Body mass index and waist circumference were significantly higher in the group with testosterone levels
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French to India Medical Travel: La radiochirurgie Gamma Knife en Inde amélior... - 0 views
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Le taux de réussite de la radiochirurgie au couteau gamma en Inde est plus élevé. Il existe un certain nombre des meilleurs hôpitaux pour la radiochirurgie au couteau gamma en Inde, capables et correctement préparés avec la technologie la plus avancée utilisée pour offrir le meilleur traitement au patient de partout dans le monde.
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shared by spineneuro on 17 Jun 22
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French to India Medical Travel: Obtenez une technologie et une expertise de n... - 0 views
frenchtoindiamedicaltravel.blogspot.com/...als-for-brain-tumor-india.html
chirurgie des tumeurs cérébrales en Inde meilleurs hôpitaux pour tumeurs cérébrales en Inde
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C'est l'une des principales raisons pour lesquelles de nombreux patients étrangers se rendent en Inde. Il a été observé que la chirurgie des tumeurs cérébrales en Inde est d'environ 60% inférieure à celle des autres pays occidentaux avancés. C'est pourquoi les patients étrangers choisissent l'Inde pour leur chirurgie des tumeurs cérébrales en raison des chirurgiens professionnels, des meilleurs hôpitaux indiens pour les tumeurs cérébrales et des coûts abordables.
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shared by Nathan Goodyear on 10 May 12
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Relationship between endogenous testosterone and cardiovascular risk in early postmenop... - 0 views
www.metabolismjournal.com/...abstract
testosterone women high elevated CRP inflammation BMI obesity overweight post-menopausal CVD
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An association of testosterone with CRP (r = 0.416, P = .004) and ET-1 (r = 0.323, P = .031) was observed
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JISSN | Full text | International Society of Sports Nutrition position stand: creatine ... - 0 views
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the energy supplied to rephosphorylate adenosine diphosphate (ADP) to adenosine triphosphate (ATP) during and following intense exercise is largely dependent on the amount of phosphocreatine (PCr) stored in the muscle
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About two thirds of the creatine found in skeletal muscle is stored as phosphocreatine (PCr) while the remaining amount of creatine is stored as free creatine
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The body breaks down about 1 – 2% of the creatine pool per day (about 1–2 grams/day) into creatinine in the skeletal muscle
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The magnitude of the increase in skeletal muscle creatine content is important because studies have reported performance changes to be correlated to this increase
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"loading" protocol. This protocol is characterized by ingesting approximately 0.3 grams/kg/day of CM for 5 – 7 days (e.g., ≃5 grams taken four times per day) and 3–5 grams/day thereafter [18,22]. Research has shown a 10–40% increase in muscle creatine and PCr stores using this protocol
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Additional research has reported that the loading protocol may only need to be 2–3 days in length to be beneficial, particularly if the ingestion coincides with protein and/or carbohydrate
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A few studies have reported protocols with no loading period to be sufficient for increasing muscle creatine (3 g/d for 28 days)
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Most of these forms of creatine have been reported to be no better than traditional CM in terms of increasing strength or performance
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Recent studies do suggest, however, that adding β-alanine to CM may produce greater effects than CM alone
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These investigations indicate that the combination may have greater effects on strength, lean mass, and body fat percentage; in addition to delaying neuromuscular fatigue
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Green et al. [24] reported that adding 93 g of carbohydrate to 5 g of CM increased total muscle creatine by 60%
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Steenge et al. [23] reported that adding 47 g of carbohydrate and 50 g of protein to CM was as effective at promoting muscle retention of creatine as adding 96 g of carbohydrate.
