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Windows Customer Support Number

Windows technical support number 1-800-261-4071 - 0 views

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Windows technical customer services support help

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  • Windows Customer Support Number on 05 Jul 16
     
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Windows technical customer services tech support help

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  • Windows Customer Support Number on 13 Jul 16
     
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Nathan Goodyear

Fat-free mass index and fat mass index percentiles in Caucasians aged 1898 y - 0 views

www.nature.com/...0802037a.html

FMI FFMI body composition BMI fat mass index

shared by Nathan Goodyear on 27 Jul 16 - No Cached
  • BMI is the sum of FFMI+FMI
  • FMI were significantly higher in elderly subjects as compared to younger ones
  • During menopause and aging39,40 changes in FFM and FM are not adequately picked up by changes in BMI
  • ...8 more annotations...
  • One advantage of FMI, as compared to the BMI concept, is that it amplifies the relative effect of aging on body fat
  • We believe that the definition of obesity based on relative body fat (ie percentage) remains of great value for the definition of obesity. However, in a situation in which a patient is losing weight without substantially changing his/her relative body fat (as is the case with crash diets), the calculation of FMI will quantitatively reveal the amount of body fat store lost.
  • high sensitivity of FMI (respectively FFMI) to a slight change of body fat stores
  • Sarcopenic obesity has been defined as a low FFM associated with a high body fat
  • relative FFM lower than 73% (ie a relative body fat greater than 27%) in men and a FFM lower than 62% (ie a body fat greater than 38%) in women.
  • FMIs greater than 8.2 kg/m2 in men and 11.8 kg/m2 in women would define the 'overfat' status (rather than the overweight range) in terms of fat mass
  • In young women, FMI averaged 5.5 kg/m2 (range 5th-95th percentile: 3.5-8.7 kg/m2) ie 38% higher than in males
  • the average FMI for young men was 4.0 kg/m2
  • Nathan Goodyear on 27 Jul 16
     
    good review of FMI, FFMI, and BMI.
Windows Customer Support Number

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Nathan Goodyear

Large Differences in Testosterone Excretion in Korean and Swedish Men Are Strongly Asso... - 0 views

jcem.endojournals.org/...687.full

Testosterone epi-Testosterone metabolism UGT2B17 SNP korean swedish

shared by Nathan Goodyear on 20 Feb 12 - No Cached
  • Nathan Goodyear on 20 Feb 12
     
    men with UGT2B17 found to be poor metabolizers of endogenous Testosterone.  Normally, epi-Testosterone and Testosterone exist in a relative 1:1 ratio,  However, in these individuals with this SNP, they will have slightly elevated Testosterone levels due to disrupted phase II testosterone metabolism (glucuronidation).  This is found in 60% of Asian men, 50% of black men, and 1% in white men.
Nathan Goodyear

Reduction of Inflammatory Cytokine Concentrations and Improvement of Endothelial Functi... - 0 views

circ.ahajournals.org/...804

obesity overweight visceral adiposity adipose tissue cytokines adipocytokines TNF-alpha IL-6 P-selectin ICAM-1 VCAM-1 CVD cardiovascular disease weight loss weight loss

shared by Nathan Goodyear on 30 Mar 12 - No Cached
  • Nathan Goodyear on 30 Mar 12
     
    adipose tissue releases inflammatory markers (cytokines IL-6, TNF-alpha, V-CAM-1, ICAM-1, and P-selectin). Associated endovascular disfunction and eventually cardiovascular disease.  A direct link between obesity induced inflammation and endovascular dysfunction.  Weight loss in these obese women reduced secretion of the associated inflammatory cytokines and thus decreased vascular dysfunction.
Nathan Goodyear

Testosterone and glucose metabolism in men: current concepts and controversies - 0 views

