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Nathan Goodyear

Longitudinal relationships of circul... [J Clin Endocrinol Metab. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24628559

Testosterone low T free Estradiol Estrone muscle mass strength elderly men male hormone hormones men's health

shared by Nathan Goodyear on 24 Mar 14 - No Cached
  • Nathan Goodyear on 24 Mar 14
     
    Declining Testosterone, calculated free Testosterone, Estradiol, and Estrone levels appear to be associated with muscle mass/strength decline in elderly men.  This points to a global decrease in HPA function rather than an individual, specific hormone deficiency.
Nathan Goodyear

Testosterone Dose-Response Relationships with Cardiovascular Risk Markers in Androgen-D... - 0 views

press.endocrine.org/...jc.2013-4160

testosterone cardiovascular women female hormone hormones CVD disease

shared by Nathan Goodyear on 19 May 14 - No Cached
  • Nathan Goodyear on 19 May 14
     
    Study finds no worsening in cardiovascular biomarkers in women on Testosterone.  The women in this study were chose due to low Testosterone.  Testosterone was given IM at 4 different doses.  This is in contrast to other studies that have looked at endogenous Testosterone level.  Studies have shown increasing endogenous T levels in women is associated with increased CVD.  Studies on exogenous are lacking.  This points to limited risk associated with CVD and T therapy in women.   One caveat.  Two of the authors of this study have ties to the maker of the Testosterone enanthate used in this study.  Why is this important?  Prior studies have shown significant decrease in adverse event reporting in those funded by pharma--bias.
Nathan Goodyear

Race differences in obesity and its relationship to the sex hormone milieu : Hormone Mo... - 0 views

www.degruyter.com/...34F8BE807519B51BD841611C00492B

androgens women men male female hormone hormones Testosterone bioavailable Testosterone obesity

shared by Nathan Goodyear on 24 Nov 14 - No Cached
  • increased abdominal and visceral adipose tissue (VAT) – found in women and marked by low sex hormone binding globulin (SHBG) and high bioavailable testosterone (BT) – is related to the metabolic risk profile
  • In men, increased BT is related to decreased abdominal obesity and a decrease in the metabolic risk profile
  • Nathan Goodyear on 24 Nov 14
     
    Only abstract available here.  Race (black vs white) is associated with changes in obesity effects on adrogenicity, particularly in women.  One wonders if this is a result of other variables i.e.vitamin D.
My Wellness

Studies Find Big Benefits in Marriage - 0 views

mywellness.in/does-marriage-elongate-life

emotional health love marriage relationships

shared by My Wellness on 31 Dec 14 - No Cached
  • My Wellness on 31 Dec 14
     
    One of the strongest and consistent benefits of marriage is better physical health and its consequence longer life,Marriage Increases the Quality of Life, Sexual fulfillment.
Nathan Goodyear

Prevalence of Hyperuricemia and the Relationship between Serum Uric Acid and Metabolic ... - 0 views

www.jstage.jst.go.jp/..._article

uric acid metabolic syndrome triglycerides waist circumference hormones hormone inflammaiton

shared by Nathan Goodyear on 27 Aug 14 - No Cached
  • Nathan Goodyear on 27 Aug 14
     
    Waist circumference and triglycerides correlate with serum uric acid levels.  Men in this study had higher hyperuricemic rates compared to women.  Elevated uric acid levels were associated with increased MetS in both sexes and higher normal uric acid levels were also associated with a higher risk of MetS.
Nathan Goodyear

Testosterone dose-response relationships in hyster... [Menopause. 2013] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24281237

Testosterone women hysterectomy menopause

shared by Nathan Goodyear on 29 Nov 13 - No Cached
  • Nathan Goodyear on 29 Nov 13
     
    One of the main instances for which women need Testosterone, is post-hysterectomy.  This study confirms that.  This study found benefit in those with and without the removal of the ovaries.
Nathan Goodyear

