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Nathan Goodyear

The Gut Microbiota and Type 1 Diabetes - 0 views

www.ncbi.nlm.nih.gov/...PMC4761565

diabetes type I diabetes gut gut flora gut health gut microbiome gut microbiota dysbiosis

shared by Nathan Goodyear on 17 Oct 16 - No Cached
  • A study by Bosi and colleagues suggested that the increased gut permeability preceded the clinical onset of T1D
  • gut permeability may be an important player in the development of T1D but, as yet, the findings in human studies have shown association but causation will be more difficult to prove.
  • Early childhood (≤ 3 month) introduction to cereals [10, 11] and cow's milk [48] were shown to promote beta cell autoimmunity
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  • These findings suggest that prebiotics and probiotics could be potential therapeutic tools to improve gut integrity in various intestinal inflammatory and autoimmune diseases including T1D
  • Nathan Goodyear on 17 Oct 16
     
    another great review article of gut dysbiosis, altered gut permeability and type I diabetes.
Nathan Goodyear

The Effect of Microbiota and the Immune System on the Development and Organization of t... - 0 views

www.gastrojournal.org/...fulltext

ENS enteric nervous system gut gut health gut bacteria gut microbiome gut-brain brain Parkinson's disease nervous system

shared by Nathan Goodyear on 30 Nov 16 - No Cached
  • Nathan Goodyear on 30 Nov 16
     
    great read on the enteric nervous system and it interaction with the host immune system and the brain.
Nathan Goodyear

Gender and sex hormones in multiple sclerosis pathology and therapy - 0 views

www.ncbi.nlm.nih.gov/...PMC2689399

hormones MS multiple Sclerosis Estriol progesterone

shared by Nathan Goodyear on 11 Jan 17 - No Cached
  • It is now well recognized that the disease manifestation is reduced in pregnant women with relapsing-remitting MS
  • This occurs particularly during the third trimester when levels of estrogens (estradiol and estriol) and progesterone (see Table 2) are elevated up to about 20 times
  • This seems well correlated with a decrease in active white matter lesions detected by MRI
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  • This clinical improvement is however followed by temporary rebound exacerbations at post-partum, when the hormone levels decline
  • a shift from Th1 to Th2 immune response, expansion of suppressive regulatory T lymphocytes and decrease in the number of circulating CD16+ natural killer (NK)-cells
  • Th1 lymphocytes secrete proinflammatory cytokines (e.g. IL-2, IFNgamma, lymphotoxin) while Th2 cells secrete anti-inflammatory cytokines (e.g. IL-4, IL-5, IL-10), which favor humoral-mediated responses
  • Th2 cytokines are associated with down-regulation of Th1 cytokines and this Th2 shift is believed to provide protection from allograft rejection during pregnancy as well as from Th1-mediated autoimmune disease
  • it is worth noting that the levels of other hormones with anti-inflammatory activity (1,25-dihydroxy-vitamin D3, norepinephrine, cortisol) also increase by 2 to 4 times during late pregnancy
  • 1,25-dihydroxy vitamin D3 induces regulatory T-cell function important for development of self-tolerance
  • breast-feeding does not alter the relapse rate in women with MS
  • Leptin is a pleiotropic hormone produced primarily by adipocytes but also by T lymphocytes and neurons
  • Several lines of evidence indicate that leptin contributes to EAE/MS pathogenesis, influencing its onset and clinical severity, by acting as a proinflammatory cytokine which promotes regulatory T cell (Treg) anergy and hyporesponsiveness, resulting in increased Th1 (TNFalpha, INFgamma) and reduced Th2 (IL-4) cytokine production
  • circulating leptin levels are increased in relapsing-remitting MS patients (men and women analyzed together) while the CD4+CD25+Treg population decreases
  • As the leptin plasma concentrations are proportional to the amount of fat tissue, obese/overweight individuals produce higher levels of leptin
  • Nielsen et al found that estradiol and progesterone exert neuroprotection against glutamate neurotoxicity, while MPA antagonizes the neuroprotective effect of estradiol and exacerbated neuron death induced by glutamate excitotoxicity
  • Nathan Goodyear on 11 Jan 17
     
    very good review of the differences in MS and hormones between the sexes.
kyra smith

