causes of chronic pancreatitis in industrialized countries, excessive use of alcohol plays a leading role. Significantly less common causes of this suffering are cholelithiasis and its complications (choledocholithiasis, stricture of the large duodenal papilla).
The pathogenesis of the disease is not well understood, although it is now firmly established that its key the link is the replacement of the epithelial tissue of the pancreatic acini with a connective tissue. According to the scientific work of the last decade, cytokines (mediators of inflammation) also play an important role.
By severityChronic pancreatitis is divided into three forms:
1. Severe course: frequent and prolonged exacerbations (more than 5 times per year) with severe pain syndrome. Body weight is sharply reduced until exhaustion caused by pancreatic diarrhea. Accompany complications - diabetes, stenosis of the duodenum as a consequence of the enlarged head of the pancreas.
2. The average severity: exacerbation 3-4 times a year, proceed for a long time with severe pain syndrome, in the analysis of feces - increase fats, muscle fibers, protein, body weight can decrease, the exocrine function of the gland can be reduced.
3. A mild course: exacerbations occur rarely (1-2 times a year), are brief, pains are not expressed significantly, easy to stop, weight loss does not occur, the exocrine function of the gland is not broken.
Chronic pancreatitis occurs in 0.2-0.6% of people. At the same time, the number of patients is constantly increasing, which is associated with the growth of alcoholism.
Acute and chronic form
There are two main types of disease - acute and chronic.
In most cases, acute pancreatitis occurs against the background of alcohol abuse, cholelithiasis (up to 30% of cases), as well as due to poisoning (intoxication), a viral disease or surgery on the gastrointestinal tract. Acute pancreatitis can also occur as an exacerbation of chronic pancreatitis.
In turn, without proper treatment, acute form pancreatitis can pass into chronic pancreatic pancreatitis.
However, chronic pancreatitis can also occur as an independent disease, without a preliminary acute phase. In this case, the causes of chronic pancreatitis can be primarily caused by diseases of the bile excretory ways - cholecystitis (inflammation of the gallbladder), dyskinesia of the biliary tract, cholelithiasis.
Symptoms of Chronic Pancreatitis
Chronic pancreatitis occurs with periods of exacerbation, when the symptoms of the disease become more active in the form of pain, nausea, digestive disorders and others, and remission, when the patient feels satisfactory.
The main symptom of chronic pancreatitis is severe pain. Its location depends on the place of the pancreas lesion - it can left or right hypochondrium or pain in the pit of the stomach (under the ribs in the middle).
Usually, pain occurs 40 minutes or an hour after eating, especially if the food was too fatty or sharp. The pain may increase in the prone position, as well as give to the left shoulder blade or shoulder, the lower abdomen or the heart region. Often the only position in which a patient may be - sitting with a lean forward.
1. If the entire pancreas is affected, the pain in the form of a "belt" grips the entire upper abdomen.
2. When the head of the pancreas is affected, pain occurs in the right hypochondrium.
3. When the body of the gland is damaged, pain occurs in the epigastric region.
4. If the tail of the pancreas is affected, then the pain is felt in the left hypochondrium or to the left of the navel.
When the pancreas is affected, the production of digestive enzymes decreases, the work of the entire digestive system is disrupted. Therefore, nausea, belching and heartburn are symptoms that always accompany chronic pancreatitis.
Exacerbation of chronic pancreatitis
During an exacerbation chronic pancreatitis acquires the symptoms of acute pancreatitis, therefore it is best to treat it in a hospital, under the supervision of specialists. Symptoms of exacerbation may be pronounced or, conversely, erased.
The patient usually complains of pain in the epigastric region or in the right hypochondrium, which can occur both after eating and on an empty stomach. Possible manifestations of dyspepsia (bloating, diarrhea, rumbling in the abdomen, nausea).
Upon examination, the doctor notes the appearance of a white coating on the tongue, a decrease in body weight. The skin of the patient is dry, scaly. In the abdominal region, red spots may appear, and subcutaneous hemorrhages may appear on the sides of the abdomen.
Diagnostics
To assess the functioning of the pancreas, coprologic tests with Elastase-1 are used (the norm is more than 200 μg / g of feces). Due to the defeat of the incremental apparatus of this gland in patients in about a third of cases, violations of carbohydrate metabolism develop.
For differential diagnosis, ultrasound and X-ray studies are often used in medical practice.
Complications
Early complications of chronic pancreatic pancreatitis are: obstructive jaundice due to violation of gallbladder outflow, portal hypertension, internal bleeding due to ulceration or perforation of the hollow organs of the digestive tract, infections and infectious complications (abscess, parapancreatitis, phlegmon retroperitoneal tissue, inflammation of the biliary tract).
Complications of a systemic nature: multiorgan pathologies, functional failure of organs and systems (renal, pulmonary, hepatic), encephalopathy, DIC syndrome. With the development of the disease, esophageal bleeding, weight loss, diabetes, malignant neoplasms of the pancreas can occur.
Forecast
Strict adherence to the diet and diet, complete abstinence from alcohol intake, strict adherence to recommendations for medical treatment significantly reduce the frequency of exacerbations, translate the process into a rarely recurring variant with slow progression. In some patients it is possible to achieve a noticeable and persistent remission.
Chronic pancreatitis is characterized by a progressive course, but the cessation of the effects of causative factors and adequate therapy slow the progression of the disease, significantly improve the quality of life of patients and prognosis.
Treatment of chronic pancreatitis
In most cases with chronic pancreatitis treatment consists of several methods that have a complex effect:
• diet;
• elimination of pain syndrome;
• restoration of digestion, elimination of pancreatic enzyme deficiency;
• stop the inflammatory process;
• restoration of pancreatic tissue;
• prevention of complications.
In this list, a kind of standard for the treatment of chronic pancreatitis pancreatitis, which is adhered to by all doctors. Only medicinal preparations can differ, at their choice individual features of an organism of the patient are considered.
Surgery
Patients with chronic pancreatitis, as a rule, are not shown surgical intervention.
However, with severe pain that is not amenable to treatment with medications, and especially with the pseudotumorous form of chronic pancreatitis, operation is recommended - sphincterotomy (dissection and expansion of the opening of the pancreatic duct).
Treatment of exacerbation of chronic pancreatitis
Chronic pancreatitis treatmentWhen the inflammation worsens, the patient is shown an urgent hospitalization. The first days after the attack, the patient can consume only non-carbonated alkaline water.
Intravenous injections of analgesics and drugs that relieve muscle spasm. Since pancreatitis in the acute stage is often accompanied by repeated vomiting and diarrhea, large fluid losses are compensated for by droppers from saline.
The scheme of treatment of a chronic form provides for complete starvation during a period of exacerbation of the disease. In this regard, intravenously injected glucose solution.
As a drug treatment, enzymes are also prescribed if the type of pancreatitis is hypoxecretory. In the case of excessive release of enzymes by the pancreas, drugs are prescribed to reduce the secretory function. Drugs for treatment are largely determined by the type of disease. Therefore only the attending physician can prescribe those or other medicines.
The standards of treatment of chronic pancreatitis in the acute stage are unchanged and effective. The three principles that medicine has been guided by for many years - hunger, cold and tranquility - are those "three whales" on which the successful treatment of this disease is held.
After the normalization of the condition, the attending physician should take the patient to a strict diet, which the person suffering from pancreatitis must observe constantly.
Diet
In order that the pancreas can normally cope with its functions, a patient with chronic pancreatitis must comply with the diet. Therapeutic diet is an important part of complex therapy not only for acute pancreatitis, but also for chronic.
First and foremost, the right diet contributes to the elimination of factors that can provoke an exacerbation of chronic pancreatitis (alcoholic beverages, smoking, coffee, fatty or fried foods, smoked meats, various starter cultures, spicy foods, chocolate and others).
Fish, mushroom or meat broths are prohibited. To eat it is necessary in small portions (no more than 300 g for one reception), low-calorie food, 5-6 times a day. Do not eat cold or hot.
Drink water that neutralizes acidity in the stomach (Borjomi, Essentuki No. 17). Limitation of daily intake of fat, up to 60 grams per day, carbohydrates to 300-400 g per day, proteins 60-120 grams per day. Limitation of salt intake per day to 6-8 g.
Folk remedies
The most common and available treatment of pancreatitis by folk remedies, but even in this case, a professional consultation of a doctor is needed.
1. Golden mustache. To prepare the decoction you will need one sheet of 25 cm long, or 2 sheets of 15 cm. They should be crushed and poured into 0.7 liters of water. Then the remedy is placed on a quiet fire for a quarter of an hour, after which it is insisted for a day in a warm place. Take 25 ml of warm broth during the remission of the disease.
2. Potatoes and carrots. For cooking, you need five small potatoes and two medium carrots. Vegetables should be washed in cold water, but not cleaned. The main thing - remove all the eyes from the potato and wash again. Squeeze out the juice from the vegetables. You should have a glass of juice, if less, add vegetables in the same proportion. This medicated mixture should be drunk within a week. Do this before dinner once a day. Then make a gap for a week and then repeat the treatment. Treatment of pancreatitis in this way consists of three courses.
3. Washed andoat filled with waterit is infused for about 24 hours, then it is dried and crushed into flour. Next, the flour is diluted with water, boiled for 3-5 minutes and infused for 20 minutes. Ready jelly is taken daily in a warm fresh form.
4. Mix together for 3 tbsp. l. herbsSt. John's wort, motherwort, add 6 tbsp. l. dry flowers of the immortelle. All mix well. Then 1 tbsp. l. herbs pour 1 tbsp. boiling water, cover, wrap, leave for 40-50 minutes. Strain, drink 1 tbsp. before meals, for half an hour. But no more than 3 times a day. National treatment continue for 2 months.
5. We will need bitter wormwood, burdock root, elecampane root, calendula flowers, chamomile medicine, St. John's wort, weed grass marsh, tripartite string, medicinal sage and field horsetail (10 grams of each ingredient). All components are crushed and thoroughly dried. Then 2 tbsp. spoon collection pour 250 ml of boiling water, warmed under a closed lid in a water bath for about half an hour and insisted 10 minutes, then filtered and brought to 250 ml of boiled water. Take the herbal mixture three times a day for half a glass for half an hour before meals.
If you suspect a development of acute pancreatitis, home treatment is not permissible, since such actions can provoke the appearance of various complications.
How to choose probiotics for the intestine: a list of drugs.
Effective and inexpensive cough syrups for children and adults.
Modern non-steroidal anti-inflammatory drugs.
Review of tablets from the increased pressure of the new generation.
Antiviral drugs are inexpensive and effective.
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Dermarolling before and after pictures
Microneedling really works! Have a look at some photos our customers sent us or were posted on our dermarolling forum.
dermaroller before and after photo
skin rejuvenation
This man is 70 years old!
Dermaneedling pioneer Dr. Desmond (Des) Fernandes dermarolled his own face more than 50 times. The result: Skin that looks decades younger than his age, in spite of the South African sun. His results prove that dermarolling is both long-term safe and effective. Recent YouTube interview with Dr. Fernandes so you can see that he really looks like that.
Dermaroller review
Are the most expensive dermarollers really the best? Whatever they claim, all dermarollers are made in China and South Korea. The most expensive ones are often the worst. We are brand-independent and sell those rollers we found to offer the best value for money.
dermaroller test and review
Home » Candida
No miracle, no mineral, no solution (Jim Humble’s MMS scam)
I never knew what MMS really was. I had read it stood for “Miracle Mineral Supplement” or “Miracle Mineral Solution”, so I suspected it to be a mineral supplement containing Magnesium and Phosphorus or something. I do not frequent alternative health forums and never visit sales sites for “miracle” products – they are a dime a dozen and it’s impossible to keep up with the latest scam – so I had no idea what MMS was, until yesterday.
It turns out that MMS, instead of curing cancer, causes cancer!
MMS is Sodium chlorite, a common form of household bleach, a toxic industrial disinfectant, a powerful oxidant (= free radical) that causes cancer when ingested in small quantities and massive organ damage or death when taken in significant quantities. There also is a “MMS2″, containing another form of bleach, used to scrub swimming pools’ walls for disinfection (it’s not added to the actual water because it would make people sick).
I thought: “How come people haven’t been dropping dead from that stuff in droves – it’s so heavily promoted that it must be killing off gullible folks left, right and center?”
The answer is simple: One bottle contains only 4 fl. oz. (118 ml), of which 22.4% is Sodium Chlorite (better known as household bleach):
You’d have to drink a couple of those small bottles to be lethally poisoned, so I guess that is rare, since the instructions say not to take more than 15 drops per day. Not that we should pay much attention to the treacherous FDA but just to show that it’s not just me who says MMS is poison: The FDA said this about Miracle Mineral Supplement:
“The product, when used as directed, produces an industrial bleach that can cause serious harm to health. The product instructs consumers to mix the 28 percent sodium chlorite solution with an acid such as citrus juice. This mixture produces chlorine dioxide, a potent bleach used for stripping textiles and industrial water treatment. High oral doses of this bleach, such as those recommended in the labeling, can cause nausea, vomiting, diarrhea, and symptoms of severe dehydration.”
Jim Humble disagrees and claims the active ingredient in MMS is Chlorine dioxide, but that’s a toxic gas, not a mineral. A mineral is a naturally occurring substance that is solid and stable at room temperature. Chlorine dioxide is thus not a mineral at all.
Even the FDA sometimes says the right thing, like a broken clock showing the correct time twice a day. Canada banned the sale of MMS because a Canadian who took it nearly died. Other countries banned its sale as well. By itself no proof of a bad product, as Stevia is illegal nearly everywhere as well, as a sweetener.
25 mg of Sodium chlorite per bottle. That would make the bottle and its packaging an order of magnitude more expensive than the cost of the bleach it contains.
When I see products heavily advertised using terms like “miracle”, I always look at their profit margin. When it is above a thousand percent, alarm bells go off and I investigate. I did that with the $4 dermarollers sold for $80 (2,000% profit) and I am now doing it with a tiny bottle with 20 cents of bleach sold for $20 as “Miracle Mineral Solution” or “Miracle Mineral Supplement” (MMS). 10,000% profit – you’d truly expect a miracle.
Let’s not dwell too long on the man behind MMS, “Bishop” James V. Humble. He usually appears with a gemstone on his forehead nowadays, to appeal to magical thinkers. He bought his Bishop title from a religious title mill “Church” of which both the founder and his successor were criminally investigated for child rape. He needed that title so that it was easier for him to start a tax-exempt “Church”. Instead of attacking the vendor, we should judge his claims on their merit: James Humble claims that MMS cures all disease known to mankind including Malaria, Diabetes, Influenza, Crohn’s disease, Herpes, Arteriosclerosis, Tuberculosis, CFS, Hepatitis A, B and C, Cancer and of course AIDS. Everything except dying of old age. MMS enlarges breasts too! “A teenage girl, overweight with depression and failure to develop breasts, was given MMS. The next day her breasts started to grow.” Yes people, MMS truly works wonders. If not for your health or breast size, then certainly for Mr. Humble’s finances. Bishop Humble the Bleach Healer. Funny how he had a massive spinal tumor removed in early 2009. MMS clearly didn’t work for him.
A cure for all ills, where have we heard that before? Every couple of years someone becomes wealthy with a miracle cure. It seems none of these miracle cures work, because millions of people keep buying one after the other and they still feel the need to email me and tell me they tried all those magical potions – fruitlessly. People should first get educated on what could be the cause of their health problem, instead of wasting money on “miracle solutions”.
I have not been able to find any references to studies done with MMS that suggest that even one sick person has been cured, neither did I find any evidence based in science that would suggest that MMS could kill pathogens in the body, as opposed to on surfaces. The ravingly positive testimonials are fake, published by spammers, MMS resellers and affiliates. In fact there is ample evidence that MMS (bleach) taken orally causes, not cures, cancer. MMS contains hundreds of times more bleach than allowed in drinking water and that rule is for a good reason: Bleach is a powerful oxidant and free radical, and the reason people are advised to eat antioxidants is because they neutralize oxidants. Why do oxidants need to be neutralized? Because they cause cellular damage. Cellular damage leads at best to premature aging and at worst to cancer. Oxidants ravage RNA, leading to cell apoptosis, tissue necrosis and, if the immune system has a bad day – cancer. More about how MMS causes cancer here.
Mr. Humble the magical potion millionaire says that MMS “kills all bacteria, pathogens, viruses, cancer cells” and whatnot, but – another great miracle – the gut flora is left in peace! Mr. Humble abuses microbiological terms like “aerobic” and “anaerobic” to make you believe that that’s actually possible. As far ar Mr. Humble is concerned, the invention of Penicillin was a waste of time. A few drops of bleach in your lemonade cures Tuberculosis, Cancer and AIDS and enlarges your boobies too.
From http://www.health-science-spirit.com/MMS.html
“Jim Humble, a chemist and metallurgist accidentally discovered the MMS by using a whole bottle of Stabilized Electrolytes of Oxygen (S.E.O.) to immediately cure a companion of malaria during a jungle expedition. S.E.O. contains about 3 % sodium chlorite. Humble gradually realized that S.E.O. is too weak”.
Let’s ignore the fact that Jim Humble is no chemist, but focus on the claim: Malaria was instantly cured by drinking a 3% bleach solution, but 3% was too weak. It was in fact extremely much too weak, since Jim increased the concentration in his Miracle Mineral Supplement roughly tenfold. Then how come Malaria was instantly cured? That page contains so much baloney and downright ridiculous gobbledegook that I could debunk every sentence as hilarious nonsense but it would take an article ten times this size. Just as one crazy man can ask more questions than ten wise men can answer, it takes quite some scientific reasoning, backed up by references, to refute the baloney in those claims. Such as the claim that Lyme disease is caused by a virus, instead of the bacterium Borrelia burgdorferi (s.l.) And that bleach can’t damage body cells. The abject advice is given to rinse out burns with the MMS bleach, causing of course even deeper tissue damage, increasing the risk of permanent scars. There are countless web pages devoted to the crapolic MMS cult. Literally every sentence is nothing but lies, disinformation, pseudoscience and psychological manipulation.
Mr. Humble bought his Bishop title from a religious title mill. Hoping to get rich quick, he started as a gold prospector in Africa, but he found a richer goldmine in sick people’s gullibility and he now is a billionaire. He says he has more than 5 million customers. Say that each customer buys on average 5 bottles during their lifetime, that’s 5,000,000 x 5 x $20 = five hundred million dollars. Tax-free, since “Bishop” Jim Humble owns the “Genesis II Church of Health and Healing”. Yup, if you don’t want to pay taxes, do as Ron Hubbard of Scientology did: Start your own cult. James Humble made at least twice that amount and is a billionaire because it’s not just bleach he sells. Books, DVD’s, ebooks, courses, seminars, consultations, the lot. On top of that, he sells pastor titles. His pastors give away MMS on street corners, but they “solicit donations” in return that go to a numbered offshore account belonging to Mr. Humble. For his “legal defense fund”. Sick but rich individuals are asked up to donate up to one million dollars to the “Church” as a sign of gratefulness for their “cure”.
Because various countries would like to arrest Mr. Humble for causing the deaths of their citizens, he exiled himself to the Dominican Republic, a country without extradition treaties. Imagine the splendor of his mansions and the beauty of his mistresses. The man is more liquid than Bill Gates. The best Cuban cigars are but a short yacht trip away. Mr. Humble can afford the world’s best lawyers, wealth managers, tax attorneys, search engine optimization experts, web designers and forum spammers. He employs his own private army of affiliates – ready to rip their enemies – anyone with a brain – to shreds. I think I should also launch a “miracle supplement”.. Caustic soda, anyone? (Kills all pathogens stone dead, leaves the body alone because “its got electrolytes!“)
Why MMS does not kill pathogens in the body, but the body itself
On the MMS disinfo pages it is claimed:
“When a chlorine dioxide ion contacts a harmful pathogen, it instantly rips up to five electrons from the pathogen, in what can be likened to a microscopic explosion… harmless to us, but terminal for pathogens.”
The big lie here is the “harmless to us” Because this also happens with the first human cell the bleach ion encounters. Since the chance that those ions touch a body cell before they touch a pathogen is almost infinitely high, in reality, when you drink bleach, all it does is cause cell damage to your own body, leaving virtually no bleach left to kill any pathogens. So it’s a double lie. All damage is done to your own body, and none to any pathogens – except perhaps some in your throat. Bleach indeed kills pathogens – but the catch is that bleach absolutely can’t distinguish between your cells and bacterial/viral/fungal/parasitical cells. It kills the first cell it stumbles upon. It denatures the first protein it sees, cuts through DNA like a hot knife through butter. The problem is that the average person just doesn’t grasp this simple scientific principle. When confronted with the incessant barrage of lies coming out of James Humble’s multi-level marketing machine, it’s all too easy for a little seed of hope to grow and from there it’s a small step to pulling out a credit card.
“Bishop” James Humble is a criminal, plain and simple. Megalomaniac liar as he is, he claims to have saved the lives of 100,000 people. I say on the contrary: He undoubdedly has contributed to the death of many sick people who could otherwise be saved. By promising them that MMS cures all disease, he encourages patients to cease unpleasant, but life-saving treatments in favor of his bleach. With his admitted 5 million customers, if just one in a hundred suffered from cancer and only one in a thousand of those decided against that extra treatment that could save their lives, then we have over four dozen poor sods who died because they believed that quack’s lies. Such cynical, yes psychopatic liars must be cut out of society. The damage they do is too great. It’s not the billion dollars stolen from the weakest in our midst. It’s not the spreading of magical belief systems-for-profit on an industrial scale. It’s the globally spread hope and faith in a poison that makes the sick sicker and bereaves children prematurely of their ailing parents and grandparents – not to mention those deluded individuals who administer this vile broth to their toddlers in the hope they’ll stop crying – because that happens too. MMS is good for you and totally harmless, right? And when it’s harmless and good for you, the more the better, right?