Relationship between non-alcoholic fatty liver ... [World J Urol. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25189458

NAFLD BPH LUTS men male fatty liver liver metabolic syndrome

shared by Nathan Goodyear on 09 Sep 14 - No Cached
  • Nathan Goodyear on 09 Sep 14
     
    Men with NAFLD have higher incidence of lower urinary tract symptoms including BPH.
Nathan Goodyear

Hypothalamic-Pituitary-Testicular Axis Disruptions in Older Men Are Differentially Link... - 0 views

press.endocrine.org/...jc.2007-1972

low T low Testosterone low T Testosterone aging LH hormone hormones men male SHBG

shared by Nathan Goodyear on 03 Sep 14 - No Cached
  • 0.4–2% annual decline
  • the age trend in free T was more substantial (−1.3% per annum)
  • The core hormonal pattern with increasing age is suggestive of incipient primary testicular dysfunction with maintained total T and progressively blunted free T associated with higher LH.
  • ...16 more annotations...
  • Obesity was associated with progressively lower total and free T independent of the simultaneous decrease in SHBG.
  • our data highlight the fact that LH was unchanged or even lower in older men in the face of lower T in obesity, suggesting that there may be a failure at the hypothalamic-pituitary level.
  • a change in BMI from nonobese to obese may be equivalent to a 15 yr fall in T.
  • This pattern supports the hypothesis that different underlying mechanisms influence the functions of the HPT axis: age predominantly affects testicular function, whereas obesity impairs hypothalamic/pituitary function.
  • the effects of aging on testicular function can be moderated by increased LH compensation for many decades
  • obesity impairs hypothalamic/pituitary function independent of age, arguably an adaptive response for which there should be no compensatory mechanism.
  • the concurrent but opposite (and separate) effects of obesity and age on SHBG
  • SHBG was negatively associated with increasing strata of obesity
  • Obesity is associated with insulin resistance (28), and the increased circulating insulin inhibits hepatic SHBG synthesis
  • the SHBG increase with age may be related to relative IGF-I deficiency (27), although this has not been directly proven.
  • Obesity is associated with peripheral and central insulin resistance (30) and proinflammatory cytokine production (TNFα and IL-6) from adipocytes (31) and central nervous system endocannibinoid release (32), all of which are potential candidates for abrogating hypothalamic endocrine and downstream reproductive axis functions.
    • Nathan Goodyear
      Nathan Goodyear on 03 Sep 14
       
      The HPA axis effect may be the result of inflammation.
  • The relationship between obesity and T can be bidirectional: low T may be the cause rather than consequence of obesity
  • chronic alcohol abuse is known to suppress LH (40), our data showed no significant association among the three hormones or SHBG and alcohol intake.
  • increase in total T in smokers occurs through a primary increase in SHBG with a compensatory rise in LH
  • the effects of obesity (BMI or waist circumference) was by far the most important determinant of variance in total T, whereas age per se was important for SHBG, LH, and free T with comorbidity and smoking being comparatively minor contributors
  • It is noteworthy that these predisposing lifestyle and health factors are modifiable. This implies that the apparent age-related decline in T may constitute a barometer of health and thus be potentially preventable and/or reversible.
  • Nathan Goodyear on 03 Sep 14
     
    Age induced decline in Testosterone is more associated with a decline in leydig cell function and thus elevated LH will be associated.  In contrast, obesity is more of a HPA axis disruption and thus LH may be normal to low.  The pulse amplitude is decrease.  No change in pulse frequency is noted.   With obesity, a decline in TT and fT was independent of SHBG. Aging is associated with a greater decrease in fT versus TT.
Nathan Goodyear

The relationship between testosterone, metabolic syndrome, and mean carotid intima-medi... - 0 views

informahealthcare.com/...13685538.2014.958458

low T Testosterone low T low Testosterone aging male metabolic syndrome metabolic syndrome IMT carotid intima-media thickness men hormone hormones

shared by Nathan Goodyear on 12 Sep 14 - No Cached
  • Nathan Goodyear on 12 Sep 14
     