Clinical Data Management Services & System - WorkSure® - 0 views

www.worksure.org/...clinical-data-management

Clinical Data Management System

shared by kyra smith on 16 Jan 17 - No Cached
  • kyra smith on 16 Jan 17
     
    Clinical Data Management System (CDM) is leading clinical development industry into a new innings of transformation. It also now faces an elevating attention from the safety and regulatory sectors, which have never been seen earlier. For the biopharmaceutical and medical devices companies, ineffectual data management can make it impossible to market the products efficiently in the multifaceted business and regulatory milieu.
Nathan Goodyear

Gut Endotoxin Leading to a Decline IN Gonadal function (GELDING) - a novel theory for t... - 0 views

www.ncbi.nlm.nih.gov/...PMC4918028

GELDING theory GELDING LPS gut gut health inflammation low T low Testosterone Testosterone hypogonadism obesity

shared by Nathan Goodyear on 30 Jun 16 - No Cached
  • GELDING theory (Gut Endotoxin Leading to a Decline IN Gonadal function)
  • trans-mucosal passage of bacterial lipopolysaccharide (LPS) from the gut lumen into the circulation is a key inflammatory trigger underlying male hypogonadism
  • Obesity and a high fat/high calorie diet are both reported to result in changes to gut bacteria and intestinal wall permeability, leading to the passage of bacterial endotoxin (lipopolysaccharide- LPS) from within the gut lumen into the circulation (metabolic endotoxaemia), where it initiates systemic inflammation.
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  • Endotoxin is known to reduce testosterone production by the testis, both by direct inhibition of Leydig cell steroidogenic pathways and indirectly by reducing pituitary LH drive, thereby also leading to a decline in sperm production.
  • Nathan Goodyear on 30 Jun 16
     
    Ever heard of the GELDING theory?  This involves the link between LPS endotoxin from the gut and low Testosterone in obese men.
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
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  • 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

Direct and Indirect Inhibition of Th1 Development by Progesterone and Glucocorticoids - 0 views

www.jimmunol.org/...1087.abstract

progesterone immune system Th1 Th2

shared by Nathan Goodyear on 20 Apr 12 - No Cached
  • Nathan Goodyear on 20 Apr 12
     
    Progesterone found to modulate the immune system.  Progesterone decreases Th1 activity to increase Th2.  This has significant immune mediated disorders/disease.
Nathan Goodyear

The World Is Fat - Obesity Rates in Developed Countries from the OECD - NYTimes.com - 0 views

economix.blogs.nytimes.com/...the-world-is-fat

obesity US USA overweight countries

shared by Nathan Goodyear on 18 Mar 12 - No Cached
  • Nathan Goodyear on 18 Mar 12
     
    Scary statistics.  USA is #1.  But, this is the one category, that we don't want to be #1 in.
Nathan Goodyear

JCI - Chronic inflammation in fat plays a crucial role in the development of obesity-re... - 0 views

www.jci.org/19451

inflammation obesity overweight WAT adipose tissue fat insulin resistance type II diabetes DM

shared by Nathan Goodyear on 20 Mar 12 - No Cached
  • Nathan Goodyear on 20 Mar 12
     
    how inflammation contributes to obesity.  Nice discussion of the inflammatory signaling that leads to obesity.  This occurs predominately in white adipose tissue WAT.  This leads to insulin resistance and type II DM.
Nathan Goodyear

Figure 1 : Endogenous kynurenines as targets for drug discovery and developme... - 0 views

www.nature.com/...nrd870_F1.html

Tryptophan metabolism

shared by Nathan Goodyear on 14 Dec 11 - No Cached
  • Nathan Goodyear on 14 Dec 11
     
    nice diagram of Tryptophan metabolism
Nathan Goodyear

Development and validation of stable-isotope dilution liquid chromatography-tandem mass... - 0 views

onlinelibrary.wiley.com/...full

hormone hormones liquid chromatography saliva salivary testing test evaluation BHRT progesterone

shared by Nathan Goodyear on 26 Nov 11 - No Cached
  • Nathan Goodyear on 26 Nov 11
     
    LC-ESI-MS/MS) for hormone evaluation has been validated for hormone testing.  Progesterone was used in this study.
Nathan Goodyear

Cell Metabolism - Orexin Is Required for Brown Adipose Tissue Development, Differentiat... - 0 views

www.cell.com/...S1550-4131(11)00340-8

orexin brown-fat weight-loss overweight obesity brown fat

shared by Nathan Goodyear on 01 Dec 11 - No Cached
  • Nathan Goodyear on 01 Dec 11
     
    orexin plays a role in weight gain through regulation of brown fat differentiation.  Low brown fat predisposes one to obesity.  Higher brown fat increases metabolism and thus increases fat burning capacity
Nathan Goodyear

