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Biomedical subjects

J T Lamont

Publications and source records attributed to J T Lamont.

15 recordsLinked to original sources
PubMed1991

Choline, an essential nutrient for humans.

Choline is required to make essential membrane phospholipids. It is a precursor for the biosynthesis of the neurotransmitter acetylcholine and also is an important source of labile methyl groups. Mammals fed a choline-deficient diet develop liver dysfunction; however, choline is not considered an essential nutrient in humans. Healthy male volunteers were hospitalized and fed a semisynthetic diet devoid of choline supplemented with 500 mg/day choline for 1 wk. Subjects were randomly divided into two groups, one that continued to receive choline (control), and the other that received no choline (deficient) for three additional wk. During the 5th wk of the study all subjects received choline. The semisynthetic diet contained adequate, but no excess, methionine. In the choline-deficient group, plasma choline and phosphatidylcholine concentrations decreased an average of 30% during the 3-wk period when a choline-deficient diet was ingested; plasma and erthrocyte phosphatidylcholine decreased 15%; no such changes occurred in the control group. In the choline-deficient group, serum alanine aminotransferase activity increased steadily from a mean of 0.42 mukat/liter to a mean of 0.62 mukat/liter during the 3-wk period when a choline-deficient diet was ingested; no such change occurred in the control group. Other tests of liver and renal function were unchanged in both groups during the study. Serum cholesterol decreased an average of 15% in the deficient group and did not change in the control group. Healthy humans consuming a choline-deficient diet for 3 wk had depleted stores of choline in tissues and developed signs of incipient liver dysfunction. Our observations support the conclusion and choline is an essential nutrient for humans when excess methionine and folate are not available in the diet.

Choline↗
PubMed1990

Lipid binding to gastric mucin: protective effect against oxygen radicals.

Gastric mucus forms a viscous gel overlying the gastric mucosa and is thought to protect the underlying mucosa from noxious agents such as acid, proteases, and bile salts. A common property of mucin, the principal glycoprotein in mucous secretions, is its ability to bind lipids. The purpose of this study was to determine if lipids bound to gastric mucin protect the mucin from oxygen radical attack. Pig gastric mucin, partially purified by Sepharose 4B gel chromatography, was found to contain large amounts of free fatty acids and cholesterol as well as lesser amounts of sphingomyelin and phospholipids. Purified mucin obtained by density-gradient ultracentrifugation in a CsCl gradient contained only trace amounts of fatty acids but no other lipids. Exposure to the oxygen radical-generating system iron/ascorbate caused a marked reduction in viscosity of purified mucin but did not affect partially purified mucin, suggesting that bound lipids shielded the mucin from attack by oxygen radicals. Using discontinuous sucrose-gradient ultracentrifugation in the presence of liposomes containing [3H]palmitic acid, we demonstrated that mucin is capable of binding fatty acids. We also observed a striking increase in solution viscosity of gastric mucin at low pH, a feature that might contribute to the ability of mucin to form a protective diffusion barrier for the underlying epithelium.

Animals↗
PubMed1989

Comparative study of Clostridium difficile toxin A and cholera toxin in rabbit ileum.

The purpose of this study was to compare the effects of Clostridium difficile toxin A and cholera toxin on fluid secretion, intestinal permeability, and arachidonate metabolites in rabbit ileum. Injection of 25 micrograms of either purified toxin into 10-cm ileal loops caused significant increases in fluid secretion and intestinal permeability to mannitol as well as release of prostaglandin E2 into the lumen. Toxin A, but not cholera toxin, caused a severe inflammatory reaction of the lamina propria and necrosis of enterocytes as well as increased release of leukotriene B4. The toxin A-mediated increases in prostaglandin E2 and leukotriene B4 could be blocked by prior instillation of 10 mg of 5-aminosalicylic acid into ileal loops. 5-Aminosalicylic acid also significantly diminished the expected increase in mannitol permeability after both toxins, but had no significant inhibitory effect on fluid secretion or, in the case of toxin A, intestinal inflammation. Our results indicate that C. difficile and cholera enterotoxins differ substantially in their effects on the rabbit intestine. Clostridium difficile toxin A, an inflammatory toxin, produces a striking infiltration of the lamina propria with neutrophils that is associated with increased release of leukotriene B4. In contrast, cholera toxin does not cause inflammation or leukotriene B4 release. Increased release of prostaglandin E2 occurs after exposure to both toxins and appears to be correlated with increased intestinal permeability.

Animals↗
PubMed1988

Postoperative jaundice.

Jaundice in the postoperative patient is a common complication of surgery that may be a confusing and potentially serious problem. The surgical patient is subjected to a variety of stresses, such as hypotension, infection, drugs, and anesthetic agents, many of which are potentially hepatotoxic. Management of the patient with postoperative jaundice can be difficult because the precise cause of the hepatic insult is frequently indeterminate. It is important for the clinician to recognize the patterns of liver injury that may occur in the postoperative period in order to initiate appropriate management.

Biliary Tract Diseases↗
PubMed1987

Interaction between oxygen radicals and gastric mucin.