    Low Testosterone is associated with increased IMT.  Low T is associated with Mets.  MetS is associated with low T.  MetS is associated with increased IMT.
Nathan Goodyear

International Journal of Impotence Research - Obesity, low testosterone levels and erec... - 0 views

www.nature.com/...ijir200842a.html

low T low Testosterone men male hormone hormones ED erectile dysfunction Testosterone diabetes metabolic syndrome obesity

shared by Nathan Goodyear on 27 Jan 15 - No Cached
  • Studies have shown that ED may be an early biomarker of general endothelial dysfunction, atherosclerosis and CVD
  • testosterone treatment of hypogonadal young and older men improves sexual function, increases lean mass and decreases fat mass
  • In men with low serum testosterone (for example, <8 or 230 nmol l−1) with obesity, metabolic syndrome and diabetes mellitus, treatment with testosterone is warranted
  • ...12 more annotations...
  • In obese middle-aged men, testosterone treatment reduced visceral adipocity, insulin resistance, serum cholesterol and glucose levels
  • testosterone replacement has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure in hypogonadal men with the metabolic syndrome as well as type 2 diabetes mellitus
  • Testosterone significantly inhibits lipoprotein lipase activity, which reduces triglycerides uptake into adipocytes in the abdominal adipose tissue
  • testosterone treatment decreased endogenous inflammatory cytokines (tumor necrosis factor-α and IL-1β) and lipids (total cholesterol) and increased IL-10 in hypogonadal men
  • Testosterone treatment reduced leptin and adiponectin levels in hypogonadal type 2 diabetic men after 3 months of testosterone replacement
  • available data clearly show a relationship between obesity, low testosterone levels and ED
  • Obesity adversely affects endothelial function and lowers serum testosterone levels through the development of insulin resistance and metabolic syndrome
  • Metabolic disturbances as well as production of cytokines and adipokines by inflamed fat cells may be causal factors in the development of ED
  • The onset of ED and the associated risk of CVD may be delayed through lifestyle modifications that affect obesity, such as diet and exercise
  • Very low testosterone levels contribute to the development of ED in obesity, metabolic syndrome and type 2 diabetes mellitus
  • Obesity is associated with low total testosterone levels that can be explained at least partially by lower sex hormone-binding globulin (SHBG) in obese men
  • epidemiological studies have shown a negative correlation between BMI and total testosterone and to a lesser extent with free and bioavailable (biologically active) testosterone levels
  • Nathan Goodyear on 27 Jan 15
     
    Obesity is associated with low Testosterone and ED in men.
Nathan Goodyear

PLOS ONE: Testosterone, Sex Hormone-Binding Globulin and the Metabolic Syndrome in Men:... - 0 views

journals.plos.org/...article

Testosterone metabolic syndrome total Testosterone free Testosterone SHBG men male hormone hormones

shared by Nathan Goodyear on 03 Mar 15 - No Cached
  • Nathan Goodyear on 03 Mar 15
     
    Meta-analysis finds that men with low total Testosterone, free Testosterone, and SHBG are more at risk for MetS than those with elevated levels.
Nathan Goodyear

Spectrum of metabolic dysfunction in relationship with hyperandrogenemia in obese adole... - 0 views

eje-online.org/...1093.long

PCOS polycystic ovarian syndrome CRP inflammation insulin insulin resistance women female hormone hormones androgens Testosterone hyperandrogenism