A PGC1-[agr]-dependent myokine that drives brown-fat-like development of white fat and ... - 0 views

www.nature.com/...nature10777.html

Irisin hormone weight-loss PGC1-alpha white fat WAT brown thermogenesis

shared by Nathan Goodyear on 23 Jan 12 - No Cached
  • Nathan Goodyear on 23 Jan 12
     
    Irisin, new recognized hormone, found to stimulate PGC1-alpha conversion of white fat to brown fat.  This increases thermogenesis and fat burning.
Nathan Goodyear

Targeting gut microbiota in obesity: effects of prebiotics and probiotics : Article : N... - 0 views

www.nature.com/...nrendo.2011.126.html

LPS lipopolysaccharides gut microbiota dysbiosis inflammation obesity metabolic endotoxemia health probiotics

shared by Nathan Goodyear on 18 Jan 12 - No Cached
  • gut microbes have a role in the host's metabolic homeostasis
  • lipopolysaccharide (LPS)
  • Associations between circulating LPS level, consumption of a high-fat diet and the presence of obesity and type 2 diabetes mellitus have been confirmed in humans
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  • associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
  • A link between energy intake (high-fat diet) and metabolic endotoxemia has also been described
  • high-fat diet induces metabolic endotoxemia in healthy individuals.
  • metabolic endotoxemia is associated with systemic and adipose tissue inflammation in pregnant women with obesity
  • A growing amount of evidence indicates that changes in the integrity of the intestinal barrier occur both in the proximal and the distal part of the gut, which can contribute to the entrance of LPS into the systemic circulation
  • intestinal endocannabinoid system
  • The low-grade systemic inflammation that characterizes the obese phenotype is controlled by peptides that are produced in the gut. These peptides are influenced by the presence or absence of the gut microbiota
  • these findings suggest that the gut microbiota modulates the biological systems that regulate the availability of nutrients, energy storage, fat mass development and inflammation in the host, which are all components of the obese phenotype
  • Nathan Goodyear on 18 Jan 12
     
    good look of how the the gut health, or lack there of, can influence energy homeostasis and contribute to obesity.  This article points to the presence of LPS playing a role in metabolic endotoxemia.  It does discuss the importance of the microbiota and their possible role in the low-grade systemic inflammation condition that is obesity.
Nathan Goodyear

Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 0 views

www.sciencedirect.com/...S0014579307012082

inflammation insulin resistance IR PPAR TNF-alpha IL-6 IL-10 IL-1Beta JNK GLT-4 Resistin adiponectin Gherlin NF-kapppB iNOS lkkb obesity TLR-4

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • A subsequent study by Yuan et al. showed that Tnf treatment of 3T3L1 adipocytes induces insulin resistance and that this could be prevented by pretreatment of cells with aspirin
  • Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
  • Insulin is a pleiotropic hormone
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  • the percentage of macrophages in a given adipose tissue depot is positively correlated with adiposity and adipocyte size
  • Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes
  • Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NFκB activation by reducing IKK activity [38]
  • adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression
  • One theory holds that the expansion of adipose tissue leads to adipocyte hypertrophy and hyperplasia and that large adipocytes outstrip the local oxygen supply leading to cell autonomous hypoxia with activation of cellular stress pathways
  • The use of the anti-inflammatory compounds, salicylate and its derivative aspirin, for treating symptoms of T2DM dates back over 100 years
  • elevated levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states
  • overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses
  • Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity
  • In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter
  • macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the “classically activated” pro-inflammatory macrophage, to the M2 state or the “alternatively activated” non-inflammatory cell
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes iNOS (reviewed in [33]
  • Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes.
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • elevated JNK activity in liver, adipose tissue and skeletal muscle of obese insulin resistant mice, and knockout of Jnk1 (Jnk1−/−) leads to amelioration of insulin resistance in high fat diet
  • Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance
  • C-reactive protein (CRP)
  • these studies highlight the possibility that increased iNOS activity plays a direct role in the pathogenesis of insulin resistance
  • the important role of Ikkb in the development of obesity and inflammation-induced insulin resistance.
  • It is probable that local concentrations of inflammatory mediators, such as FFAs, Tnf or other cytokines/adipokines contribute to this polarity switch
  • Tnf and other cytokines/chemokines are symptomatic of inflammation, and while they propagate and/or maintain the inflammatory state, they are not the initial cause(s) of inflammation
  • Tlr4, in particular, is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria
  • Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system.
  • Tlr4 stimulation results in the activation of both Ikkb/NFκB and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1, etc. (reviewed in [57
  • Nathan Goodyear on 10 Jan 12
     