Several countries have already put out arrest warrants for this thug.
“Jim Humble is wanted in Malawi Africa and other African countries surrounding it, and has at least two arrest warrants out for him, regarding the poisoning and death of several people who have died due to taking this procedure and giving them false information. On his websites he is careful not to say it cures just helps conditions, but in Africa he says it does cure all, the problem is he has been saying it cures everything from aids to hep and more, these peoples immune systems are already compromised so if they take this in heavy doses they become very ill or die!”
From that same page:
“I’m a chemist, and I can tell you for a fact that chlorine dioxide will attack anything that it can grab electrons from. That includes healthy cells in the body, such as the stomach and gut lining. That causes irritation which results in nausea, vomiting and diarrhea as the body desperately tries to rid itself of the poison you have ingested. Chlorine dioxide cannot tell a toxin or a bacterium from a healthy human cell, it will happily damage any of them. If you took enough MMS to get blood concentrations of chlorine dioxide high enough to kill a single pathogen, you would probably die, though that would take about 400 ml or a couple of bottles full. Antibiotics are far more potent at killing bacteria than MMS, and far less toxic. Dicloxacillin, for example, is 100 times more potent at killing bacteria than MMS, and 20 times less toxic.”
Noone knows exactly what this man is up to. He say he’s working with prison authorities in African countries to do experiments on prisoners, to give but one example.
MMS affiliates and magical thinkers alike will be saying: “Bishop Humble is the victim of a Big Pharma/FDA witchhunt, they want to neutralize him because he found the cure for all disease!” Sure. When I start selling caustic soda as the cure to all ills, I’ll also eventually be “witch-hunted”. The real witch hunting is done on MMS forums. Anyone who speaks against MMS is immediately banned, like Rhys Morgan, a boy with Crohns disease who explained why he thinks MMS can’t cure disease – on the contrary.
MMS doesn’t work, period. It can’t work, because it would have to violate a few laws of nature to do so. Ions would have to have brains and legs to direct them to pathogens, instead of random body cells. Of course you can believe in miracles and believe “Bishop Humble” on his honest-to-God word, since this do-gooder, in his own words, descends from a line of priests all the way to Jesus. Some people buy into Humble’s snake oil and innocent people are the victim of that.
MMS bleach is being given to autistic babies orally and as enemas by Kerri Rivera, with the dose increased until they get very sick – this woman should stop causing harm to small children:
Video streaming by Ustream
Kerri Rivera should stop deceiving parents and parents should do their own research. Research into scientific facts, not anecdotes and unsubstantiated claims.
Articles debunking MMS:
http://healthwyze.org/index.php/component/content/article/460-the-debate-between-healthwyzeorg-and-jim-humble-about-whether-mms-is-a-fraud.html?showall=1
http://www.nation.co.ke/oped/Editorial/Miracle%20supplement%20dangerous%20to%20Kenyans%20%20/-/440804/1014118/-/1luiwo/-/
http://www.smh.com.au/national/deadly-chemical-being-sold-as-miracle-cure-20100108-lyvl.html
http://lizditz.typepad.com/i_speak_of_dreams/2010/08/bleachgate-or-mineral-miracle-solution.html
http://www.guardian.co.uk/science/2010/sep/15/miracle-mineral-solutions-mms-bleach
http://www.guardian.co.uk/science/the-lay-scientist/2010/sep/17/miracle-mineral-solutions-mms
http://noodlemaz.wordpress.com/2010/08/12/bleachgate-the-plot-thickens/
http://www.sott.net/articles/show/213275-MMS-Miracle-Mineral-Solution-or-Trojan-Horse-Your-Body-and-DNA-Decide
http://blogs.plos.org/takeasdirected/2010/09/19/bleachgate-more-miracle-mineral-solution-madness/
http://www.nation.co.ke/News/Malaria%20drug%20endangers%20Kenyan%20lives%20/-/1056/1012418/-/11e26ja/-/
http://cenblog.org/terra-sigillata/2010/09/20/bleachgate-uk-and-kenyan-press-raising-awareness-of-miracle-mineral-solution/
http://noodlemaz.wordpress.com/2010/08/16/link-roundup-bleachgate/
http://blogs.mirror.co.uk/investigations/2010/10/the-miracle-mineral-solution-c.html
http://parafort.com/ri/?p=1154
http://www.sott.net/articles/show/207643-Down-the-Rabbit-Hole-The-Assassination-of-JFK-Bishop-Jim-Humble-And-The-Nexus-Conference
http://curezone.com/forums/am.asp?i=1109319:
“Anyone on the board been cured of cancer, herpes, AIDs, hepatitis? I haven’t read about it. And as for the 1000’s of people cured of Malaria in Africa? I’m a researcher. I research everything, and I’m good at it. I have spent months trying to find info on the Malaria cures in Africa. The government of Malawi knows nothing about it. It isn’t in any of the African newspapers. There is no evidence whatsoever, other than Jim Humble’s word. And how is it that it can cure Malaria in 4 hours, AIDS in a day, and you guys have been taking it for months and nothing but nausea and diarrhea? People keep saying, “Jim Humbel says that it’s pathogen die off”, or “Jim Humble says to increase the dose” He isn’t a doctor, he isn’t even a chemist. He hasn’t seen the patient, how does he know? I think that the referral to a cult comes from the book that Humble wrote about him having lived 100’s of previous lives and the difference between him and others is that he remembers.”
The articles of association of the “Genesis Church of Healing” of this criminal genius show that it’s nothing but a tax-exempt multinational corporation that intends to aquire real estate and business holdings worldwide:
http://genesis2church.com/articles-of-association/
If you have at least 1200 dollars to spare, the sleazeball will relieve you of your cash in a “private consultation”:
http://www.mareaweb.net/mms/NEWS011.htm
Jim Humble in his gold-digging days:
Update 1
Humble’s army of affiliates have gone into full-blown attack mode and even come with threats of violence. In an attempt to educate this poor ignorant soul, Jim Humble sent me a PDF he made. That PDF purports to explain exactly how MMS destroys pathogens on a molecular level. After reading it, I became strengthened in my belief that Mr. Humble knows full well that his MMS is a fraud, because someone who’s able to use all the scientific-sounding terms such as “electron shell” and even draw a (falsified) 3D model of one, clearly has done some research into the chemistry involved. Meaning, he is educated enough to know the truth, but he chose to misrepresent it in order to sound credible. If he would merely have come with vague claims that could still be attributed to ignorance. Someone who publishes a very scientific looking PDF full of three dimensional models of the quantum mechanics of molecules and who uses all the applicable professional lingo, but who lies about the facts every step of the way clearly is a deliberate fraudster. Me calling him a ruthless thug was appropriate, and I am not taking it back. People are dying because of this scam. I fervently hope that Humble will sue me, because the outcome will prove once and for all that his whole setup is a scam:
1. Humble claims that electron shells fully envelop covalently bonded molecules (or polyatomic ions). That is a gross misrepresentation of basic chemistry that nicely helps draw the wool over our eyes.
2. Humble claims that by pulling some of the electrons out of their outer shells, that the entire molecule will disintegrate into separate atoms. That is nonsense for many reasons, one of them being the threedimensional electron orbital structure of molecules and hence the need of a lot of electron-pulling in many places simultaneously – impossible to do unless half of the blood serum would be replaced by MMS.
3. Humble claims that part of the MMS “curing mechanism” involves the creation of free oxygen atoms, and that that free oxygen is totally harmless because “it can not oxidize things but become part of the water or carbon dioxide in the body”. This is complete nonsense. An oxygen atom will immediately destroy the first random molecule it comes into contact with – whether it be that of a pathogen or that of your body.
4. Then follows a claim on how oxygen “can’t do damage to the body”, because its oxidation strength is “only 0.95 Volts”. This claim is patently false. Oxygen is very harmful – so harmful in fact that breathing pure oxygen for just a few hours will result in permanent brain damage due to central nervous system oxygen toxicity. Every IC ward nurse knows this, and adjusts the supply of supplemental oxygen such that the patient never breathes pure oxygen, or even 50% or 40% oxygen. The devices used are designed in a way that the patient can never breathe pure oxygen, because it would kill in less than a day. Under higher pressures than atmospheric pressure, Oxygen can kill in minutes. Every NITROX SCUBA diver knows that. Even the 21% oxygen in our air damages our cells and tissues all the time, and our body has to repair that damage all the time. It has even been postulated that the oxygen in the air we breathe is a small contributor to causing lung cancer.
5. Humble also says that the Chlorine split off by his carcinogenic concoction is nothing to worry about, because it “turns into harmless table salt by combining with Sodium in the body”. Well, no. There is no free Sodium (Na+) in the body for the Chlorine atom to attach to. Instead, it will severely damage the nearest protein molecule or DNA strand or anything else it touches.
6. Humble claims that there is a big difference between the proteins in bacteria, viruses, fungi and parasites and in the proteins in our bodies. He says that MMS kills only the proteins in the pathogens, but not in our bodies. But he is wrong. There is no such fundamental difference. All proteins react the same to free radicals.
There are many more wild, unsubstantiated claims and plain untruths in that PDF. For the layperson, it looks like an impressive explanation of fundamental biochemistry principles. For anyone with a basic knowledge of highschool chemistry, it is unadulterated baloney. Basically, Humble claims that “All pathogens and all diseases and all sick cells are anaerobic and MMS kills only those because it is a weak oxidizer and therefore can only oxidize weak pathogens and anearobics are weak but it oxidises them very powerfully like an explosive because MMS is basically an explosive but can’t oxidize any cells or tissues in the body.” (From a Project Camelot interview). Then he affirms that MMS can cure any disease, including cancer. If you believe that then I have a bridge to sell you on the Moon.
Update 2
The MMS criminals started to spam people with Lyme disease that MMS will cure them. I was forwarded such an email:
MMS-Lyme-spam
The email claims that MMS is sent from God to Jim Humble’s Church and that their “Sacramental Protocols” (using MMS) will cure all disease of mankind. If you believe that, I’ve got some prime real estate to sell you – on Pluto. Another gem from the same email from that psychopath:
Humble-psychopathy
You have a helpful point of view or interesting info to add?
Email [email protected] for possible publication below.
Dallas McMillan:
This is a great article – I’ve been researching MMS on the net – this is clearly a large scale scam posing as a grass roots, medicine for the masses movement.IT would be SO easy to do a trial of MMS to assess effectiveness – even a small case study of 10 people with Malaria, or AIDS, or small breasts, or whatever they claim to cure.What I find so scary is how easily people get sucked into this – it really does appear to be a cult movement. Sadly the state of scientific literacy is so poor that people find the testimonials to be evidence.I’m amazed at just how little evidence they present – they haven’t even tried to falsify a few decent case studies.It shows they are really a MLM movement, and all they need is new suckers to keep making the people at the top wealthy.
Christian Becker:
Interesting. Only learned about MMS a few days ago and was like “What the hell?”. Although I don’t really understand what your problem with the FDA is (I’m not from the US), I think this article should be read by those people who really think that shoving bleach up or down their bodily orifices will do any good. Granted, I’m not sure these deluded people will believe (as if you needed to “believe” it) anything you say.I’d like to point out a small mistake: The actual bleach (ClO2) is a radical, but not an ion. Chlorite, which disproportionates to chloride and chlorine dioxide, is an ion, though, but it’s not the (in)effective agent.
poo:
I have small boobs … I took mms … guess what, I still have small boobs!! ;)
Mms for me seemed to do nothing whatsoever ever for any health complaints and I stopped taking it after I got sick. Any one who has ever taken the stuff will know how much of a battle it is to drink the foul smelling potion down … uggg … it truely is disgusting!!!! Cure your ills but eating REAL food, organic unprocessed natural food.
Peace4All:
I fully believe in Sarah’s breakdown. Unknowingly, she has provided me the push to always do my own search to seek out the truth about products and their claims. Plus, I am naturally curious and crave information as I do on mostly every topic, but oddly I didn’t do it much on products. “Bishop” Humble, you should be ashamed of yourself. It’s people like you that creates such an evil world we live in now.
Republishing this article is prohibited. Violations are subjected to a copyright license fee.
C60 in olive oil
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ABCB11
ABCB11
Reviewed June 2012
What is the official name of the ABCB11 gene?
The official name of this gene is “ATP-binding cassette, sub-family B (MDR/TAP), member 11.”
ABCB11 is the gene's official symbol. The ABCB11 gene is also known by other names, listed below.
Read more about gene names and symbols on the About page.
What is the normal function of the ABCB11 gene?
The ABCB11 gene provides instructions for making a protein called the bile salt export pump (BSEP), which is found in the liver. Bile salts are a component of bile, which is used to digest fats. Bile salts are produced by liver cells and then transported out of the cell by BSEP to make bile. The release of bile salts from liver cells is critical for the normal secretion of bile.
Does the ABCB11 gene share characteristics with other genes?
The ABCB11 gene belongs to a family of genes called ABC (ATP-binding cassette transporters). It also belongs to a family of genes called ATP (ATPases).
A gene family is a group of genes that share important characteristics. Classifying individual genes into families helps researchers describe how genes are related to each other. For more information, see What are gene families? in the Handbook.
How are changes in the ABCB11 gene related to health conditions?
benign recurrent intrahepatic cholestasis - caused by mutations in the ABCB11 gene
Mutations in the ABCB11 gene can cause benign recurrent intrahepatic cholestasis type 2 (BRIC2). People with BRIC2 have occasional episodes of impaired bile secretion that lead to severe itching (pruritus) and yellowing of the skin and whites of the eyes (jaundice). On occasion, people with BRIC2 have later been diagnosed with a more severe condition called progressive familial intrahepatic cholestasis type 2 (described below) when their symptoms worsened.
Affected individuals have a mutation in both copies of the ABCB11 gene. Mutations in the ABCB11 gene that cause BRIC2 lead to a 40 to 50 percent reduction of bile salt transport. The resulting buildup of bile salts in the liver leads to the signs and symptoms of BRIC2. It is unclear what causes the episodes to begin or end.
progressive familial intrahepatic cholestasis - caused by mutations in the ABCB11 gene
More than 100 mutations in the ABCB11 gene have been found to cause a severe form of liver disease called progressive familial intrahepatic cholestasis type 2 (PFIC2) that usually leads to liver failure. Development of this condition requires a mutation in both copies of the ABCB11 gene. Mutations in the ABCB11 gene that cause PFIC2 result in a 70 percent reduction to complete absence of bile salt transport out of the liver. The lack of transport causes bile salts to build up in liver cells, leading to liver disease and its associated signs and symptoms.
Mutations that lead to the production of a short, nonfunctional protein or cause no protein to be produced tend to be associated with severe liver disease that appears earlier in life. People with no functional BSEP protein also seem to be at a greater risk of developing a type of liver cancer called hepatocellular carcinoma.
intrahepatic cholestasis of pregnancy - associated with the ABCB11 gene
Women with a change in the ABCB11 gene are at risk of developing a condition called intrahepatic cholestasis of pregnancy. Affected women typically develop impaired bile secretion (cholestasis) and pruritus during the third trimester of pregnancy, and these features disappear after the baby is born. A common variation (polymorphism) in the ABCB11 gene is found more often in women who develop this condition than women who do not. This variation leads to a change in a single protein building block (amino acid) in the BSEP protein. Specifically, the amino acid valine is replaced by the amino acid alanine at position 444 of the protein (written as V444A). This change leads to a reduction in the amount of BSEP protein in liver cells. In rare cases, an uncommon change (a mutation) in one copy of the ABCB11 gene is found in women with intrahepatic cholestasis of pregnancy. A single mutation in this gene increases the risk of developing intrahepatic cholestasis of pregnancy. These mutations likely reduce the amount or function of the BSEP protein.
In women with either type of genetic change, enough BSEP function remains for sufficient bile secretion under most circumstances. Studies show that the hormones estrogen and progesterone (and products formed during their breakdown), which are elevated during pregnancy, further reduce the function of BSEP, resulting in impaired bile secretion and the signs and symptoms of intrahepatic cholestasis of pregnancy. Many factors, however, likely contribute to the risk of developing this complex disorder.
Where is the ABCB11 gene located?
Cytogenetic Location: 2q24
Molecular Location on chromosome 2: base pairs 168,922,825 to 169,031,322
The ABCB11 gene is located on the long (q) arm of chromosome 2 at position 24.
The ABCB11 gene is located on the long (q) arm of chromosome 2 at position 24.
More precisely, the ABCB11 gene is located from base pair 168,922,825 to base pair 169,031,322 on chromosome 2.
See How do geneticists indicate the location of a gene? in the Handbook.
Where can I find additional information about ABCB11?
You and your healthcare professional may find the following resources about ABCB11 helpful.
You may also be interested in these resources, which are designed for genetics professionals and researchers.
What other names do people use for the ABCB11 gene or gene products?
• ABC16
• ABCBB_HUMAN
• bile salt export pump
• BRIC2
• BSEP
• PFIC2
• PFIC-2
• progressive familial intrahepatic cholestasis 2
• sister p-glycoprotein
• SPGP
Where can I find general information about genes?
The Handbook provides basic information about genetics in clear language.
These links provide additional genetics resources that may be useful.
What glossary definitions help with understanding ABCB11?
alanine ; amino acid ; ATP ; benign ; bile ; breakdown ; cancer ; carcinoma ; cell ; familial ; gene ; hepatocellular carcinoma ; jaundice ; liver cancer ; liver failure ; mutation ; polymorphism ; progesterone ; protein ; secretion ; valine
You may find definitions for these and many other terms in the Genetics Home Reference Glossary.
See also Understanding Medical Terminology.
References (16 links)
The resources on this site should not be used as a substitute for professional medical care or advice. Users seeking information about a personal genetic disease, syndrome, or condition should consult with a qualified healthcare professional. See How can I find a genetics professional in my area? in the Handbook.
Reviewed: June 2012
Published: November 24, 2014
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The Pregnancy Pain in the Behind You Need to Know About
Everything is going fine for you and your bump when all of a sudden pregnancy becomes a pain in the butt. Literally. Many moms-to-be are struck by pain in the behind or lower back – and then find that the pain runs down their legs. When the pregnancy pain known as sciatica strikes it can be a temporary annoyance – or it can become hard to move.
What is sciatica?
The sciatic nerve is the biggest nerve in the body. It starts in your lower back and extends all the way down to your ankles. When the sciatic nerve becomes compressed it is called sciatica.
What causes sciatica?
Sciatica can occur for a variety of reasons throughout life, but it is common during pregnancy. Several things can cause the sciatic nerve to become compressed during pregnancy, including weight gain, your bulging uterus, a shifting center of gravity, or your baby's head resting in exactly the wrong place.
pregnancy pain
Image via Unsplash/ Alexander Krivitskiy
{ MORE: Jessica Simpson's Severe Pregnancy Swelling is All of Us }
What does sciatica feel like?
Sciatica starts in the lower back or buttocks and sends a sharp, shooting pain down your leg. It will probably feel different than any other pain you have experienced, even if you have had lower back pain throughout your pregnancy.
How common in sciatica?
Very! Most pregnant women will experience at least one episode of sciatica during their pregnancy.
How severe is sciatica?
It varies greatly from mother to mother. For some women, the pain will occur only once or will be transient. However, for others, the pain may be severe and long-lasting taking them off their feet completely. Thankfully, severe sciatica is rare.
Can sciatica be prevented?
Unfortunately, there is really no way to prevent sciatica. It will either strike or it won’t. Just be prepared to recognize what’s going on when it happens.
What can I do if sciatica strikes?
As with any pregnancy-related concern, call your doctor or midwife for advice, especially before taking any medication or starting any new exercise. However, there are several things other moms have found helpful in dealing with sciatica during pregnancy that you may find helpful too. Getting off your feet, sleeping on the unaffected side, using warm compresses, yoga, acupuncture, acetaminophen, a pregnancy massage, and a pregnancy girdle are things other moms have said have helped them cope with sciatica.
Can sciatica hurt my baby?
No! Sciatica may be very uncomfortable for the mother, but it is not at all harmful for the baby.
{ MORE: This Care Box Is the Perfect Gift for Moms Expecting a Rainbow Baby }
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If this pregnancy pain in the butt strikes, take a deep breath, take a load off your feet, and know that this too will pass.