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Studies suggest that increasing skeletal muscle creatine uptake may enhance the benefits of training
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Long-term CM supplementation appears to enhance the overall quality of training, leading to 5 to 15% greater gains in strength and performance
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Nearly all studies indicate that "proper" CM supplementation increases body mass by about 1 to 2 kg in the first week of loading
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short-term adaptations reported from CM supplementation include increased cycling power, total work performed on the bench press and jump squat, as well as improved sport performance in sprinting, swimming, and soccer
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Long-term adaptations when combining CM supplementation with training include increased muscle creatine and PCr content, lean body mass, strength, sprint performance, power, rate of force development, and muscle diameter
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subjects taking CM typically gain about twice as much body mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to 12 weeks of training) than subjects taking a placebo
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The gains in muscle mass appear to be a result of an improved ability to perform high-intensity exercise via increased PCr availability and enhanced ATP synthesis, thereby enabling an athlete to train harder
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there is no evidence to support the notion that normal creatine intakes (< 25 g/d) in healthy adults cause renal dysfunction
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One cohort of patients taking 1.5 – 3 grams/day of CM has been monitored since 1981 with no significant side effects
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Sex, Receptors, and Attachment: A Review of Individual Factors Influencing Response to ... - 0 views
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testosterone promotes both OTR binding in the hypothalamus (Johnson et al., 1991) as well as production of AVP (Delville et al., 1996), which has many opponent actions to OT
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The mineral selenium proves itself as powerful anti-cancer medicine - 0 views
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In a December 1996 article in the Journal of the American Medical Association, Dr. Larry Clark presented evidence that supplemental selenium could reduce cancer death rates by as much as 50%
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patients receiving selenium had a 67% decrease in cancer of the prostate, a 58 percent decrease in colon or rectal cancer and a 45% decrease in lung cancer
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An article in the Journal of the American Medical Association (JAMA) by Clark et al. (1996) showed that 200 mcg of supplemental selenium a day reduced overall cancer mortality by 50% in humans compared to a placebo group not receiving supplemental selenium
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In a recent five-year study of nearly 30,000 rural Chinese people, researchers from the NCI found that daily doses of these three nutrients reduced cancer deaths by 13%.
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In a study in Cancer Letters (Evangelou et al. 1997), animals with malignant tumors given high doses of vitamins C and E and selenium manifested a significant prolongation of the mean survival time. Complete remission of tumors developed in 16.8% of the animals
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cities and states with high selenium content in the soil also had significantly lower rates of cancer, especially of the digestive and urinary systems.
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In one study of hundreds of men, a daily intake of 200 micrograms of selenium cut the incidence of prostate cancer by 60 percent.
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The statistics for breast cancer are particularly striking. "The higher the selenium, the lower the breast cancer
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In Yugoslavia, scientists studied 33 patients with breast cancer. These women had selenium levels in their bloodstream only half those of healthy volunteers.
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The overall reduction in cancer incidence was 37% in the selenium-supplemented group; a 50% reduction in cancer mortality was observed over a 10-year period
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The following are the site-specific reductions in cancer incidence observed in the study: colon-rectal cancers (58%), lung cancer (46%), and prostate cancer (63%)
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It was determined that, as the male population ages, selenium levels decrease, paralleling an increase in prostate cancer
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Diagnosing Growth Hormone Deficiency in Adults - 0 views
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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
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The glucagon stimulation test (GST) is a reliable, safe alternative to the ITT in the diagnosis of GHD
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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.
