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Tynor Hot and Cold Pack - 0 views

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    Tynor Hot and Cold Pack is a convenient device to provide hot fomentation or cold compress. Hot fomentation of the injured or inflamed area enhances the threshold of pain and thus reduces the perception of pain. It has a synergistic effect along with pain relieving drugs. Raising temperature of the injured tissue also enhances the blood profusion and the healing process. Hot fomentation has a relaxing effect. Cold compress helps in reduction of inflammation in injuries, protects by slowing the metabolic rate around the tissue, reduce oedema and bleeding. Cold compress helps in immediately lowering fever, in very high fever conditions. It can be used after an acute injury or surgical procedure. No heat or cryo burns. Requires no holding. Reusable. Easy application. Appealing aesthetics. Tynor Hot and Cold Pack Features Multi functionality Reduce swelling and odema at the site of injury. Muscles spasm and pain. Headache and minor injuries. Versatile design Can be used as either cold or hot pack. Reusable in either hot & cold condition. Temperature range - Can be used from 0 Cº to 75Cº. Longer temperature retention time. Fabric cover ensures no cryo burns or hot skin burns. Physical features Non-toxic, and biodegradable. Gel remains soft and flexible upto 0 degree. Durable, and puncture resistant. Soft, "frost free" PVC cover. Flexible conforms to the body contours. Easy to clean and maintain. Excellent workmanship. Good aesthetics. Elastic belt Holds the pack against the body, No need to hold by hand. Enhances convenience. Tynor Hot and Cold Pack Measurements
Nathan Goodyear

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors i... - 0 views

  • The presence and activity of PR significantly affect the prognostic value of ER.
  • The observed loss of PR protein expression in a subset of ER+/PR+ breast cancers, because of hypermethylation or deletion of the PR gene locus, results in the loss of ER prognostic value
  • These findings emphasize the clinical value of assessing both PR and ER expression in breast cancer samples
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  • PR is an essential modulator of ER-regulated genes but also that it significantly contributes to the prognostic value of ER in ER+/PR+ breast cancers
  • PR-regulated genes have independent prognostic value, and the presence of PR correlates with favorable clinicopathological outcomes
  • this study demonstrates that progestin-activated PR redirects ER chromatin binding and functions as a genomic estrogen agonist and as a phenotypic estrogen antagonist in ER+/PR+ breast cancer cells and human tumors
  • Approximately 80% of ER+ breast cancers are also positive for PR,
  • In isolation, both hormones activate or inhibit cellular processes in similar directions, although the magnitude of these effects is less for progestin alone than for estrogen alone
  • PR-mediated antagonism of estrogenic phenotypes is well documented
  • joint activation of ER and PR antagonized ER-regulated oncogenic processes
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    WOW!!  study finds that progesterone through PR activity antagonizes ER protein expression by the cell.  This has huge implications in breast cancer and possible prostate cancer.  But then again, women don't need progesterone; only estrogen.  The presence of PR correlates with improved clinicopathological outcomes.  The authors do seem to get confused about progesterone and progestins.  They are not one in the same.
hadiyasafdar

How Does fillers and Facelift Surgery Work? - Cosmetic Surgeon - Medium - 0 views

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    Who wouldn't love to look young and beautiful? Minor signs of ageing can make us panic because such signs start appearing one after the other making you look older and less pretty as would look without them. Wrinkles and lines appear because your skin loses its elasticity and volume over time. We know that ageing is an inevitable process but we wish to delay it and look youthful for more and more time.
Nathan Goodyear

Angiogenic Factors and Natural Killer (NK) Cells in the Pathogenesis of Preeclampsia - 0 views

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    Abnormal NK cell activity in the placenta plays a likely role in the development of preeclampsia. This proposes an immunologic role in the development of preeclampsia.  This process is similar to the literatures link between maternal NK and RPL.
Nathan Goodyear

Urological Research, Volume 15, Number 3 - SpringerLink - 0 views

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    aromatization of androstenedione to estrogen shown to play role in prostatitis, BPH, and prostate cancer.  In this study, they looked at aromatase inhibition to slow this process.
Nathan Goodyear

The relation of proinsulin, insulin, and proinsulin... [Diabetes. 1997] - PubMed - NCBI - 0 views

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    insulin resistance promotes increased processing of proinsulin to insulin
Nathan Goodyear

IOS Press - Journal Article - 0 views

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    neuroinflammaiton, also described as excitotoxicity, found in the brains of children/young adults that lived in high air pollution areas.  Neuroinflammation (IL-6, IL-1, TNF-alpha, IFN-gamma...) found in the brains of these children and young adults.  This is the same process found in Alzheimers and other excitotoxicity disease states.  Addtionally, it is also involved in most chronic diseases of aging.
Nathan Goodyear