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The Pregnancy Pain in the Behind You Need to Know About
Jamie is a Beltway Insider who loves channeling her pre-motherhood love of traveling into spending time exploring all D.C. has to offer with her brood of two girls and two boys ages 9, 7,5, and a baby. She is a reformed lawyer turned full-time kid wrangler who enjoys photographing her everyday chaos and anything salted caramel. Since life is never dull, she loves writing about the issues and events going on in her life at any given time, including caring for a daughter with special needs and th ... More
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Open Access
Two-stage hepatectomy after autologous CD133+ stem cells administration: a case report
• Eloisa Franchi1,
• Maria C Canepa1,
• Andrea Peloso1,
• Letizia Barbieri1,
• Laura Briani1,
• Gabor Panyor1,
• Paolo Dionigi1 and
• Marcello Maestri1Email author
World Journal of Surgical Oncology201311:192
DOI: 10.1186/1477-7819-11-192
Received: 22 December 2012
Accepted: 5 August 2013
Published: 13 August 2013
Abstract
Liver resection is the mainstay of treatment for patients with primary and metastatic liver tumors. However, a large majority of patients present for initial medical evaluation with primary and metastatic liver tumors when their cancer is unresectable. Several trials have been undertaken to identify alternative treatments and complementary therapies. In the near future, the field of liver surgery will aim to increase the number of patients that can benefit from resection, since radical removal of the tumor currently provides the sole chance of cure. This paper reports the case of a patient with an advanced colonic cancer in the era of stem cell therapyIn 2011, a 57 years old white Caucasian man with a previous history of non-Hodgkin lymphoma (NHL) was diagnosed with colon cancer and bilobar liver metastases. Following neoadjuvant therapy, the patient was enrolled in a protocol of stem cell administration for liver regeneration. Surgery was initially performed on the primary cancer and left liver lobe. An extended right lobectomy to S1 was then performed after a portal vein embolization (PVE) and stem cell stimulation of the remaining liver. The postoperative course was uneventful and the patient was free of disease after 12 months. Extreme liver resection can provide a safer option and a chance of cure to otherwise unresectable patients when liver regeneration is boosted by PVE and stem cell administration.
Keywords
Liver surgery Portal vein embolization Stem cells Liver regeneration Colon cancer Liver metastases
Background
The treatment of choice for both primary and metastatic liver tumors is radical resection [1]. However, up to 45% of patients present for initial medical evaluation when the parenchymal diffusion of cancer requires more surgical resection than is possible. An accepted evaluation of prospective resection is that 30% of the liver must remain in order for its function to be unaffected, or a safer 40% if there is an underlying disease (for example, chronic hepatitis, diabetes) or previous chemotherapy treatment [2].
Portal vein embolization (PVE) has been proposed as a tool to stimulate liver regeneration when prospective surgical resection is over the limit [3]. This technique relies on the portal injection of several agents into the cancer liver lobes. Commonly, patients present with a large tumor in the right liver lobe and a left lobe that is too small for radical resection. Following PVE, the contralateral segments experience a degree of hypertrophy in the range of 15 to 25%, depending on liver status.
When a patient has a tumor that is technically resectable but the remaining liver is small, PVE can stimulate growth, which can be observed until the volume is within the necessary limit. The process is continuous and the remaining tissue will continue to grow. Studies have reported that the liver can take 150 days to develop a volume large enough to allow surgical resection [4]. However, during this time the disease can continue its progression, and patients could die while waiting. Furthermore, PVE does not prevent the tumor growth inside the occluded portal lobe, and there are concerns regarding its potential when diffusion of cancer is faster than expected [5]. Therefore, a procedure is needed to gain volume as swiftly as possible, while minimizing waiting list time to avoid any advantage for the cancer.
Several recent studies have suggested that stem cells play a key role in the field of tissue regeneration [6]. The liver reacts to any lesion by several naturals paths. Thus, several populations of cells cooperate through different pathways, and their role depends on the nature of the stimulus and the extent of damage. A normally functioning liver will undergo a slow turnover of functional mass based on the proliferation of hepatocytes. Adult hepatocytes proliferate after a normal liver resection when the residual parenchyma can tolerate the damage, while supplying the needs of the whole body. When the loss of tissue is greater, the liver seems to have a pool of sleeping cells that have been found mainly in rodents, called ‘oval cells’ [7]. Such cells are relatively undifferentiated and several studies have demonstrated that they can play a role when the normal hepatocytes are not able to repair by normal mechanisms. These emergency cells can possibly differentiate toward the hepatocyte or biliary cell lines. When the liver suffers an extreme insult, both acute and chronic, stem cells can be mobilized from the bone marrow to participate in the repair [8]. These cells are CD34+ and their number grows steadily after extended liver resections [9], while they do not appear after normal abdominal surgery (that is, gastrointestinal or pancreatic operations). Among this population, CD133+ cells are a subset with special liver engraftment potential [10]. The CD133+ phenotype is typical of some cell lines with multipotent differentiation capacity. Recently, CD133+ cells have been proposed to augment liver regeneration after PVE in selected patients [11, 12].
This paper presents a case of two-stage hepatectomy of synchronous liver metastases from colon cancer.
Case presentation
A 57 -year-old white Caucasian man was diagnosed with non-Hodgkin lymphoma (NHL) in 1991 (Figure 1). The NHL was treated by a standard protocol of chemotherapy and radiotherapy. The treatment was successful and achieved a complete response. Thereafter, the patient reported good health and normal quality of life. In March 2011, a routine follow-up examination revealed a sigmoid cancer and bilobar multiple liver metastases. In Vittorio Emanuele hospital, Catania, Italy, the oncology team decided to commence a FOLFOX combination chemotherapy regimen. This treatment of six cycles had some success and re-evaluation deemed the disease as stable.
https://static-content.springer.com/image/art%3A10.1186%2F1477-7819-11-192/MediaObjects/12957_2012_Article_1409_Fig1_HTML.jpg
Figure 1
Timeline of the patient’s course of disease. After the onset of NHL, the patient had a prolonged period of good health. The colon cancer with synchronous metastases was initially considered unresectable. NHL, non-Hodgkin lymphoma.
The patient was then referred to the liver unit at Fondazione IRCCS Policlinico San Matteo, University Hospital, Pavia, Italy. An additional computed tomography (CT) scan was undertaken to define the extent of the disease (Figures 2 and 3). The multidisciplinary liver team decided the patient should undergo a two-stage resection, with PVE of the right liver lobe after removal of the primary tumor and hepatic segment 3 (S3), because the patient had a future liver remnant volume (FLRV) of <40% (total liver volume (TLV) = 1,281 cm3; FLRV = 328 cm3; 25.6%). This percentage is regarded as below the limit for liver resection when a patient has chronic disease or has received chemotherapy. Due to the patient’s history of NHL, the chance of undergoing radical surgery remained questionable, and a protocol of boosted regeneration by autologous administration of CD133+ stem cells was proposed. The local ethics committee authorized the procedure as a compassionate treatment and the patient signed a specific consent form.
https://static-content.springer.com/image/art%3A10.1186%2F1477-7819-11-192/MediaObjects/12957_2012_Article_1409_Fig2_HTML.jpg
Figure 2
A CT scan demonstrated advanced bilobar disease. (A) Cancer nodule in the left lobe and (B, C, D) multiple gross deposits in the right lobe of the liver. The tumor also infiltrates S1. CT, computed tomography.
https://static-content.springer.com/image/art%3A10.1186%2F1477-7819-11-192/MediaObjects/12957_2012_Article_1409_Fig3_HTML.jpg
Figure 3
Volumetric preoperative study. (A, B, C) The study demonstrated a future liver remnant volume (D: FLRV) below the minimum of 40% of total liver volume (TLV). This percentage is generally accepted as the lower limit to allow an extended liver resection with a reasonable probability of success when there is an underlying disease, such as chronic hepatitis, cirrhosis or previous chemotherapy. FLRV, future liver remnant volume; TLV, total liver volume.
In July 2011, the patient was admitted to the surgical ward and underwent a combined resection of the colon and liver (S3). An intraoperative ultrasound (IOUS) was performed to confirm the extent of liver disease and map the major biliovascular structures. The pathology confirmed the R0 result on colon cancer and S3, with one positive lymph node out of 14 in the sigmoid specimen. After an uneventful postoperative course, the patient was discharged on the eighth postoperative day.
In August 2011, the patient was readmitted and received granulocyte-colony stimulating factor (G-CSF) at 10 μg/kg of body weight per day to mobilize CD133+ cells from the bone marrow into the blood stream. From the third day of treatment and then daily, a blood sample was taken and CD133+ cells were counted by cytofluorometry. A leukapheresis was performed when the CD133+ cells reached n = 15/μL (on the fifth day of treatment, in this case). The CD133+ cells were purified by immunomagnetic separation (CliniMACS, Miltenyi Biotec Ltd, Surrey, UK). On the same day the right liver was embolized by routine percutaneous technique, the CD133+ suspension was seeded in the prospective remaining left liver parenchyma. The procedure was tolerated quite well and the patient was discharged on the third postoperative day.
Fifteen days later, a volumetric CT scan was undertaken to evaluate the FLRV. The scan demonstrated a growth on the left segment with a FLRV of 772 cm3 (60%), which was considered sufficient for radical resection of the tumor burden (Figure 4). A Chevrolet-shaped laparotomy was performed. The IOUS confirmed the tumor in the right lobe with involvement of S1 and part of S4. The liver ligaments were cut and a cava dissection up to the hepatic vein was performed. The hilum was dissected, and the right portal branch, right hepatic artery and bile duct were ligated and sectioned. The right hepatic vein was isolated free at its caval origin and cut between vascular clamps. The stumps were closed with running polypropylene sutures. The parenchyma was transected by cavitron ultrasonic surgical aspirator (CUSA; Valleylab, Boulder, CO, USA). Small vessels were sealed by harmonic scalpel, while those greater than 3 mm were closed by silk ligatures or titanium clips. The resection was extended to the very lateral portion of S4 and to S1 (Figure 5).
https://static-content.springer.com/image/art%3A10.1186%2F1477-7819-11-192/MediaObjects/12957_2012_Article_1409_Fig4_HTML.jpg
Figure 4
CT scan, resected liver and specimen. (A, B) After the portal vein embolization (PVE) and administration of autologous CD133+ cells, the future liver remnant volume (FLRV) reached 772 cm3 (15 days after the procedure). The (C) resected liver and (D) specimen are shown. CT, computed tomography; FLRV, future liver remnant volume; PVE, portal vein embolization.
https://static-content.springer.com/image/art%3A10.1186%2F1477-7819-11-192/MediaObjects/12957_2012_Article_1409_Fig5_HTML.jpg
Figure 5
A CT scan was obtained after surgery. The outcome was unremarkable with normal liver function. The resected area is highlighted by the hemostatic clips left in situ. CT, computed tomography.
The postoperative course was unremarkable and the patient was discharged on the eighth postoperative day. The pathology report demonstrated R0 surgical outcome. Later, the oncology team prescribed a course of chemotherapy (Figure 1). On December 2012, the patient was alive and well, and free from disease at follow-up CT scans.
Conclusions
Once regarded a risk [13, 14], liver surgery is today routine practice for the treatment of several primary and metastatic tumors. However, when the numbers of patients that are deemed eligible for surgery are assessed, a vast majority do not qualify because of anatomy, the number of lesions and amount of FLRV.
PVE is recognized as a tool to stimulate liver regeneration before a liver resection is performed [15]. However, the amount and speed of regeneration can vary with each case, and a number of patients have died while waiting to gain a remaining liver large enough to allow a resection. Recently, stem cells have offered a choice of treatment for several diseases and a possible aid even in the field of liver surgery, with preliminary clinical studies demonstrating a favorable effect when administered after liver damage [16].
We started a clinical study to offer stem cell administration to selected patients. To qualify, the patient must have primary or metastatic liver malignancy, a FLRV below the cutoff for safe resection (<30% or <40% if the patient has an underlying liver condition) and a contraindication to the routine PVE. The patient reported in this case had a previous history of NHL, which was treated by chemotherapy. Thus, the patient’s ability to regenerate after an extended resection was questionable and the case was deemed marginal.
Patients with hematological cancers and metastatic onset of new oncological disease are frequently considered unsuitable for further aggressive surgical treatments. Even with this single case report, the result was appealing and we have begun a local trial on autologous CD133+ stem cells. It must be recognized that there are still concerns about the use of adult stem cells in clinical practice. For example, a patient with cancer can have cancer stem cells in circulation. Thus, we are extensively testing any possible risk of cancer spreading, and to date there has been no evidence that CD133+ autologous administration can negatively affect the biology of the disease. However, this is only a case report and the safety of such procedures must be carefully validated in controlled trials.
While liver regeneration is likely to be boosted by local deposition of specific cells, the question arises about whether regeneration can be any different from the naïve parenchyma. Concerning the hepatic functional reserve, there have been no evident changes after the administration of CD133+ stem cells. These are probably effective in increasing the amount of hepatic parenchyma, but the quality of the regenerated tissue remains the same. Again, this issue requires specific studies which we hope to perform at leading centers. The long-term outcome of this case has not yet been defined and the patient is still undergoing follow-up, but it is important to add that the autologous portal administration of CD133+ cells did not cause any immediate or late adverse effect. Similarly, other reports do not highlight special complications [11].
This report suggests that some cell populations can stimulate hepatic regeneration and their use should be taken into consideration for patients who need extreme liver surgery. We believe that a prospective approach to regenerative medicine in this field will allow an improved indication to resection, while offering a chance of cure to otherwise unresectable patients. Further studies are required to ensure safety and effectiveness of the therapeutic tool against the risk of liver failure after extended resections.
Consent
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Abbreviations
CT:
Computed tomography
CUSA:
Cavitron ultrasonic surgical aspirator
FLRV:
Future liver remnant volume
G-CSF:
Granulocyte colony-stimulating factor
IOUS:
Intraoperative ultrasound
NHL:
Non- hodgkin lymphoma
PVE:
Portal vein embolization
TLV:
Total liver volume.
Declarations
Authors’ Affiliations
(1)
Fondazione IRCCS Policlinico San Matteo, University of Pavia
References
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Copyright
© Franchi et al.; licensee BioMed Central Ltd. 2013
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Herbs
Herb Garden
A Medicinal Herb Garden is a term often used to describe reference resources useful for medics, herbalists, and botanists of all levels, and serving as a basic guidance for the general public, not as a source for cultivation, consumption, or substitution of a medical treatment or a guide to self-medication.
Online Herb Gardens provide objective information including monographs with a brief summary for each herb and photographs. On-land Herb Gardens offers the same, but approaching nature. The Bonnefont Cloister in New York is an example of an Herb Garden dating from the late 13th century, containing more than 250 species of plants which were grown during the middle Ages.
The following are just a few examples of Herb Gardens monographs:
Arnica (Arnica chamissonis)
Also known as North American Arnica is a perennial plant, lanky habit, growing to approximately 30 to 60 cm in height, and has yellow daisy-like flowers.
Preparations of Arnica are used externally for sunburns, superficial and limited burns, and diaper rashes. Arnica drugs consist of the dried capitulum's.
Roman Chamomile (Chamaemelum Nobile)
Also known as Roman chamomile, chamomile, Manzanilla, lawn chamomile or Anthemis nobilis, is a perennial plant found in dry fields and around gardens and cultivated grounds native to Western Europe, the Azores and North Africa, but also as an escape from cultivation in North America. Flowers in June to August consisting of a prominent yellow solid central disk and silver white rays. The fruit is an achene.
Used medicinally by the ancient Egyptians, the plant has anti-inflammatory activity and antispasmodic effect. The part used is the flower in aromatic, cosmetic, culinary, decorative, and medicinal industry, baths and skin lotions, hair treatments, teas and other products.
German chamomile (Matricaria recutita)
Also known as Bodegold or chamomilla recutita and sometimes mistakenly called Matricaria chamomilla. This is a sweet-scented annual plant native to Europe and western Asia that grows up to 60 cm. Found wild along roadsides, in fields and cultivated in gardens. The white ray-flowers are often bent down to make the disk-flowers even more prominent.
The medicinal part is the flower. As a tea, it is used for lumbago, rheumatic problems, insomnia, and rashes, tending to reduce inflammation and to facilitate bowel movement without acting directly as a purgative. Used as a wash or compress for skin problems and inflammations, including inflammations of mucous tissue. As a vapor it is used to alleviate cold symptoms or asthma, and as a salve it can be used for hemorrhoids and wounds. German chamomile is also used in shampoos to bring out highlights in blond hair and as additive in liqueurs such as Benedictine, or aromatic bitters.
Valerian (Valeriana officinalis)
Is a perennial plant, native to Europe and the temperate zones of Asia, common in damp woods, ditches, and along rivers, grows up to 90 to 120 cm in height. The fresh root has a mop like appearance.
Valerian oil is used in the flavor, fragrance and pharmaceutical industries. The principle compounds of medicinal interest are said to be valepotriates which is supposed to have sedative and anti-spasmolytic effects used for centuries to treat restlessness and nervous disturbances in sleep. The dried roots are used in drug preparations.
Soapwort (Saponaria officinalis L.)
Also known as Soapwort, bouncing bet is a perennial plant native of Southern Europe, also found as a weed spreads via underground stolons. Leaves are dark green and three-nerved.
Self-fertile flowers are pink with five notched petals.
Boiling the whole plant soap can be obtained so it is used as a gentle effective cleaner. The root can be tried for later use in preparations used externally to treat itchy skin.
Yarrow (Achillea millefolium)
Also known as yarrow, milfoil, woundwort, field hop. Asteraceae is a perennial plant found all over the world in waste places, fields, meadows, pastures, and along roadsides and railroad embankments. Leaflets are sharply cleft, fernlike foliage and flowers from June to October, white pinkish rays and yellow disks turning to brown, arranged in convex or flat compound corymbs.
Tea of yarrow is used for stomach problems. The plant contains compounds that inhibit seed germination and have sex-pheromone qualities antispasmodic, astringent, antibacterial proven mosquito repellent. Flower and leaves are used in bitters and vermouth, approved by the FDA for use in alcoholic beverages.
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How Do You Tell The Difference Between The Common Cold And Seasonal Allergies?
Question: How do you tell the difference between the common cold and seasonal allergies?
Answer: In general, allergies tend to start more with watery eyes, irritated eyes, a little bit of an itching sensation or a clogging in the ear, and some nasal congestion, or maybe even a sore or scratchy throat, but not severe.
Colds tend to come on a little bit more severely, more of a sore throat, more of a fatigue, more of a thicker and irritating mucus that people can have, more of an earache.
So in terms of the differentiation, the colds at first at least tend to be more severe, but if allergies go on for longer, then they can get to those levels, and it becomes more important to see a doctor and consider should I be treating this as just allergies or should I be treating this as a cold.
Certainly if you have a higher fever, if you have more of a headache, if you have a lot of thicker or yellow or green mucus, then those are generally more signs of an infection which may be a virus or even bacteria, and you might need more treatment than that, so if you're having more of those symptoms that tell you that you're really feeling sick rather than just bothered by the allergy symptoms or fatigued, then that would be a time to see your doctor.
Next: What Kind Of Testing Is Available To Determine To What One Is Allergic?
null
Previous: I Know I Have Seasonal Allergies. Should I See A Doctor Or Can I Leave It Untreated?
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5eff3d1f6f98e57329caed0ceb9053d3
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7,616,284,421,837,918,000
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Skip to Content
UW Health SMPH
American Family Children's Hospital
SHARE TEXT
diclofenac transdermal
Pronunciation: dye KLOE fen ak
Brand: Flector Patch
What is the most important information I should know about diclofenac transdermal?
Multum donot
Do not use this medication if you have ever had asthma or a severe allergic reaction caused by aspirin, diclofenac (Cataflam, Voltaren), or another non-steroidal anti-inflammatory drug (NSAID). Do not use diclofenac just before or after having heart bypass surgery (also called coronary artery bypass graft, or CABG).
Before using this medication, tell your doctor if you are allergic to any drugs, or if you have heart disease, congestive heart failure, high blood pressure, a history of heart attack or stroke, a history of stomach ulcer or bleeding, liver or kidney disease, a blood clotting disorder, asthma or polyps in your nose, or if you smoke.
While the risk of absorbing diclofenac transdermal into your bloodstream is low, an NSAID may cause life-threatening heart or circulation problems such as heart attack or stroke, especially if you use it long term.
Multum emt
Get emergency medical help if you have chest pain, weakness, shortness of breath, slurred speech, or problems with vision or balance.
This medicine may also cause serious effects on the stomach or intestines, including bleeding or perforation (forming of a hole). These conditions can be fatal and can occur without warning while you are using diclofenac transdermal, especially in older adults.
Multum emt
Call your doctor at once if you have symptoms of stomach bleeding such as black, bloody, or tarry stools, or coughing up blood or vomit that looks like coffee grounds.
What is diclofenac transdermal?
Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID). It works by reducing hormones that cause inflammation and pain in the body.
Diclofenac transdermal skin patch is used to treat pain caused by minor sprains, strains, or bruising.
Diclofenac transdermal may also be used for other purposes not listed in this medication guide.
What should I discuss with my healthcare provider before using diclofenac transdermal?
While the risk of absorbing diclofenac transdermal into your bloodstream is low, an NSAID can cause life-threatening heart or circulation problems such as heart attack or stroke, especially if you use it long term.
This medicine may also cause serious effects on the stomach or intestines, including bleeding or perforation (forming of a hole). These conditions can be fatal and can occur without warning while you are using diclofenac transdermal, especially in older adults.
Multum donot
Do not use this medication if you have ever had asthma or a severe allergic reaction caused by aspirin, diclofenac (Cataflam, Voltaren), or another NSAID. Do not use diclofenac just before or after having heart bypass surgery (also called coronary artery bypass graft, or CABG).
If you have any of these other conditions, you may need a dose adjustment or special tests to safely use this medicine:
• a history of drug allergies;
• a history of heart attack, stroke, or blood clot;
• heart disease, congestive heart failure, high blood pressure;
• a history of stomach ulcer or bleeding;
• liver or kidney disease;
• a bleeding or blood clotting disorder;
• asthma;
• polyps in your nose; or
• if you smoke.