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Obesity, particularly marked obesity, is associated with blunted GH secretion in response to provocative stimuli
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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
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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
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Oral, in contrast to transdermal oestrogen, lowers IGF-1 levels and is associated with increased GH levels
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Adequate pituitary replacement with thyroxine and hydrocortisone are needed for optimal GH production
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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
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the GST is safe, with almost no contraindications, it causes nausea and sometimes vomiting in 15–20% of subjects
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shared by Nathan Goodyear on 04 Mar 15
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Fifty- two-Week Treatment With Diet and Exercise Plus Transdermal Testosterone Reverses... - 0 views
onlinelibrary.wiley.com/...full
diet exercise nutrition diabetes metabolic syndrome men male hormone hormones low T low Testosterone
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there appears to be a positive correlation between serum testosterone levels and insulin sensitivity in men across the full spectrum of glucose tolerance (Pitteloud et al, 2005), and this relationship is at least partially direct and not fully dependent on (changes in) elements of the MetS
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supervised D&E alone led to significant improvements in testosterone concentrations, glycemic control, and components of the MetS
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diet control, exercise, and testosterone supplementation may be beneficial in the management of men with T2D
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androgen-deprivation therapy in males with prostatic cancer may be associated with an increased risk for T2D, which may be caused by negative effects on insulin sensitivity
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insulin sensitivity, measured by HOMA, improved in both groups and with a significantly greater degree when testosterone was added to supervised D&E
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Fasting insulin concentrations, a good representative of insulin sensitivity, did show a significant correlation with changes in circulating androgen levels, an observation in support of Pitteloud et al (2005), who showed a direct relationship between insulin sensitivity and circulating testosterone concentrations using the hyper-insulinemic euglycemic clamp technique
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52 weeks of testosterone treatment also significantly improved circulation levels of adiponectin and hsCRP, key serum markers of insulin sensitivity and hepatic steatosis
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The changes in both adiponectin and hsCRP were significantly correlated with the therapy-induced changes in bioavailable testosterone
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serum PSA concentrations did not differ between the 2 treatment groups, indicating that short-term testosterone administration appears to be acceptably safe
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shared by Nathan Goodyear on 19 Mar 15
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Unintended effects of statins from observational studies in the general population: sys... - 0 views
www.ncbi.nlm.nih.gov/...PMC3998050
statin therapy statins myopathy cholesterol side effects diabetes liver liver enzymes
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One cohort study (Women’s Health Initiative) of higher quality and larger sample size found stronger evidence of an increased risk of self-reported T2DM (OR=1.47; 95% CI 1.32 to 1.64) for the groups of women who reported statin use at baseline and three years later
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Smeeth et al. found an increased risk of incident liver disease in the first year after the index date
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The cumulative incidence of T2DM after three years of statin treatment was 6.25%, corresponding to an excess risk of 2.25%
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We found no increased risk of peripheral neuropathy, depression, common eye diseases, renal disorders or arthritis associated with taking statins. Studies of higher quality did not show previously reported protective effects of statins on fractures, venous thrombo-embolism or pneumonia
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Statin use associated with increased myopathy, liver dysfunction, and type II Diabetes. The authors conclude that the absolute risk is very low, yet OR was 1.47 for type II Diabetes (translated 47% increased odds of developing Diabetes as a result of statins) and OR of 2.63 in risk of myopathy (translated 163% increased odds of developing myopathy as a result of statins). Seems the authors "low risk" statement is just applies to those without symptoms/side effects. Physicians need to do a better job of understanding risks and customizing therapies.
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shared by Nathan Goodyear on 12 Nov 14
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BMC Cancer | Full text | A lactate shuttle system between tumour and stromal cells is a... - 0 views
www.biomedcentral.com/...352
cancer prostate cancer CAFs cancer associated fibroblasts mono-carboxylate transporters
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Under hypoxic conditions, tumour cells primarily use glycolysis for energy, producing lactate, which is expelled to the tumour microenvironment, allowing tumours to continue their glycolytic activity
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Sonveaux et al. showed that lactate, which is generally considered a waste product, is preferred over glucose by oxidative tumour cells as their primary energy source
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MCT4 is a low-affinity transporter, which is abundant in highly glycolytic muscle cells and is one of the many target genes of hypoxia-inducible factor 1 alpha (HIF-1α)
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Other targets of HIF-1α include glucose transporter-1 (GLUT-1), the main transporter involved in glucose uptake [9,10]; lactate dehydrogenase V (LDHV), which is responsible for the conversion of pyruvate into lactate; pyruvate dehydrogenase kinase isozyme 1 (PDK1), which is responsible for the phosphorylation and consequent inactivation of pyruvate dehydrogenase (PDH); and carbonic anhydrase IX (CAIX), a hypoxia-related protein involved in pH regulation [11]. Alpha-methylacyl-CoA racemase (AMACR), pristanoyl-CoA oxidase (ACOX-3) and D-bifunctional protein (DBP), are also important fatty acid oxidation-related proteins in prostate cancer
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the essential role played by the cross-talk between stroma and epithelium in carcinogenesis and prostate cancer progression has been increasingly recognised
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strong membranous expression of MCT1 was consistently observed in cancer cells, suggesting a role for MCT1 in the transport of lactate into tumour cells from the acidic extracellular matrix, suggesting that lactate might be used as a fuel by oxidative cancer cells.
