Ironic insult added to copper injury

M L Schilsky – 30 December 2003 – Several clinical studies have suggested that excess hepatic iron accumulation is a progressive factor in some liver diseases including chronic viral hepatitis and hemochromatosis. However, it is not known whether iron‐induced hepatotoxicity may be directly involved in hepatitis, cirrhosis, and liver cancer. The Long‐Evans Cinnamon (LEC) rat, which accumulates excess copper in the liver as in patients with Wilson's disease, is of a mutant strain displaying spontaneous hemolysis, hepatitis, and liver cancer.

B7/BB‐1 expression and hepatitis activity in liver tissues of patients with chronic hepatitis C

K Mochizuki, N Hayashi, K Katayama, N Hiramatsu, T Kanto, E Mita, T Tatsumi, N Kuzushita, A Kasahara, H Fusamoto, T Yokochi, T Kamada – 30 December 2003 – Cytotoxic T lymphocytes (CTL) are closely related to the mechanism of liver injury in chronic viral hepatitis. Recently, it has been suggested that antigen‐specific T cell activation requires both presentation of antigen by major histocompatibility complex (MHC) molecules and the delivery of costimulatory signals.

Adenovirus‐mediated expression of cytokine‐induced neutrophil chemoattractant in rat liver induces a neutrophilic hepatitis

J J Maher, M K Scott, J M Saito, M C Burton – 30 December 2003 – C‐X‐C chemokines are potent chemoattractants that are believed to mediate neutrophilic inflammation in several organs. Recent studies suggest a role for C‐X‐C chemokines in the pathogenesis of neutrophilic hepatitis but do not prove causation. We investigated the biological consequences of hepatic chemokine production in vivo by transiently overexpressing cytokine‐induced neutrophil chemoattractant (CINC), a member of the C‐X‐C chemokine family, in intact rats.

Protective effect of L‐carnitine in ammonia‐precipitated encephalopathy in the portacaval shunted rat

G Therrien, C Rose, J Butterworth, R F Butterworth – 30 December 2003 – L‐carnitine administration prevents the neurological symptoms of acute ammonia toxicity. To further evaluate its efficacy in the prevention of hepatic encephalopathy in hyperammonemic conditions, L‐carnitine (16 mmol/kg, intraperitoneally [i.p.) was administered 1 hour before ammonium acetate (NH4OAc) (8.5 mmol/kg, subcutaneously) to portacaval shunted (PCS) rats. Cerebrospinal fluid (CSF) ammonia, lactate, and amino acid levels were measured in relation to deteriorating neurological status in these animals.

Nitric oxide does not reverse pulmonary hypertension associated with end‐stage liver disease: A preliminary report

M A Ramsay, A Schmidt, H A Hein, A T Nguyen, K Lynch, C A East, K J Ramsay, G B Klintmalm – 30 December 2003 – Pulmonary hypertension is a well known, though uncommon complication of end‐stage liver disease (ESLD). Patients with severe pulmonary hypertension and ESLD undergoing orthotopic liver transplantation (OLT) may develop right ventricular failure and death. This study investigates the reversibility of pulmonary hypertension by the inhalation of nitric oxide in patients under evaluation for OLT.

Detection of type 2‐like T‐helper cells in hepatitis C virus infection: Implications for hepatitis C virus chronicity

S Tsai, Y Liaw, M Chen, C Huang, G C Kuo – 30 December 2003 – One striking clinical feature of hepatitis C virus (HCV) infection is that more than 50% of patients with acute hepatitis C will develop chronic infection. To investigate its possible mechanisms, we examined the activation of type 2‐like T‐helper (Th2‐like) cells relating to the development of chronicity.

Altered hepatocellular Ca2+ regulation during hemorrhagic shock and resuscitation

S Rose, A Pizanis, M Silomon – 30 December 2003 – The present study evaluated the effect of the benzothiazepine Ca2+ channel blocker diltiazem (DZ) on altered hepatocellular Ca2+ regulation and oxidant injury during hemorrhagic shock/resuscitation. In anesthetized, male Sprague‐Dawley rats, hemorrhagic shock was induced by rapid blood withdrawal and maintaining the mean arterial blood pressure at 40 mm Hg over 60 minutes. Rats were then resuscitated with 60% of shed blood and threefold the shed blood volume of Ringer's lactate.

Chronic alcohol intoxication induces hepatic injury through enhanced macrophage inflammatory protein‐2 production and intercellular adhesion molecule‐1 expression in the liver

A P Bautista – 30 December 2003 – This study tested the hypothesis that prolonged consumption of alcohol directly or indirectly, through endotoxin influx in the circulation, stimulates the Kupffer cells to produce macrophage inflammatory protein‐2 (MIP2) and up‐regulates the expression of adhesion molecules, i.e., CD18 on PMNs and its counter‐receptor, intercellular adhesion molecule‐1 (ICAM‐1), on hepatic cells.

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