Necrosis versus apoptosis in acetaminophen-induced hepatotoxicity
β Scribed by Klaus Schulze- Osthoff; Heike Bantel
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 632 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ Synopsis
Shorter duration and lower dose of peginterferon alfa-2a therapy results in inferior HBeAg seroconversion rates compared with the duration and dose of 48 weeks and 180 lg: NEPTUNE study.
π SIMILAR VOLUMES
We read with interest the study by Sola `et al., 1 who found that 39 patients (67%) had a very alarming decrease in their serum sodium levels ! 5 mEq/L during terlipressin treatment for acute variceal bleeding (AVB). We, however, feel that some of their observations may require a closer look by the
Research into the pathogenesis of acetaminophen (paracetamo1)-induced hepatotoxicity has concentrated on the generation of toxic metabolites by the hepatocytes. It has, however, recently been shown that human macrophages cultured with acetaminophen secrete increased quantities of tumour necrosis fac
Recent evidence suggests that macrophages and/or other nonparenchymal cells may release important mediators contributing to the hepatic necrosis induced by high doses of acetaminophen (APAP). The nature and causative role of these mediators has remained elusive, however. To investigate the role of t
Cimetidine has been shown to protect against acetaminophen-mediated hepatotoxicity in both rats and mice. In contrast to cimetidine, ranitidine recently has been determined to potentiate the hepatotoxic action of acetaminophen in Fischer 344 rats. The present studies were designed to characterize th