HEALTH MANAGEMENT. Key protein associated with acute liver failure identified USC scientists

New research from the Keck help school of medicine which can University of Southern California (USC) to avoid damage to the liver caused by medication such as acetaminophen and other stressors.
Paracetamol, better known as Tylenol, can reduce pain and fever. The over-the-counter drug is an important part in many cold and flu remedies and prescription painkillers such as Percocet and vicodin. TESCO HEALTH INSURANCE

However, paracetamol (acetaminophen) the most common cause of drug-induced liver disease is metabolized by the liver, and liver failure, acute in the United States and Britain. The Tylenol maker announced in July that it was the maximum recommended daily dose to 3,000 mg to prevent that reduces accidental overdose.
Doctors at the Keck School of Medicine of USC found a protein in the mitochondria of liver cells in mice, if to silence brought, protects against liver toxicity normally associated with excess doses of acetaminophen.
They found that the protein SAB or SH3 binding protein 5, bonds with the enzyme JNK (c-Jun N-terminal kinase). JNK regulates cellular metabolism, and survival in response to stress, protects of the cells for short intervals enabled. JNK kills but also cells that are activated for a long time. HEALTH INFORMATION TECHNOLOGY

"Because the short-term activation of JNK survival of the cell is associated with, SAB is potentially a better target than inhibition of JNK, which could have adverse effects", Neil Kaplowitz, m.d., the study investigator and Professor of medicine at the Keck said school.
Researchers have long believed that acetaminophen to toxic metabolites, which was converted in excess, overpower liver cells, to die. In a study of 2008, Kaplowitz, who holds, that the Keck School Thomas H. brem Chair of medicine and Veronica p. Budnick Chair for liver disease and other USC members, that the theory – enabled, found that it not the metabolite, but rather the permanent activation of JNK, which damaged the organ. By the inhibition of JNK activation in mice, has been damage to the liver, which avoided by high doses of acetaminophen. HEALTH MANAGEMENT

In the current study, published online by the journal of biological chemistry in August SAB silent in mice, the scientists that had prevented successfully but no effect on the metabolism of paracetamol, injury of the liver. Tested the impact damage on liver apoptosis or programmed cell death due to inflammatory proteins, the SAB silencing in many diseases and tissue - involved are to protected the liver in this case. AHM HEALTH INSURANCE

"We proved that long-lasting activation of JNK aims is to SAB and a prerequisite for the subsequent death of liver cells", Kaplowitz said. "We then showed that it is a universal effect." Development of a drug against cell death to protect, it could be argued, aim JNK - but this is a double-edged sword. This provides a new goal: create a drug, that inhibit the interaction between JNK and SAB. " WPA HEALTH INSURANCE

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