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Nathan Goodyear

Acute effects of interferon-alpha administration on testosterone concentrations in heal... - 0 views

www.eje-online.org/...371.short

interferon hepatitis Hepatitis C low T low Testosterone Testosterone FAI free Androgen Index men male hormone hormones

shared by Nathan Goodyear on 22 Apr 15 - No Cached
  • Nathan Goodyear on 22 Apr 15
     
    Interferon therapy in men with hepatitis C was found to decrease total Testosterone and Free Androgen index at the level of the gonads; this was independent of the HPA in this study.
Nathan Goodyear

Sexual dysfunction in males with chronic hepatitis C and antiviral therapy: interferon-... - 0 views

joe.endocrinology-journals.org/...345.long

hepatitis Hepatitis C HCV interferon low T low testosterone deficiency men male hormone hormones depression

shared by Nathan Goodyear on 22 Apr 15 - No Cached
  • Nathan Goodyear on 22 Apr 15
     
    Study of men with hepatitis C and interferon therapy found decrease in free and total Testosterone levels in men.  The study results suggest a non-HPA effect, which suggests more of a peripheral effect at the level of the TEsticles.
Nathan Goodyear

Induction of interferon and activation of NK cells and macrophages in mice by oral admi... - 0 views

www.ncbi.nlm.nih.gov/...2581116

Germanium NK cells immune system interferon

shared by Nathan Goodyear on 30 May 18 - No Cached
  • Nathan Goodyear on 30 May 18
     
    Orally administered Germanium, at 300 mg/kg) found to increase NK activity and activation of macrophages via Interferon in mouse animal model.
Nathan Goodyear

Effect of silymarin (milk thistle) on liver disease in patients with chronic hepatitis ... - 0 views

www.ncbi.nlm.nih.gov/...22797645

milk thistle hepatitis C hepatitis liver disease HCV

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    study finds milk thistle unsuccessful in lower ALT in HCV patients that had failed interferon therapy.  The dosing used in this study was low.
Nathan Goodyear

http://www.diabetologia-journal.org/files/Narendran.pdf - 0 views

www.diabetologia-journal.org/...Narendran.pdf

exercise inflammation growth hormone GH IGF-1 TNF-alpha IL-6 IL-1beta IL-1Ra interferon-gamma diabetes islet cells

shared by Nathan Goodyear on 28 Oct 14 - No Cached
  • Nathan Goodyear on 28 Oct 14
     
    Exercise is not just for calories out.  Exercise increases growth hormone, IGF-1, glucagon-like peptide 1, IL-6, and IL-1ra.  The effect is to GH increases beta islet cell mass and protects beta cell lines against IL-1beta, Interferon-gamma and TNF-alhpa induced apoptosis.  IL-6 increased production increases GLP-1 and IL-1ra which counters IL-1beta.  Interleukin-1beta induces islet cell apoptosis and thus IL-1ra counters this pro-inflammatory signal.
Nathan Goodyear

Epigallocatechin-3-gallate ameliorates experimental autoimmune encephalomyelitis by alt... - 0 views

www.researchgate.net/...lance_among_CD4_T-cell_subsets

EGCG epigallocatechin-3-gallate autoimmune disease MS cytokine cytokines inflammation

shared by Nathan Goodyear on 22 Jan 14 - No Cached
  • Nathan Goodyear on 22 Jan 14
     
    EGCG found to reduce cytokine production in animal model of MS, experimental autoimmune encephalomyelitis.  Specifically, EGCG reduced interferon gamma, IL017, IL-6, IL-1beta, TNF-alpha and decreased Th1 and Th17 cells with an increase in Treg cells.
Nathan Goodyear

Sex hormones as immunomodulators in heal... [Int Immunopharmacol. 2001] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...11407317

Lupus SLE inflammation Sex hormones hormone Estradiol Testosterone

shared by Nathan Goodyear on 31 Jul 13 - No Cached
  • Nathan Goodyear on 31 Jul 13
     
    Estradiol in mice predisposed to Lupus have increased inflammation and characteristics of Lupus.  In contrast, Estradiol in those without predisposition, do not.  Clearly this is an inflammatory signaling problem.  Studies have shown an Interferon gamma signaling deficit in those with Lupus.  Testosterone decreases the above inflammation signaling.
Nathan Goodyear

