Elevated miR-33a and miR-224 in steatotic chronic hepatitis C liver biopsies.

Aim: To assess the expression of selected microRNAs (miRNA) in hepatitis C, steatotic hepatitis C, noninfected steatotic and normal liver tissues.

Methods: The relative expression levels of miR-21, miR-33a, miR-96, miR-122, miR-125b, miR-221 and miR-224 were determined in 76 RNA samples isolated from 18 non-steatotic and 28 steatotic chronic hepatitis C (CHC and CHC-Steatosis, respectively) cases, 18 non-infected, steatotic liver biopsies of metabolic origin (Steatosis) and 12 normal formalin-fixed paraffin-embedded liver tissues using TaqMan MicroRNA Assays. All CHC biopsy samples were obtained prior to initiating therapy.

The role of pancreatic ductal secretion in protection against acute pancreatitis in mice*.

Objectives: A common potentially fatal disease of the pancreas is acute pancreatitis, for which there is no treatment. Most studies of this disorder focus on the damage to acinar cells since they are assumed to be the primary target of multiple stressors affecting the pancreas. However, increasing evidence suggests that the ducts may also have a crucial role in induction of the disease.

The crucial role of early mitochondrial injury in L-lysine-induced acute pancreatitis.

Aims: Large doses of intraperitoneally injected basic amino acids, L-arginine, or L-ornithine, induce acute pancreatitis in rodents, although the mechanisms mediating pancreatic toxicity remain unknown. Another basic amino acid, L-lysine, was also shown to cause pancreatic acinar cell injury. The aim of the study was to get insight into the mechanisms through which L-lysine damages the rat exocrine pancreas, in particular to characterize the kinetics of L-lysine-induced mitochondrial injury, as well as the pathologic responses (including alteration of antioxidant systems) characteristic of acute pancreatitis.

A new severe acute necrotizing pancreatitis model induced by L-ornithine in rats.

Objective: Intraperitoneal administration of large doses of L-arginine is known to induce severe acute pancreatitis in rats. We therefore set out to determine whether metabolites of L-arginine (L-ornithine, L-citrulline, and nitric oxide) cause pancreatitis.

Design: The authors conducted an in vivo animal study.

Effect of melatonin on the severity of L-arginine-induced experimental acute pancreatitis in rats.

Aim: To determine the effect of melatonin pre- and post-treatment on the severity of L-arginine (L-Arg) -induced experimental pancreatitis in rats.

Methods: Male Wistar rats (25) were divided into five groups. Those in group A received two injections of 3.

Changes in lipid metabolism in chronic hepatitis C.

Aim: To investigate the relationship between certain biochemical parameters of lipid metabolism in the serum and steatosis in the liver.

Methods: The grade of steatosis (0-3) and histological activity index (HAI, 0-18) in liver biopsy specimens were correlated with serum alanine aminotransferase (ALT), total cholesterol and triglyceride levels in 142 patients with chronic hepatitis C (CH-C), and 28 patients with non-alcoholic fatty liver disease (NAFLD) without hepatitis C virus (HCV) infection. The serum parameters were further correlated with 1,797 age and sex matched control patients without any liver diseases.

The proteasome inhibitor MG132 protects against acute pancreatitis.

The cell-permeant MG132 tripeptide (Z-Leu-Leu-Leu-aldehyde) is a peptide aldehyde proteasome inhibitor that also inhibits other proteases, including calpains and cathepsins. By blocking the proteasome, this tripeptide has been shown to induce the expression of cell-protective heat shock proteins (HSPs) in vitro. Effects of MG132 were studied in an in vivo model of acute pancreatitis.

A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis.

Aim: To assess the effect of our novel cell-permeable nuclear factor-kappaB (NF-kappaB) inhibitor peptide PN50 in an experimental model of acute pancreatitis. PN50 was produced by conjugating the cell-penetrating penetratin peptide with the nuclear localization signal of the NF-kappaB p50 subunit.

Methods: Pancreatitis was induced in male Wistar rats by administering 2X100 mug/kg body weight of cholecystokinin-octapeptide (CCK) intraperitoneally (IP) at an interval of 1 h.

[Clinicopathologic observations on chronic hepatitis C therapy with interferon-alpha].

Introduction: Chronic hepatitis C is a progressive liver disease. It may lead to cirrhosis within 15-20 years, on the grounds of which hepatocellular carcinoma may develop in around 4% of the cases. The entity can thus be regarded a premalignant condition.

Ethanol administration generates oxidative stress in the pancreas and liver, but fails to induce heat-shock proteins in rats.

Background: Heat-shock proteins (HSP) play an essential role in the sequestration and reparation of denatured cellular proteins. Because ethanol treatment can result in oxidative stress-induced protein damage, it is possible that expression of HSP is altered after ethanol consumption. Dose-response and time-course studies were performed to investigate whether acute and chronic intragastric ethanol administration can induce tissue damage, oxidative stress and expression of the heat-shock proteins HSP60 and HSP72 in the pancreas and liver of male Wistar rats.

NF-kappaB activation is detrimental in arginine-induced acute pancreatitis.

The transcription factor nuclear factor kappaB (NF-kappaB) has been shown to have a critical role in the pathogenesis of sodium taurocholate- and cerulein-induced acute pancreatitis by regulating the expression of many proinflammatory genes in the pancreas. Heat shock proteins (HSPs), on the other hand, protect the pancreas against cellular damage. The aims of the present study were: (i) to investigate pancreatic NF-kappaB activation, proinflammatory cytokine synthesis, and cytoprotective HSP induction during L-arginine- (Arg-) induced acute pancreatitis in rats, and (ii) to establish whether pretreatment with pyrrolidine dithiocarbamate (PDTC) or methylprednisolone (MP) can block the activation of pancreatic NF-kappaB and determine their effects on the severity of Arg-induced acute pancreatitis.

Assessment of histological features in chronic hepatitis C.

Background/aims: Hepatitis C virus infection is an important disease with a high chronicity rate (50-80%), leading to end-stage liver cirrhosis and hepatocellular carcinoma. In this study, the characteristic histological findings were compared with the epidemiological features of hepatitis C virus infection in liver biopsy material.

Methodology: Liver biopsies were studied from 106 patients (60 males, 46 females, aged 11-81 years, mean: 43) found positive for hepatitis C antibody by a second-generation ELISA method.