Risk of hepatitis C virus infections through household contact with chronic carriers: Analysis of nucleotide sequences

Masao Honda, Shuichi Kaneko, Masashi Unoura, Kenichi Kobayashi, Seishi Murakami – 1 June 1993 – We evaluated the risk of hepatitis C virus transmission through household contact with chronic carriers using nucleotide sequence analysis. Chronic hepatitis C patients (76 patients) were divided into two groups: familial transmission of hepatitis C virus was studied in group A (53 patients); group B (23 patients) served as nonfamilial controls for group A.

Distribution of body water in patients with cirrhosis: The effect of liver transplantation

Darrell H. G. Crawford, June W. Halliday, W. G. E. Cooksley, Therese L. Murphy, Suzanne D. Golding, Jennifer D. Wallace, Ross C. Cuneo, Steven V. Lynch, Russell J. Strong, Lawrie W. Powell – 1 June 1993 – We compared total body water and intracellularextracellular distribution of body water between male patients with mild liver disease without ascites (n = 9), male patients with severe liver disease and gross ascites (n = 6) and a group of age‐, sex‐, height‐ and weight‐ matched controls (n = 6).

Blood‐brain barrier permeability is markedly decreased in cholestasis in the rat

Jacqueline B. Wahler, Mark G. Swain, Richard Carson, Nora V. Bergasa, E. Anthony Jones – 1 June 1993 – The blood‐brain‐barrier plays an essential role in regulating the entrance of substances into the brain. To date, permeability of the blood‐brain barrier has not been studied in models of cholestatic liver injury, although levels of substances known to enhance vascular permeability (bile acids, substance P, histamine) are elevated in cholestasis.

Bile acid synthesis from newly synthesized vs. preformed cholesterol precursor pools in the rat

Jürgen Scheibner, Michael Fuchs, Michael Schiemann, Gisela Tauber, Erwin Hörmann, Eduard F. Stange – 1 June 1993 – The present study defines the origin of cholesterol subserving bile acid synthesis in male rats with an extracorporal bile duct by labeling newly formed cholesterol with tritiated water. Within 6 hr after interruption of the enterohepatic circulation, the bile acid pool was depleted. At this early time point the proportion from de novo cholesterol was 8% and 12% for biliary cholesterol and cholate, but 18% and 19% for muricholate and chenodeoxycholate, respectively.

Brain indoles in human hepatic encephalopathy

Hanan Al Mardini, Emma J. Harrison, Paul G. Ince, Kim Bartlett, Christopher O. Record – 1 June 1993 – The neurotransmitter serotonin has a profound effect on the control of sleep; thus excess serotonin activity in the brain could be responsible for impaired consciousness in hepatic encephalopathy. Furthermore, an increased brain level of 5‐hydroxyindoleacetic acid has been a consistent finding in various animal models of the condition.

Reduction of cerebral perfusion precedes rise of intracranial pressure in rats with ischemic fulminant liver failure

Vijay Shah, Steve Webster, Jeanne Gottstein, Andres T. Blei – 1 June 1993 – In fulminant liver failure, brain edema may progress to intracranial hypertension. However, the rise in intracranial pressure is a late event in this sequence. We investigated the relationship between cerebral perfusion and development of intracranial hypertension in a well‐characterized model of fulminant liver failure, the rat subjected to hepatic devascularization (n = 11).

Long‐term ethanol consumption alters the hepatic response to the regenerative effects of tumor necrosis factor‐α

Paul A. Akerman, Piera M. Cote, Shi Qi Yang, Craig McClain, Steve Nelson, Gregory Bagby, Anna Mae Diehl – 1 June 1993 – The pathogenesis of chronic alcoholic liver disease is uncertain, but it may reflect an impaired wound healing response to ethanol‐induced liver injury. Cellto‐cell communication such as that mediated by the cytokine tumor necrosis factor is necessary for successful liver regeneration and complete recovery from liver injury. Hence disruption of intercellular regenerative signaling may contribute to the pathogenesis of chronic alcoholic liver disease.

Effect of ursodeoxycholic acid on the kinetics of cholic acid and chenodeoxycholic acid in patients with primary sclerosing cholangitis

Gerda Rudolph, Richard Endele, Martin Senn, Adolf Stiehl – 1 June 1993 – Treatment of patients with cholestatic liver diseases with ursodeoxycholic acid has been shown to have beneficial effects that may be related to a shift in the balance between hydrophilic and hydrophobic bile acids in favor of hydrophilic bile acids. During treatment of patients with primary sclerosing cholangitis with ursodeoxycholic acid, plasma concentrations of some endogenous bile acids decrease.

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