shared by Nathan Goodyear on 10 Mar 15 - No Cached
  • subjects with hyperandrogenemic phenotypes displayed the greatest degree of hyperinsulinemia, β-cell function, and chronic inflammation
  • The rise in serum androgens is accompanied by excess insulin secretion, suggesting that insulin directly stimulates ovarian androgen production
  • The degree of hyperinsulinemia does not seem to be directly correlated with the development of HS
  • ...7 more annotations...
  • higher androgen and insulin levels stimulate hair growth
  • genetic and epigenetic changes may be involved in the pathogenesis of PCOS
  • HA has been identified as an important risk factor for MS and dyslipidemias in premenopausal women and adolescents
  • In our study, HA was found to be an independent risk factor for MS as previously reported by Coviello et al.
  • obesity and HA, and not insulin resistance, are the major determinants of chronic inflammation and risk of atherosclerosis in adolescents with PCOS
  • use of an inflammation marker may help identify high-risk females with PCOS
  • hyperandrogenemic PCOS phenotypes have greatest degree of hyperinsulinemia, insulin resistance, and inflammation
  • Nathan Goodyear on 10 Mar 15
     
    Elevated androgens are associated increasing insulin, insulin resistance, and inflammation (as measured by CRP).
Nathan Goodyear

Annals of Occupational and Environmental Medicine | Full text | The Relationship of Liv... - 0 views

www.aoemj.com/5

lead liver enzymes liver ALT AST environmental toxins

shared by Nathan Goodyear on 09 Mar 15 - No Cached
  • Nathan Goodyear on 09 Mar 15
     
    Lead and organic solvent exposure associated with increased liver function tests, indicating liver damage.
Nathan Goodyear

Relationship of thyroid hormone levels and cardiov... [Endocrine. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...23546612

thyroid hormone hormones rT3 reverse T3 cardiovascular disease diabetes

shared by Nathan Goodyear on 16 Aug 14 - No Cached
  • Nathan Goodyear on 16 Aug 14
     
    Patients with type II Diabetes and h/o of CVE  have higher rT3 in study.  The Endocrinologist that said reverse T3 is completely irrelevant needs to read more studies and stop listening to opinion.
Nathan Goodyear

Estrogen Receptor Signaling and Its Relationship to Cytokines in Systemic Lupus Erythem... - 0 views

www.hindawi.com/...317452

autoimmune disease autoimmune Estrogen estrogen receptors ER alpha ER beta ER-alpha ER-beta hormone hormones SLE LUPUS inflammation cytokines

shared by Nathan Goodyear on 07 Jul 14 - No Cached
  • Nathan Goodyear on 07 Jul 14
     
    Nice review of the literature of Estrogens, estrogen receptors and their effect on cytokine production and Lupus.
Nathan Goodyear

Relationship between Low Free Testosterone Levels and Loss of Muscle Mass : Scientific ... - 0 views

www.nature.com/...srep01818.html

low T Testosterone low T low Testosterone free Testosterone sarcopenia muscle mass men male hormone hormones

shared by Nathan Goodyear on 13 Aug 14 - No Cached
  • Nathan Goodyear on 13 Aug 14
     
    Study finds low free Testosterone and low calculated free Testosterone was associated with sarcopenia in Japanese men.  This association was not found with Total Testosterone.
Nathan Goodyear

Inverse relationship between serum levels of interleukin-1beta and testosterone in men ... - 0 views

www.researchgate.net/...stable_coronary_artery_disease

low T low T low Testosterone Testosterone inflammation men male hormone hormones IL-1beta IL-10 cytokines

shared by Nathan Goodyear on 13 Aug 14 - No Cached
  • Nathan Goodyear on 13 Aug 14
     
    low Total Testosterone and bioavailable Testosterone is associated with increased IL-1beta and IL-10.  This points to low T having a more direct link to increased systemic inflammation in men.
Nathan Goodyear

