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Biomedical subjects

S Kibrick

Publications and source records attributed to S Kibrick.

At least 19 recordsLinked to original sources
PubMed1979

Migration of epithelial cells in the small intestine of mice perorally infected with coxsackievirus B5.

The rate of cell migration in the small intestine during enteric viral infections has not been assessed previously. CD-1 mice (33 days old) were infected perorally with 1.0 X 10(8) plague-forming units of coxsackievirus B5 and 12 hr later were injected intraperitoneally with 2 micron Ci of [3H]thymidine/g of body weight. After 2, 12, 24, 48, 60, and 72 hr, mice were killed, and the small intestine was removed. Specimens obtained at each interval were examined by radioautography; similar specimens were titrated for virus by plaque assay in HeLa cells. In mice perorally infected with coxsackievirus B5, epithelial cells migrated from crypt to villus tip in 60 hr, as compared with 48 hr in uninfected control mice and 24 hr previously reported for mice perorally infected with enteric bacteria (e.g., Salmonella typhimurium). Virus was recovered from intestinal tissue, but no inflammatory response in the limina propria was apparent. These observations are consistent with previous report that substrate absorption rates may be altered during viral and bacterial enteric infection.

Animals↗
PubMed1977

Pathophysiological aspects of coxsackievirus B intestinal infection.

Our findings reveal that intestinal infection with coxsackie B5 results in decreased intestinal epithelial cell division in association with an increase in carbohydrate (glucose) and amino acid (leucine) absorption in the small intestine. These findings are contrasted with those occurring during Salmonella infection, which results in increased intestinal cell division rate but decreased carbohydrate (glucose) absorption. The changes in intestinal function and physiology that have been described occurred during an asymptomatic viral infection characterized by normal intestinal histology. A reasonable hypothesis is that these pathophysiological changes may be due not only to a variety of local factors but also to hormonal effects induced by systemic spread of coxsackievirus B.

Animals↗
PubMed1976

Susceptibility of mice to group B coxsackie virus is influenced by the diabetic gene.

A positive correlation was found between genetic predisposition to diabetes in the mouse and susceptibility to group B Coxsackie virus in this host. Male mice of the inbred strain C57BL/Ks and the following genetic variants were used; mice homozygous for the autosomal recessive gene for diabetes (db/db), the phenotypically normal heterozygous (db/+), and the normal mice which lacked the diabetic gene (+/+). The mortality response of the +/+ mice to intraperitoneal inoculation with Coxsackie virus B4 differed from the response of the two genetic variants (db/db and db/+) derived from this strain. The db/+ variant was more susceptible to Coxsackie virus B4 than the parental background strain (+/+). The db/db variant was more susceptible than either of the other genotypes. Pathological findings of the pancreas of the three genotypes during the acute stage of infection closely paralleled the genotypically dependent susceptibility of the host.

Animals↗
PubMed1976

Infection of hypercholesterolemic mice with Coxsackievirus B.

Adult male mice were made hypercholesterolemic by a diet high in cholesterol, cholic acid, animal fat, and sucrose. After three months on this diet, animals were infected with 5 X 10(9) plaque-forming units of coxsackievirus B5. Control groups consisted of uninfected hypercholesterolemic mice and infected mice maintained on a standard laboratory diet. Infection in the hypercholesterolemic animals was associated with leukopenia, severe fatty metamorphosis and focal necrosis in the liver, cholelithiasis, ileus, cardiomyolysis, and lack of inflammatory response. These mice died within seven to 14 days. Uninfected hypercholesterolemic animals had lesser degrees of fatty liver and cholelithiasis, and all survived. Infected mice maintained on a standard diet also survived. Titers of virus in representative tissues were lower in the hypercholesterolemic than in the normal mice, an indication that replication of virus was not solely responsible for the lethal outcome of the infections. These experiments demonstrate that hypercholesterolemia may alter host defenses against group B coxsackievirus in the mouse.

Animals↗
PubMed1976

Maturation of intestinal defenses against peroral infection with group B coxsackievirus in mice.

The intestinal tract of adult mice provides effective protection against peroral infection with group B coxsackievirus. This protective function consists of at least two separate components. One is a barrier effect that prevents virus from passing through the mucosal side of the gut into the circulation. It becomes clearly evident at 18 days of life and is present thereafter. The other is a clearance mechanism that acts to eliminate virus from the enteric tract after infection has occurred. This is first demonstrable at about 14 to 18 days and also persists. The appearance of these protective functions coincides with the known development of enzymatic and morphological changes in the gut associated with the transition from suckling to weanling.

Administration, Oral↗
PubMed1976

Measurement of intestinal absorption in mice by a double-label radioisotope perfusion technic.

The use of the standard chemical technic for measuring intestinal glucose absorption was compared with a new double-label radioisotope technic. Glucose absorption and water flux in the mouse small intestine were measured by both methods. The results indicated that the 2 approaches yield almost identical values. The radioisotope technic utilized [14C] polyethylene glycol to measure water flux and [3H] glucose. The technic was found to be reliable, rapid, and applicable to small samples and other substrates. It is particularly suited to absorption studies in small animals such as the mouse, where sample size is limited. The study also showed that the polyethylene glycol recovery rate from the mouse intestine was 97.8%, indicating that it is a valid absorption marker in this species.

Animals↗
PubMed1975

Differential action of deoxynucleosides on mammalian cell cultures infected with herpes simplex virus types 1 and 2.

Cytopathic effects induced by eight serologically defined isolates of herpes simplex virus type 2 (tested on human amnion cells) were markedly inhibited by thymidine at a concentration of 5 mM; eight serologically defined isolates of herpes simplex virus type 1, however, were not significantly inhibited. A similar effect was seen with thymidine, deoxyguanosine, and deoxycytidine at 1-mM concentrations in tests with rabbit kidney cultures. The inhibitory effect of thymidine was not blocked by the simultaneous presence of deoxycytidine, which has been shown by others to release mammalian cells from thymidine suppression. Differential suppression of herpes simplex cytopathic effects by these deoxynucleosides provides further evidence of biochemical differences between herpes simplex types 1 and 2. This phenomenon offers a basis for rapid differentiation of type 1 from type 2.

Cells, Cultured↗