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E C Schafer

Publications and source records attributed to E C Schafer.

5 recordsLinked to original sources
PubMed1990

Hyperammonemic encephalopathy in urinary diversion with urea-splitting urinary tract infection.

We present two cases of hyperammonemic encephalopathy secondary to urea-splitting urinary tract infection with urinary diversion. One patient had a ureterosigmoidostomy, the other an ileal loop diversion. Neither patient had significant underlying liver disease, but both had considerable muscle atrophy that may have predisposed them to develop hyperammonemia. Medical therapy did not provide long-term control of symptoms. In both cases, hyperammonemic encephalopathy resolved after revision of their urinary diversions. The probable mechanism of the metabolic derangements produced by urea-splitting urinary tract infections is reviewed. We suggest that patients with urinary diversion who develop hyperammonemic encephalopathy secondary to a urea-splitting urinary tract infection be treated with surgical revision of the urinary system to improve drainage and decrease bowel contact time.

Acidosis↗
PubMed1985

Laser endoscopy.

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Endoscopy↗
PubMed1977

Toxicity of dieldrin to bobwhite quail in relation to sex and reproductive status.

In a study of dieldrin toxicity to breeding and nonbreeding bob-white quail (Colinus virginianus), breeding birds of both sexes on long photoperiods were more susceptible to dieldrin poisoning than nonbreeding birds, although some differences were not statistically significant at the .10 level. Shortened photoperiods caused gonadal regression, weight loss, and additional mortalities among dieldrin-treated birds previously in breeding condition. Dieldrin did not influence food consumption, body weight, or egg production until about a week or less before death of individual birds. Dieldrin brain residues were higher among birds that died during the study than among survivors sacrificed at its termination. Among those that died, neither dieldrin treatment level, reproductive status, nor sex seemed related to brain residue levels. Nevertheless, within those factors, levels were slightly higher in the birds that died later in the test.

Animals↗
PubMed1977

Role of acetaldehyde in the ethanol-induced impairment of glycoprotein metabolism in rat liver slices.

The mechanism responsible for ethanol-induced changes in the glycosylation of proteins was investigated in rat liver slices. Ethanol (5 to 50 mM) decreased [1-14C]glucosamine and [14C]leucine incorporation into total liver and microsomal proteins and greatly inhibited incorporation into medium (secretory) proteins. Pyrazole prevented the inhibition of glycoprotein synthesis by ethanol. Additions of methylene blue or pyruvate, which corrected the disordered redox state caused by ethanol oxidation, did not reverse the inhibitory effects of ethanol on glycosylation. Sorbitol, which mimics ethanol in generating reducing equivalents in the hepatocyte, also inhibited glycosylation; however, fructose, the immediate oxidation product of sorbitol, similarly inhibited glycoprotein synthesis without altering the redox state. When low levels of acetaldehyde (0.12 to 0.70 mM) were maintained in the medium by means of infusion, a significant inhibition of glycoprotein synthesis was observed. Acetate did not impair glycosylation. These data suggest that the ethanol-induced impairment of glycoprotein synthesis and secretion is a consequence of ethanol metabolism and further suggest that this inhibition is attributable to acetaldehyde formation rather than to the altered redox state resulting from ethanol oxidation.

Acetaldehyde↗