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Our hypothesis is in agreement with those of Fiaschi et al.[17], who describe the metabolic reprogramming of CAFs towards the Warburg phenotype as a result of contact with prostate cancer cells
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Using in vitro studies, they showed lactate production and efflux by de novo expressed MCT4 in CAFs and also demonstrated that, upon contact with CAFs, prostate cancer cells were reprogrammed towards aerobic metabolism, with an increase in lactate uptake via the lactate transporter MCT1.
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pharmacological inhibition of MCT1-mediated lactate uptake dramatically affected PCa cell survival and tumour outgrowth
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In this model, “energy transfer” or “metabolic coupling” between the tumour stroma and epithelial cancer cells fuels tumour growth and metastasis via oxidative mitochondrial metabolism in anabolic cancer cells
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the concomitant expression of MCT1 in tumour cells and MCT4 in fibroblasts in the same tissue is clinically significant, and associated with poor prognosis.
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Intravenous Ascorbate as a Tumor Cytotoxic Chemotherapeutic Agent - 0 views
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Ascorbic acid and its salts (AA) are preferentially toxic to tumor cells in vitro (6 — 13) and in vivo
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Increases animal and human resistance to infectious agents by enhancing lymphocyte blastogenesis, enhancing cellular immunity, strengthening the extracellular matrix, and enhancing bactericidal activity of neutrophils and modulation of complement protein
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Strengthens the structural integrity of the extracellular matrix which is responsible for stromal resistance to malignant invasiveness
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In 1977, Bram et al reported preferential AA toxicity for several malignant melanoma cell lines, including four human-derived lines
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Noto et al reported that AA plus vitamin K3 had growth inhibiting action against three human tumor cell lines at non-toxic levels
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The AA begins to reduce cell proliferation in the tumor cell line at the lowest concentration, 1.76 mg/dl, and is completely cytotoxic to the cells at 7.04 mg/dl
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preferential toxicity of AA for tumor cells. >95% toxicity to human endometrial adenocarcinoma and pancreatic tumor cells (ATCC AN3-CA and MIA PaCa-2) occurred at 20 and 30 mg/dl, respectively.
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No toxicity or inhibition was demonstrated in the normal, human skin fibroblasts (ATCC CCD 25SK) even at the highest concentration of 50 mg/dl.
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Cameron and Pauling have published extensive suggestive evidence for prolonged life in terminal cancer patients orally supplemented (with and without initial intravenous AA therapy) with 10 g/day of AA
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the long-term, oral dosage used in those experiments (10 g/day), while substantial and capable of producing immunostimulatory and extracellular matrix modulation effects, was not high enough to achieve plasma concentrations that are generally cytotoxic to tumor cells in culture
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5 — 40 mg/dl of AA is required in vitro to kill 100% of tumor cells within 3 days. The 100% kill levels of 30 mg/dl for the endometrial carcinoma cells and 40 mg/dl for the pancreatic carcinoma cells in Figure 2 are typical
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1 h after beginning his first 8-h infusion of 115 g AA (Merit Pharmaceuticals, Los Angeles, CA), the plasma AA was 3.7 mg/dl and at 5 h was 19 mg/dl. During his fourth 8-h infusion, 8 days later, the 1 h plasma level was 158 mg/dl and 5 h was 185 mg/dl
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plasma levels of over 100 mg/dl have been maintained in 3 patients for more than 5 h using continuous intravenous infusion
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In rare instances of patients with widely disseminated and rapidly proliferating tumors, intravenous AA administration (10 — 45 g/day) precipitated widespread tumor hemorrhage and necrosis, resulting in death
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Although the outcomes were disastrous in these cases, they are similar to the description of tumor-necrosis-factor-induced hemorrhage and necrosis in mice (52) and seem to demonstrate the ability of AA to kill tumor cells in vivo.