Chronic hepatitis C infection and sex hormone levels: effect of disease severity and re... - 0 views

www.ncbi.nlm.nih.gov/...16732861

hepatitis low T low Testosterone liver Hepatitis C HCV Testosterone hormone hormones male man SHBG

shared by Nathan Goodyear on 22 Apr 15 - No Cached
  • Nathan Goodyear on 22 Apr 15
     
    hepatitis associated with a decline in total Testosterone.  This was a positive correlation with worsening hepatitis.  Free Testosterone was not effected.  Interesting, SHBG increased.
Nathan Goodyear

Activation of CNS Inflammatory Pathways by Interferon-alpha: Relationship to Monoamines... - 0 views

www.ncbi.nlm.nih.gov/...PMC2655138

IFN-alpha Interferon-alpha IL-6 CNS inflammation inflammatory depression serotonin 5-hydroxyindoleacetate

shared by Nathan Goodyear on 14 Sep 11 - No Cached
  • Nathan Goodyear on 14 Sep 11
     
    mechanism of peripheral inflammation , via IFN-alpha and IL-6, contribution to depression
Nathan Goodyear

Oncolytic virotherapy promotes intratumoral T cell infiltration and improves Anti-PD-1... - 0 views

www.cell.com/...S0092-8674(17)30952-2

immunotherapy cancer RIGVIR oncolytic therapy PD-1 check point inhibitors

shared by Nathan Goodyear on 23 Oct 18 - No Cached
  • Nathan Goodyear on 23 Oct 18
     
    Study found that viral oncolytic therapy improved efficacy of PD-1 check point inhibitors by 62%. Increased CD8 expression, interferon-gamma...Interesting, starting CD8 levels played no role in predicting outcome.
Nathan Goodyear

Germane facts about germanium sesquioxide: I. Chemistry and anticancer properties. - Pu... - 0 views

www.ncbi.nlm.nih.gov/...15165414

cancer germanium

shared by Nathan Goodyear on 04 Jun 18 - No Cached
  • Nathan Goodyear on 04 Jun 18
     
    only abstract available here.  Great review and discussion of the research behind Germanium Sesquioxide and its immune effects in the fight against cancer.  Primary effects are via increase in Interferon gamma and increase in NK cell activity; but it also inhibits tumor growth and metastatic potential. The germanium compound is specific to the sesquioxide compound.
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
  • ...54 more annotations...
  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

Natural Killer Cells in Pregnancy and Recurrent Pregnancy Loss: Endocrine and Immunolog... - 0 views

