Be more intelligent than you've ever been before with in-depth knowledge about your operation - and the market at large - like you've never had before.
This study is misleading. Their conclusion is that D2 and D3 are equivalent in raising 25-OH vitamin D via po form preferentially over the IM form. However, when you look at the results, the response of D3 was statistically significant over that of D2. That is the conclusion: vitamin D3 is the optimal form of vitamin D.
IV germanium augments NK activity in mouse blood providing anti-tumor activity. Different activity found with po and intra-peritoneal injection--augmentation of cytotoxic macrophages. Prolongation of life was not found in the IV arm.
The data show that pharmacologic ascorbate concentrations produced Asc•− selectively in extracellular fluid compared with blood and that H2O2 formation occurred when Asc•− concentrations were >100 nM in extracellular fluid.
These data validate the hypothesis that ascorbate is a prodrug for selective delivery of reactive species to the extravascular space
pharmacologic ascorbate as a prooxidant drug for therapeutic use.
Recently we reported that pharmacologic ascorbic acid concentrations produced H2O2 concentrations of ≥25 μM, causing cancer cell death in vitro
We found that H2O2 concentrations generated in vivo were those that caused cancer cell death in vitro
When ascorbate was given parenterally, Asc•−, the product of a loss of one electron from ascorbate, was detected preferentially in extracellular fluid compared with blood
Asc•− generation in extracellular fluid depended on the ascorbate dose and the resulting concentrations
With i.v. administration of ascorbate, Asc•− concentrations were as much as 12-fold greater in extracellular fluid compared to blood and approached 250 nM
In blood, such Asc•− concentrations were never produced and were always <50 nM
These data are all consistent with the hypothesis that pharmacologic ascorbate concentrations in vivo serve as a prodrug for selective delivery of H2O2 to the extracellular space
After oral ingestion, control of intracellular and extracellular ascorbate concentrations is mediated by three mechanisms: intestinal absorption, tissue transport, and renal reabsorption
intestinal absorption, or bioavailability, declines at doses >200 mg
also at ≈60 μM, renal reabsorption approaches saturation, and excess ascorbate is excreted in urine
Parenteral administration bypasses tight control
When tight control is bypassed, H2O2 forms in the extracellular space
in vivo validation of ascorbate as a prodrug for selective H2O2 formation
Temporarily bypassing tight control with parenteral administration of ascorbate allows H2O2 to form in discrete time periods only, decreasing likelihood of harm, and provides a pharmacologic basis for therapeutic use of i.v. ascorbate
H2O2 formation results in selective cytotoxicity
Tumor cells are killed with exposure to H2O2 for ≤30 min
In vitro, killing is mediated by H2O2 rather than Asc•−
In addition to cancer treatment, another potential therapeutic use is for treatment of infections. H2O2 concentrations of 25–50 μM are bacteriostatic
This study looked at post menopause women and found that those with PCOS had an increase in CAD and worse cardiovascular event survival. PCOS is a metabolic syndrome, in part, driven by elevated androgens in women.
Looking To Sell Your Infusion IV Pumps? Willow Medical will purchase your infusion iv pumps. We will buy all of your quality iv pumps. We offer competitive pricing and will purchase from companies and individuals. Sell infusion pumps to Willow Medical today!
Great article from 2008 that discusses glycemic index and glycemic load. What is great about this article is the supplementary appendix listing the above for > 1000 items.
low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier
oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
malnutrition progressing to cachexia is another common manifestation of cirrhosis
Malnutrition can be mitigated with BCAA supplementation
Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease
Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
BCAAs metabolites inhibit proteolysis
Patients with cirrhosis have both insulin deficiency and insulin resistance
BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization
Coadministration of BCAAs and glucose has been found to be particularly useful
BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves
BCAA administration has also been shown to have a positive effect on liver regeneration
A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells
BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding
The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation
Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
patients taking BCAA supplementation report improved quality of life
BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
BCAAs make up 20-25% of the protein content of most foods
Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran
In addition to BCAAs from diet, oral supplements of BCAAs can be used
Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy
Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs
Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia
BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver
patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
the serum BCAA concentration is strongly correlated with the serum albumin level
Group items tagged 