Multum nopreg
FDA pregnancy category C. Tell your doctor if you are pregnant or plan to become pregnant during treatment. Using diclofenac during the last 3 months of pregnancy may harm the unborn baby. Do not use this medication during pregnancy unless your doctor has told you to.
Multum nobrfeed
It is not known whether diclofenac transdermal passes into breast milk or if it could harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.
How should I use diclofenac transdermal?
Use exactly as prescribed by your doctor. Do not use in larger or smaller amounts or for longer than recommended. Using extra skin patches will not make the medication more effective. Follow the directions on your prescription label.
Apply the skin patch directly to the area of pain. The skin patch can be worn for up to 12 hours and then removed. Apply a new patch at that time if pain continues. Do not wear a skin patch while taking a bath or shower or while swimming.
Multum donot
Do not apply diclofenac transdermal on an open skin wound, or on areas of eczema, infection, skin rash, or burn injury.
Multum icon27
Wash your hands after applying or removing a skin patch.
If the patch falls off, try sticking it back on, or use medical tape to hold it on.
Multum external
After removing a skin patch fold it in half, sticky side in, and throw it away in a place where children or pets cannot get to it. Keep both used and unused skin patches out of the reach of children or pets.
If you use this medication long-term, your blood may need to be tested often. Your blood pressure may also need to be checked. Visit your doctor regularly.
Multum emt
The diclofenac transdermal patch may burn your skin if you wear the patch during an MRI (magnetic resonance imaging). Remove the patch before undergoing such a test.
Multum rt
Store at room temperature away from moisture and heat. Do not take a skin patch out of the patch envelope until you are ready to use it. Reseal the envelope for storage.
What happens if I miss a dose?
Apply a skin patch as soon as you remember, and wear it for 12 hours before applying a new one. Do not use extra patches to make up the missed dose. Do not wear a diclofenac skin patch for longer than 12 hours.
What happens if I overdose?
Multum emt
Seek emergency medical attention or call the Poison Help line at 1-800-222-1222.
What should I avoid while using diclofenac transdermal?
Multum noalcohol
Avoid drinking alcohol. It may increase your risk of stomach bleeding.
Avoid taking aspirin, oral (pill form) diclofenac (Cataflam, Voltaren), or other NSAIDs without your doctor's advice. This includes ibuprofen (Advil, Motrin), naproxen (Aleve, Naprosyn), indomethacin, piroxicam (Feldene), nabumetone (Relafen), etodolac (Lodine), and others.
Multum donot
Ask a doctor or pharmacist before using any over-the-counter cold, allergy, or pain medicine. Many combination medicines contain aspirin or other medicines similar to diclofenac (such as ibuprofen, ketoprofen, or naproxen). Taking certain products together can cause you to get too much of this type of medication. Check the label to see if a medicine contains aspirin, ibuprofen, ketoprofen, or naproxen.
Multum avoideyes
Avoid getting this medication near your eyes. If this does happen, rinse with water and call your doctor if you have eye irritation that lasts longer than 1 hour.
What are the possible side effects of diclofenac transdermal?
Multum emt
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.
Although the risk of serious side effects is low when diclofenac is applied to the skin, you should be aware of side effects that can occur if the medication is absorbed into your bloodstream.
Multum donot
Stop using this medicine and call your doctor at once if you have a serious side effect such as:
• chest pain, slurred speech, problems with vision or balance, and feeling weak or short of breath;
• bloody or tarry stools, coughing up blood or vomit that looks like coffee grounds;
• fever, chills, body aches, flu symptoms;
• pale or yellowed skin, dark colored urine, confusion;
• swelling or rapid weight gain;
• urinating less than usual or not at all;
• nausea, upper stomach pain, itching, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes);
• skin rash, bruising, severe tingling, numbness, pain, muscle weakness;
• fever, sore throat, and headache with a severe blistering, peeling, and red skin rash; or
• the first sign of any skin rash, no matter how mild.
Less serious side effects may include:
• mild nausea, vomiting;
• diarrhea, constipation;
• upset stomach, heartburn, gas;
• dizziness; or
• mild itching, burning, redness, or other skin irritation where the patch was worn.
This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
What other drugs will affect diclofenac transdermal?
Tell your doctor about all other medicines you use, especially:
• a blood thinner such as warfarin (Coumadin);
• cyclosporine (Gengraf, Neoral, Sandimmune);
• lithium (Eskalith, Lithobid);
• methotrexate (Rheumatrex, Trexall);
• a diuretic (water pill);
• steroids (prednisone and others); or
• heart or blood pressure medication such as benazepril (Lotensin), enalapril (Vasotec), lisinopril (Prinivil, Zestril), quinapril (Accupril), ramipril (Altace), and others.
It is not likely that other drugs you take orally or inject will have an effect on topically applied diclofenac. But many drugs can interact with each other. Tell your doctor about all medications you use. This includes prescription, over-the-counter, vitamin, and herbal products. Do not start a new medication without telling your doctor.
Where can I get more information?
Your pharmacist can provide more information about diclofenac transdermal.
Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.
Every effort has been made to ensure that the information provided by Cerner Multum, Inc. ('Multum') is accurate, up-to-date, and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. Multum information has been compiled for use by healthcare practitioners and consumers in the United States and therefore Multum does not warrant that uses outside of the United States are appropriate, unless specifically indicated otherwise. Multum's drug information does not endorse drugs, diagnose patients or recommend therapy. Multum's drug information is an informational resource designed to assist licensed healthcare practitioners in caring for their patients and/or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. The absence of a warning for a given drug or drug combination in no way should be construed to indicate that the drug or drug combination is safe, effective or appropriate for any given patient. Multum does not assume any responsibility for any aspect of healthcare administered with the aid of information Multum provides. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions about the drugs you are taking, check with your doctor, nurse or pharmacist.
Copyright 1996-2013 Cerner Multum, Inc. Version: 3.01. Revision date: 2/17/2011.
Your use of the content provided in this service indicates that you have read, understood and agree to the End-User License Agreement, which can be accessed by clicking on this link.
This information does not replace the advice of a doctor. Healthwise, Incorporated disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use. How this information was developed to help you make better health decisions.
Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated.
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Table 5
Quotes relating to knowledge and understanding
Lay understanding and explanation – "And I don't know what the cause of them is and was, I mean, I speculated and thought, could it be this and could it be that... I've been taking HRT and whether it coincided with that... prior to recently I suppose I had considered that they were caused by stress... Stress is a major thing with me, sort of getting very anxious and tense... Hormones was one of the things that I kept tossing about, they weren't migraines... I thought maybe it's diet, some of the things that I'm eating that could be triggering these things." (Patient 2107, Female, 52)
Lay understanding and explanation – "... I know my first... migraine that I ever had... was on the first day at first year at school... So whether it was because it was a stressful situation, or whether it was because I was starting to develop at that age, I don't know." (Patient 9423, Female, 40)
Seeking of information – "It might be the library if I'm on a particular quest for something... Or I might buy a magazine or, you know, any of the journals, nursing things... " (Patient 2466, Female, 53)
Seeking of information – "I'd like to know why. You know, I've heard different reasons for it but I haven't heard a proper reason for it. You know, why that, why that causes your headache. It would be nice to know." (Patient 552, Male, 38)
Worry – "Well, my friend, well, I suppose it was this chair he sat in and took a brain haemorrhage. My nephew had a brain haemorrhage...and I'm just frightened there's something going on." (Patient 4211, Female, 56)
Leiper et al. BMC Family Practice 2006 7:27 doi:10.1186/1471-2296-7-27
Open Data
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how to stop smoking
Cure For Baldness
Official Website
How To Stop Smoking For Hair And Health
Smoking does not only damage the health of the body, but also can damage the health of the hair. And the reason is because in the cigarettes contain chemicals that can damage the hair. Therefore if we want to be healthy try to figure out how to stop smoking.
Smoking may be enjoyable for those who are already addicted. But it would be so painful for others who do not like smoke, because they have to inhale cigarette smoke, which result from the activity of smoking. Have we thought that those who do not like smoke, was forced to inhale cigarette smoke? Do not we feel sorry for them?
Just look at those who have a healthy body, because they are diligent exercise and of course free from cigarettes. Do we not want to like them? Indeed when we smoke, consciously or not, we are actually damaging our own bodies. But the majority of smokers ignore this. In fact, smokers know the harmful effects caused by smoking. However because they are addicted, they will continue to smoke even though they know the risks. Below are some tips for you about how to stop smoking for hair and health.
Here how to stop smoking for hair and health
Strong intention
Intend within you that from now on you will stop smoking. Reinforce your intention that you will not be tempted, even though you see people smoking in front of you. Keep in your mind, that the person who is smoking is the one who is destroying his own body and remember that there are so much dangerous chemicals inside of cigarette that will destroy your health and even its will interfere your hair growth, so your hair will becomes dull, brittle, branches, hair loss, even can lead to baldness at young age. Keep in your mind that without smoking is much better.
Confident
You should be confident that you will stop smoking, and no one will be able interfere with your intention to quit smoking. And keep in your mind that cigarette is the health and hair growth destroyer, so there is no reason that can force you to keep smoking.
Positive hobbies
Make it an activity or hobby that can fill our spare time with something useful and possibly could be something great. For example, learn a musical instrument, sports, painting, etc. Or maybe you could create a tool or something that can be beneficial for everyone. Fill your activities with positive things and eat foods that are healthy and beneficial for the body and for your hair.
Consistent
If you've been able to stop smoking, keep in your mind that we will not be tempted again to smoke. Grow our confidence that no one can shake our intention to stop smoking. And you must remember besides damaging your health, smoking kills your hair growth as well.
Those are some tips about how to stop smoking, may be useful for us. Stop smoking immediately, so that every part of our body including our hair, being healthy and strong. And the main thing is at least you can reduce the causes of disease in your body and you can live your life with a healthier, so hopefully you can enjoy your life much better.
Visit: www.CureYourBaldnessToday.com
baldness motto
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Febrile Seizure Treatment Options for Children
Febrile Seizure Treatment Options for Children
Febrile seizures are the most common type of seizures seen in children, 2-5% of children have a febrile seizure during their childhood. (Christopher, Westermeyer, 2017). Standard western treatment includes fever reducing drugs, antibiotics and anti-epileptic drugs but...
Nutrition and Eastern Medicine Theory
Nutrition and Eastern Medicine Theory
Nutrition Eastern Medicine theory suggests that diet has a direct and profound influence on the health and well being of an individual. The principles were developed over 2000 years ago and are still relevant to today’s patient. When the digestive system is not...
Easing Anxiety and Depression with Eastern Medicine
Easing Anxiety and Depression with Eastern Medicine
Anxiety As described by the Mayo Clinic: Experiencing occasional anxiety is a normal part of life. However, people with anxiety disorders frequently have intense, excessive and persistent worry and fear about everyday situations. Often, anxiety disorders involve...
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Designed to provide the optimum absorption of CBD into the blood stream by employing a patented slow release delivery system. It’s well accepted that CBD is most effective when taken sublingualy, however most oils when taken in this way are swallowed and broken down by your body. The Gel-Tab™. is placed under the tongue and the CBD is slowly absorbed resulting in higher rates of CBD being absorbed than what would be achieved with a normal oil
I found your article to be very informative. My son has refractory Epilepsy and Type 1 Diabetes. I am very interested in CBD but I am concerned about how it will interact with the 3 AED’s he is currently taking as well as how it will affect his blood glucose levels as he is on an insulin pump. Do you know of anyone with a similar combination of issues? How they have handled introducing CBD to their regime? And if they are seeing positive results?
CBD may help reduces REM behavior disorder in people with Parkinson’s disease. REM behavior disorder is a condition that causes people to act out physically during dreaming and REM sleep. Typically, during REM, the body is largely paralyzed, a state known as REM atonia. This immobilization keeps sleepers from reacting physically to their dreams. In REM behavior disorder, this paralysis doesn’t occur, leaving people free to move—which can lead to disruptive sleep and to injuring themselves or their sleeping partners. Cannabis may also work to reduce pain and improve sleep quality in people with Parkinson’s disease.
Despite, its low potency, the effects of this product were faster. In about an hour, my back pain was relieved considerably enough for me to work around and do daily chores. Remember though, this product did not, even with regular use, bring down my back pain to a level that was to my absolute liking. However, it did help me a lot with my sleep terrors and anxiety.
On the other hand, we have a depression. It is normal to be sad at some point. But, if you are feeling down longer than 2 weeks, this means that you suffer from depression, so you will need a treatment. There are a lot of different types of depression, but basically, all of them have the same symptoms and the same side effects. Depression makes you sad, unable to do things and makes you feel hopeless.
There’s also been a lot of talk lately about “microdosing” CBD. This refers to an incremental process of finding your minimum effective dose. You can do this with any concentration of CBD oil, but lower concentrations will take longer. In a 2017 article in Rolling Stone, Dr. Dustan Sulak outlines his protocol for microdosing. You can begin this process by asking yourself three questions:
Some manufacturers ship CBD products nationally, an illegal action which the FDA has not enforced in 2018, with CBD remaining as the subject of an FDA investigational new drug evaluation and is not considered legal as a dietary supplement or food ingredient as of November 2018.[70] CBD is openly sold in head shops and health food stores in some states where such sales have not been explicitly legalized.[71][72]
So am I to assume, due to no response/deleted comment that my simple question was too difficult to answer? With all the technical & correct information you have on you GREAT website, can someone (?) not simply correct or acknowledge the FACT the your NOT using nano-particle size product? I am truly interesting (for my wife) in CBD, have done my research, and I love working with numbers which is why if found this discrepancy. Comments welcome, but avoidance is disturbing.
I started using marijuana as a teen. The main reason that kept me using it was the fact that it made my stomach stop hurting. I thought I just had anxiety problems or an ulcer. I have no Idea It’s one of the reason that supress the pain I feel after I read this article from http://www.ilovegrowingmarijuana.com/cbd-in-medic…. Since reading is not my thing back then.
I suffer with migraines, fibromyalgia, and arthritis. I pretty much hurt anytime I move. I’m on a regimen of meds, but ordered the Virgin Cannibis Hemp Oil (off of Amazon) and have had it two days. I took 3 tablespoons a day, gagging it down. I couldn’t bring myself to take it today, but I didn’t notice a difference after the second day, and I suppose I would notice something. Was it too soon, or should I be trying a different product? I really need something to alleviate the level of pain during movement, as it’s causing me to be more sedentary.
Once again, there is no side effect on the overall health and all of this is more than just safe to know and to use. Keep in mind that hemp oil is more than just safe to use at all times and the sleep-related advantage is more than just noticeable. The combination of all the benefits hemp oil has on the human body will make you much stronger when it comes to depression and anxiety. Also, you will be able to defend yourself much better than other people from the same issues and you will be able to win the battle. BTW, check our best cbd oil for pain.
Sedatives, sometimes called tranquilizers, are exactly what they sound like. The purpose is to make the brain less excitable and to cause a sort of mild sedation. This approach, just as the other one, does help a lot of people. The problem with this type of drug, though, is that they usually cause a good bit of drowsiness, and in extreme cases can lead to dependency.
All this talk about THC lands us nicely in the whole “Full Spectrum vs. Pure Isolate” debate. Once you begin shopping for CBD products, you’ll notice a lot of jargon that gets thrown around without much explanation. Now that we’ve introduced THC into the conversation, we can talk about the difference between, and relative benefits of, Full Spectrum CBD and CBD Isolate (and the lesser-known contender: Broad Spectrum).
For example, CBD can increase CB1 receptor density so that there’s just too many CB1 receptors for THC to bind to, thus taking the edge off the potential psychoactivity of weed, while still retaining all the opioid-like painkilling effects. In case you are concerned about this meaning you have to buy more weed or take more hits if you’re using CBD oil, you should also know that CBD can extend the duration of the effects of THC by inhibiting the cytochrome P-450 enzymes that would cause you to more rapidly metabolize THC.
For the past couple of years, the field has been experiencing a boom in cannabidiol-related research. What has permeated the scientific consensus stems from efforts undertaken to explain effects of THC, with descriptions of cannabidiol just a by-product of the initial purpose. For example, CBD was thought to have been simply a precursor of THC, mainly due to the structural similarities between the two.
I wanted to know something about your part in the absorption of CBD. You talked about how CBD is non water-soluble and the best way to get the full effect is to either take a large amount OR vaporize it which you considered to be annoying or unnecessary. I on the other hand have no quarrels with doing this as I am an occasional smoker. Since you didn’t elaborate much on vaporizing, does this imply that it is still an adequate route to getting a better effect of CBD?
Instead, CBD acts as an agonist on an entirely different receptor called the 5-HT1A receptor, and this is how CBD actually works as an antidepressant with anti-anxiety and neuroprotective effects. It also serves as what is called an “allosteric modulator” of your opioid receptors, which is how it works to remove pain and reduce the effects of chronic inflammation. Other positive medical effects of CBD (there’s over 60 of them, if you care to read up on them here) are due to increased intracellular calcium release and agonism of another receptor called the PPAR-γ receptor.
This product is not for use by or sale to persons under the age of 18. This product should be used only as directed on the label. It should not be used if you are pregnant or nursing. Consult with a physician before use if you have a serious medical condition or use prescription medications. A Doctor's advice should be sought before using this and any supplemental dietary product. All trademarks and copyrights are property of their respective owners and are not affiliated with nor do they endorse this product. These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure or prevent any disease. By using this site, you agree to follow the Privacy Policy and all Terms & Conditions printed on this site. United States Holds This Patent On CBD
Holland & Barrett was one of the first retailers on the British high street to stock cannabis oil, however LloydsPharmacy now also stocks it. They have chosen to stock Celtic Wind Crops due to the fact that the company grows the hemp and manufactures the product themselves (so it's completely traceable) as well as the fact that their CBD products contain all the other added natural compounds within the hemp plant, which may yield added health benefits for users.
58. Rock EM, Bolognini D, Limebeer CL, et al. Cannabidiol, a non-psychotropic component of cannabis, attenuates vomiting and nausea-like behaviour via indirect agonism of 5-HT(1A) somatodendritic autoreceptors in the dorsal raphe nucleus. Br J Pharmacol. 2012;165:2620–2634. doi: 10.1111/j.1476-5381.2011.01621.x. [PMC free article] [PubMed] [CrossRef]
Reflecting the next morning, I was most surprised by the fact that I never felt "high" in any way—there was never a moment of It's kicking in; I can feel it now like with pain medications or even anti-anxiety drugs. Considering it takes time, consistency, and the right dosage to experience the full effect, I continued taking the oil once a day for the next six days. Here's what went down.
Our bodies are thought to produce endocannabinoids by the billions every day. “We always thought the ‘runner’s high’ was due to the release of dopamine and endorphins. But now we know the euphoria is also from an endocannabinoid called anandamide,” its name derived from the Sanskrit word for bliss, says Joseph Maroon, M.D., clinical professor and vice chairman of neurosurgery at the University of Pittsburgh Medical Center. We produce these natural chemicals all day, but they fade quickly because enzymes pop up to destroy them. That’s where CBD comes in: By blocking these enzymes, CBD allows the beneficial compounds to linger. This is why Amanda Oliver, 31, a career consultant in Charleston, SC, pops a CBD gummy bear each night before bed. “I used to lie there tossing and turning as my mind raced from work projects to whether I had set the home alarm,” Oliver says. One piece of candy with 15 mg of CBD is enough to shut off her brain and facilitate sleep. She also swears by the CBD oil she takes at the height of her period, which she says quells her debilitating cramps.
Green Roads World isn’t your standard cut-&-dry CBD reseller. They actually custom the oil to help treat your medical condition. Green Roads World employees a team of physicians, chemists and other health care professionals to provide affordable and reliable medications that are dosed to perfection for each patient. Green Roads has been voted on numerous Top 5 CBD lists due to their high quality products. They have truly done amazing things with their process of removing lipids and fats to create a 99% pure CBD crystal.
By eating healthy food and walking every day we both lost a needed 35 lbs. I never experienced the dreaded “munchies” that some get on this medicine.Smoking marijuana is reported to have an appetite stimulating effect. When I built up a tolerance to the THC, even though I was ingesting large amounts, I did not get an intense “high” like whatwould happen if a person were smoking it. For me, it produced a deep sense of well being.
I have sporadic back spasms for year I see a chiropractor monthly for maintenance (it help) and deal with daily Knee & hip joint pain due to my job (heavy mechanic/steel work with lots of walking). after reading all the great reviews on CBD oil I want to get off the daily ibuprofen regiment and try CBD oil. I would like to try it as a gel cap but would like some advise on dosage size. I also want to know how often I should take the CBD treatments. any and all advise is appreciated
The anxiolytic effect of THC is well documented, with other cannabinoids (especially CBD) also providing relief (if less potent). The exact pathways of the process have not been identified. A preliminary study published in 2013 in the International Neuropsychopharmacology Journal has set the foundations for further research linking CBD to future treatments for depression and psychosis.[25]
Now don’t get me wrong – some will indeed claim that cannabis is addictive. For example, the Boggs Act of 1951 established mandatory sentences for drug users and also claimed that cannabis was addictive. But since then, testimony given by Dr. Harris Isbell, Director of Research at the Public Health Service hospital in Lexington, Kentucky exposed this as false, explaining how cannabidiols from marijuana are not physically addictive.