Reduced Activation and Increased Inactivation of Thyroid Hormone in Tissues of Critical... - 0 views

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    critical illness is associated with low TSH, reduced T3, and increased rT3 production.  Inflammation is critically involved in this process.  This study from JCEM shows how unreliable TSH and T4 are.
Nathan Goodyear

The neurophysiology of brain injury. [Clin Neurophysiol. 2004] - PubMed - NCBI - 0 views

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    Just the abstract is available online, but the neurophysiology of brain injury is well discussed here.  This process takes time.  In fact, most TBIs are mild and often go unreported/unrecognized until neurological deficits begin.
Nathan Goodyear

The Complex Role of Estrogens in Inflammation - 0 views

  • These studies suggest inflammation-dependent up-regulation of ERβ relative to ERα.
  • up-regulation of ERβ relative to ERα under hypoxic conditions, which might lead to a preponderance of signaling through ERβ pathways
  • it seems that E2 at periovulatory to pregnancy levels inhibited proinflammatory cytokines from PBMCs
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  • it is clear that E2 can stimulate antibody production by B cells, probably by inhibiting T cell suppression of B cells
  • In cycling women, the largest quantities of Ig were detected before ovulation
  • In contrast, E2 at high concentrations leads to a suppression of B-lymphocyte lineage precursors
  • E2 at periovulatory to pregnancy serum levels is able to stimulate antibody secretion under healthy conditions but also in autoimmune diseases, whereas similar serum levels of E2 lead to a suppression of bone marrow B cell lineage precursors
  • In chronic inflammatory disorders, where B cells play a decisive role, E2 would promote the disease when autoaggressive B cells are already present, whereas chronically elevated E2 would inhibit initiation of an autoimmune disease when no such B cells are available. This might be a good reason why particularly B cell-dependent diseases such as SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis appear in women in the reproductive years, predominantly, in the third or fourth decades of life
  • Th17 cells are thought to be the main responsible cells for chronic inflammatory tissue destruction in autoimmune diseases
  • IFN-γ, IL-12, and TNF were allocated to Th1 reactions
  • IL-4, IL-5, and IL-10 to Th2 responses
  • antiinflammatory T regulatory cells producing TGF-β and proinflammatory T helper type 17 cells (Th17) producing IL-17
  • no direct effects of estrogens on Th17 cells or IL-17 secretion have been described until now.
  • So-called Th17 cells producing IL-17 are the main T cells responsible for chronic inflammation.
  • Because IFN-γ has been allocated a Th17-inhibiting role (Fig. 1⇑), its increase by E2 at pregnancy doses and the E2-mediated inhibition of TNF must be viewed as a favorable effect in chronic inflammation
  • in humans and mice, E2 at periovulatory to pregnancy levels stimulates IL-4, IL-10, and IFN-γ but inhibits TNF from CD4+ T cells
  • In humans and mice, E3 and E2, respectively, at pregnancy levels inhibit T cell-dependent delayed type hypersensitivity
  • increased IL-4, IL-10, and IFN-γ in the presence of low TNF support an antiaggressive immune response
  • secretion of IL-1β is increased at periovulatory/proestrus to early pregnancy levels, whereas IL-1 secretion is inhibited at high pregnancy levels
  • The dichotomous effect of E2 on IL-1β and TNF at high and low concentrations is most probably due to inhibition of NF-κB at high concentrations
  • experiments with mouse and rat macroglial and microglial cells demonstrate that E2 at proestrus to pregnancy levels exerts neuroprotective effects by increasing TGF-β and by inhibiting iNOS and NO release, and reducing expression of proinflammatory cytokines and prostaglandin E2 production.
  • E2 at periovulatory to pregnancy levels inhibits NF-κB activation, which must be viewed as an antiinflammatory signal
  • It was shown that E2 concentrations equal to or above 10−10 m are necessary to inhibit NF-κB activation
  • important proinflammatory cytokines are typically inhibited at periovulatory (proestrus) to pregnancy levels of E2, which is evident for IL-6, IL-8, and TNF
  • low E2 concentrations were demonstrated to have no or even stimulatory effects
  • This renders a woman in the postmenopausal phase to a more proinflammatory situation
  • most in vitro studies demonstrated a stimulatory effect of E2 on secretion of IL-4, IL-10, and TGF-β typically at periovulatory to pregnancy levels
  • E2 at periovulatory to pregnancy levels has an ameliorating effect on chronic inflammatory diseases as long as B cell-dependent immunity or an overshooting fibrotic tissue repair process do not play a crucial pathogenic role. However, when the B cell plays an important role, E2 might even stimulate the disease process as substantiated by flare-ups in SLE during pregnancy
    • Nathan Goodyear
       
      SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis
  • Short-term administration of E2 at pregnancy levels was shown to induce an inflammatory response specific to the lateral prostate of the castrated male rat
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    great review of the complex interaction between Estrogens and inflammation.  Reference here is in females.
Nathan Goodyear

'Metabolic syndrome' in the brain: deficiency in omega-3 fatty acid exacerbates dysfunc... - 0 views

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    diets with high high-fructose corn syrup and low omega-3 shown to slow cognitive processing in rat model.  This is basically, metabolic syndrome of the brain, as it is the result of hyperinsulinemia.
Nathan Goodyear

T cells in systemic sclerosis: a reappraisal. - ResearchGate - 0 views

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    Article looks at the role of IL-6 in fibrosis in scleroderma.  The fibrosis in scleroderma appears to be a Th2 driven process.
Nathan Goodyear

ERβ Impedes Prostate Cancer EMT by Destabilizing HIF-1α and Inhibiting VEGF-M... - 0 views

  • Loss of ERβ1 expression also resulted in a significant increase in migration and invasion (Figure 2F), functions characteristic of an EMT
  • we hypothesized that ERβ functions as a “gatekeeper” of the epithelial phenotype
  • breast and prostate are different with respect to ER expression and function
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    The process of androgen deprivation therapy needs to be re-evaluated.  Why?  First, the CVD side effects associated with the androgen depletion.  Second, the depletion of 3 beta androstanediol that has been shown to bind to ER beta and inhibit growth.  As in this study that finds that ER beta activity slows prostate cancer through destabilizing of HIF-1 alpha and by inhibiting VEGF.
Nathan Goodyear

Potential Prostate Cancer Drug Target: Bioactivation of Androstanediol by Conversion to... - 0 views

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    Article discusses the the conversion of 3-alpha-diol back to DHT and this role in prostate cancer in androgen deprivation therapy.  What we now know is that this metabolite interacts with ER alpha receptor to promote proliferation.  Carcinogenesis appears to be primarily an estrogen driven process and her in prostate cancer, the androgen metabolites are promoting proliferation through estrogen receptors.
Nathan Goodyear

Morning free and total testosterone in HIV-infected men: implications for the assessmen... - 0 views

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    low T is found in 20-70% of men with HIV.  What is interesting about this article is that Total Testosterone was found to be a poor assessment of biological active Testosterone.  Free Testosterone assessed in the am was shown to be a better functional assessment in these men.  Serum is a poor choice though.  The process of equilibrium dialysis to calculate free Testosterone is filled with variables that will effect reliability.  Increases SHBG was found associated.
Nathan Goodyear

Dihydrotestosterone may inhibit hypothalamo-pi... [Neurosci Lett. 2004] - PubMed - NCBI - 0 views

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    Mouse study finds that DHT metabolite provides negative feedback to HPA via 3beta androstaendiol.  What is interesting is that this signaling occurred through ER beta.  Androgen signaling processed through estrogen receptors.
Nathan Goodyear

Estrogen signaling and disruption of androgen metab... [Prostate. 2007] - PubMed - NCBI - 0 views

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    Cadmium exposure/toxicity promotes prostate tumor growth and it does this via a AR independent process.  The authors propose that it is via estrogen receptors and estrogen signaling from DHT metabolites.
Nathan Goodyear

Androgen Deprivation Therapy, Insulin Resistance, and Cardiovascular Mortality: An Inco... - 0 views

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    Androgen deprivation therapy is associated with increased diabetes, metabolic syndrome, insulin resistance, and cardiovascular mortality.  The longer the duration of therapy, the more the progression of metabolic dysfunction.  This process seems similar to chemotherapy i.e. secondary cancer due to chemotherapy.  The treatment of one disease, prostate cancer in this case, leads to an increase in the risk of the #1 killer in men--logic seems severely flawed there.
Nathan Goodyear

Estrogen attenuates glutamate-induced cell death by inhibiting Ca2+ influx through L-ty... - 0 views

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    Estradiol inhibits glutamate mediated influx of calcium and thus cell death in cell line.  Glutamate, the principle excitatory neurotransmitter, is involved in neurodegeneration through activation of calcium channels.  This study of cell line cultures found that Estradiol inhibits this process.  I question whether this is applicable to both men and women.  Time will tell.
Nathan Goodyear

Progesterone enhances transthyretin expressio... [J Mol Neurosci. 2011] - PubMed - NCBI - 0 views

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    Postmenopausal cognitive decline is a common complaint.  Declining Estradiol and progesterone have been implicated, in part, to this cognitive decline.  This study finds that progesterone increases expression of Transthyretin, a protein that processes amyloid Beta protein.  This amyloid Beta protein is associated with damage found in Alzheimer's. 
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