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toxic effects of AA on one normal cell line were observed at 58.36 mg/dl and the lack of side effects in patients maintaining >100 mg/dl plasma levels
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Although it is very rare, tumor necrosis, hemorrhage, and subsequent death should be the highest priority concern for the safety of intravenous AA for cancer patients.
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Cathcart (55) who describes no ill effects with doses of up to 200 g/d in patients with various pathological conditions
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following circumstances: renal insufficiency, chronic hemodialysis patients, unusual forms of iron overload, and oxalate stone formers
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Screening for red cell glucose-6-phosphate dehydrogenase deficiency, which can give rise to hemolysis of red blood cells under oxidative stress (57), should also be performed
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any cancer therapy should be started at a low dosage to ensure that tumor hemorrhage does not occur.
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a scorbutic rebound effect can be avoided with oral supplementation. Because of the possibility of a rebound effect, measurement of plasma levels during the periods between infusions should be performed to ensure that no such effect takes place
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Every effort should be made to monitor plasma AA levels when a patient discontinues intravenous AA therapy.
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Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views
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MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
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This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
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Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
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It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
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The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
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It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
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The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
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Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
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Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
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The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
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Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
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Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
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It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
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Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
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Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
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weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
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Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
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Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
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In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
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individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
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Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
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Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
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It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
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it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
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The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
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Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
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Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
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It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
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inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
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Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days
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shared by Nathan Goodyear on 30 Jan 18
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Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2... - 0 views
www.nature.com/...s41698-017-0044-8
cancer cancer stem cells liver cancer vitamin C IV vitamin C oncology
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Chen et al. have revealed that ascorbate at pharmacologic concentrations (0.3–20 mM) achieved only by intravenously (i.v.) administration selectively kills a variety of cancer cell lines in vitro, but has little cytotoxic effect on normal cells.
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Ascorbic acid (the reduced form of vitamin C) is specifically transported into cells by sodium-dependent vitamin C transporters (SVCTs)
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differential sensitivity to VC may result from variations in VC flow into cells, which is dependent on SVCT-2 expression.
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high-dose VC significantly impaired both the tumorspheres initiation (Fig. 4d, e) and the growth of established tumorspheres derived from HCC cells (Fig. 4f, g) in a time-dependent and dose-dependent manner.
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The antioxidant, N-acetyl-L-cysteine (NAC), preventing VC-induced ROS production (a ROS scavenger), completely restored the viability and colony formation among VC-treated cells
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Interestingly, the combination of VC and cisplatin was even more effective in reducing tumor growth and weight
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Consistent with the in vitro results, stemness-related genes expressions in tumor xenograft were remarkably reduced after VC or VC+cisplatin treatment, whereas conventional cisplatin therapy alone led to the increase of CSCs
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Interestingly, at extracellular concentrations greater than 1 mM, VC induces strong cytotoxicity to cancer cells including liver cancer cells
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we hypothesized that intravenous VC might reduce the risk of recurrence in HCC patients after curative liver resection.
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Intriguingly, the 5-year disease-free survival (DFS) for patients who received intravenous VC was 24%, as opposed to 15% for no intravenous VC-treated patients
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In this study, based on the elevated expression of SVCT-2, which is responsible for VC uptake, in liver CSCs, we revealed that clinically achievable concentrations of VC preferentially eradicated liver CSCs in vitro and in vivo
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Additionally, we found that intravenous VC reduced the risk of post-surgical HCC progression in a retrospective cohort study.