Hi Colleen, it's almost a year later and I'm wondering how you're doing. I'm experiencing a recurrence of Stage 3 ovarian, originally diagnosed in 2011. I've decided to get some chemo, not sold on another 6 cycles though. As a new MMJ patient, I'm still going to go through with Rick Simpson Oil (THC+CBD,) and I just joined a program with my local dispensary to get CBD capsules for $2 each when I order them at least 30 at a time. I hope you're doing well!! I'm off to do more research on dosing. **NOTE: If you have ANY experience with CBD treatment of ovarian cancer, PLEASE respond. Thank you!!
It’s also important to select CBD oil products based on your concentration preferences. Some forms of CBD oil – such as vapors and tinctures – normally have higher-than-average concentrations, whereas sprays and topicals tend to have lower concentrations. Remember: higher concentration means more pronounced effects, but not necessarily mean higher quality.
It’s also nearly impossible to overdose on CBD. Kind of like water, dark chocolate, and steamed kale, it has an unusually low level of toxicity. In the last 6,000 years, CBD hasn’t killed anyone via overdose, which is particularly impressive when you compare it to non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, Advil and Tylenol, which can wreak havoc on your gut lining, liver and kidneys. Or aspirin (salicylic acid) which kills over 1,000 people every year. Or alcohol, which kills over 110,000 people a year. No one’s ever died from CBD.
In fact, numerous studies have looked at the relationship between CBD and pain, and the results are promising. Researchers have looked at various kinds of pain – from joint pain to cancer pain. One finding is that CBD increases levels of glutamate and serotonin – both neurotransmitters that play a role in pain regulation. And CBD’s anti-inflammatory properties help by tackling the root cause of much chronic pain.
Anxiety Disorder Association of America (ADAA) conducts research every year to find out the statistics increase or decrease. The studies conducted over a period of 10 years have revealed that 54 percent of the women while 46 percent of the men suffer from the anxiety disorders. But some studies also believe that the numbers of men who suffer from the anxiety issues are much higher than that of the women. It is just that they do not report their problem to the doctors or do not seek out for help until something significant problem occurs.
“The brain has these receptors that respond to endocannabinoids, which are neurotransmitters that are naturally produced in the body and brain,” says Jerald Simmons, a neurologist at Houston’s Comprehensive Sleep Medicine Associates. “Some of the cannabinoids in the marijuana plant are very similar to the endocannabinoids in the brain, and they act on the same receptors.”
Thanks for your interest in our products. Unfortunately due to strict FDA regulations I am unable to make claims on our products based on your specific needs, I can however share our top selling products in each category. Please view the links below:http://cbdoilreview.org/product/elixinol-cbd-oil-extract-x-pen-1000mg/http://cbdoilreview.org/product/endoca-hemp-oil-drops-1500mg/http://cbdoilreview.org/product/elixinol-hemp-oil-drops-regular-300mg/http://cbdoilreview.org/product/elixinol-cbd-hemp-oil-capsules-900mg/https://cbdoilreview.org/product/vape-bright-starter-pack-200-mg/This is also a great link to some pages that you may find helpful https://cbdoilreview.org/cbd-cannabidiol/I hope this helps and if you have any further questions please feel free to reach out to us at [email protected]
I have chronic pain, severe recurring depression, no energy, no motivation, just really just tired of pain and tired of being tired… I have tried medical weed for severe pain, it worked, it also gave me energy. But have smoked street weed ND I get paranoid. Dont want that, yes I have sleeping problems. Just tired of all the damn pills, that I know I will pay for later. I broke my back 5yrs ago caught mrsa, I just want to feel better. Is there any help? I’m about to give up. Ty
In addition to fighting inflammation in the body, CBD oil may reduce anxiety by directly affecting the brain. Studies have found that CBD actually lowers activity in the amygdala and increases prefrontal cortex activation, two parts of the brain involved in anxiety. There is also evidence that CBD is able to activate hippocampus neurogenesis, aka regenerate new neurons! This activates CB1 receptors, which has a positive balancing impact on GABA and glutamate levels, associated with reducing anxiety.
Zuardi, A. W., Crippa, J. A., Hallak, J. E., Bhattacharyya, S., Atakan, Z., Martin-Santos, R., … & Guimarães, F. S. (2012). A critical review of the antipsychotic effects of cannabidiol: 30 years of a translational investigation [Abstract]. Current Pharmaceutical Design, 18(32), 5,131–5,140. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22716160
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By Dr. Peter Kadile
I have discussed and educated about the importance of regular hand washing in the prevention of getting sick or spreading disease.
Hey Doc, my wife is insistent that we take the bedspread or comforter off the bed when we stay at a hotel because it is dirty and rarely washed. Even when we stay at a five star hotel? James, Rancho Mirage
James, it may be easy to forget about preventive hygiene when staying at a hotel, especially a more expensive five star hotel, but a recent study conducted by the online trip calculator service, Travelmath, found that three star hotels were cleaner than five star hotels. The dirtiest surfaces in the hotels were found to be on the bathroom counter, remote control, desk and phone. It’s unclear why the five star hotels harbored more bacteria on the surfaces studied, but just because you pay more for a more luxurious hotel doesn’t necessarily mean it is cleaner. As far as the bedspread is concerned, it rarely gets thrown in the daily wash with the bedsheets. A good routine to perform every time you stay at a hotel would be to immediately remove the bedspread and put it in the closet. Wipe down the bathroom counter, desk, phone and remote control with antibacterial wipes or spray. Since the remote is the most commonly handled item in the hotel room, consider placing it in a clear plastic bag before you use it.
Dear Dr. Kadile, I work in the fitness industry as a personal trainer. I frequently work at several different gyms with different clients in one day. Is using hand sanitizer between gyms and clients as good as washing my hands? – Lyn, La Quinta
Lyn, gyms and fitness equipment are notoriously full of nasty germs, since not everybody uses a towel or wipes down the equipment after using it.
Hand sanitizers are generally made up of alcohol, glycerin, water and maybe some fragrance added. The alcohol is the main germ fighter. A good hand sanitizer should have an alcohol concentration of at least 60 percent. Hand sanitizer is beneficial if hand washing is unavailable, but it is not as good. Using a hand sanitizer is good in addition to hand washing. Really, the best way to clean your hands is with soap and water. Washing gets rid of most germs and breaks up oils and removes dirt, which can hide bacteria and germs. Hand sanitizer simply works on the surface of the skin, whereas hand washing will get the water and soap into the small cracks and crevices of the skin. You’ve got the right idea in cleansing your hands between clients, but hand washing is better than hand sanitizer.
A common carrier of germs that we rarely think about is our cell phone. Have you ever used your cell phone in the restroom? Have you ever seen somebody using their cell phone in the restroom? Have you heard a person talking on the cell phone while they used the bathroom, then set their cell phone on the bath room counter, wash their hands, then pick it up again? Disgusting when you think about it.
Whatever our hands touch, our cell phones touch. Cell phones have been found to have 18 times more harmful bacteria than a public restroom. Our phones get warm from the battery and we also tend to store them in warm, dark places such as purses and pockets. The warmth or heat can make them good breeding grounds for bacteria. So if you are diligent about washing your hands, don’t forget about your cell phone! Rubbing alcohol and cotton swabs can be used to clean your phone and there are also cleaning products specifically available for use on cell phones.
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halofantrine-oral Related Diseases & Conditions
Medications are used to manage a variety of conditions. Our doctors have compiled a list of ailments that the medication halofantrine-oral may be used to treat or manage.
• Malaria Malaria is an infectious disease transmitted by the bite of an infected Anopheles mosquito. Symptoms of malaria include chills,...learn more »
In This Article
Malaria Article
• Malaria facts
• What is malaria?
• What are malaria symptoms and signs?
• How is malaria transmitted?
• Where is malaria a particular problem?
• What is the incubation period for malaria?
• How is malaria diagnosed?
• What is the treatment for malaria?
• Is malaria a particular problem during pregnancy?
• Is malaria a particular problem for children?
• Is it possible to prevent malaria?
• What is the prognosis (outcome) for people with malaria?
• Is there a vaccine for malaria?
• Where can people get more information about malaria?
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Open Access Highly Accessed Open Badges Research article
Identification of tyrosine-phosphorylated proteins associated with metastasis and functional analysis of FER in human hepatocellular carcinoma cells
Haiyu Li12, Zhenggang Ren1*, Xiaonan Kang2, Lan Zhang1, Xuefei Li12, Yan Wang1, Tongchun Xue1, Yuefang Shen1 and Yinkun Liu12*
Author Affiliations
1 Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, PR China
2 Institute of Biomedical Sciences, Fudan University, Shanghai 200032, PR China
For all author emails, please log on.
BMC Cancer 2009, 9:366 doi:10.1186/1471-2407-9-366
The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2407/9/366
Received:2 March 2009
Accepted:16 October 2009
Published:16 October 2009
© 2009 Li et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background-
Aberrant activity of tyrosine-phosphorylated proteins is commonly associated with HCC metastasis. Cell signaling events driven by these proteins are implicated in numerous processes that alter cancer cell behavior. Exploring the activities and signaling pathways of these proteins in HCC metastasis may help in identifying new candidate molecules for HCC-targeted therapy.
Methods-
Hep3B (a nonmetastatic HCC cell line) and MHCC97H (a highly metastatic HCC cell line) were used in this study, and the tyrosine-phosphorylated proteins expressed in these cell lines were profiled by a phosphoproteomics technique based on LC-MS/MS. Protein-protein interaction and functional clustering analyses were performed to determine the activities of the identified proteins and the signaling pathways closely related to HCC metastasis.
Results-
In both cell lines, a total of 247 phosphotyrosine (pTyr) proteins containing 281 pTyr sites were identified without any stimulation. The involvement of almost 30% of these in liver or liver cancer has not been reported previously. Biological process clustering analysis indicated that pTyr proteins involved in cell motility, migration, protein autophosphorylation, cell-cell communication, and antiapoptosis functions were overexpressed during metastasis. Pathway clustering analysis revealed that signaling pathways such as those involved in EGFR signaling, cytokine- and chemokine-mediated signal transduction, and the PI3K and JAK-STAT cascades were significantly activated during HCC metastasis. Moreover, noncanonical regulation of the JNK cascade might also provide new targets for HCC metastasis. After comparing the pTyr proteins that were differentially expressed during HCC cell metastasis, we selected FER, a nonreceptor tyrosine kinase, and validated its role in terms of both expression and function. The data confirmed that FER might play a critical role in the invasion and metastasis of HCC.
Conclusion-
The identification of pTyr proteins and signaling pathways associated with HCC metastasis could provide useful information for selecting new molecular intervention targets. Moreover, FER might serve as a novel drug target in future HCC therapy.
Background
Hepatocellular carcinoma (HCC) is one of the most malignant solid tumors and ranks fourth in terms of mortality and fifth in terms of morbidity among various human cancers worldwide [1]. The short-term prognosis of this condition has dramatically improved due to early diagnosis and surgical resection, transplantation, and local ablation therapy. However, long-term survival is still poor due to frequent intrahepatic metastasis and distant metastasis. Therefore, determining the mechanism of HCC metastasis is a major challenge and impeding the progression of this tumor at an early stage is essential for improving the prognosis of HCC.
Protein tyrosine phosphorylation is an important posttranslational modification that plays a critical role in signal transduction associated with cell proliferation, survival, apoptosis, mobility, adhesion, etc. Tyrosine-phosphorylated proteins (also known as phosphotyrosine proteins, pTyr) include a wide range of signal molecules, such as receptor tyrosine kinases, adapter proteins, and scaffold proteins, which are known to be involved in the cancer metastatic process [2-7]. Aberrant expression and activity of pTyr proteins in the cell signaling pathway have been reported in various human cancers [5,6,8-11]. In recent years, several kinase inhibitors have been introduced for molecular target therapy in clinical oncology. These act by interfering with the activity of specific signaling pathways [9,10,12]. Therefore, exploring and analyzing the expression profiles of pTyr proteins in HCC cells by a high-throughput method would be extremely useful for obtaining insights into the mechanisms of HCC metastasis and recurrence. Such studies would also help in identifying new drug targets for HCC therapy.
In the post-genome era, proteomics techniques based on LC-MS/MS enable us to study the complete range of signal proteins present in a set of cells or tissues under specific conditions [13-15]. In this study, pTyr proteins were identified, and a comparative study was performed between a nonmetastatic HCC cell line (Hep3B) and an HCC cell line with high metastatic potential (MHCC97H). Several biological processes and signaling pathways were found to be strongly correlated with HCC metastasis. Among the differentially expressed pTyr proteins, FER, a nonreceptor tyrosine kinase, appears to be an important protein involved in HCC metastasis.
Methods
Cell culture
The Hep3B cell line (nonmetastatic human HCC cells) was obtained from Cornell University, USA, and grown in MEM medium supplemented with 10% fetal bovine serum (PAA) in a 5.0% CO2 incubator at 37°C. The MHCC97H cell line (highly metastatic human HCC cells) was established in the Liver Cancer Institute, Zhongshan Hospital, Fudan University [16]. These cells were sustained in DMEM medium supplemented with 10% fetal bovine serum (PAA) in a 5.0% CO2 incubator at 37°C. The two cell lines have an integrated HBV DNA genome and exhibit positive alpha-fetoprotein (AFP) expression. These cell lines are commonly used as model cell lines in HCC studies [17-20].
Immunoprecipitation of pTyr proteins
Cells that had grown to approximately 90% confluency were subcultured. The subcultured cells were grown to approximately 80% confluency and starved in serum-free medium for 12 h to reduce the phosphorylation background resulting from the culture conditions. The cells were placed in a 10-cm dish, washed twice with chilled PBS, and lysed by incubation in 1 ml modified RIPA lysis buffer (150 mM NaCl, 50 mM Tris-HCl (pH 7.4), 1% NP-40, 0.25% sodium deoxycholate, and 1 mM EDTA supplemented with 1 mM sodium orthovanadate, 10 mM sodium fluoride, 10 mM glycerophosphate, and 5 mM sodium pyrophosphate) for 30 min on ice. The cell lysate was cleared by centrifugation at 15,000 rpm for 30 min at 4°C, and the protein concentration was determined by the DC Protein Assay kit (Bio-Rad).
Anti-pTyr specific immuoprecipitation was performed with two different anti-pTyr antibodies. The phosphotyrosine monoclonal antibody pTyr-100 (Cell Signaling Technology) and/or 4G10 (Upstate) was noncovalently conjugated to Protein A-agarose (Sigma) at a concentration of 1 mg/ml beads by overnight incubation at 4°C with gentle shaking. After coupling, the antibody resin was washed twice with PBS and then three times with modified RIPA buffer (5 bead volumes of buffer for each wash). To confirm that efficient coupling had been achieved, an aliquot of the antibody resin was boiled in SDS-PAGE sample buffer for 5 min, and the yield of the released antibody was determined by running it along side a purified antibody standard on SDS-PAGE. The gels were stained with Coomassie blue. The immobilized antibody (400 μl, 400 μg) was added in the form of a 1:1 slurry in modified RIPA buffer to 50 mg cell lysate (1 mg/ml) that had been precleared with 800 μl Protein A-agarose at 4°C for 6 h. The mixture was incubated overnight at 4°C with gentle shaking. The immunocomplex beads were then harvested by centrifugation at 3,000 rpm and 4°C for 5 min and washed three times with 10 bead volumes of modified RIPA buffer. Finally, pTyr-containing proteins were eluted three times with 500 μl of elution buffer (8 M urea, 50 mM NH4HCO3, and 20 mM ethylamine) for 5 min each at 96°C, and the eluates were combined.
Desalting and tryptic digestion of pTyr-containing proteins
The pTyr-containing proteins were reduced and alkylated by the ProteoPrep™ Reduction and Alkylation Kit (Sigma) according to the manufacturer's instructions. Briefly, the protein sample was reduced by incubation with 5 mM ributylphosphine (TBP) at room temperature for 30 min. The protein solution was then alkylated by adding 15 mM iodoacetamide and incubating in the dark for 1 h at room temperature. The excess iodoacetamide in the reaction mixture was quenched by additional incubation with 5 mM TBP for 15 min at room temperature. Subsequently, the protein mixture was desalted on a PD-10 desalting column, as recommended by the manufacturer (GE Healthcare), and the buffer was exchanged with a 50 mM NH4HCO3 solution. Trypsin (modified sequencing grade; Promega, Madison, WI) digestion was performed at a 1:50 trypsin-to-protein ratio (w/w) for 16 h at 37°C. The tryptic peptides were then dried in a Speed Vac.
Immobilized metal affinity chromatography (IMAC)
Phosphopeptides from trypic digestion were further enriched with the Magnetic Phosphopeptide Enrichment Kit (Clontech), according to the manufacturer's instructions but with a slight modification. First, the tryptic peptides were reconstituted in an appropriate volume of the binding/washing buffer and incubated with the washed and equilibrated beads for 30 min at room temperature by gentle shaking. The supernatant was then removed from the beads by a magnetic separator. The beads containing the phosphopeptides were washed three times with the wash buffer. Finally, the phosphopeptides were eluted three times using a total of 100 μl of elution buffer. The eluates were then filtered through an 0.22-μm filter and dried in a Speed Vac.
Nanoflow LC-MS/MS protein identification and database searches
The pTyr peptides enriched by IMAC were analyzed using an LTQ mass spectrometer (Thermo Electron Corp., San Jose, CA) equipped with a nanoelectrospray ion source. The m/z ratios of the peptides and their fragmented ions were recorded by the mass spectrometer. The peak lists for the MS2 and MS3 spectra were generated from the raw data by Bioworks version 3.3 (Thermo Electron) using the following parameters: the mass range was 600-3500, intensity threshold was 1000, and minimum ion count was 10. The generated peak lists were searched by the Sequent program (included in Bioworks) against the nonredundant human protein database of the human International Protein Index (IPI) (ipi.HUMAN.3.3.fasta). The MS/MS spectra were searched with a precursor ion mass tolerance of 2 Da and fragment ion mass tolerance of 1 Da. Full tryptic specificity was applied, two missed cleavages were allowed, and static modification was set for the alkylation of Cys with iodoacetamide (+57). To search the MS/MS data, dynamic modifications were set for oxidized Met (+16) and phosphorylated Ser, Thr, and Tyr (+80). Neutral losses of water and ammonia from the b and y ions were considered in the correlation analysis. To identify phosphopeptides on the basis of the MS/MS or MS/MS/MS spectra, the sequences must meet the following filter criteria: cross-correlation value (Xcorr) > 1.5, 2.0, and 2.5 for singly, doubly, and triply charged ions, respectively; uniqueness scores of matches (deltaCn) > 0.1; and peptide mass tolerance of 5 ppm.
Bioinformatics analysis of pTyr proteins
For functional annotation and protein-protein interaction (PPI) analysis, the identified pTyr proteins were submitted to the Human Protein Reference Database (HPRD). This database contains extensive information on human proteins, including domain architecture, protein functions, PPIs, posttranslational modifications (PTMs), enzyme-substrate relationships, subcellular localization, tissue expression, and disease association of genes [21-23]. This allows the identified pTyr proteins to be classified into subclasses based on their biological processes and molecular functions. The expression of these proteins was also evaluated under normal and liver cancer conditions using the records in the HPRD. Based on the PPI information available in the HPRD, a PPI network was generated using the Cytoscape version 2.6.1 software [24,25]. This is an open-source bioinformatics software platform for visualizing molecular interaction networks and biological pathways. It allows these networks to be integrated with annotations, gene expression profiles, and other state data. Cytoscape contains some web plug-ins for downloading/linking a network from/to several databases such as pathwayCommons, IntAct, and NCBI Entrez Gene. Moreover, this software contains several plug-ins that allow computational analyses and functional enrichment, such as clusterMaker, BubbleRouter, and BinGO. In this study, functional clustering and signaling pathway analyses of proteins were carried out by running the BinGO, pathwayCommons, and BubbleRouter programs in Cytoscape. BinGO is a tool for determining the Gene Ontology (GO) categories that are statistically overrepresented in a set of genes or a subgraph of a biological network [26]. It returns the correct p-value after using two different methods to account for multiple testing. In this study, the result was evaluated by the p-value from the Hypergeometric test, and the correct p-value was calculated using the Benjamini & Hochberg False Discovery Rate (FDR) correction.
RNAi and transfection
A 21-nt long double-stranded siRNA for FER was designed on the basis of reported data. It was derived from the human FER cDNA (accession no. J03358) 5'-AAA GAA ATT TAT GGC CCT GAG-3' (nt 84-104) [27] and was synthesized by Jikai Biotechnical Company (Shanghai, China). The selected siRNA sequences were submitted for a BLAST search against the human genome sequence to confirm the specificity of the siRNA. An unrelated silencing sequence was selected and synthesized as a negative control.
For siRNA transfection, 3 × 105 MHCC97H cells were seeded in a 6-well plate 1 day prior to transfection. Transfection was performed with the Lipofectamine 2000 Plus transfection agent (Invitrogen) according to the manufacturer's instructions. First, 200 pmol siRNA was diluted in 250 μl Opti-MEM (Gibco-Invitrogen) and mixed with 40 μl Plus transfection agent. This was left for 20 min at RT. Next, Lipofectamine 2000 was diluted in 250 μl Opti-MEM and left for 5 min at RT. The two solutions were then mixed and left at RT for 20 min. After aspirating the medium, the cells were washed twice with PBS and added to 1.5 ml of new Opti-MEM and transfection mixture. After transfection for 4-6 h, the medium was exchanged with the standard cell medium. The experiments with FER RNAi were initiated 48 h after transfection.
