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Biomedical subjects

R A Willson

Publications and source records attributed to R A Willson.

At least 37 records · Page 2Linked to original sources

Splenic abscess. A rare complication of Crohn's colitis.

This report describes a patient with Crohn's disease of the colon who presented with a rare extraintestinal complication: splenic abscess. Additional features of this case were the association of multiple extraintestinal manifestations of Crohn's disease, including iritis, ankylosing spondylitis, and pericholangitis, and polymicrobial bacteremia. This report emphasizes the cryptic nature of splenic abscess presentation, the more frequent association of extraintestinal manifestations of Crohn's disease with intraabdominal complications, and the association of polymicrobial anaerobic bacteremia with obstructive gastrointestinal complications.

Abscess↗

A comparison of hepatocyte size distribution in untreated and phenobarbital-treated rats as assessed by flow cytometry.

Flow cytometric analysis of narrow forward angle light scatter was used to examine the effect of phenobarbital treatment on hepatocyte size. Light scatter analysis of freshly isolated hepatocytes and of hepatocytes separated by means of centrifugal elutriation into five subpopulations (fractions 1-5) was performed on both untreated and phenobarbital-treated rats. The frequency distribution histogram of forward scatter intensity produced by freshly isolated hepatocytes from untreated rats was used as the baseline. This histogram was arbitrarily divided into four regions; referred to as region 1 (small cells) to region 4 (large cells). Subsequent analysis of the light scatter histograms derived from elutriated fractions of both untreated and phenobarbital-treated animals was performed using these baseline regions. Analysis showed that small cells were enriched in elutriated fraction 1, and large cells in elutriated fraction 5. Phenobarbital treatment was associated with a uniform shift to a higher intensity light scatter (relative increase in cell size) within each of the four selected regions. Our findings suggest that phenobarbital does not have a selective hypertrophic effect on these subpopulations of rat hepatocytes.

Animals↗

Liver support systems: the low clearance of model hepatic excretory anions by charcoal hemoperfusion.

The removal of cholephilic anions (unconjugated bilirubin, bromosulfophthalein, and indocyanine green) by charcoal hemoperfusion was assessed in normal dogs. None of these model excretory compounds was effectively removed by the charcoal columns. In vitro studies suggested that poor removal of the anions was related to albumin binding in that, when the anions were in molecular solution, their extraction by the charcoal column was high; however, when albumin was added, their extraction was negligible. Therefore, if the removal from plasma of strongly bound toxins is important in the treatment of acute hepatitic failure, additional support devices may have to be encompassed into the ultimately hepatic support system.

Animals↗

Experimental hepatic injury: the sequential changes in drug metabolizing enzyme activities after administration of acetaminophen.

Experimental hepatic necrosis was induced in phenobarbital pretreated rats by means of the intraperitoneal administration of an acetaminophen-dimethyl sulfixide (DMSO) mixture. Cytochrome P-450 content and the specific activities of aminopyrine demethylase, aniline hydroxylase and bilirubin glucuronyl transferase diminished over the three-day study period, as compared with control animals. The reductions, however, were generally modest; not uniform for all the enzymes assayed; and correlated poorly with histologic necrosis and standard liver function tests. It is concluded that in acute liver disease changes in the hepatic in vitro drug metabolizing enzyme capacity may not be closely related to cellular necrosis, per se, and the degree of change in enzyme activities will vary from one enzyme system to another. These findings may explain, in part, the often inconsistent alterations in the disposition and elimination of drugs described in associated liver disease.

Acetaminophen↗