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Three hundred thirty-nine participants (55.3%) received 2 g intravenous VC for 4 or more days after initial hepatectomy
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As the key protein responsible for VC uptake in the liver, SVCT-2 played crucial roles in regulating the sensitivity to ascorbate-induced cytotoxicity
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we also observed that SVCT-2 was highly expressed in human HCC samples and preferentially elevated in liver CSCs
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we revealed that VC treatment dramatically reduced the self-renewal ability, expression levels of CSC-associated genes, and percentages of CSCs in HCC, indicating that CSCs were more susceptible to VC-induced cell death
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as a drug for eradicating CSCs, VC may represent a promising strategy for treatment of HCC, alone or particularly in combination with chemotherapeutic drugs
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In HCC, we found that VC-generated ROS caused genotoxic stress (DNA damage) and metabolic stress (ATP depletion), which further activated the cyclin-dependent kinase inhibitor p21, leading to G2/M phase cell cycle arrest and caspase-dependent apoptosis in HCC cells
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we demonstrated a synergistic effect of VC and chemotherapeutic drug cisplatin on killing HCC both in vitro and in vivo
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Intravenous VC has also been reported to reduce chemotherapy-associated toxicity of carboplatin and paclitaxel in patients,38 but the specific mechanism needs further investigation
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Our retrospective cohort study also showed that intravenous VC use (2 g) was related to the improved DFS in HCC patients after initial hepatectomy
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several clinical trials of high-dose intravenous VC have been conducted in patients with advanced cancer and have revealed improved quality of life and prolonged OS
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high expression (grade 2+/3+) of SVCT-2 was in agreement with poorer overall survival (OS) of HCC patients (Fig. 1c) and more aggressive tumor behavior
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these data suggest that SVCT-2 is preferentially expressed in liver CSCs and is required for the maintenance of liver CSCs.
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pharmacologic concentrations of plasma VC higher than 0.3 mM are achievable only from i.v. administration
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The viabilities of HCC cells were dramatically decreased after exposure to VC in dose-dependent manner
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These results verify that VC inhibits tumor growth in HCC PDX models and SVCT-2 expression level is associated with VC response
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qPCR and IHC analysis demonstrated that expression levels of CSC-associated genes and percentages of CSCs in PDXs dramatically declined after VC treatment, confirming the inhibitory role of VC in liver CSCs
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shared by Nathan Goodyear on 03 Jun 18
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High Progesterone Receptor Expression in Prostate Cancer Is Associated with Clinical Fa... - 0 views
www.ncbi.nlm.nih.gov/...PMC4344236
prostate cancer progesterone progesterone receptor hormones cancer prostate
![](/images/link.gif)
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Our large-sized study demonstrates a wide distribution of PGR in stromal and epithelial cells of both benign and malignant prostate tissue
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In line with our findings, several have also reported a high PGR expression in TE of PCa [9,10,23,25]. In contrast, others have demonstrated a total lack of PGR expression in TE
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In our work univariate analysis demonstrated a high PGR expression in TS to be associated with clinical failure in PCa patients. So far we have not yet demonstrated the mechanism underlying this association
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Several non-genomic proliferative actions of progesterone have been proposed in tumor cells of other organs, including breast [35–37], astrocytoma [38] and osteosarcoma [39] cell lines. However, such results are contradicted by suggestions of anti-proliferative actions of progesterone in endometrial cancer
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Latil and co-workers found a decreased PGR expression in clinically localized tumors and increased PGR expression in hormone-refractory tumors, when compared with normal prostate tissue
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Our findings provide further support to these findings, indicating that PGR plays a role in the pathogenesis of PCa
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Ki67 and PGR in TE were correlated with CF (S3 Text), indicating an association between PGR and proliferative activity
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The PGR is, like the glucocorticoid receptor, similar to androgen receptor with 88% sequence homology in the ligand-binding domain
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progesterone induced expression of androgen receptor-regulated genes could be a potential mechanism contributing to the development of castrate resistant PCa
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A possibility of different roles by the two PGR isoforms in normal prostate tissue and PCa, as is suggested for the estrogen receptors [13], must also be taken into account
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STudy finds that increased Progesterone receptor expression on epithelial and stromal cells is associated with increased clinical failure of therapy. Several proposed mechanisms: 88% homologous with androgen receptor suggesting cross-stimulation and via progesterone induced increased androgen receptor gene stimulation i.e. epigenetics.
13More
Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer - 0 views
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The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis
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The most important reason for the poor performance of cancer drugs is the remarkable heterogeneity and adaptability of cancer cells. The molecular characteristics of histologically identical cancers are often dissimilar and molecular heterogeneity frequently exists within a single tumour.
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Because GO is far more efficient in generating ATP compared with GLY (producing 36 vs 2 ATP per glucose
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molecule), cancer cells upregulate glucose receptors and significantly increase glucose uptake in an attempt to ‘catch up
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early carcinogenesis often occurs in a hypoxic microenvironment, the transformed cells have to rely on anaerobic GLY for energy production.