Oxidative Stress and Its Relationship With Adenosine Deaminase Activity in Various Stag... - 0 views

www.ncbi.nlm.nih.gov/...PMC3547448

Adenosine Deaminase ADA cancer breast cancer superoxide disumutase glutathione peroxidase oxidative stress inflammation

shared by Nathan Goodyear on 10 Nov 14 - No Cached
  • Reduced SOD activity might be responsible for excessive accumulation of superoxide anions leading to increased free radical mediated injury. Increased free radical production has been shown to be responsible for chromosomal damage leading to mutagenecity, cell proliferation and carcinogenesis. SOD activity showed marked improvement after mastectomy indicating the lowering of oxidative stress.
  • The increased production of reactive oxygen species causes oxidative stress leading to cell proliferation and hence increased inflammatory conditions
  • Superoxide dismutase is an important antioxidant enzyme which decomposes the harmful superoxide anions into hydrogen peroxide thus protects the body from the action of free radicals
  • ...20 more annotations...
  • Females suffering from breast cancer had significantly decreased Superoxide dismutase (SOD) and reduced glutathione (GSH) levels in comparison to normal females
  • ADA seems to be a promising marker of inflammation in breast cancer thereby suggesting that it can be used as a diagnostic tool to detect the stage of breast cancer along with cytopathological studies
  • In conclusion, our study confirmed the role of oxidative stress in the pathogenesis of breast cancer.
  • Another potent antioxidant molecule is reduced glutathione. It acts as reductant which converts hydrogen peroxide into water and reduces lipid peroxidation products into their corresponding alcohols and thus mediates protective action.
  • In the present study, significantly low SOD activity has been observed in female patients suffering from carcinoma breast both pre as well as post operative in comparison to healthy females.
  • We observed significantly decreased SOD activity and GSH levels in patients belonging to clinical stage 4 as compared to those having stages 1, 2 or 3 of breast cancer.
  • Increased ADA activity in breast cancer patients has also been reported
  • The compromised antioxidant defence system produces the oxidative stress which in turn creates the inflammatory response shown by concomitant increased adenosine deaminase (ADA) activity in female patients.
  • Experimental and epidemiological evidences implicate the involvement of oxygen derived free radical in the pathogenesis of breast cancer.
  • Antioxidant status was highly depressed in advanced stages of breast cancer as compared to initial stage.
  • In the present study, significantly low GSH levels were observed in female patients of carcinoma breast as compared to normal females
  • Walia et al. (1995) reported increased ADA activity in breast cancer patients as compared to age matched normal subjects.
  • These free radicals are able to cause damage to membrane, mitochondria and macromolecules including proteins, lipids and DNA and actively take part in cell proliferation. This cascade in turn generates the inflammatory response and causes the progression of the disease.
  • increased oxidative stress gives rise to inflammation which could further aggravates the disease
  • Breast carcinoma involves a cascade of events that are highly inflammatory.
  • Marked oxidative stress in stage 4 of breast cancer indicated advancement of the disease, hence checking oxidative stress at initial stage could be helpful for controlling the progression of the disease.
  • They concluded that ADA is a better probable parameter for detection of breast cancer
  • Adenosine deaminase enzyme (ADA) catalyzes the conversion of adenosine to inosine which finally gets converted to uric acid
  • serum ADA activity tends to increase with advancing age,
  • Prevalence of oxidative stress gives rise to inflammation.
  • Nathan Goodyear on 10 Nov 14
     
    Study finds a reduction in SuperOxide Dismutase and Glutathione Perioxidase in advancing breast cancer.  Cancer is a high oxidative stress disease that results in inflammation, mitochondrial dysfunction and proliferation.  Adenosine Deaminase (ADA) is proposed to be another biomarker to assess tumor stage.  
Nathan Goodyear