joe.endocrinology-journals.org/...R37.full

shared by Nathan Goodyear on 04 Feb 14 - No Cached
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      80% of E2 production in men, that will cause low T in men, comes from SQ adiposity.  This leads to increase in visceral adiposity.
  • Only 5% of men with type 2 diabetes have elevated LH levels (Dhindsa et al. 2004, 2011). This is consistent with recent findings that the inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
  • Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion
  • ...32 more annotations...
  • kisspeptin has emerged as one of the most potent secretagogues of GNRH release
  • Consistent with the hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
  • Figure 4
  • Interestingly, a recent 16-week study of experimentally induced hypogonadism in healthy men with graded testosterone add-back either with or without concomitant aromatase inhibitor treatment has in fact suggested that low oestradiol (but not low testosterone) may be responsible for the hypogonadism-associated increase in total body and intra-abdominal fat mass
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      This does not fit with the research on receptors, specifically estrogen receptors.  These studies that the authors are referencing are looking at "circulating" levels, not tissue levels.
  • A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
  • Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
  • This is supported by observational studies showing that weight gain and development of diabetes accelerate the age-related decline in testosterone
  • Weight loss can reactivate the hypothalamic–pituitary–testicular axis
  • The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
  • Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
  • Several observational and randomised studies reviewed in Grossmann (2011) have shown that weight loss, whether by diet or surgery, leads to substantial increases in testosterone, especially in morbidly obese men
  • This suggests that weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
  • There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
  • in those men in whom glycaemic control worsened, testosterone decreased
  • successful weight loss combined with optimisation of glycaemic control may be sufficient to normalise circulating testosterone levels in the majority of such men
  • weight loss, optimisation of diabetic control and assiduous care of comorbidities should remain the first-line approach.
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      This obviously goes against marketing-based medicine
  • In part, the discrepant results may be due to the fact men in the Vigen cohort (Vigen et al. 2013) had a higher burden of comorbidities. Given that one (Basaria et al. 2010), but not all (Srinivas-Shankar et al. 2010), RCTs in men with a similarly high burden of comorbidities reported an increase in cardiovascular events in men randomised to testosterone treatment (see section on Testosterone therapy: potential risks below) (Basaria et al. 2010), testosterone should be used with caution in frail men with multiple comorbidities
  • The retrospective, non-randomised and non-blinded design of these studies (Shores et al. 2012, Muraleedharan et al. 2013, Vigen et al. 2013) leaves open the possibility for residual confounding and multiple other sources of bias. These have been elegantly summarised by Wu (2012).
  • Effects of testosterone therapy on body composition were metabolically favourable with modest decreases in fat mass and increases in lean body mass
  • This suggests that testosterone has limited effects on glucose metabolism in relatively healthy men with only mildly reduced testosterone.
  • it is conceivable that testosterone treatment may have more significant effects on glucose metabolism in uncontrolled diabetes, akin to what has generally been shown for conventional anti-diabetic medications.
  • the evidence from controlled studies show that testosterone therapy consistently reduces fat mass and increases lean body mass, but inconsistently decreases insulin resistance.
  • Interestingly, testosterone therapy does not consistently improve glucose metabolism despite a reduction in fat mass and an increase in lean mass
  • the majority of RCTs (recently reviewed in Ng Tang Fui et al. (2013a)) showed that testosterone therapy does not reduce visceral fat
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      visceral and abdominal adiposity are biologically different and thus the risks associated with the two are different.
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      yet low T is associated with an increase in visceral adiposity--confusing!
  • testosterone therapy decreases SHBG
  • testosterone is inversely associated with total cholesterol, LDL cholesterol and triglyceride (Tg) levels, but positively associated with HDL cholesterol levels, even if adjusted for confounders
  • Although observational studies show a consistent association of low testosterone with adverse lipid profiles, whether testosterone therapy exerts beneficial effects on lipid profiles is less clear
  • Whereas testosterone-induced decreases in total cholesterol, LDL cholesterol and Lpa are expected to reduce cardiovascular risk, testosterone also decreases the levels of the cardio-protective HDL cholesterol. Therefore, the net effect of testosterone therapy on cardiovascular risk remains uncertain.
  • data have not shown evidence that testosterone causes prostate cancer, or that it makes subclinical prostate cancer grow
  • compared with otherwise healthy young men with organic androgen deficiency, there may be increased risks in older, obese men because of comorbidities and of decreased testosterone clearance
  • recent evidence that fat accumulation may be oestradiol-, rather than testosterone-dependent
Nathan Goodyear

The Androgen Derivative 5α-Androstane-3β,17β-Diol Inhibits Prostate Cancer Ce... - 0 views

cancerres.aacrjournals.org/...5445.full

prostate cancer 3-beta androstanediol DHT metabolite E-cadherin ER beta ER-beta male hormone hormones men

shared by Nathan Goodyear on 27 Jan 14 - No Cached
  • In the early stages, prostate cancer growth is dependent on circulating androgens
    • Nathan Goodyear
      Nathan Goodyear on 27 Jan 14
       