Cell invasion assay in vitro
The MHCC97H cell invasion assay was performed in a 24-well plate according to a previously described protocol but with slight modifications [28]. Briefly, 100 μl of Matrigel (1 mg/ml) was added to the upper chamber of a 24-well transwell plate, and the plate was incubated at 37°C for at least 4-5 h to induce gelling. The upper chamber that was coated with Matrigel was washed three times using warm serum-free medium, and 200 μl of cell suspension containing 1 × 105 cells was placed in the chamber. Simultaneously, the lower chamber of the transwell plate was filled with 600 μl of the cell supernatant from 3T3 cells supplemented with 10% FBS. After cell invasion for 30 h at 37°C, the noninvaded cells at the top of the transwell plate were scraped off with a cotton swab. All invaded cells were stained with the Giemsa staining solution and counted under a microscope. The mean value of three independent experiments was used for the t-test to calculate the statistical significance.
TMA construction and immunohistochemical staining
A tissue microarray (TMA) was assembled using 100 HCC cases, consisting of 50 cases each of HCC with or without metastasis studied over a follow-up period of 2~5 years. For each case, 2 core samples of hepatoma tissue were acquired from a donor paraffin block provided by the Pathology Diagnosis Department of Zhongshan Hospital. Serial tissue sections (4 μm thick) were cut from the TMAs for immunohistochemical analysis.
For immunohistochemical staining, the slides were deparaffinized in xylene and rehydrated through a graded series of ethanol concentrations. Intrinsic peroxidase was blocked by using 3% hydrogen peroxide for 15 min. A solution of 5% BSA in PBST (PBS + 0.125% Tween 20) was used to block nonspecific antibody binding, and anti-FER antibodies (Sigma-ATLAS) were used at the concentration recommended by the manufacturer. The slides were kept overnight at 4°C. After washing three times with PBST for 5 min, the slides were incubated with the secondary antibody for 30 min at room temperature. Following three additional washes in TBST, the slides were developed by DAB staining. The sections were scanned at low magnification. The immunostaining score was estimated on a scale of 0 to 3 based on the percentage and intensity of the stained tumor cells, using the criterion given on the ATLAS web http://www.proteinatlas.org webcite. Whether the stain was distributed on the membrane or in the cytoplasm was also recorded and assessed at high magnification. The immunoreactivity was scored semiquantitatively by counting the area and density of stained cells using the Image-Pro Plus 5.0 software. Manual correction was then performed to normalize the score. Statistical analysis was performed with the SPSS13.0 software using the nonparametric Mann-Whitney U test.
Results
pTyr protein capture and the expression profiles of Hep3B and MHCC97H cells
To optimize the enrichment of pTyr proteins, two different antibodies against pTyr proteins were tested for their ability to immunoprecipitate pTyr-containing proteins from the samples. The results showed that 4G10 and pTyr-100 had different protein immunoblotting profiles (Figure 1). The data illustrate the similarities and differences in the pTyr proteins recognized by both antibodies. They also support the use of multiple antibodies to improve the detection of pTyr proteins. In subsequent experiments, a combination of two antibodies was chosen, which was expected to increase the types and quantities of captured pTyr proteins. Figure 1 show that the pTyr proteins in the two cell lines differed in terms of distribution and quantities, suggesting that different pTyr proteins may be involved in HCC metastasis depending on their metastatic potentials.
thumbnailFigure 1. Comparison of pTyr proteins profile detected using pTyr-100 and 4G10 antibodies in two HCC cell lines with differently metastatic potential. Protein extracts from two HCC cell lines were separated by SDS-PAGE (20 ug protein per lane) and analyzed by Western blot with anti-pTyr antibodies, 4G10 and pTyr100.
Enrichment and identification of phosphopeptides
After anti-pTyr immunoprecipitation, tryptic digestion, and IMAC enrichment, the eluted phosphopeptides were analyzed by LC-MS/MS using an LTQ instrument as shown in Figure 2. As described in Materials and Methods, MS/MS spectra were used to search the human IPI 3.3 database with the SEQUENT (version 3.5) software to identify the amino acid sequence and phosphorylation sites. The MS/MS spectra of CAV1, STAT3, CTTN, and FER are shown in Figure 3. In total, 83 pTyr proteins containing 92 pTyr sites were identified in Hep3B cells. The expression of 39 of these has not been reported previously in liver or liver cancer tissues. Similarly, 164 pTyr proteins containing 189 pTyr sites were identified in MHCC97H cells, and the expression of 81 of these was recorded in liver or liver cancer tissues. Among the identified pTyr proteins, 72 pTyr proteins from Hep3B cells and 153 pTyr proteins from MHCC97H cells were differentially expressed. All of the identified pTyr proteins and sites in the two cell lines are listed in Table S1 - S3 in additional file 1. A few phosphoserine/threonine-containing peptides were recovered because their original protein was tyrosine phosphorylated.
Additional file 1. Supplemental Tables S1 -S3. Table S1: Common tyrosine phosphorylated proteins and sites from MHCC97H and Hep3B cell lines. Legend: The data in this table show the detailed information of the common tyrosine phosphorylated proteins and sites identified by LC-MS/MS in MHCC97H and Hep3B cell lines. Table S2: Tyrosine phosphorylated proteins and sites from MHCC97H cell line. Legend: The data in this table show the detailed information of the differentially expressed tyrosine phosphorylated proteins and sites identified by LC-MS/MS in MHCC97H cell line. Table S3: Tyrosine phosphorylated proteins and sites from Hep3B cell line. Legend: The data in this table show the detailed information of the differentially expressed tyrosine phosphorylated proteins and sites identified by LC-MS/MS in Hep3B cell line.
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thumbnailFigure 2. Scheme of enrichment and identification of pTyr proteins. Cells were firstly lysed in modified RIPA buffer. pTyr proteins and their interacting partners were then immunoprecipitated by anti-pTyr antibodies. Eluted proteins were further digested into peptides and used to IMAC for second phosphopeptides enrichment. The sample was lastly analyzed by LC-MS/MS.
thumbnailFigure 3. MS/MS spectra of the pTyr proteins, CAV1, STAT3, CTTN and FER.
Functional annotation of pTyr proteins
To understand the functions of the pTyr proteins identified in this study, these proteins were submitted to the HPRD database, functionally annotated based on the GO terms, and classified according to their molecular functions (outlined in Tables 1 & 2; for detailed information, see Table S4 in the additional file 2). A comparative study on the classification of pTyr proteins in these two cell lines revealed that the differential distribution in biological processes mainly involved protein, nucleic acid, and enzyme/energy metabolism. In terms of the functions at the molecular level, these proteins acted as translation regulators, enzymes, kinases/proteinases, calcium-binding proteins, cytoskeletal-associated proteins, and adhesion molecules. However, there were obvious differences between the Hep3B and MHCC97H cell lines.
Additional file 2. Supplemental Table S4. Table S4: Functional classification and distribution of tyrosine phosphorylated proteins from Hep3B and MHCC97H cell. Legend: The data provided display the detailed information in response to function and distribution of tyrosine phosphorylated proteins, which were identified by LC-MS/MS in MHCC97H and Hep3B cell lines.
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Table 1. Functional classification of identified pTyr proteins based on biological process in Hep3B and MHCC97H cell
Table 2. Functional classification of identified pTyr proteins based on molecule function in Hep3B and MHCC97H cell
Protein interaction analysis
A computer-deduced biological PPI network map can represent and indicate the interaction network that exists in a set of proteins. In this, the node molecules represent proteins, while the edges indicate the interactions between proteins. The PPI network can either create PPIs between proteins submitted from MS/MS identification data (root proteins) or it can predict new PPIs between the submitted protein and other proteins from previously published literature. At present, this is believed to be a promising strategy for extrapolating new functions and interactions of biomolecules. To analyze the functional implications of the protein cohorts identified in this study, pTyr proteins that were differentially expressed in Hep3B and MHCC97H cells were subjected to PPI analysis. The 72 proteins that were only expressed in the Hep3B cell line generated a network containing 235 nodes and 224 edges. Similarly, the 153 proteins that were only expressed in the MHCC97H cell line generated a network containing 542 nodes and 596 edges (Figure 4A, 4B upper box). To view the interactions between the root proteins in each network, two simple networks (the Hep3B and MHCC97H networks) that only contained root proteins and linker proteins (interactional proteins found in protein databases, and it bridges two other proteins in the PPI network) were elaborated (Figure 4).
thumbnailFigure 4. Simple PPI network for pTyr proteins (root proteins) identified by MS/MS spectrometry with their linker proteins in Hep3B and MHCC97H cell. Small box represents every complete PPI network for all nodes in two HCC cell lines. A: Hep3B-network B: MHCC97H-network. Pink ellipase node denoted linker proteins, blue and yellow ellipase node represented respectively root proteins in Hep3B and MHCC97H.
In the two simple networks, linker proteins, including CEBPB, EP300, MAPK1, MAPK3, MYC, PRKCB1, RPS6KA1, and SMARCA4, were shared. These were involved in some important signaling pathways such as the TNF-alpha-NF-kB signaling pathway, androgen-receptor signaling pathway, MAPK cascade, apoptosis pathways, Wnt-signaling pathways, cell cycle-G1 to S control, etc. These pathways play important roles in cell growth, differentiation, cell-cycle control, and apoptosis. The results suggested that the common pTyr proteins involved in these pathways may be associated with HCC pathogenesis.
Moreover, comparison of these two simple networks revealed that FER (a nonreceptor tyrosine kinase) was probably a protein of biological importance in HCC cell metastasis. It existed as only a dual function protein (root and linker-like protein) in these two simple networks. It linked four root proteins--CTNND1, CTTN, STAT3, and CAV1 (see highlighted diamond node and red edge in Figure 4B), in the MHCC97H network; however, it was absent in the Hep3B network. Interestingly, one each of these four proteins played a key role in cytoskeletal regulation, cell adhesion, signal regulation, and transportation. Thus, based on the results, it is reasonable to suppose that FER is an important pTyr protein and was therefore selected for sequential functional validation.
Functional clustering analysis
To fully predict the coherent function, all node proteins from the PPI networks of the MHCC97H and Hep3B cells were clustered according their GO attributes in biological process and signaling pathways.
Biological process clustering analysis showed that in relation to tumorigenesis and metastasis, identified pTyr proteins were abnormally overrepresented in the two PPI networks, especially in the MHCC97H cells (Figure 5). These were mainly involved in cell division, differentiation, development, proliferation, phosphorylation, cell communication, blood vessel morphogenesis, DNA metabolic processes, antiapoptosis functions, intracellular protein transport, cell migration, cell adhesion, and cellular localization. More importantly, biological processes related to cancer metastasis, including cell motility, migration, antiapoptosis functions, cell localization, and cell communication, differed significantly between the two HCC cell lines (p < 1.00E-05).
thumbnailFigure 5. Histogram of functional cluster analysis based on biological process for all nodes proteins from PPI networks of Hep3B and MHCC97H cell lines. The numbers of proteins assigned to every functional groups and the significance of the statistical difference are shown.
On the other hand, pathway cluster analysis suggested that there was considerable overall alteration in signal transduction during HCC cell metastasis (p = 8.23E-10 to p = 4.20E-25). The maximum difference between the two cell lines was observed in the transmembrane receptor tyrosine kinase signaling pathway, cell surface receptor-linked signal transduction pathway, and protein kinase cascade (Figure 6). In particular, the difference was prominent in the epidermal growth factor receptor (EGFR) signaling pathway, cytokine- and chemokine-mediated signaling pathway, and JAK-STAT and phosphoinoside 3-kinase (PI3K) cascades. It should be noted that the JNK cascade has a negative relationship with HCC metastasis in signaling pathway clustering (overrepresented in the Hep3B cell line rather than in the MHCC97H cell line). Surprisingly, the regulatory pattern of protein amino acid phosphorylation in the two cell lines was completely reversed. In MHCC97H cells, autophosphorylation was upregulated, while in Hep3B cells, dephosphorylation was upregulated (details of pathway clustering were outlined in Table S5a, S5b in the additional file 3).
Additional file 3. Supplemental Table S5. Table S5a: Pathway clustering for node proteins in PPI network of MHCC97H cell. Table S5b: Pathway clustering for node proteins in PPI network of Hep3B cell. Legend: The two tables summarize detailed information of pathway clustering results generated from BinGO program, which was run to explore the functional regulation of node proteins in PPI network of MHCC97H and Hep3B cell.
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thumbnailFigure 6. Pathway cluster analysis for all node proteins from networks of Hep3B (A) and MHCC97H (B) cell lines. Every ellipase node size represents the number of proteins assigned to each pathway; node color indicates correct p-value of each pathway from statistical test, orange denotes higher relative levels of overrepresented pathways with less p-value and yellow indicates lower levels of overrepresented pathways with bigger p-value, and white node denotes no change on a pathway.
Verification of the pTyr proteins
FER, CAV1, and CTNND1 were closely connected proteins in the MHCC97H network but were absent in the Hep3B network. These proteins were selected and tested for their expression in the two cell lines by using western blot assays. As shown in Figure 7, the total amount of these three proteins or the phosphorylated forms of these three proteins generally increased in the MHCC97H and Hep3B cell lines in response to their metastatic potential. This was consistent with the MS/MS results. These proteins were weakly expressed in Hep3B cells, and their amounts were below the detection limit of the MS assay.
thumbnailFigure 7. FER, CTNND1, CAV1 and their phosphorylated version expression in two HCC cell lines. First, equal protein lysates from two HCC cells lines were subjected to SDS-PAGE electrophoresis and subsequent Western blotting using anti-FER, CTNND1, CAV1 and actin antibodies (lower panel). Then in parallel experiment, equal protein lysates from two cell lines were immunoprecipitated using anti-pTyr 4G10 and pTyr100 antibodies, followed by reacting with FER, CTNND1 and CAV1 antibodies in Western blot assay (upper panel). This represents three independent experiments.
The functions of FER were further verified by cell invasion experiments. FER expression in MHCC97H cells was knocked-down by treatment with a specific siRNA. The results showed that the invasive ability of treated MHCC97H cells was significantly weaker than that of the control cells, and only a few cells could pass though the matrigel-coated filter (Figure 8). This indicated that FER played a role in cell invasion in vitro. TMA analysis was performed to determine the expression level of FER in HCC tissues. The TMA was constructed from a total of 100 HCC cases, consisting of 50 liver cancer tissues each from patients with and without distant lung metastasis after liver cancer exairesis. TMA analysis showed that tumor tissue cells with distant pulmonary metastasis had higher FER expression levels than those without distant metastasis (p < 0.001, Figure 9). This was similar to the expression pattern observed in the cell lines.
thumbnailFigure 8. Invasion activity reduction of MHCC97H cell by FER knockdown. A: Matrigel invasion assay of MHCC97H cell. Image was viewed at ×200 and migrated cells were stained with purple, representing three independent experiments. B: Western blot assay of FER expression after siRNA in MHCC97H cell, representing three independent experiments. In comparison analysis, data was shown as Mean ± SD and statistics significance was calculated from the Student's test among every groups. Two asterisk denotes p < 0.01.
thumbnailFigure 9. Expression of FER in HCC tissue. A: immunohistochemical staining of paraffin-embeded human HCC tissues showing different FER expression pattern in various samples (up panel is viewed at ×200 and low panel is viewed at ×50). B: comparison of FER staining in metastasis and non-metastatis HCC tissue (data was shown as the Mean ± SD).
Discussion
Bioinformatics analysis based on computer calculations and the application of biological software is a very effective and essential supplement in proteomics research. It is a powerful tool that has been extensively used for MS/MS data analysis, such as PPI studies, functional clustering, pathway mapping, and prediction of protein function and structure [11,28-34]. In this study, we examined the expression profiles of pTyr proteins in two HCC cell lines (MHCC97H and Hep3B) that have different metastatic potentials. For this purpose, we used an LC-MS/MS-based proteomics technique. We also compared and analyzed the interactions and functions of these proteins by PPI and functional clustering analyses based on their GO attributes that were determined by biological process clustering and signaling pathway analysis. The results revealed that some cell functions related to cancer metastasis were significantly upregulated in HCC metastasis, especially those involved in cell motility, migration, localization, communication, antiapoptosis processes, and protein autophosphorylation. These alterations have been partly reported in previous studies on cancer metastasis [35-38]. High motility and migration are prerequisites for the successful metastasis of tumor cells and their transfer to the target site, penetration into the basement membrane and blood vessels, and movement from poorly oxygenated sites to rich oxygenated sites [3,39]. Antiapoptosis is a pivotal mechanism by which cancer cells are protected from elimination by means of various steps of a metastatic process [40]. At present, there are large amounts of data that highlight the importance of this process in cancer metastasis (reviewed in [40-43]). Protein amino acid autophosphorylation is a specific attribute of tyrosine kinase, and its upregulation in the highly metastatic MHCC97H cells confirmed that alteration of tyrosine phosphorylation was in fact involved in HCC metastasis. Western blot analysis of the pTyr protein profile also confirmed these results. More importantly, we found that alteration in cell communication was the most obvious cellular event in HCC metastasis. Since cell communication driven by signal transduction controls all cell behavior and activity, aberrations in signal transduction could be a crucial factor leading to HCC metastasis and could also trigger changes in cancer cell behavior. Therefore, it is very important to explore the events that occur during the activation and regulation of the signaling pathway in HCC metastasis. For this purpose, a pathway clustering analysis was performed for the node proteins of the PPI networks in Hep3B and MHCC97H cell lines. The results revealed that EGFR signal transduction, cytokine- and chemokine-mediated signaling, and the PI3K and JAK-STAT cascades were closely related with HCC metastasis since these processes were significantly upregulated. These analytical results were similar to those obtained for liver metastasis of breast cancer [11,29]. EGFR is an Erb-family transmembrane receptor tyrosine kinase. This receptor is shared by multiple ligands, including EGF, TGF, EGFF-like factor, and amphiregulin [44]. EGFR-mediated signaling has been implicated in a variety of human cancers and is a key regulator of the cell proliferation, migration, metastasis, angiogenesis, and antiapoptosis processes [45,46]. Recently, some studies have reported that EGFR inhibitors are effective first-line therapeutic agents in the treatment of some metastatic cancers [47,48]. EGFR is a potential therapeutic target in HCC treatment [49,50]. The JAK-STAT cascade, which is another example, is a critical signaling pathway that plays an important role in cell proliferation, differentiation, survival, motility, and apoptosis [51]. Recently, it was reported that sustained activation of the JAK-STAT cascade was involved in hepatocarcinogenesis and metastasis [52,53]. The data showed that increasing activity of the JAK-STAT cascade was associated with aberrant methylation silencing of the suppressor of cytokine signaling (SOCS), which is a negative regulator of the JAK-STAT pathway [54]. However, another study also suggested that constitutive activation of STAT3 was closely related to HCC metastasis and was the main factor leading to the upregulation of the JAK-STAT cascade [55]. Consistent with these results, our MS/MS results also indicated STAT3 activation. Unexpectedly, the JNK cascade was found to be negatively associated with HCC metastasis, thereby deviating from its canonical functions. This indicates that the role of this cascade in HCC metastasis should be re-evaluated. Negative regulation of the JNK cascade was recently reported in prostate and ovarian cancers [56,57]. Researchers showed that JNKK1, an upstream kinase of JNK, could persistently phosphorylate JNK and activate the stress-activated protein kinase signaling pathway (SAPK) to induce cell apoptosis and decrease tumor metastasis. Moreover, the SAPK pathway also showed a negative correlation with HCC metastasis in this study. Therefore, these two pathways might play synergetic roles in HCC metastasis. In other words, cluster analysis of signaling pathways may provide some important information for predicting the functions of the pTyr proteins involved in HCC metastasis. These results have been obtained by bioinformatics studies and need to be verified experimentally prior to practical application.
In our study, FER, a nonreceptor tyrosine kinase, was shown to be significantly involved in the HCC metastatic process. FER was initially discovered in 1988 during studies on the proto-oncogene protein Fes/Fps [58]. Since then, its involvement has been reported in growth factors/cytokine-mediated signaling as well as in the integrin/E-cadherin-mediated signaling pathways. It also plays a critical role in cytoskeletal regulation, cell adhesion, migration, and proliferation [59-61]. In this study, we examined the total and phosphorylated forms of FER; these were found to be overexpressed in the MHCC97H cell line but not in the Hep3B cell line. Similar expression patterns were observed for CTNND1 and CAV1, which are related to FER, and the results were also validated by western blotting and MS/MS analyses. FER and CTNND1 were shown to be involved in cadherin and integrin-mediated cell adhesion. Under normal circumstances, FER could indirectly sustain CTNNB1 dephosphorylation to ensure cadherin-mediated adhesion stability. When FER is overexpressed and phosphorylated, it can directly induce CTNNB1 and CTNND1 phosphorylation, resulting in the loss of cadherin-mediated adhesion [61,62]. This suggests that increasing metastasis may be associated with CTNNB1 in some cancers. Moreover, CTNND1 had been implicated in the metastasis and pathogenesis of several human cancers [63]. It was shown that overexpression and phosphorylation of CTNND1 in the cytoplasm could promote cadherin-deficient tumor metastasis by regulating the activity of the small GTPase [64,65]. CAV1 is an important marker protein of caveolae and regulates signal transduction as a scaffolding protein. Recently, CAV1 was found to be an independent predictor of decreased survival in breast and rectal cancers and was significantly associated with the presence of distant metastasis in colon cancer patients [66]. CAV1 could also sustain cadherin-mediated adhesion stability. It functioned by modulating the level and/or subcellular distribution of cadherin and CTNND1 by inhibiting Src kinase activity [67]. Nevertheless, FER was identified as a Src substrate and is involved in tumor transformation [59]. In this study, these three proteins displayed similar expression patterns in the two cell lines studied and also interacted directly in the MHHCC97H network. Therefore, we hypothesize that FER may be a key regulator in the adhesion event involving these three proteins and may participate in HCC metastasis. We also examined the influence of FER on cell invasion activity in vitro. The data illustrated that the knock-down of FER by RNAi significantly reduced MHCC97H cell invasion activity, suggesting that FER could positively contribute to HCC metastasis. To verify this, we further examined FER expression in HCC tumor tissues from patients with diverse distant metastasis outcomes after tumor excision. The results showed that FER overexpression frequently occurred in tumor cells with distant pulmonary metastasis, indicating that FER is strongly associated with HCC distant pulmonary metastasis.