Cancer cells metabolically "fertilize" the tumor microenvironment with hydrogen peroxid... - 0 views

www.ncbi.nlm.nih.gov/...PMC3180189

cancer reverse warburg effect warburg effect NF-kapppB HIF-1alpha Cav-1 H2O2

shared by Nathan Goodyear on 12 Nov 14 - No Cached
  • reducing oxidative stress with powerful antioxidants, is an important strategy for cancer prevention, as it would suppress one of the key early initiating steps where DNA damage and tumor-stroma metabolic-coupling begins. This would prevent cancer cells from acting as metabolic “parasites
  • Oxidative stress in cancer-associated fibroblasts triggers autophagy and mitophagy, resulting in compartmentalized cellular catabolism, loss of mitochondrial function, and the onset of aerobic glycolysis, in the tumor stroma. As such, cancer-associated fibroblasts produce high-energy nutrients (such as lactate and ketones) that fuel mitochondrial biogenesis and oxidative metabolism in cancer cells. We have termed this new energy-transfer mechanism the “reverse Warburg effect.
  • Then, oxidative stress, in cancer-associated fibroblasts, triggers the activation of two main transcription factors, NFκB and HIF-1α, leading to the onset of inflammation, autophagy, mitophagy and aerobic glycolysis in the tumor microenvironment
  • ...38 more annotations...
  • oxidative stress and ROS, produced in cancer-associated fibroblasts, has a “bystander effect” on adjacent cancer cells, leading to DNA damage, genomic instability and aneuploidy, which appears to be driving tumor-stroma co-evolution
  • tumor cells produce and secrete hydrogen peroxide, thereby “fertilizing” the tumor microenvironment and driving the “reverse Warburg effect.”
  • This type of stromal metabolism then produces high-energy nutrients (lactate, ketones and glutamine), as well as recycled chemical building blocks (nucleotides, amino acids, fatty acids), to literally “feed” cancer cells
  • loss of stromal caveolin (Cav-1) is sufficient to drive mitochondrial dysfunction with increased glucose uptake in fibroblasts, mimicking the glycolytic phenotype of cancer-associated fibroblasts.
  • oxidative stress initiated in tumor cells is transferred to cancer-associated fibroblasts.
  • Then, cancer-associated fibroblasts show quantitative reductions in mitochondrial activity and compensatory increases in glucose uptake, as well as high ROS production
  • These findings may explain the prognostic value of a loss of stromal Cav-1 as a marker of a “lethal” tumor microenvironment
  • aerobic glycolysis takes place in cancer-associated fibroblasts, rather than in tumor cells, as previously suspected.
  • our results may also explain the “field effect” in cancer biology,5 as hydrogen peroxide secreted by cancer cells, and the propagation of ROS production, from cancer cells to fibroblasts, would create an increasing “mutagenic field” of ROS production, due to the resulting DNA damage
  • Interruption of this process, by addition of catalase (an enzyme that detoxifies hydrogen peroxide) to the tissue culture media, blocks ROS activity in cancer cells and leads to apoptotic cell death in cancer cells
  • In this new paradigm, cancer cells induce oxidative stress in neighboring cancer-associated fibroblasts
  • cancer-associated fibroblasts have the largest increases in glucose uptake
  • cancer cells secrete hydrogen peroxide, which induces ROS production in cancer-associated fibroblasts
  • Then, oxidative stress in cancer-associated fibroblast leads to decreases in functional mitochondrial activity, and a corresponding increase in glucose uptake, to fuel aerobic glycolysis
  • cancer cells show significant increases in mitochondrial activity, and decreases in glucose uptake
  • fibroblasts and cancer cells in co-culture become metabolically coupled, resulting in the development of a “symbiotic” or “parasitic” relationship.
  • cancer-associated fibroblasts undergo aerobic glycolysis (producing lactate), while cancer cells use oxidative mitochondrial metabolism.
  • We have previously shown that oxidative stress in cancer-associated fibroblasts drives a loss of stromal Cav-1, due to its destruction via autophagy/lysosomal degradation
  • a loss of stromal Cav-1 is sufficient to induce further oxidative stress, DNA damage and autophagy, essentially mimicking pseudo-hypoxia and driving mitochondrial dysfunction