      This is in contrast to studies that show poor prognosis with Lower T at time of diagnosis of prostate cancer
  • 5α-reductase not only provides a potent amplification of the androgenic signal ( 4– 6), but it also prevents estrogen formation by subtracting testosterone from the action of aromatase ( 7, 8), thus blocking activation of the estrogen receptor subtypes (ERα and ERβ; refs. 9, 10)
  • ERβ is the prevailing subtype ( 11), and a growing body of evidence points to the protective role of this receptor in prostate cancer
  • ...3 more annotations...
  • It has been shown that the transformation of the dihydrotestosterone to 5α-androstane-3α,17β-diol (3α-diol) and 5α-androstane-3β,17β-diol (3β-Adiol), generates two metabolites unable to bind the androgen receptor, but possessing a very high affinity for the estrogen receptors
  • the effects of testosterone may result from the balance between the androgenic and the estrogenic molecules originating from its catabolism.
  • Recent data have been published postulating a direct estrogenic role of the 3β-hydroxylated derivatives of dihydrotestosterone in the prostate development and homeostasis
  • Nathan Goodyear on 27 Jan 14
     
    Here is the full article.
Nathan Goodyear

Oestrogen and colorectal cancer: mechan... [Int J Colorectal Dis. 2013] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...23319136

estrogen estriol estradiol estrone colon cancer ER beta ER-beta

shared by Nathan Goodyear on 19 Nov 13 - No Cached
  • Nathan Goodyear on 19 Nov 13
     
    Estrogen early protects against colon cancer, but estrogen increases proliferation late.  The problem here is the estrogens involved.  If ER beta is shown to be highly expressed in the colon, then Estriol would be of benefit as it preferentially binds to ER beta at a rate of 5:1 and Estradiol at a rate of 1:1.  Estriol is currently used in Europe in advanced breast cancer.
Nathan Goodyear

http://www.ccsenet.org/journal/index.php/cco/article/viewFile/26281/16499 - 0 views

www.ccsenet.org/...16499

TK-1 cancer thymidine kinase 1

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  • Nathan Goodyear on 28 Mar 15
     
    another thumbs up for TK-1.  This finds serum and tumor TK-1 differentiate from normal, healthy tissue.
Nathan Goodyear

ω-3 Fatty Acid Supplementation as a Potential Therapeutic Aid for the Recover... - 0 views

advances.nutrition.org/...268.full

omega 3 DHA EPA fish oil TBI traumatic brain injury concussions concussion brain injury

shared by Nathan Goodyear on 30 Aug 15 - No Cached
  • There is a growing body of preclinical literature suggesting that ω-3 FAs, and DHA in particular, may play a therapeutic role in mTBI
  • the potential for ameliorating or possibly even preventing the complications associated with concussions
  • DHA is the predominant ω-3 FA present in the brain, and, consistent with this finding, DHA, and not EPA, has been demonstrated to be critical for brain development and cognitive function throughout life
  • ...7 more annotations...
  • the concentration of EPA in the brain is negligible (77–80), suggesting that EPA plays a limited role in mediating the beneficial effects of LCPUFA supplementation on mTBI pathology
  • the current state of the science regarding LCPUFA supplementation for the treatment of concussion is based primarily on animal models
  • there is evidence that the amount of DHA in brain tissue is decreased after mTBI (65, 66), suggesting an elevated need for DHA in mTBI recovery.
  • the well-established role of DHA in supporting the structure and function of the brain throughout the lifespan (26, 27, 46, 47, 53) provides encouragement that LCPUFAs may also prove beneficial in the context of concussion recovery.
  • no therapies are currently available to aid the recovery from this injury
  • Previously discussed reports outlining the use of ω-3 FAs in the recovery from severe TBIs (reviewed in Ref. 92) described the use of very-high doses of LCPUFAs (16.2 g/d EPA plus DHA) in the recovery of these patients
  • Within the context of mTBIs/concussions, translating a DHA intake used in several rat studies of mTBI recovery (40 mg ⋅ kg−1 ⋅ d−1 DHA) (57, 63, 64) using body surface area conversion methods (93) amounts to an estimated human intake of 387 mg/d DHA
  • Nathan Goodyear on 30 Aug 15
     
    nice review of the evidence of n-3, particularily DHA, in concussions and concussion recovery.
wheelchairindia9

Karma Ergo 115 Wheelchair - 0 views

disabilityproduct.in/...Karma-S-Ergo-115-Wheelchair

Ergo S-Shape Seating System For Handicapped foldable and easy to store Karma Ergo 115 Wheelchair detachable foot rest washable and dry able cushions Karma Ergo 305 Wheelchair footrest for maximum safety

shared by wheelchairindia9 on 04 Sep 15 - No Cached
  • wheelchairindia9 on 04 Sep 15
     