The gastrointestinal epithelium is continuously exposed to reactive oxygen metabolites that are generated within the lumen. In spite of this exposure, the healthy epithelium appears unaffected, suggesting efficient mechanisms for protection against these potentially cytotoxic oxidants. The objective of this study is to characterize the interaction between purified gastric mucin and hydroxyl radicals generated from the interaction between ferric iron and ascorbic acid. We found that both native and pronase-treated mucin effectively scavenged hydroxyl radical and that the scavenging properties were not significantly different. The effective concentration of mucin required for a 50% reduction in malondialdehyde production was approximately 10 mg/ml for both native and pronase-treated mucin. In addition, the iron-ascorbic system produced a dramatic decrease (greater than 50%) in the specific viscosity of mucin that was inhibited by catalase, deferoxamine, and mannitol. Superoxide dismutase had no effect. These data suggest that hydroxyl radicals derived from the iron-catalyzed decomposition of hydrogen peroxide are responsible for the depolymerization of native mucin. We propose that mucin may provide protection to the surface epithelium of the gastrointestinal tract by scavenging oxidants produced within the lumen; however, it does so at the expense of its viscoelastic properties.

Animals↗
PubMed1984

Clostridium difficile colitis.

Clostridium difficile has become one of the commonest pathogens of the lower intestinal tract. This organism appears unique in that infection almost always occurs during or after antibiotic therapy, suggesting that some component of the normal microflora prevents colonization by C. difficile. Once it has overgrown in the colon, C. difficile releases several toxins which cause tissue damage and diarrhea. Infection can range from a simple self-limited diarrheal illness to fulminant colitis with perforation and megacolon. Assay of stool filtrates reveals the presence of cytotoxin in nearly all patients with antibiotic-associated pseudomembranous colitis, and in approximately one third to one half of those with less severe infections. Effective therapy is available in the form of oral vancomycin, although the expense of this antibiotic has led to the use of oral metronidazole or bacitracin, which appear to be equally efficacious and considerably cheaper. Although we have learned a great deal about C. difficile in the past decade, a number of fascinating puzzles remain. We know very little about the immune response to this organism or its toxin, or whether a vaccine might someday be feasible. Similarly, we have very little insight into what effects antibodies exert on the normal colonic flora and how these effects allow C. difficile infection in a small percentage of patients. Studies of this pathogen will undoubtedly lead to a fuller understanding of the enormously complex and still mysterious microbial ferment which lives within our gastrointestinal tract.

Adult↗
PubMed1983

Cysteamine and prostaglandin F2 beta stimulate rat gastric mucin release.

Gastric mucin glycoproteins form an adherent gel over the surface epithelium that is thought to protect the stomach against chemical and physical damage. The purpose of this study was to measure the release of mucin glycoproteins from rat stomach after treatment with cysteamine and prostaglandin F2 beta, two structurally unrelated drugs that have been shown to protect the stomach against the noxious effects of alcohol and other damaging agents. Gastric mucin was separated into soluble (washout) and insoluble (adherent) phases before colorimetric quantitation of total mucin, protein-bound hexose, and sialic acid. Cysteamine produced a dose-dependent increase in release of soluble and gel mucin. Prostaglandin F2 beta caused a dose-dependent release of hexose-containing mucin but had no effect on sialic acid-containing glycoproteins. Sepharose 4B chromatography of both the soluble and adherent mucus revealed that greater than 90% was a high molecular weight glycoprotein fraction. N-Ethylmaleimide, a known inhibitor of cytoprotection by cysteamine, had no effect on mucin secretion. Similarly, indomethacin inhibited mucin secretion by cysteamine but did not significantly influence cytoprotection. Thus the secretion of mucin by cytoprotective agents is unlikely by itself to explain the ability of the stomach to resist chemical or physical damage.

Animals↗
PubMed1982

Diarrhea we can treat: antibiotic-associated colitis.

C. difficile, a gram-positive anaerobic bacillus, has emerged in the past five years as a common cause of hospital-acquired diarrhea. The organism usually gains entry to the host during or after antibiotic treatment, which presumably alters the normal barrier function of the colonic microflora. The organism produces a cytotoxin that can be identified in stool samples by its ability to alter the cellular morphology of tissue culture cells. Infection with C. difficile produces a spectrum of diseases ranging from mild diarrhea to fulminating colitis. An important bedside clue is the presence of pseudomembranes in the rectum or sigmoid at proctosigmoidoscopy. The disease may also occur in patients with chronic inflammatory bowel disease where it may be confused with a relapse of the underlying disease. Treatment with vancomycin is effective, but 10% to 15% of patients may experience relapse. The major mode of transmission appears to be environmental acquisition rather than person-to-person spread.

Anti-Bacterial Agents↗
PubMed1974

Cell surface galactosyltransferase and lectin agglutination of thymus and spleen lymphocytes.

Lectin agglutination and cell surface galactosyltransferase (EC 2.4.1.67; 1-O-alpha-D-galactosyl-myo-inositol:raffinose galactosyltransferase) enzyme activity have been studied with thymus and spleen lymphocytes of neonatal rats. Thymus lymphocytes were more agglutinable by concanavalin A than by wheat germ agglutinin, whereas spleen lymphocytes were more agglutinable by wheat germ agglutinin than by concanavalin A. Thymus lymphocytes, but not spleen lymphocytes, of neonatal rats could be blast transformed by concanavalin A. Cell surface galactosyltransferase activity was present on both types of lymphocytes, but was greatly increased on thymus cells after blast transformation. The differences in lectin agglutination suggest a difference in the surface membranes of thymus and spleen lymphocytes. The increase in cell surface galactosyltransferase activity with blast transformation of thymus lymphocytes may be related to the exteriorization of the Golgi apparatus into the plasma membrane.

Agglutination↗