2 mm) along with a loss of normal five-layer pattern (Fig. 1). The proximal uninvolved esophagus revealed a normal 5-layered wall pattern (Fig. 2). Triamcinolone

acetonide (40 mg/mL diluted 1:1 with saline solution; 0.5 mL at each site) was injected at the proximal margin as well as in the strictured segment. Thereafter, endoscopic dilatation was performed and the patient has since been asymptomatic. Corrosive selleckchem injury of the gastrointestinal tract (GIT) is an important health problem, especially in developing countries. The injury and inflammation of the GIT caused by corrosives can cause hemorrhaging and perforation in an acute setting and strictures in the delayed phase. Corrosive induced GIT strictures are difficult to manage as they require more endoscopic dilatation sessions and are more likely to recur. The factors responsible for this clinical course are unclear but the intense fibrosis and consequent esophageal wall thickening may be responsible for it. EUS could provide more detailed information compared with conventional endoscopy as it images the full thickness of the GIT wall. It has been shown in an acute setting that the involvement of muscularis propria on EUS predicts stricture formation

with an accuracy of 100%. Theoretically, EUS may also be helpful in the management of patients with corrosive strictures but its role needs to be studied. One may predict the response to dilatation by measuring the wall selleck chemical thickness on EUS (Fig. 1)

as well as more precisely injecting intralesional steroids in the thickest GIT wall under EUS guidance. However, this hypothesis needs to be tested in prospective studies. Contributed by “
“A surgeon needs to address Cell Cycle inhibitor four issues on surgical evaluation for a liver transplant candidate. These are: (1) necessity; (2) suitability; (3) strategy; and (4) informed consent. A surgeon’s “eye-ball” test is sometimes more important than consulting many specialists. A creative strategy is key, especially if you practice in extreme organ shortage areas. “
“Sabio G, Cavanagh-Kyros J, Ko HJ, Jung DY, Gray S, Jun JY, et al. Prevention of steatosis by hepatic JNK1. Cell Metab 2009;10:491-498. (Reprinted with permission.) Nonalcoholic steatosis (fatty liver) is a major cause of liver dysfunction that is associated with insulin resistance and metabolic syndrome. The cJun NH2-terminal kinase 1 (JNK1) signaling pathway is implicated in the pathogenesis of hepatic steatosis and drugs that target JNK1 may be useful for treatment of this disease. Indeed, mice with defects in JNK1 expression in adipose tissue are protected against hepatic steatosis. Here we report that mice with specific ablation of Jnk1 in hepatocytes exhibit glucose intolerance, insulin resistance, and hepatic steatosis. JNK1 therefore serves opposing actions in liver and adipose tissue to both promote and prevent hepatic steatosis.