Once it is confirmed that FER is a potential regulator in HCC metastasis, the next step is to understand the mechanism by which it regulates HCC cell metastasis. To date, there are few reports on the functional regulation of FER in cancer, and the main focus has been on cell adhesion. FER was shown to play a key role in the coordinate regulation of E-cadherin-mediated cell-cell adhesion and integrin-mediated focal adhesion. It could move between the two adhesion pathways to trigger adhesion transition [59,61]. In a study on FER function using the Trojan peptide, researchers showed that FER that had dissociated from the cadherin complex could translocate to the integrin complex where it reduced p130CAS phosphorylation and interrupted integrin-mediated focal adhesion by affecting the phosphorylation of p130CAS binding partners, including PTP-PEST, PTP1B, FAK, and Crk [62]. FER was also reported to be an upstream tyrosine kinase for CTTN (cortactin) as well as Src and Fyn [68,69]. Phosphorylation of CTTN by FER is very critical for its recruitment to the cadherin and integrin complex [70]. CTTN mainly participates in cytoskeletal regulation and plays a pivotal role in tumor metastasis [71,72]. Recently, CTTN was shown to be an essential regulator of matrix metalloproteinase secretion and extracellular matrix degradation [73]. In another study, it was shown that phosphorylation of tyrosine residues in CTTN was strongly associated with the potential to induce metastasis in nude mice [74]. Whether CTTN phosphorylation by FER also has the same effects in HCC metastasis needs to be confirmed in future studies.
The results of this study suggested that FER is involved in HCC distant metastasis, and we have discussed the main mechanism and signaling pathways associated with FER functional regulation. The results from bioinformatics analysis also imply that FER is altered in MHCC97H cells in comparison with Hep3B cells. As a new functional molecule, the effect of FER on HCC metastasis remains unknown. It is possible that FER can alter the metastatic potential of HCC cells by one or several of the mechanisms mentioned here. Further studies are required to explore the exact role of FER in HCC cell invasion and metastasis. These would be both exciting and challenging.
Conclusion
The tyrosine phosphorylation data presented in this study is a useful resource for studying HCC metastasis and is an effective supplement for the PTyr database reported. Many of the identified pTyr proteins, including protein kinases and proteinases, could be useful for selecting intervention targets in future studies. The presence of multiple molecules and signaling pathways that are overrepresented in HCC cells with high metastatic potential suggests that HCC metastasis is a complex process and that the biological strategies for HCC metastasis treatment should be customized. In this study, FER was shown to be an important protein in HCC metastasis. We hope to obtain more evidence for the role of FER and its mechanism of action in HCC metastasis. This molecule may be a new drug target in future HCC therapy.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
HYL, ZGR and YKL contributed to design, analysis, interpretation of data. HYL performed the experiment. XNK helped to analyze the MS/MS data. LZ gave a hand in Western blot assay. XFL participated in cell invasion assay. YFS involved in cell culture. YW and TCX constructed TMA. HYL drafted the manuscript, YKL and ZGR revised it critically and gave smart suggestion for important content. All authors read and approved the manuscript.
Acknowledgements
We would like to thank Mr Yao Jun (Fudan University, Shanghai, China) for LC-MS/MS identification and Mr Yang Zhang (Fudan University, Shanghai, China) for assistance with bioinformatics analysis. This work was supported by grants from National Natural Science Foundation of China (NO.30672416) and National High Technology Research and Development Program of China (863 Program) (NO. 2006AA02A308).
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Pre-publication history
The pre-publication history for this paper can be accessed here:
http://www.biomedcentral.com/1471-2407/9/366/prepub
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Comscore
R29's Ultimate Cold & Flu Survival Guide
• Opener
Yep, it's officially winter, and with that comes lots of warm fuzzy knits, darkness at 4 p.m.… and the inevitable dawning of cold and flu season. Germs and bugs wreak havoc on our jam-packed schedules, our skin, and every other element of our lives. Not to mention, double-fisting Gatorade and Tylenol PM isn't exactly our idea of fun. Naturally, we want to protect ourselves from getting sick, to avoid spreading nasty germs around, and to get better as quickly as possible if those bugs manage to sneak past our well-crafted defenses.
That's why we consulted two doctors who know how to prevent and treat colds and flus: Dr. Eduardo Dolhun, MD, founder of the Dolhun Clinic and creator of Drip Drops ORS, and Dr. John Cranshaw, also of the Dolhun Clinic and former Chief of Medicine at St. Luke’s Hospital in San Francisco. They've got everything you ever wanted to know about colds, flus, and keeping yourself healthy. Follow their advice and a sniffle-proof, fever-free season could be yours.
Like this post? There's more. Get tons of beauty tips, tutorials, and news on the Refinery29 Beauty Facebook page!
Illustrations by
• 1
How can I keep myself from getting sick? And do I really need a flu shot?
You're not imagining it — people really do catch colds more often as the temperature drops. That's because the viruses that lead to colds and flus thrive in cooler temperatures, leading to higher transmission rates. Short of avoiding all human contact, the best way to protect yourself from colds is to practice good hygiene. Keep your hands clean, lay off the cigarettes (smoking increases the risk of catching a cold), and avoid rubbing your eyes. ("A sick person rubs his nose, touches the elevator button, you touch the button, and then you touch your eyes," Dolhun explains. "Suddenly, the virus is in your respiratory system.")
Both doctors agree that the flu shot is a must. “This year looks to be a bad one for flu," Cranshaw says. "The flu has already had more exposure than usual, and the strain we are seeing, H3N2, is particularly nasty." The good news? This brutal bug is among one of three strains included in this year's vaccine. It's recommended for flu-vulnerable people such as pregnant women and the elderly, but it's a smart move for everyone.
Not convinced? Crenshaw recalls a patient who turned down the vaccine because he was young and healthy, only to catch the flu. "The next time I saw him, he was on a ventilator in the ICU, and then he was dead," he says. "I don't like to push anything on my patients, but when people ask about the flu shot, I share that story."
• 2
What kills more germs, soap or hand sanitizer?
Eliminating germs is key for preventing sickness, but unfortunately, most of us don't wash our hands well enough. "When your doctor recommends hand-washing, it doesn't mean just a quick squirt of soap," Cranshaw says. "It means applying a good amount, then rubbing it on your hands for at least 20 seconds." And, forget about anti-bacterial soaps. "They're a marketing phenomenon," Dolhun says. "A regular bar of Ivory soap outperforms so-called anti-bacterial soaps."
Still, both doctors agree that hand sanitizers are more effective than soap. "Alcohol gels and hand sanitizers are the best," Dolhun says. "Put them in your purse, stash them everywhere, and use them." Look for an alcohol content level of between 60 and 70 percent, which studies have shown to be most effective in killing germs.
• 3
What about vitamins and supplements?
Supplements can keep any cold at bay, right? Wrong. "I always caution against breaking the bank and buying a bunch of supplements that don't work," says Dolhun. "That said, zinc has been proven to help boost the immune system." Cranshaw agrees, adding that vitamin C, echinacea, and zinc are the most promising supplements — but still, they're no magic bullet. "The data on the effectiveness of these is pretty poor at best," he admits.
Managing stress and paying attention to nutrition, however, can help you stay strong. “The best way to boost your immune system is to be happy and smile," says Dolhun. “But after that, make sure your hydration is good. Eat lots of fresh vegetables and fruits." Garlic and green tea have the potential to help, but your best bet is to catch up on Z's. "Proper sleep helps you maximize your immune defenses," he adds. "Sleep deprivation makes you more susceptible to illness." If you want to stay strong, head to bed early.
• Ugh, I'm sick. Now what should I do?
Once you've fallen ill, the key is to treat the illness right away. "After 72 hours, even medical-grade antivirals won't be as effective," Dolhun says. When it comes to treatment, the best you can hope for is to relieve symptoms — no over-the-counter treatment will shorten the duration or severity of your illness. While some prescription medications can help, the doctors tend to recommend those only for high-risk people. "We're already seeing resistant viruses," Cranshaw says. "The more people who take them, the less effective they'll be. And these medications aren't widely effective to begin with."
When it comes to feeling better in the meantime, turns out that Mom was right: you should rest up and drink fluids. Try chicken soup, tea with honey, or an oral rehydrating solution like Drip Drops. Proper hydration is key, since that helps move mucus out of the body. "If you let mucus stagnate, it becomes a petri dish," Dolhun adds. "That's when you can develop a secondary infection — why you can start to feel better and all of a sudden, you feel worse."
And, while it's usually a good idea to stay fit, now's the time to ease off the workouts. Let your body's energy go to fighting the sickness. "Listen to your body," Dolhun says. "If you're feeling crummy, you should rest. I see people go from zero to 60 in no time after they've been sick, but I recommend ramping things up slowly."
• What kind of medicine will help me most?
It all depends on what you're hoping to treat. Fevers exist to help your immune system fight the virus, but pain relievers minimize the discomfort they cause. Dr. Dolhun usually recommends Advil (ibuprofen) over Tylenol (acetaminophen). "Both help with pain and fever reduction, but I generally recommend ibuprofen because it can help with that stuffiness that people feel," he says. If you have any gastrointestinal problems, kidney issues, or liver disease, though, go with acetaminophen — it's easier on the stomach. Just check other products for acetaminophen, Dolhun says, since too much can cause liver failure. "People have suffered from accidental overdoses when taking Tylenol with other cold treatments that already contain the same ingredient," he warns. Read labels carefully before popping a pill.
As far as over-the-counter cough medicines go, bad news: they're not all that, says Cranshaw. "I'm not a big believer in cough medicines," he says. "They haven't been shown to be very effective." For a runny nose, look for a decongestant like Benadryl, which can dry things up a bit. Got a sore throat? Gargle with salt water and take an appropriate pain reliever. "Sore throat is pain, just like a headache is pain, he adds. "I take Advil or Aleve when I have a sore throat, and it gets me through the night pretty well."
• Feed a cold, starve a fever — what does that mean?
According to Dolhun, this age-old advice has more to do with how the patient is feeling than a way to treat the illness. "When you have a cold — versus a high fever, which generally means the flu — you’re not as sick. Focus on staying at home and hydrating, getting proper nutrition, and just getting better." Running a fever? Focus on hydration, even if you're too ill to get food down.
As far as eating chicken soup goes, both Dolhun and Cranshaw say it's a go. "Naturally made chicken soup has a lot of sodium, so it hydrates really well," says Dolhun. "That's what you need when you get sick." Herbal teas (he likes Celestial Seasonings Red Zinger) and honey can also help. "In this fast-paced, push-through-it culture, some of the basics are often forgotten," he says. "So be gentle on yourself and give yourself a lot of TLC. Give your body a fighting chance."
• When should I call my doctor?
Most colds just need time to clear up, but you should contact a doctor if you have a severe cough, a high fever that won't go away, or you've been sick for a week. "For somebody otherwise healthy, your doctor will probably say, 'Yep, you have a cold. Go home and take care of yourself,'" says Cranshaw. "Anybody who is really miserable — getting worse, not able to keep food or fluids down, or with a fever over 101 degrees — should talk to a doctor or nurse. I bet they'll appreciate hearing from you."
One last note: even though you may start to feel better, you could be contagious for at least 24 hours after a fever disappears. "You shed those viruses even after the fever is gone," Cranshaw says. So stay home for one extra sick day, and you may keep others from getting sick, too.
MORE SLIDESHOWS
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Never one to shy away from bold prints and embellishments, Cynthia Rowley packs a punch of color into this season's resort wears. Rowley's wonderfully over-the-top styling maybe shouldn't work, but it does, and we simply can't look away. Moroccan-infused tunics, kaleidoscope and madras prints, embroidery, and oversized, read
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What Makes You Sleep?
Although you may put off going to sleep in order to squeeze more activities into your day, eventually your need for sleep becomes overwhelming and you are forced to get some sleep. This daily drive for sleep appears to be due, in part, to a compound known as adenosine. This natural chemical builds up in your blood as time awake increases. While you sleep, your body breaks down the adenosine. Thus, this molecule may be what your body uses to keep track of lost sleep and to trigger sleep when needed. An accumulation of adenosine and other factors might explain why, after several nights of less than optimal amounts of sleep, you build up a sleep debt that you must make up by sleeping longer than normal. Because of such built-in molecular feedback, you can’t adapt to getting less sleep than your body needs. Eventually, a lack of sleep catches up with you.
The time of day when you feel sleepy and go to sleep is also governed by your internal “biological clock” and environmental cues - the most important being light and darkness. Your biological clock is actually a tiny bundle of cells in your brain that responds to light signals received through your eyes. When darkness falls, the biological clock triggers the production of the hormone melatonin.
This hormone makes you feel drowsy as it continues to increase during the night. Because of your biological clock, you naturally feel the most sleepy between midnight and 7 a.m. You may also feel a second and milder daily “low” in the midafternoon between 1 p.m. and 4 p.m. At that time, another rise occurs in melatonin production and might make you feel sleepy.
Your biological clock makes you the most alert during daylight hours and the most drowsy in the early morning hours. Consequently, most people do their best work during the day. Our 24/7 society, however, demands that some people work at night. Nearly onequarter of all workers work shifts that are not during the daytime, and more than two-thirds of these workers have problem sleepiness and/or difficulty sleeping. Because their work schedules are at odds with powerful sleep-regulating cues like sunlight, night shift workers often find themselves drowsy at work, and they have difficulty falling or staying asleep during the daylight hours when their work schedules require them to sleep.
The fatigue experienced by night shift workers can be dangerous.
Major industrial accidents - such as the Three Mile Island and Chernobyl nuclear power plant accidents and the Exxon Valdez oil spill - have been caused, in part, by mistakes made by overly tired workers on the night shift or an extended shift.
Night shift workers also are at greater risk of being in car crashes when they drive home from work. One study found that one-fifth of night shift workers had a car crash or a near miss in the preceding year because of sleepiness on the drive home from work. Night shift workers are also more likely to have physical problems, such as heart disease, digestive disturbances, and infertility, as well as emotional problems. All of these problems may be related, at least in part, to the workers’ chronic sleepiness. See “Working the Night Shift” for some helpful tips.
Other factors can also influence your need for sleep, including your immune system’s production of cellular hormones called cytokines.
These compounds are made in large quantities in response to certain infectious diseases or chronic inflammation and may prompt you to sleep more than usual. The extra sleep may help you conserve the resources needed to fight the infection. Recent studies confirm that being well rested improves the body’s responses to infection.
People are creatures of habit, and one of the hardest habits to break is the natural wake and sleep cycle. A number of physiological factors conspire to help you sleep and wake up at the same times each day. Consequently, you may have a hard time adjusting when you travel across time zones. The light cues outside and the clocks in your new location may tell you it is 8 a.m. and you should be active, but your body is telling you it is more like 4 a.m. and you should sleep. The end result is jet lag - sleepiness during the day, difficulty falling or staying asleep at night, poor concentration, confusion, nausea, and general malaise and irritability. See “Dealing With Jet Lag”.
Working the Night Shift
Try to limit night shift work, if that is possible. If you must work the night shift, the following tips may help you:
• Increase your total amount of sleep by adding naps and lengthening the amount of time you allot for sleep.
• Use bright lights in your workplace.
• Minimize your shift changes so that your body’s biological clock can adjust to a nighttime work schedule.
• Get rid of sound and light distractions in your bedroom during your daytime sleep.
• Use caffeine only during the first part of your shift to promote alertness at night.
If you are unable to fall asleep during the day, and all else fails, talk with your doctor to see if it would be wise for you to use prescribed, short-acting sleeping pills to help you sleep during the day.
Provided by ArmMed Media
Revision date: June 20, 2011
Last revised: by Jorge P. Ribeiro, MD
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Monthly Archives: May 2023
The Art of Plant-Based Healing: Nurturing Wellness Through Natural Remedies
Plant-based healing is a masterpiece woven from the threads of nature’s bounty, a testament to the profound relationship between flora and human well-being. In a world where the allure of synthetic remedies is strong, the ancient wisdom of natural healing through plants shines as a beacon, illuminating a path to holistic wellness.
Unveiling the Power of Plant-Based Healing
At the heart of plant-based healing lies the recognition that nature is not just a backdrop to our lives; it is a dynamic source of healing energy. Plants, adorned with intricate compounds and bioactive elements, have long been revered for their ability to restore balance within the body. This natural synergy between humans and the botanical world forms the foundation of a profound healing art.
Tapping into Ancient Wisdom
The practice of plant-based healing draws inspiration from ancient traditions that have cherished the therapeutic potential of herbs for centuries. From Ayurveda’s intricate
Read the rest
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November 26, 2015
ABCDEFGHIJKLMNOPQRSTUVWXYZ
Ear Health
Health Home >> Ear Health >> Ear health overview
Ear health: FAQs
How can I prevent swimmer's ear?
To help prevent an outer ear infection, also known as swimmer's ear or, dry your ears well after swimming or showering. You can try using a hair dryer set on the lowest setting for a few minutes. Swimming caps will help prevent water getting into the ear while swimming. You can also use eardrops with acetic acid or alcohol after swimming to neutralize possible infections. If these measures don't work, contact your doctor.
What are the signs and symptoms of a middle ear infection?
The most common symptoms of middle ear infections are fever and pain. You may also have difficulty sleeping. When children and infants have an ear infection, they may become irritable, tug on their ear, or change their feeding or eating patterns.
Why didn't my child get prescribed an antibiotic for an ear infection?
If your child is not at high risk for complications of an ear infection and has mild symptoms, your doctor may not prescribe an antibiotic. Since many ear infections are caused by a virus - which won't be affected by antibiotics - and improve in a few days without treatment, your doctor may want to wait before prescribing an antibiotic. If your child's symptoms don't improve in a few days or if they get worse, then your doctor will likely prescribe an antibiotic.
What is labyrinthitis?
Labyrinthitis is inflammation of the inner ear. The inflammation in the inner ear can cause a spinning sensation called vertigo and can throw your balance off too. The cause of labyrinthitis is usually unknown, but viral infections have been linked to inner ear inflammation.
What can I do to prevent hearing loss?
Noise-induced hearing loss is one the most common causes of hearing loss. To prevent this, turn down the volume! If someone else can hear the music that is playing on your personal music player or someone has to shout for you to hear them, you're listening to music at a volume that can damage your ears. You can also protect your hearing by making sure your ears are protected when using power tools or if your line of work involves exposure to loud noise (e.g., construction).
How are infants tested for deafness?
Infants are all screened for hearing loss or deafness at birth. At this age, otoacoustic emissions testing (OAE) is used. OAE testing generates sounds within the ear and measuring the sound produced by the inner ear to see how well your inner ear is working.
If children do not do well on an OAE test, then auditory brain stem response (ABR) testing will be used. ABR is a non-invasive test that measures the function of hearing nerves. Electrodes are attached to various places on your head (e.g., ears, forehead) and earphones generate sounds. The electrodes pick up the activity of the hearing nerves.
What are the signs that my child has hearing problems?
If your child is not responding to noises, is not speaking clearly, or is not speaking at an expected age, he or she may have hearing problem. Contact your child's doctor for an assessment.
Are hearing loss and deafness permanent?
Some forms of hearing loss are permanent and others are not. Hearing loss is usually permanent when the inner ear or nerves of the ear are damaged. When hearing loss is caused by a blockage (e.g., from wax), fluid in the middle ear, or problems with the hearing bones, it is usually temporary and resolves or improves after treatment.
What is the best way to clean your ears?
Your ears are good at cleaning themselves, so you should never put anything in your ear - especially cotton swabs - to clean them. Using a cotton swab can actually push wax further into your ear and can scratch or damage the ear canal.
If you think your ears are blocked by wax, contact your doctor or pharmacist for advice on how to clean them. If your ears are healthy, you can try to clear the earwax by applying mineral oil a few times a day for a few days and then washing the wax out by gently squirting water into the ear canal with a rubber bulb syringe.
What is tinnitus?
Tinnitus is when you hear a sound in your ear that is not actually present. The type of sound varies from person to person and can include ringing, buzzing, roaring, or hissing. If you think you have tinnitus, contact your doctor. Although no cause is found for most cases of tinnitus, sometimes the cause is an underlying medical problem that can be treated.
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Temperature discomforts and sleep
Read this tip to make your life smarter, better, faster and wiser. LifeTips is the place to go when you need to know about Symptoms and Signs and other Fibromyalgia topics.
Why does my body seen out of sync with the actual temperature?