    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

JCI - Inflammatory links between obesity and metabolic disease - 0 views

www.jci.org/57132

obesity overweight weight-loss inflammation metabolic disease

shared by Nathan Goodyear on 04 Jan 12 - No Cached
  • metainflammation
  • The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
  • It is clear that inflammation participates in the link between obesity and disease
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  • Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
  • adipose tissue macrophage (ATM)
  • Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
  • increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
  • The M2 activation state is intrinsically linked to the activity of PPARδ and PPARγ
  • well-known regulators of lipid metabolism and mitochondrial activity
  • Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
  • inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
  • Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
  • JNK, TLR4, ER stress)
  • NAFLD is associated with an increase in M1/Th1 cytokines and quantitative increases in immune cells
  • Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
  • DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
  • saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
  • Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
  • Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
  • Placental inflammation is a characteristic of maternal obesity
  • a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
  • Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
  • Nod-like receptor (NLR) family of PRRs
  • ceramides and sphingolipids
  • The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
  • adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
  • Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)
  • NF-κB, obesity also activates JNK in insulin-responsive tissues
  • Nathan Goodyear on 04 Jan 12
     
    must read to see our current knowledge on the link between inflammation and obesity.
Nathan Goodyear

New Developments and Novel Therapeutic Perspectives for Vitamin C - 0 views

jn.nutrition.org/...2171.abstract

vitamin C IV intravenous therapy treatment cancer cardiovascular

shared by Nathan Goodyear on 14 Nov 11 - No Cached
  • Nathan Goodyear on 14 Nov 11
     
    vitamin C is powerful anti-oxidant that has implications in cardiovascular disease and cancer; but High serum levels of vitamin C are hard to maintain orally, but can be maintained via IV therapy
Nathan Goodyear

Accumulation of Dietary Docosahexaenoic Acid in the Brain Attenuates Acute Immune Respo... - 0 views

stroke.ahajournals.org/...2903.abstract

Omega-3 EFA DHA stroke inflammation brain injury head trauma

shared by Nathan Goodyear on 17 Nov 11 - No Cached
  • Nathan Goodyear on 17 Nov 11
     
    DHA shown to protect against post stroke inflammation and injury.  This has implications on any head injury.
ind swift

Gynecology Drugs| Pharmaceutical Formulations Development | Indian Drug Manufacturers - 1 views

www.indswiftltd.com/gyno_swift_division.php

DISTONE (IJ) 1X24

shared by ind swift on 14 Aug 12 - No Cached
ind swift liked it
  • ind swift on 14 Aug 12
     
    4 ANAPROCT CAP Each Capsule Contains: Neem (Azadirachta Indica) 25 Mg Suran (Amorphophallus Companulatus) 25 Mg Yashtimadhu (Glycirrhiza Glabra) 25 Mg Haritaki (Terminalia Chebula) 25 Mg Kumarighansatva (Aloe Vera) 50 Mg Mukta Shukti Bhasma(Pearl Oyster) 75 Mg Arishtak (Sapindus Trifoliatus) 75 Mg Saphatika Bhasma (Potash Alum) 100 Mg Daruhaldi Ghansatva(Ext.Berberis Aristata)100 Mg Capsule Anit-Haemorroidal Haemostat 5 ANAPROCT OINTMENT Lidocaine U.S.P.
Nathan Goodyear

ScienceDirect.com - Journal of Chromatography B - Simultaneous determination of salivar... - 0 views

www.sciencedirect.com/...S1570023208008131

LC-MS liquid chromatography mass mass spectroscopy saliva salivary hormone hormones testosterone DHEA

shared by Nathan Goodyear on 14 Aug 12 - No Cached
  • Nathan Goodyear on 14 Aug 12
     
    LC-MS for salivary testosterone and DHEA validated.  Also, T and DHEA were shown to have specific diurnal rhythms.  Changes in levels were also followed after DHEA therapy.
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