    Ergo Wheelchair features an ergonomic "S" shaped seat that provides the perfect shape to fit the human body to relieve pressure, increase stabilization, weight distribution and lower the risk of pressure sores and scoliosis. Ergonomic wheelchair series provides users with a large selection of ultra lightweight wheelchairs that can help improve life. This series has features that include a high strength lightweight frame, foldable and easy to store, breathable anti-bacterial, anti-staining, removable and machine washable cushion. Also includes the exclusive S-Shape Seating System, which provides increased stability, better weight distribution and lowers the risk of pressure sores and spinal injury. Karma S Ergo 115 Wheelchair: This model features our S-Shape Seating System and is our number one best seller for many reasons. At a mere 11.3 kg in weight with detachable foot rest and many features such as removable machine washable and dry-able cushions treated by AEIGIS treated anti-microbial coated seating system. Karma S-Ergo 115 Wheelchair Features: Ergonomic Handrims & S-Shape Ergonomic Seating System Fixed armrest w/ wider concave armpads Swing In & Away Footrests Backrest Pouch attached to the upholstery 24" flat free polyurethane tires, high tread, flat free wheels Seat width: 16"x17" or 18"x17" or 20"x 17" Silver 1/4" Aegis Anti-Bacterial Upholstery, washable Folding backrest / folding seat for easy traveling "Tube-in Center" foot-plate, assures better side leg support High strength, starting weight at only 11.3 kg. (w/o footrests) 7×1" Polyurethane front casters Upholstery: Black breathable mesh bottom & top AEIGIS Frame Color: Pearl Silver or Rose Red Weight Capacity of 115 kg. Karma S-Ergo 115 Wheelchair Measurements: Seat Width 16 inch., 18 inch., 20 inch. Seat Depth 17 inch. Armrest Height 8 inch. Seat Height 19 inch. Back Height 17 inch. Overall Height 36 inch. Overall Open Width 23 inch., 25 inch., 27 inch
Nathan Goodyear

Diagnosing Growth Hormone Deficiency in Adults - 0 views

www.hindawi.com/...972617

HGH GH human growth hormone growth hormone IGF-1

shared by Nathan Goodyear on 04 Nov 14 - No Cached
  • it is clear that serum IGF-1 and or IGFBP-3 can be normal in patients with undisputed GHD
  • Various investigators have reported normal IGF-1 values in 37–70% of GH deficient adults
  • The co-administration of arginine and GHRH (the combined test) is a powerful stimulus for GH production and has gained increasing acceptance as a useful method of diagnosing GHD [34]. This test has been advocated as a suitable alternative to ITT
  • ...12 more annotations...
  • The glucagon stimulation test (GST) is a reliable, safe alternative to the ITT in the diagnosis of GHD
  • An intravenous infusion of arginine (0.5 g/kg body weight) together with an intravenous bolus of GHRH (1 mcg/kg body weight) is administered [30]. Serum samples for GH are then obtained every 15–30 minutes for two hours.
  • Obesity, particularly marked obesity, is associated with blunted GH secretion in response to provocative stimuli
  • It has also been suggested that that even mildly increased BMI (25–30 kg/m2) can result in diminished stimulated GH production in 13% of healthy subjects
  • Corneli et al. have defined BMI-specific cut-off points for diagnosing adult-onset GHD using GHRH + arginine—11.5 ng/mL for those with BMI < 25 kg/m2, 8.0 ng/mL for BMI 25–30 kg/m2, 4.2 ng/mL for those with BMI > 30 kg/m2
  • GH levels are higher during the luteal phase in comparison with the follicular phase of the cycle
  • Oral, in contrast to transdermal oestrogen, lowers IGF-1 levels and is associated with increased GH levels
  • Adequate pituitary replacement with thyroxine and hydrocortisone are needed for optimal GH production
  • one cannot rely on a low IGF-1 to diagnose GHD in women taking oral oestrogen preparations.
  • Numerous GH secretagogues are available with the insulin tolerance test being the gold standard and the glucagon stimulation test or the GHRH + arginine as acceptable alternatives
  • ain et al. found the GST to be at least as good as the ITT in provoking GH secretion
  • the GST is safe, with almost no contraindications, it causes nausea and sometimes vomiting in 15–20% of subjects
  • Nathan Goodyear on 04 Nov 14
     
    Nice, more recent analysis, of HGH testing.
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