edrv.endojournals.org/...44.full

natural killer cells pregnancy loss recurrent immune system miscarriage NK

shared by Nathan Goodyear on 15 Apr 12 - No Cached
  • NK cells have been the cells most extensively studied, primarily because they constitute the predominant leukocyte population present in the endometrium at the time of implantation and in early pregnancy
  • parental chromosomal abnormalities, uterine anatomic anomalies, endometrial infections, endocrine etiologies (luteal phase defect, thyroid dysfunction, uncontrolled diabetes mellitus), antiphospholipid syndrome, inherited thrombophilias, and alloimmune causes
  • estrogen
  • ...28 more annotations...
  • progesterone
  • prolactin
  • In summary, in vivo animal experiments have shown an inhibitory role of estrogen on peripheral NK cell lytic activity, which is partly due to suppression of NK cell output by the bone marrow and partly due to suppression of individual NK cell cytotoxicity. However, in vitro studies so far have failed to show conclusively a direct effect of estrogen on NK cells.
  • At the progesterone concentrations believed to be present in the uterus [up to 10−5 m at the maternal-fetal interface (35)], studies consistently show inhibition of lymphocyte proliferation (33) and inhibition of NK cytolytic activity in vitro
  • The exact role of prolactin in NK cell regulation is unknown.
  • The overall effects of estrogen on NK cells are likely multifactorial, therefore, and depend on the type of cell affected as well as the kind of ER expressed by that cell.
  • It is known that progesterone can directly affect T cell differentiation in vitro, suppressing development of the Th1 pathway and enhancing differentiation along the Th2 pathway (44)
  • Th1 cells predominantly produce interferon-γ (IFN-γ), IL-2, and TNF-β and are involved in cell-mediated immunity. Th2 cells produce IL-4, IL-5, IL-6, IL-10, and IL-13 and stimulate humoral immunity
  • Furthermore, in response to progesterone, γδ T cells produce progesterone-induced blocking factor (PIBF) (54
  • A defining characteristic of NK cells is their ability to lyse target cells without prior sensitization and without restriction by HLA antigens.
  • NK cell function is mainly regulated by IL-2 and IFN-γ
  • IL-2 causes both NK cell proliferation and enhanced cytotoxicity. IFN-γ augments NK cytolytic activity, but does not cause NK proliferation. The two cytokines act synergistically to augment NK cytotoxicity (6).
  • The largest leukocyte population in the endometrium consists of NK cells named large granulated lymphocytes
  • there is a significant increase in the number of uNK cells throughout the secretory phase, which peaks in early pregnancy when uNK cells comprise about 75% of uterine leukocytes (62)
  • Second, uNK cell phenotype changes during the normal menstrual cycle and early pregnancy (68)
  • general proinflammatory effect of estrogen, causing an influx of macrophages and neutrophils, which is antagonized by progesterone through its receptor (70, 71).
  • The mechanism of such a progesterone-induced local immunosuppression is unclear.
  • progesterone plays an important role in proliferation and differentiation of uNK cells (32).
  • Through promotion of a uterine Th2 environment, progesterone could indirectly affect uNK cell function
  • The mechanism of this increase in uNK cell numbers has been addressed in both human and mouse models, and is likely the result of: 1) recruitment of peripheral NK cells to the uterus, and 2) proliferation of existing uNK cells
  • prolactin system plays an important role in implantation and the maintenance of pregnancy
  • the exact pathways of hormonal regulation of NK cells remain to be delineated.
  • The exact function of uNK cells has not yet been unequivocally determined
  • uNK cells express a different cytokine profile, compared with resting peripheral NK cells. mRNAs for granulocyte CSF, M-CSF, GM-CSF, TNF-α, IFN-γ, TGF-β, and leukemia inhibitory factor (LIF) have been found in decidual CD56+ cells
  • Their increased numbers in early pregnancy, their hormonal dependence, and their close proximity to the infiltrating trophoblast all suggest that they play an important role in the regulation of the maternal immune response to the fetal allograft and the control of trophoblast growth and invasion during human pregnancy
  • role of uNK cell-derived cytokines on trophoblast growth and differentiation (114, 115, 116, 117).
  • Th1 immunity to trophoblast is associated with RPL, whereas Th2 immunity is associated with a successful pregnancy
  • RPL is associated with Th1 immunity, for which NK cells are partly responsible.
  • Nathan Goodyear on 15 Apr 12
     
    dysregulated immune system plays role in recurrent miscarriage.  Specifically, this article discusses natural killer cells (NK).
Nathan Goodyear

S-adenosyl methionine improves early viral responses and interferon-stimulated gene ind... - 0 views

www.ncbi.nlm.nih.gov/...PMC3021477

SAMe Hepatitis C virus viral infection

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe shown to be beneficial as an early response treatment in Hepatitis C. Maybe as a treatment for flu?
Nathan Goodyear

World J Gastroenterol - 0 views

www.wjgnet.com/...5317.htm

hepatitis IV vitamin C IV intravenous vitamin C glutathione B-complex HCV

shared by Nathan Goodyear on 25 Sep 13 - No Cached
  • Nathan Goodyear on 25 Sep 13
     
    IV antioxidant mixture of vitamin C, glutathione, glycyrrhiza, and B-complex reduces liver enzymes.  Arm taking only oral shows no decline in liver enzymes.
Nathan Goodyear

American Journal of Gastroenterology - Abstract of article: Hepatitis-C Patients Have R... - 0 views

www.nature.com/...ajg2007533a.html

Hepatitis C hepatitis growth hormone HGH IGF-1 liver disease hormone hormones

shared by Nathan Goodyear on 22 Apr 15 - No Cached
  • Nathan Goodyear on 22 Apr 15
     
    People with chronic hepatitis C have low growth hormone production.  HGH therapy did not increase IGF-1 due to liver disease.
Nathan Goodyear

Antidepressants inhibit interferon-gamma-induced ... [Exp Neurol. 2007] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17481608

anti-depressants inflammation IL-6 depression

shared by Nathan Goodyear on 14 Sep 11 - No Cached
  • Nathan Goodyear on 14 Sep 11
     
    anti-depressants inhibit inflammatory IL-6 production from microglial cells in brain, suggesting anti-inflammatory effects of antidepressants as role in improving depression symptoms
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