Temperature discomforts and sleep
One thing that interferes with sleep - and daily life as well - is the unpredictable changes in body temperature that seem to occur with fibro patients. Use natural fiber bedding, as it will allow your skin to breathe and not trap sweat. A light down blanket or comforter and a sheet should do the trick most of the year, as it seems to adjust to body temperatures easily. During the day, dress in layers that you can put on or take off as needed.
Comments
10/5/2006 4:22:33 PM
Kim said:
If you live in a hot climate, the air conditioner clicks on and off all night causing a temperature fluctuation. Use a ceiling fan set on low to offset this fluctuation.
9/16/2007 8:54:22 AM
Mariann in TX. said:
I find cotton to be the best comfort for clothing and bedding. Anything with other fibers causes me to have more heat. And using a fan as the tip suggests does work.
Name:
URL: (optional)
Comment:
Not finding the advice and tips you need on this Fibromyalgia Tip Site? Request a Tip Now!
Guru Spotlight
Carma Spence-Pothitt
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Maximizing Your Workout at the Gym 1
Maximizing Your Workout at the Gym 2
Building a Strong Foundation
Before you hit the gym, it’s essential to have a clear plan in mind. Start by setting specific goals that you want to achieve through your workouts. Whether it’s building strength, increasing endurance, or losing weight, having a clear objective will help you stay focused and motivated.
Once you have your goals in place, it’s time to create a workout routine that aligns with those objectives. A well-rounded regimen should include a combination of cardiovascular exercise, strength training, and flexibility exercises. This balanced approach will help you build a strong foundation and prevent muscle imbalances. Learn more about the topic covered in this article by checking out the suggested external site. Inside, you’ll uncover extra information and an alternative perspective on the topic. Investigate this valuable resource!
Additionally, it’s important to prioritize proper form and technique in your workouts. This not only minimizes the risk of injury but also ensures that you’re targeting the intended muscles effectively. Consider working with a personal trainer or taking classes to learn the correct form for various exercises. Form is the foundation of a successful and safe workout.
Mind-Muscle Connection
In order to truly maximize your workout, it’s crucial to develop a strong mind-muscle connection. This means focusing on and engaging the specific muscles you’re targeting during each exercise. It’s easy to go through the motions and let momentum take over, but that won’t yield optimal results.
Take the time to mentally connect with the muscles you’re working on. Visualize them contracting and lengthening with each repetition. Concentrate on the quality of each movement and avoid simply going through the motions. This heightened awareness will not only enhance your workout but also prevent injuries and imbalances.
Vary Your Routine
While consistency is key when it comes to exercise, sticking to the same routine day in and day out can lead to a plateau in your progress. To keep your body challenged and continuously improving, it’s important to regularly change up your workout routine.
One way to introduce variety is by incorporating different types of exercises and equipment into your routine. Instead of exclusively using machines, try incorporating free weights, resistance bands, or bodyweight exercises. This will engage different muscle groups and stimulate new levels of growth and strength.
Additionally, varying the intensity and duration of your workouts can also yield great results. Incorporating interval training, high-intensity workouts, or longer endurance sessions can help elevate your fitness level and prevent monotony.
Rest and Recovery
While it may be tempting to push yourself to the limit every day, it’s important to prioritize rest and recovery. Your body needs time to repair and rebuild after intense workouts.
Make sure to include rest days in your workout schedule, allowing your muscles to recover from the stress of exercise. This doesn’t mean you have to sit on the couch all day. Active recovery, such as gentle stretching, yoga, or low-impact activities, can help promote circulation and aid in the recovery process.
Additionally, prioritize sleep as a vital component of your recovery routine. Aim for seven to eight hours of quality sleep each night to ensure your body fully rejuvenates and prepares for the next workout session.
Nutrition and Hydration
Achieving your fitness goals isn’t just about what you do in the gym; it’s also about what you put into your body. Proper nutrition and hydration play a crucial role in maximizing your workouts.
Ensure that you’re consuming a well-balanced diet that includes a variety of fruits, vegetables, lean proteins, whole grains, and healthy fats. Fueling your body with the right nutrients will provide the energy necessary for effective workouts and aid in muscle recovery.
Hydration is equally important. Dehydration can hinder your performance and result in fatigue and muscle cramps. Aim to drink at least eight cups of water throughout the day, and increase that amount during intense workouts or hot weather.
Motivation and Accountability
Finally, maintaining motivation and accountability is key to maximizing your workouts. It’s normal to experience fluctuations in motivation, so finding strategies to stay on track is essential.
Consider finding a workout buddy or joining a fitness community to hold yourself accountable and stay motivated. Having someone to exercise with not only provides social support but also adds an element of friendly competition that can push you to work harder.
Setting smaller, achievable goals along the way can also help maintain motivation. Celebrate your milestones and use them as fuel to keep going.
Conclusion
Maximizing your workout at the gym requires a holistic approach. It’s not just about the exercises you do but also about setting clear goals, focusing on form, varying your routine, prioritizing rest and recovery, fueling your body with proper nutrition and hydration, and staying motivated and accountable. By incorporating these strategies into your fitness journey, you’ll be well on your way to achieving your desired results. Enhance your study by exploring this suggested external source. There, you’ll find additional and valuable information to expand your knowledge of the topic. Gym near me https://www.liftvero.com, check it out!
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How is a migraine diagnosed?
Researchedby:
Fact-checked
by:
Last Updated: October 25, 2023
Usually, a headache with additional symptoms of sensitivity to light and sound, nausea, and worsening with physical activity is most suggestive of a migraine. A migraine with aura involves reversible neurological symptoms that can be visual or sensory (e.g., flashing lights, zig-zag lines, foggy vision).[1]
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Sài Gòn Y Khoa
HUYẾT ÁP THẤP: CÁCH ĐIỀU TRỊ VÀ PHÒNG NGỪA
Huyết áp thấp và cách khắc phục
Hiện nay, huyết áp thấp là một tình trạng khá phổ biến và tỷ lệ người bị huyết áp thấp đang ngày càng tăng. Tuy nhiên, nhiều người còn khá thờ ơ vì ko biết rằng huyết áp thấp có thể gây nguy hiểm cho tính mạng. Chính vì vậy, với những hiểu biết cơ bản về bệnh huyết áp thấp sẽ giúp chúng ta có một cách nhìn khoa học và chủ động hơn trong việc bảo vệ sức khoẻ cho chính mình.
Huyết áp thấp là một bệnh lý thường gặp, xuất hiện cả ở nam giới lẫn nữ giới, ở lứa tuổi dậy thì và người cao tuổi.
Thế nào là huyết áp thấp?
Theo Tổ Chức Y Tế Thế Giới, huyết áp thấp là biểu hiện của sự rối loạn chức năng vỏ não của trung khu thần kinh vận mạch. Bệnh huyết áp thấp có thể bao gồm huyết áp thấp triệu chứng và huyết áp thấp tư thế...
Huyết áp thấp là khi trị số huyết áp tâm thu dưới 90mmHg và huyết áp tâm trương dưới 60mmHg, mạch áp có hiệu số thường dưới 20mmHg.
Triệu chứng lâm sàng của người bị huyết áp thấp
- Mệt mỏi, hoa mắt chóng mặt, lả, có cảm giác buồn nôn và rất muốn được nghỉ ngơi.
- Khó tập trung và dễ nổi cáu, lạnh tay chân.
- Suy giảm khả năng tình dục
- Da nhăn và khô, kèm theo rụng tóc.
- Thở dốc nhất là sau khi leo lên cầu thang hay làm việc nặng.
Huyết áp thấp có nguy hiểm không?
Đây là một trạng thái bệnh lý thường gặp, xuất hiện cả ở nam giới lẫn nữ giới, ở lứa tuổi dậy thì và người cao tuổi. Theo thống kê cho thấy, nhiều trường hợp huyết áp thấp có thể dẫn tới tai biến mạch máu não, trong đó phần lớn là nhồi máu não. Ngoài ra, người bị tụt huyết áp cấp có thể gây sốc, đặc biệt nguy hiểm đến tính mạng trong những trường hợp như đang lái xe, làm việc trên tầng cao… Nếu huyết áp thấp kéo dài, còn làm cho các cơ quan thận, gan, tim, phổi suy yếu nhanh chóng. Chính vì vậy người bị huyết áp thấp không nên chủ quan, coi thường bệnh.
Khắc phục huyết áp thấp như thế nào?
Để khắc phục huyết áp thấp cần phải xác định rõ nguyên nhân gây ra tình trạng huyết áp thấp, từ đó có những biện pháp áp dụng phù hợp.
1. Nếu bị Huyết áp thấp do suy giảm hoạt động của tuyến giáp, bạn nên đến bác sỹ thăm khám, xét nghiệm máu để phát hiện ra nguyên nhân, bác sỹ sẽ giúp bạn giải quyết vấn đề một cách thấu đáo.
2. Trường hợp bị Huyết áp thấp không do nguyên nhân trên, bạn cần thực hiện các biện pháp sau:
- Ăn đủ các bữa, đặc biệt bữa sáng rất quan trọng. Các chuyên gia khuyên bạn nên ăn sáng với những thực phẩm tốt cho tim mạch và các loại nước hoa quả ép (nên thêm một chút muối) sẽ giúp máu lưu thông dễ dàng hơn.
- Nên ăn mặn hơn người bình thường (10-15g muối/ngày).
- Ngủ đủ giấc và đủ thời gian cũng góp phần quan trọng vào việc khắc phục cũng như phòng ngừa chứng cao huyết áp.
- Luyện tập thể dục nhẹ nhàng và đều đặn như đi bộ, dưỡng sinh, Yoga…
- Thường xuyên dùng các loại trà để hỗ trợ nâng cao huyết áp. Trên thị trường hiện nay có một số sản phẩm hỗ trợ tăng huyết áp, song một sản phẩm hỗ trợ tăng huyết áp tốt phải đảm bảo tốt các tiêu chí sau:
• Không gây phản ứng phụ khi người bệnh dùng thường xuyên. Điều này chỉ có thể có được nếu sản phẩm được sản xuất từ nguồn gốc thiên nhiên.
• Có tác dụng làm ấm nóng cơ thể, không gây lạnh bụng, đi ngoài, nếu không sẽ có tác dụng ngược lại, làm cho bệnh nhân càng tụt huyết áp hơn. Vì vậy sản phẩm không nên bổ sung những vị thuốc có tính hàn.
BSCK1.LƯƠNG VĂN ĐẾN
Tin tức mới
• Phòng khám Đa khoa Sài Gòn Y khoa :
Đã có lịch khám tháng 03/2015, Khoa Nội, Khoa Nhi, Khoa Sản.
• Vật Lý Trị Liệu hoạt động trở lại từ ngày 12/05/2014
Hỗ trợ trực tuyến
Dịch vụ: (08) 39561753
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1,407,540,244,891,652,400
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Pregnancy, Parenting, and Lower Back Pain
You're pregnant! Congratulations! Your body's changing-wondrously, marvelously. One unexpected and unwelcome change may be lower back pain. Recent studies suggest that two-thirds of pregnant women experience lower back pain.1
These statistics seem reasonable. The weight of the growing baby, plus the weight of the placenta and amniotic fluid, create an unbalanced load in front of the lower back. The result is irritation of spinal ligaments, muscles, and tendons, causing pain, muscle spasm, and loss of mobility.
Of course, some cases of pregnancy-related back pain have specific medical causes. Uncommon conditions such as pregnancy-associated osteoporosis, septic arthritis, and inflammatory arthritis may need to be considered.2
That said, the vast majority of cases of back pain in pregnancy are mechanical in origin.
Your doctor of chiropractic will perform a complete examination and determine the correct course of treatment, if appropriate. Once you're feeling better, you can begin
stretching and doing safe, gentle exercises that will help prevent recurrences of lower back pain. The goal is to strengthen your lower back and minimize the mechanical effects of pregnancy.
The best method of preventing back pain in the first place is being fit. This includes healthy nutrition, gaining a moderate amount of weight, and regular exercise. Your obstetrician will likely recommend vitamin and iron supplements and will monitor your weight. The average healthy woman gains between 25 and 35 pounds during the course of her pregnancy.3
Let's fast forward a few years. Your newborn is now a toddler. Parents know that if you have kids, stuff happens. You bend over to place a bulky car seat in your car. Then you place your child in it. And then, you bend over to remove the car seat from your car. If you've gone to the mall, kids want Daddy or Mommy to carry them. Pick them up, cart them around, put them down again.
What's a parent to do? It's not like you can avoid any of these activities. Your kids are kids - it's up to you to do stuff for them. The answer lies in regular exercise. "But how will I find time to exercise, when there already isn't enough time to do the things I need to do?"
That's a tough question, but if you recognize the benefits, you'll make the effort to make the time. Forty-five minutes or an hour per workout, three or four times a week, will be plenty. And, once you're in the habit of exercising, you'll notice it's easier to lift your kids, easier to bend over, easier to carry them. It's easier because you're
fitter and stronger. And healthier. And, surprisingly, you're having more fun.
1Pennick VE, Young G: Interventions for preventing and treating pelvic and back pain in pregnancy. Cochrane Database Syst Rev 18(2):CD001139, 2007.
2Sax TW, Rosenbaum RB: Neuromuscular disorders in pregnancy. Muscle Nerve 34(5):559-571, 2006.
3Jain NJ, et al: Maternal obesity: can pregnancy weight gain modify risk of selected adverse pregnancy outcomes? Am J Perinatol 24(5):291-298, 2007.
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Osca Perawat Batuk Efektif
Osca Perawat Batuk Efektif - Askep kapukonline.com update Osca Perawat Batuk Efektif - STANDARD OPERASIONAL PROSEDUR (SOP) untuk Perawat, setelah sebelumnya posting (Baca : Osca Perawat Alih Baring)
BATUK EFEKTIF
STANDARD OPERSIONAL PROSEDUR
PENGERTIAN
Latihan mengeluarkan sekret yang terakumulasi dan mengganggu di saluran nafas dengan cara dibatukkan.
TUJUAN
1. Membebaskan jalan nafas dari akumulasi sekret
2. Mengeluarkan sputum untuk pemeriksaan diagnostik laborat
3. Mengurangi sesak nafas akibat akumulasi sekret
KEBIJAKAN
1. Klien dengan gangguan saluran nafas akibat akumulasi secret
2. Pemeriksaan diagnostik sputum di laboratorium
PETUGAS
Perawat
PERALATAN
1. Kertas tissue
2. Bengkok
3. Perlak/alas
4. Sputum pot berisi desinfektan
5. Air minum hangat
PROSEDUR PELAKSANAAN
1. Tahap PraInteraksi
1. Mengecek program terapi
2. Mencuci tangan
3. Menyiapkan alat
2. Tahap Orientasi
1. Memberikan salam dan sapa nama pasien
2. Menjelaskan tujuan dan prosedur pelaksanaan
3. Menanyakan persetujuan/kesiapan pasien
3. Tahap Kerja
1. Menjaga privacy pasien
2. Mempersiapkan pasien
3. Meminta pasien meletakkan satu tangan di dada dan satu tangan di abdomen
4. Melatih pasien melakukan nafas perut (menarik nafas dalam melalui hidung hingga 3 hitungan, jaga mulut tetap tertutup)
5. Meminta pasien merasakan mengembangnya abdomen (cegah lengkung pada punggung)
6. Meminta pasien menahan nafas hingga 3 hitungan
7. Meminta menghembuskan nafas perlahan dalam 3 hitungan (lewat mulut, bibir seperti meniup)
8. Meminta pasien merasakan mengempisnya abdomen dan kontraksi dari otot
9. Memasang perlak/alas dan bengkok (di pangkuan pasien bila duduk atau di dekat mulut bila tidur miring)
10. Meminta pasien untuk melakukan nafas dalam 2 kali , yang ke-3: inspirasi, tahan nafas dan batukkan dengan kuat
11. Menampung lender dalam sputum pot
12. Merapikan pasien
4. Tahap Terminasi
1. Melakukan evaluasi tindakan
2. Berpamitan dengan klien
3. Mencuci tangan
4. Mencatat kegiatan dalam lembar catatan keperawatan
PENILAIAN PENCAPAIAN KOMPETENSI ASPEK KETRAMPILAN BATUK EFEKTIF
NO
ASPEK YANG DINILAI
BOBOT
NILAI
0
1
2
A
Alat
1
Kertas tissue
1
2
Bengkok
1
3
Perlak/alas
1
4
Sputum pot berisi desinfektan
1
5
Air minum hangat
1
B
Tahap Pra Interaksi
1
Melakukan pengecek program terapi
1
2
Mencuci tangan
1
3
Menempatkan alat di dekat pasien
2
C
Tahap Orientasi
1
Memberikan salam dan menyapa nama pasien
1
2
Menjelaskan tujuan dan prosedur pelaksanaan
2
3
Menanyakan persetujuan dan kesiapan pasien
1
D
Tahap kerja
1
Menjaga privacy pasien
1
2
Mempersiapkan pasien
3
3
Meminta pasien meletakkan satu tangan di dada dan satu tangan di abdomen
3
4
Melatih pasien melakukan nafas perut (menarik nafas dalam melalui hidung hingga 3 hitungan, jaga mulut tetap tertutup)
4
5
Meminta pasien merasakan mengembangnya abdomen (cegah lengkung pada punggung)
3
6
Meminta pasien menahan nafas hingga 3 hitungan
4
7
Meminta menghembuskan nafas perlahan dalam 3 hitungan (lewat mulut, bibir seperti meniup)
4
8
Meminta pasien merasakan mengempisnya abdomen dan kontraksi dari otot
3
9
Memasang perlak/alas dan bengkok (di pangkuan pasien bila duduk atau di dekat mulut bila tidur miring)
2
10
Meminta pasien untuk melakukan nafas dalam 2 kali , yang ke-3 : inspirasi, tahan nafas dan batukkan dengan kuat
7
11
Menampung lender dalam sputum pot
2
12
Merapikan pasien
1
E
Tahap Terminasi
1
Melakukan evaluasi tindakan
1
2
Berpamitan dengan klien
1
3
Membereskan alat-alat
1
4
Mencuci tangan
1
5
Mencatat kegiatan dalam lembar catatan keperawatan
1
TOTAL
50
Demikian artikel tentang Standard Operasional Prosedur (SOP) Osca Perawat Batuk Efektif. Semoga membantu dalam Test Osca Perawat Jateng / Jawa Tengah. Bila bermanfaat, silahkan Share kepada teman-teman anda...!!
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Osca Perawat Batuk Efektif (Osca Perawat Batuk Efektif)
4.5 stars - "Osca Perawat Batuk Efektif" Prosedur cara tindakan keperawatan Osca Batuk efektif sesuai standard operasional prosedur brikut pengertian, tujuan, alat dan bahan, prosedur pelaksanaan, aspek penilaian kompetensi
thumbnailOsca Perawat Batuk Efektif2011-10-17T00:21:00+07:00
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Thursday, May 23, 2013
Incontinence vs. Interstitial Cystitis: Which One Is It?
By Jennifer Sobol, D.O., Health Pro Wednesday, October 10, 2007
Let me start off by saying that incontinence is a completely different medical problem from Interstitial Cystitis (IC for short). I have often been asked to talk about IC during an incontinence lecture. There are many overlapping symptoms, and many people have both, but hear this now- they are completely different! I have been reluctant to discuss IC in this SharePost because they are not the same, but I thought I could address the differences here.
Interstitial Cystitis is a syndrome that I loosely refer to as "painful bladder syndrome." It has a very large spectrum of symptoms that often start off annoying and can travel the road to end-stage bladders, which can be debilitating. The following is a very brief and simplified explanation of a very complex medical condition.
Often, symptoms start with urinary frequency and urgency. Many people experience pain over their bladder especially when the bladder is filling, and often relieved after voiding. Voiding itself can be painful, however.
Many people get mild to severe bladder spasms. Over time people's bladders can get fibrotic and actually lose capacity and the ability to store an appropriate amount of urine. Treatments are pretty variable, but the mainstay usually starts with a class of medications called anticholinergics.
Anticholinergics are the medications used in overactive bladder treatments, and this is why many people think incontinence and IC are the same. I know I will probably get a lot of angry replies when I state this, but the majority of people with Interstitial Cystitis do not have incontinence. Some do, I agree, but most people do not. Again, in general, IC is a painful syndrome that can cause urgency and frequency along with other bladder symptoms.
To confuse the picture more, both women and men get IC. For a very long time, IC was only recognized as a disease that affected women. Men were diagnosed with an "analogous" disease called chronic prostatitis. We are realizing that men can also be afflicted with IC, but now it is called Chronic Prostatitis/Chronic Pelvic Pain Syndrome. The symptoms are the same, but can show up differently. For instance, men tend to have more pain with orgasm, where women more often have pain with intercourse and penetration.
Treatment for IC, as mentioned before, is often initially treated with anticholinergic medications. That is about all IC has in common with incontinence and overactive bladder. From this point, there are many different approaches to treating IC. There is only one FDA approved medication for Interstitial Cystitis, but there are many agents used for additional treatment. There are diet recommendations, as well as behavior modification treatments too.
I hope you find this information useful. I really want to emphasize that if you are having symptoms of urgency, frequency or incontinence, you really need to be evaluated by a physician to figure out the cause. You may think you have one thing going on, but it could be something else.
Secondary Causes of Incontinence
By Jennifer Sobol, D.O., Health Pro— Last Modified: 09/29/10, First Published: 10/10/07
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