Ethanol and hepatic regeneration
Gordon Baskin, George I. Henderson, Steven Schenker – 1 March 1988
Gordon Baskin, George I. Henderson, Steven Schenker – 1 March 1988
Arturo Panduro, Fouad Shalaby, Luis Biempica, David A. Shafritz – 1 March 1988 – In efforts to understand mechanisms of liver dysfunction in cirrhosis, transcription of specific genes important to liver function has been measured in the rat model of CCl4‐induced hepatic fibrosis. The relative transcription rates of albumin, α‐fetoprotein and pro‐α1‐collagen genes were studied during development of fibrosis and after fibrosis was established.
Hiroyuki Sugimoto, Shoji Yamada, Takayuki Arai, Setsuo Kobayashi, Koei Hamana, Shigeru Matsuzaki – 1 March 1988 – Polyamines and acetylpolyamines were analyzed in the liver, spleen, lung, kidney, serum and urine by high‐performance liquid chromatography on a column of cation‐exchange resin after administering various cytotoxic substances to male mice. All of the compounds tested more or less affected the tissue levels of polyamines, including putrescine, spermidine, spermine and acetylpolyamines (N1‐acetylspermidine and N1‐acetylspermine).
Douglas A. Bakan, James L. Barnhart – 1 March 1988 – The parameters which are important in causing changes in the Tl and T2 proton magnetic relaxation times of dog bile were investigated. Three factors were found to be important in causing relaxation in bile: (i) total bile salt concentration; (ii) total protein concentration, and (iii) viscosity. The T1 and T2 values of hepatic and gallbladder biles were found to be independent of specific gravity, osmolarity and electrolyte concentrations.
Fayez K. Ghishan, Harry L. Greene – 1 March 1988 – We present our experience with 18 pediatric patients with α1‐antitrypsin deficiency of the PiZZ phenotype. Fifteen patients (83%) presented with neonatal cholestatic jaundice at a mean age of 2 ± 0.6 months (±S.D.). The male:female ratio was 15:3, indicating a male predominance. All metabolic, infectious and obstructive causes of jaundice were ruled out by appropriate tests in the patients with neonatal cholestasis.
Harald F. Teutsch – 1 March 1988 – To investigate intercellular compartmentation of liver metabolism, we have recently introduced new procedures for quantitative assessment of metabolic liver cell heterogeneity both along sinusoids of portal and septal origins as well as at the level of the parenchymal unit, and also for three‐dimensional imaging of enzyme and metabolite distribution.
Kiyoshi Yamazaki, Nicholas F. Larusso – 1 March 1988 – Electropermeabilisation—i.e. subjecting cells to a short series of high‐voltage pulses—has been used to make isolated rat hepatocytes transiently permeable to small molecules. The permeabilised cells can be loaded with [14C]sucrose at 0°C and resealed by a brief incubation at 37°C. The electrical treatment does not impair cellular function, since autophagic sequestration of sucrose occurs at the same rate as in untreated cells.
Flemming Burcharth – 1 March 1988 – The records of 37 patients who had undergone splenoportography, including one group of 12 who were studied before 1976 and a second group of 25 who were studied after 1977, were reviewed. The primary difference was that in the second group, the tract in the spleen was occluded with absorbable gelatin sponge (Gelfoam) plugs as the needle was withdrawn. In addition, there were minor changes in technique, such as changes in the needle puncture angle and entry site.
Alan B. Lumsden, J. Michael Henderson, Michael H. Kutner – 1 March 1988 – Endotoxin concentrations were measured in the portal, hepatic and peripheral venous blood of two groups of patients with cirrhosis using a limulus‐based chromogenic assay. The high sensitivity of chromogenic detection allowed measurement of endotoxin as low as 10 to 15 pg per ml, an order of magnitude greater than previously possible by gelation studies. Group 1 consisted of 56 patients with cirrhosis undergoing angiographic evaluation.
Jean‐Claude Sibille, Hitoshi Kondo, Philip Aisen – 1 March 1988 – Like the rat peritoneal macrophage, the isolated Kupffer cell is capable of processing and releasing iron acquired by phagocytosis of immunosensitized homologous red blood cells. When erythrophagocytosis is restrained to levels which do not affect cell viability, about one red cell per macrophage, close to 50% of iron acquired from red cells is released within 24 hr in the form of ferritin.