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Crohn's Disease: Case Western Reserve Researchers Identify Links Between Inflammatory Disease Genes
Researchers from Case Western Reserve University School of Medicine identified a novel link between ITCH, a gene known to regulate inflammation in the body and NOD2, a gene which causes the majority of genetic Crohn"s Disease diagnoses. ITCH, when malfunctioning, causes widespread inflammatory diseases, including inflammatory bowel disease, gastritis, uncontrolled skin inflammation, and pulmonary pneumonitis. Derek Abbott, M.D., Ph.D., and his team of researchers found that ITCH also influences NOD2-induced inflammation. These findings, published in the August 11th issue of Current Biology, suggest a common pathophysiology exists between multiple inflammatory diseases. The unexpected finding of the interaction between these genes offers the possibility of a new drug target, which would be effective in treating Crohn"s disease - a chronic disorder causing inflammation of the gastrointestinal tract.

New Flu Virus Found In Canadian Pig Farm Workers
The Canadian authorities have announced that a new strain of influenza A virus has been found in two pig farm workers in the Province of Saskatchewan
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Protect Children From The Allure Of Smoking, Say Doctors
BMA Scotland has warned that children who smoke face years of tobacco addiction that can lead to life-threatening diseases and premature death. The association also called on MSPs to support the proposals contained in the Tobacco and Primary Medical services (Scotland) Bill in order to reduce children"s exposure to tobacco products.
Medical Devices

Quinine Side Effects May Be Result Of Tryptophan Deficiency

Researchers have found that the anti-malarial drug quinine can block a cell"s ability to take up the essential amino acid tryptophan, a discovery that may explain many of the adverse side-effects associated with quinine. Once confirmed, these findings would suggest that dietary tryptophan supplements could be a simple and inexpensive way to improve the performance of this important drug. Quinine is a very commonly used anti-malarial drug, yet to this day the principal mode of quinine action against the malaria parasite is still largely unclear, as is the basis for adverse reactions like nausea, headaches, and blurred vision. To address these gaps, Simon Avery and colleagues at the University of Nottingham took advantage of yeast genetics, examining the effects of quinine on a collection of 6000 yeast mutants, each one lacking exactly one of the yeast"s 6000 genes. While quite different from humans, yeast is comparable on a cellular level and yeast is frequently, and successfully, used as front-line agents in testing chemicals and small molecule drugs. Their screen revealed that strains unable to make tryptophan were extremely susceptible to quinine poisoning, which led them to identify a tryptophan transporter as a key quinine target (yeast that cannot make their own tryptophan have to rely exclusively on external s, and thus die if tryptophan transport is blocked). This discovery fits in well with evidence that quinine reactions are more severe in malnourished individuals. Unlike yeast, humans cannot make their own tryptophan and thus require dietary tryptophan, which is abundant in meat but limited in yams, a staple food crop in the tropics where malaria is prevalent. If quinine severely reduces tryptophan uptake, then it follows that people with preexisting tryptophan deficiencies would be especially at risk to this drug. The authors also note that tryptophan is important as a precursor for the brain chemical serotonin, so the enhanced tryptophan deficiency induced by quinine could explain why many of quinine"s side effects are localized to the head region. They also note that side-effects could be averted simply by taking dietary tryptophan supplements in conjunction with quinine treatments, though it is not yet known if tryptophan may affect quinine action against the malaria parasite. This study appears in the July 3rd issue of Journal of Biological Chemistry and was published online June 26. From the Article: "THE ANTIMALARIAL DRUG QUININE DISRUPTS TAT2P-MEDIATED TRYPTOPHAN TRANSPORT AND CAUSES TRP STARVATION" by Combiz Khozoie, Richard J. Pleass and Simon V. Avery Nick Zagorski American Society for Biochemistry and Molecular Biology


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