D. Azoulay, D. Castaing, A. Dennison, W. Martino, D. Eyraud, H. Bismuth – 1 January 1994 – The aim of this prospective nonrandomized study was to assess the immediate and short‐term sequelae of transjugular intrahepatic portosystemic shunting on the circulatory hyperdynamic state of the cirrhotic patient. Twelve transjugular portosystemic shunting procedures were performed in 12 cirrhotic patients for sclerotherapy failure (10 cases) and/or intractable ascites (4 cases). Self‐expandable stents 10 mm in diameter were used in all cases.

Ole Hamberg, Hendrik Vilstrup – 1 January 1994 – Glucose reduces the hepatic conversion of aminonitrogen to urea, quantified by the functional hepatic nitrogen clearance (i.e., the slope of the linear relation between urea synthesis rate and blood α‐aminonitrogen concentration). This is due to a direct effect of glucose and to inhibition of glucagon. In this study, the effect of glucose on functional hepatic nitrogen clearance was examined during spontaneous hormone responses and during hormonal control by somatostatin.

Gilles Pomier‐Layrargues, J. F. Giguère, J. Lavoie, P. Perney, S. Gagnon, M. D'Amour, J. Wells, Roger F. Butterworth – 1 January 1994 – Previous reports have suggested that “endogenous” benzodiazepines could contribute to neural inhibition in hepatic encephalopathy. RO 15‐1788 (flumazenil), a specific antagonist of brain benzodiazepine receptors, could thus reverse the neurological symptoms of hepatic encephalopathy. To test this possibility, we conducted a double‐blind, placebo‐controlled crossover trial of the efficacy of flumazenil in cirrhotic patients in hepatic coma.

Wilfried F. Seifert, Anne Bosma, Adriaan Brouwer, Henk F. J. Hendriks, Paul J. M. Roholl, Rick E. W. van Leeuwen, G. Christa F. van Thiel‐De Ruiter, Ingrid Seifert‐Bock, Dick L. Knook – 1 January 1994 – Earlier studies have shown that retinoid administration suppresses the generation of hepatic fibrosis and stimulates its regression in normal (i.e., vitamin A‐sufficient) carbon tetrachloride‐treated rats. This study focuses on the possible role of a marginal or deficient vitamin A status on carbon tetrachloride‐induced fibrosis.

Hey‐Chi Hsu, A‐Min Huang, Po‐Lin Lai, Wei‐Ming Chien, Shian‐Yang Peng, Shu‐Wha Lin – 1 January 1994 – The tumor‐suppressor gene p53 may transactivate the transcription of genes that down‐regulate cellular growth‐related genes and may become oncogenic as a result of the production of mutant proteins or the loss of its protein expression. This study reports that alterations of the highly conserved consensus intervening sequences at the splice junctions may lead to the inactivation of the p53 gene.

Paul C. Adams, Colin Bradley, Jaroslav V. Frei – 1 January 1994 – Hepatic iron and zinc concentrations were determined in 26 consecutive nonalcoholic cirrhotic patients who had previously undergone portacaval shunting and then liver transplantation and 37 control patients. Stainable iron was graded on a scale of 0 to 4; 11 shunt patients and 3 control patients had grade 2 to 4 iron staining.

Stephen D. H. Malnick, Daniel D. Bass, Alvin M. Kaye, Michel Vaubourdolle, Jacqueline Giboudeau, Olivier Chazouillères, Raoul Poupon – 1 January 1994

Laurie N. Fishman, Joel E. Lavine – 1 January 1994 – A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left‐right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left‐right asymmetry, was reversed in homozygous transgenic embryos.

Soonho Um, Osamu Nishida, Masaki Tokubayashi, Fumiko Kimura, Yukinobu Takimoto, Hideyuki Yoshioka, Ryoichi Inque, Toru Kita – 1 January 1994 – In chronic portal‐hypertensive rat models, such as portal vein constriction or cirrhosis, the portal blood flow that effectively perfuses the hepatocytes is substantially reduced because of anatomical or functional shunts. It is possible therefore that a feedback mechanism from the liver to the splanchnic bed is responsible for the splanchnic hyperemia observed in chronic portal hypertension.

Mario Strazzabosco, Carlo Poci, Carlo Spirlí, Leonardo Sartori, Alexander Knuth, Gaetano Crepaldi – 1 January 1994 – Recent studies in perfused livers and isolated hepatocytes indicate that ursodeoxycholic acid‐induced HCO3‐rich hypercholeresis originates at the ductule/duct level. The bile duct epithelium may be involved in bile alkalinization by passively reabsorbing the protonated unconjugated ursodeoxycholic acid, by directly secreting in response to an ursodeoxycholic acid‐induced increase in acid/base transporter activity or by taking up UDCA− in exchange for a base equivalent.