Risk Factors of Hypothermia During Pediatric Liver Transplantation Using a Novel Warming Method.

Background: Intraoperative hypothermia often occurs in patients under general anesthesia, including liver transplantation (LT), leading to various life-threatening conditions. This study aimed to evaluate factors causing hypothermia in patients undergoing pediatric LT.

Methods: Data were collected from patients undergoing LT who were warmed during surgery.

A safety analysis of edaravone (MCI-186) during the first six cycles (24 weeks) of amyotrophic lateral sclerosis (ALS) therapy from the double-blind period in three randomized, placebo-controlled studies.

Background: There continues to be a need for new therapies to treat ALS.

Objective: Provide an overview of safety for edaravone in ALS patients during the first six cycles of treatment.

Methods: Analysis was based on three randomised, placebo-controlled clinical trials.

Nrf2 counteracts cholestatic liver injury via stimulation of hepatic defense systems.

The transcription factor Nrf2 is a key regulator for hepatic induction of detoxifying enzymes, antioxidative stress genes and Mrp efflux transporters. We aimed to investigate whether Nrf2 activation counteracts liver injury associated with cholestasis. The role of Nrf2 activation in counteracting cholestatic liver injury was studied using a bile duct-ligation (BDL) model of Keap1 gene-knockdown (Keap1-kd) mice that represent the sustained activation of Nrf2 in the liver.

Ursodeoxycholic acid stimulates Nrf2-mediated hepatocellular transport, detoxification, and antioxidative stress systems in mice.

The protective action of ursodeoxycholic acid (UDCA) in cholestatic liver diseases may be mediated by choleresis, detoxification, and cytoprotection against oxidative stress. Nrf2, one transcription factor, serves as a cellular stress sensor and is a key regulator for hepatic induction of detoxifying enzymes, antioxidative stress genes, and numerous Mrp family members. We aimed to investigate whether UDCA induces hepatic Mrp expression along with that of detoxifying enzymes and antioxidative stress genes via the Nrf2 transcriptional pathway.

Ursodeoxycholic acid protects concanavalin A-induced mouse liver injury through inhibition of intrahepatic tumor necrosis factor-alpha and macrophage inflammatory protein-2 production.

Ursodeoxycholic acid (UDCA) is widely used for the therapy of liver dysfunction. In this study, we investigated the protective effect of UDCA in concanavalin A-induced mouse liver injury. The treatment with UDCA at oral doses of 50 and 150 mg/kg at 2 h before concanavalin A injection significantly reduced the elevated plasma levels of aminotransferases and the incidence of liver necrosis compared with concanavalin A-injected control group without affecting the concentrations of liver hydrophobic bile acids.

Protective effects of ursodeoxycholic acid on chenodeoxycholic acid-induced liver injury in hamsters.

Aim: To investigate the effects of ursodeoxycholic acid (UDCA) on chenodeoxycholic acid (CDCA)-induced liver injury in hamsters, and to elucidate a correlation between liver injury and bile acid profiles in the liver.

Methods: Liver injury was induced in hamsters by administration of 0.5% (w/w) CDCA in their feed for 7 d.

Hepatoprotective bile acid 'ursodeoxycholic acid (UDCA)' Property and difference as bile acids.

Ursodeoxycholic acid (UDCA) is a bile acid, which is present in human bile at a low concentration of only 3% of total bile acids. It is a 7beta-hydroxy epimer of the primary bile acid chenodeoxycholic acid (CDCA). UDCA is isolated from the Chinese drug 'Yutan' a powder preparation derived from the dried bile of adult bears.

Effect of cholecystokinin1 receptor antagonist loxiglumide (CR1505) on basal pancreatic exocrine secretion in conscious rats.

Introduction And Aim: To examine the involvement of cholecystokinin (CCK) in the basal pancreatic exocrine, we investigated the effect of loxiglumide (CR1505), a CCK1 receptor antagonist, on basal pancreatic exocrine secretion in conscious rats.

Methodology: After the basal collection of pancreatic juice for 1 hour, loxiglumide (10 mg/kg/h) or saline was infused via the femoral vein continuously for 2 hours.

Results: Loxiglumide significantly suppressed the basal pancreatic protein and amylase outputs.