  • loss of stromal Cav-1 is a powerful biomarker for identifying breast cancer patients with early tumor recurrence, lymph-node metastasis, drug-resistance and poor clinical outcome
  • this type of metabolism (aerobic glycolysis and autophagy in the tumor stroma) is characteristic of a lethal tumor micro-environment, as it fuels anabolic growth in cancer cells, via the production of high-energy nutrients (such as lactate, ketones and glutamine) and other chemical building blocks
  • the upstream tumor-initiating event appears to be the secretion of hydrogen peroxide
  • one such enzymatically-active protein anti-oxidant that may be of therapeutic use is catalase, as it detoxifies hydrogen peroxide to water
  • numerous studies show that “catalase therapy” in pre-clinical animal models is indeed sufficient to almost completely block tumor recurrence and metastasis
  • by eliminating oxidative stress in cancer cells and the tumor microenvironment,55 we may be able to effectively cut off the tumor's fuel supply, by blocking stromal autophagy and aerobic glycolysis
  • breast cancer patients show systemic evidence of increased oxidative stress and a decreased anti-oxidant defense, which increases with aging and tumor progression.68–70 Chemotherapy and radiation therapy then promote further oxidative stress.69 Unfortunately, “sub-lethal” doses of oxidative stress during cancer therapy may contribute to tumor recurrence and metastasis, via the activation of myofibroblasts.
  • a loss of stromal Cav-1 is associated with the increased expression of gene profiles associated with normal aging, oxidative stress, DNA damage, HIF1/hypoxia, NFκB/inflammation, glycolysis and mitochondrial dysfunction
  • cancer-associated fibroblasts show the largest increases in glucose uptake, while cancer cells show corresponding decreases in glucose uptake, under identical co-culture conditions
  • Thus, increased PET glucose avidity may actually be a surrogate marker for a loss of stromal Cav-1 in human tumors, allowing the rapid detection of a lethal tumor microenvironment.
  • it appears that astrocytes are actually the cell type responsible for the glucose avidity.
  • In the brain, astrocytes are glycolytic and undergo aerobic glycolysis. Thus, astrocytes take up and metabolically process glucose to lactate.7
  • Then, lactate is secreted via a mono-carboxylate transporter, namely MCT4. As a consequence, neurons use lactate as their preferred energy substrate
  • both astrocytes and cancer-associated fibroblasts express MCT4 (which extrudes lactate) and MCT4 is upregulated by oxidative stress in stromal fibroblasts.34
  • In accordance with the idea that cancer-associated fibroblasts take up the bulk of glucose, PET glucose avidity is also now routinely used to measure the extent of fibrosis in a number of human diseases, including interstitial pulmonary fibrosis, postsurgical scars, keloids, arthritis and a variety of collagen-vascular diseases.
  • PET glucose avidity and elevated serum inflammatory markers both correlate with poor prognosis in breast cancers.
  • PET signal over-estimates the actual anatomical size of the tumor, consistent with the idea that PET glucose avidity is really measuring fibrosis and inflammation in the tumor microenvironment.
  • human breast and lung cancer patients can be positively identified by examining their exhaled breath for the presence of hydrogen peroxide.
  • tumor cell production of hydrogen peroxide drives NFκB-activation in adjacent normal cells in culture6 and during metastasis,103 directly implicating the use of antioxidants, NFκB-inhibitors and anti-inflammatory agents, in the treatment of aggressive human cancers.
  • Nathan Goodyear on 12 Nov 14
     
    Good description of the communication between cancer cells and fibroblasts.  This theory is termed the "reverse Warburg effect".
Nathan Goodyear

Relationship between low free testosterone levels and loss of muscle mass. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...23660939

free Testosterone total Testosterone muscle Testosterone sarcopenia muscle loss men male hormone hormones

shared by Nathan Goodyear on 05 Apr 15 - No Cached
  • Nathan Goodyear on 05 Apr 15
     
    low free Testosterone associated with muscle loss in men compared to no association with total Testosterone in Japanese men.
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