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Dichloroacetate activated the pyruvate dehydrogenase, which resulted in increased delivery of pyruvate into the mitochondria
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DCA increased GO and depolarised the mitochondria, returning the membrane potential towards the levels of the non-cancer cells, without affecting the mitochondria of non-cancerous cells
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induction of apoptosis by DCA in non-small cell lung cancer, breast cancer and glioblastoma cell lines
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DCA was shown to induce apoptosis in endometrial (Wong et al, 2008) and prostate (Cao et al, 2008) cancer cells
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shared by Nathan Goodyear on 18 May 17
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Hyperbaric oxygen therapy promotes neurogenesis: where do we stand? - 0 views
www.ncbi.nlm.nih.gov/...PMC3231808
hbot hyperbaric therapy hyperbaric brain TBI stroke neurogenesis neuorplasticity
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activated by hypoxia, HIF-1α causes the transcription of its regulated downstream genes, including erythropoietin (EPO) and VEGF which are known to promote neurogenesis
- ...10 more annotations...
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The safety of HBOT was also evaluated and it was pointed out that, if given at proper paradigms, like 1.5 ATA for 60 minutes, HBOT will not cause oxygen toxicity
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Rockswold et al., on the other hand, found that HBOT might be potentially beneficial for severe TBI patients
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McDonagh et al., concluded that there was insufficient evidence to establish the effectiveness of HBOT in the treatment of TBI
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The first multicenter, randomized, double-blind, controlled trial in 2009 found that 40-hour HBOT of 24% oxygen at 1.3 ATM produced significant improvement in children's overall functioning, receptive language, social interaction, eye contact, and sensory/cognitive awareness compared to those received slightly pressurized room air
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Another study in 2010 on 16 autism patients, adopting a similar treatment paradigm, showed no effect on a wide array of behavioral evaluations
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To date, there is little evidence that HBOT causes malignant growth or metastasis. A history of malignancy should therefore not be considered as a contraindication for HBOT
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HBOT enhances the production of reactive oxygen species (ROS) and causes oxidative stress in body tissues
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Excessive accumulation of oxidative stress may contribute to neurodegenerative processes and cell death in the brain, as seen in diseases like Alzheimer's disease (AD) and Parkinson's disease (PD)
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process that results in a functional improvement of cellular stress resistance, survival, and longevity in response to sub-lethal levels of stress
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training exercise sprints running epigenetics PLIN2 PLIN5
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Study finds sprint interval training increases PLIN 2 and PLIN 5 as in endurance training. PLIN2/5 are increased and play role in intramuscluar triglyceride breakdown. Increased IMTG is found in IR. This aids insulin resistance. Other studies have found that SIT increased PLIN5 > ET. Exercise impacts muscle and fat through epigenETics.
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Chirurgie cardiaque robotique en Inde Cost Of Robotic Heart Surgery India Best Robotic Heart Surgeons of India Minimally Invasive cardiac surgeon in India
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La chirurgie cardiaque robotisée en Inde s'est avérée être une aubaine pour les patients nationaux comme pour les patients du monde entier, réalisée par des chirurgiens cardiaques peu invasifs en Inde avec la plus grande précision. Il est disponible dans les meilleurs hôpitaux pour la chirurgie cardiaque robotique en Inde et est effectué par des chirurgiens cardiaques mini-invasifs en Inde.
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TAVR de l'Inde chirurgiens TAVR de l'Inde Avantages de la chirurgie Tavi_Tavr
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En offrant un traitement médical de la plus haute qualité au prix du remplacement de la valve aortique par cathéter trans (Tavr) Inde, l'Inde s'est imposée comme l'un des centres les plus populaires pour obtenir des traitements du monde entier. Pour un rendez-vous accéléré et une consultation avec notre consultant Veuillez appeler le +91-9370586696 ou vous pouvez nous envoyer un courrier Identifiant de l'e-mail : - enquiry@indiacardiacsurgerysite.com