Reply:
Alejandro Forner, Ramón Vilana, Jordi Bruix – 5 August 2010
Reply:
Hui Xu, Liang‐Hu Qu – 5 August 2010
Reply:
Elizabeth K. Speliotes, Joseph M. Massaro, Christopher J. O'Donnell, Caroline S. Fox – 5 August 2010
Activation of the mammalian target of rapamycin signaling pathway in hepatocellular carcinoma
Ishwaria M. Subbiah, Robert E. Brown, Michael B. Fallon – 2 August 2010
Drug therapy: Rifaximin1
Jasmohan S. Bajaj, Oliviero Riggio – 29 July 2010
Hepatic venous outflow obstruction in pediatric living donor liver transplantation using left‐sided lobe grafts: Kyoto university experience
Seisuke Sakamoto, Hiroto Egawa, Hiroyuki Kanazawa, Toshiya Shibata, Aya Miyagawa‐Hayashino, Hironori Haga, Yasuhiro Ogura, Mureo Kasahara, Koichi Tanaka, Sinji Uemoto – 29 July 2010 – The goals of this study were to evaluate the incidence of hepatic venous outflow obstruction (HVOO) in pediatric patients after living donor liver transplantation (LDLT) using left‐sided lobe grafts and to assess the therapeutic modalities used for the treatment of this complication at a single center.
Mycobacterium tuberculosis infection in liver transplantation
Baligh R. Yehia, Emily A. Blumberg – 29 July 2010 – Mycobacterium tuberculosis can cause significant infections in liver transplant candidates and recipients. Its nonspecific clinical features and prolonged growth time in culture make the diagnosis difficult, and treating tuberculosis (TB) remains challenging because of significant toxicities and drug‐drug interactions. The diagnosis of a latent TB infection may be accomplished with tuberculin skin testing and with the newer interferon‐γ release assays, although this infection may be underrecognized because of host factors.
Is increasing the copy number of the microRNA precursor in a vector really helpful for further improving the level of mature microRNA in stable cells?
Fang Wang, Fu Yang, Ling Zhang, Shuhan Sun – 29 July 2010
Uric acid potentially links fatty liver and high blood pressure
Hong‐Fang Ji, Liang Shen – 29 July 2010
Phosphoinositide 3‐kinase/protein kinase B signaling pathway is involved in estradiol 17β‐d‐glucuronide–induced cholestasis: Complementarity with classical protein kinase c
Andrea C. Boaglio, Andrés E. Zucchetti, Enrique J. Sánchez Pozzi, José M. Pellegrino, Justina Elena Ochoa, Aldo D. Mottino, Mary Vore, Fernando A. Crocenzi, Marcelo G. Roma – 29 July 2010 – Estradiol 17β‐D‐glucuronide (E217G) is an endogenous, cholestatic metabolite that induces endocytic internalization of the canalicular transporters relevant to bile secretion: bile salt export pump (Bsep) and multidrug resistance–associated protein 2 (Mrp2). We assessed whether phosphoinositide 3‐kinase (PI3K) is involved in E217G‐induced cholestasis.