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.

1 June 1993

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).

Jurgen Ludwig, Etsuko Hashimoto, Hiroshi Obata, William P. Baldus – 1 June 1993

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.

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.

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.

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).

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.

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.