Raman Venkataramanan, and Timothy R. Sterling, on behalf of the ATS Hepatotoxicity of Antituberculosis

Drug-induced liver injury (DILI) is a major cause of late-stage clinical drug attrition, market withdrawal, black-box warnings, and acute liver failure. Consequently, it has been an area of focus for toxicologists and clinicians for several decades. In spite of considerable efforts, limited

the attitudes of Turkish students studying at the department of English Language and Literature towards cultural aspects in language teaching and learning. The data were collected through a Likert type questionnaire in which all participants were asked questions to respond with the purpose of finding

Drug-induced liver injury (DILI) is a significant concern in drug development due to the poor concordance between preclinical and clinical findings of liver toxicity. We hypothesized that the DILI types (hepatotoxic side effects) seen in the clinic can be translated into the development

The Author(s) 2014. This article is published with open access at Springerlink.com Abstract Causality assessment is a critical step in estab-lishing the diagnosis of drug induced liver injury (DILI) during drug development. DILI may resemble almost any type of liver disease, and often presents a

Individual vulnerability to drug-induced liver injury (DILI)might result fromdeficiencies in the detoxification process, which determines the level of exposure to the reactive metabolite. We evaluated whether a genetically determined reduction in the ability to detoxify electrophilic compounds

with nevirapine hypersensitivity (15 drug-induced liver injury [DILI], 33 SJS/TEN, 20 hypersensitivity syndrome, and 46 nevirapine-induced rash plus 3 with both DILI and SJS phenotype) and 155 age-, sex- and ethnicity-matched nevirapine-exposed controls. HLA typing for 5 loci (A, B, C, DRB1, and DQB1

cause of acute liver injury, drug induced steatosis and steatohepatitis are considered a rare form of drug induced liver injury (DILI). The complex mechanism leading to hepatic steatosis caused by commonly used drugs such as amiodarone, methotrexate, tamoxifen, valproic acid, glucocorticoids, and others

Early and accurate pre-clinical and clinical biomarkers of hepatotoxicity facilitate the drug development process and the safety monitoring in clinical studies. We selected eight known model compounds to be administered to male Wistar rats to identify biomarkers of drug induced liver injury (DILI

, and some degree of open-access scheduling. Practices that managed no-shows well encouraged walk-ins and work-ins and overbooked resident schedules either equally or based upon individual no-show rates. Practice exemplars of both types were highly committed to addressing the no-shows problem and were dili