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Biomedical subjects

M S Martin

Publications and source records attributed to M S Martin.

At least 55 records · Page 3Linked to original sources

Insulin-induced insulin resistance of alpha-aminoisobutyric acid transport in cultured human skin fibroblasts.

Cultured fibroblasts derived from skin biopsies were used to develop a system for studying insulin resistance in human tissue in vitro. Uptake of alpha-aminoisobutyric acid by cultured human skin fibroblasts was found to occur by a combination of saturable and nonsaturable processes. Insulin stimulated uptake by decreasing the Km of the saturable transport system from 0.58 mM to 0.26 mM. The maximal velocity of saturable uptake was 16.6 nmol/10(7) cells/min in both the presence and absence of insulin. Uptake of alpha-aminoisobutyric acid at 0.2 mM was studied in human skin fibroblasts with and without chronic exposure to insulin for 4 days at an initial concentration of 10 micrograms/ml. Unstimulated uptake was increased from 17 to 20 nmol/10(8) cells/min, and the increase in uptake due to maximal stimulation by insulin was unchanged at 16 nmol/10(8) cells/min in the cells exposed chronically to insulin. The apparent Km for insulin was increased from 80 microunits/ml to 2400 microunits/ml in the insulin-exposed cells. Thus, chronic exposure to insulin induces resistance of alpha-aminoisobutyric acid uptake by decreasing the apparent affinity for insulin.

Adult↗

Proliferative effect of lithocholic acid on rat liver cell in culture.

In contrast to cholic acid, deoxycholic acid and chenodeoxycholic acid, lithocholic acid (LCA) enhances the growth of rat liver cells in culture. Enhanced proliferation of LCA-treated rat liver cells persists even 12 days after LCA was removed. These findings could suggest a mutagenic effect of LCA, or a metabolite, on rat liver cells.

Animals↗

Mediated transport and metabolism of lactate in rat aorta.

1. Under appropriate conditions L- and D-lactate enter the cells of rat aorta and are metabolized. Oxidation of lactate to CO2 occurs under aerobic conditions. 2. L- and D-lactate are taken up into the cells when oxygen, glucose, or both oxygen and glucose are present in the incubation medium. Both L- and D-lactate are excluded from the cells when neither oxygen nor glucose is present. 3. D,L-Glyceraldehyde prevents the uptake of L-lactate. The effect is apparently not due to the inhibition of glucose metabolism by L-glyceraldehyde. 4. L-lactate (20 mM) markedly inhibits the uptake of 5 mM D-lactate, but 20 mM D-lactate fails to inhibit the uptake of 5 mM L-lactate. 5. Raising the pH of the incubation medium markedly depresses the uptake of L-lactate. 6. The results provide evidence that L- and D-lactate enter the cells of rat aorta by a mediated transport system.

Animals↗

Venezuelan encephalitis virus infection in neotropical bats. I. Natural infection in a Guatemalan enzootic focus.

A serological survey of 939 Neotropical bats of 22 species from an enzootic focus of Venezuelan encephalitis (VE) virus on the Pacific lowlands of Guatemala during 1971--1975 revealed VE virus specific antibodies in seven species, three belonging to the genus Artibeus. VE virus was isolated from the blood of one Uroderma bilobatum. Antibody frequency was considerably lower in bats than in terrestrial mammals, and tended to vary within any given species from locality to locality and from year to year. At the village of La Avellana where VE virus was most active, antibody rates in the two best-sampled Artibeus species were 0.14 in 1971, 0.11 in 1972, 0.03 in 1973, and 0.11 in 1975. The positive rate of 0.10 over all years at La Avellana for the genus Artibeus suggests that these and possibly other bats regularly are infected by VE virus, and may possibly serve as alternate hosts to maintain virus circulation if most terrestrial animals become immune.

Animals↗

Venezuelan encephalitis virus infection in neotropical bats. II. Experimental infections.

Eighty-nine Neotropical bats of five species were inoculated subcutaneously with epizootic or enzootic strains of Venezuelan encephalitis (VE) virus. Viremia was detected in 92.5% of all bats, but no illness attributable to virus infection was observed. Detectable viremias averaged slightly over 4 days in Artibeus jamaicensis and A. lituratus, and 2.8 days in Phyllostomus discolor, and maximal viremia titers in these three species averaged 6.9, 6.6, and 4.6 log10 SMicLD50 per ml of blood, respectively. In general Artibeus developed and maintained detectable levels of both hemagglutination-inhibition (HI) and neutralizing antibody for as long as tested (up to 506 days), although HI antibody to enzootic VE virus strains disappeared in some A. lituratus. The detectable antibody response of P. discolor was slower and of lower magnitude and shorter duration than that of Artibeus, although individual P. discolor which had lost detectable HI and N antibody resisted challenge. Vertical passage of antibody was observed in three A. lituratus offspring. Artibeus jamaicensis were found to be only slightly less susceptible to VE virus infection than a U.S. subspecies of the cotton rat (Sigmodon hispidus). No virus was recovered by mouse inoculation of organ pools of bats killed as early as 2 days and as late as 299 days after the last day of detectable viremia.

Animals↗

[Experimental models: nutrition and intestinal cancers].

Experimental models of colonic carcinoma chemically induced in rats explored the effects of several factors involved in colon carcinogenesis: high fat level of the diet, quality and quantity of fat, fecal excretion of neutral and acid steroids, intestinal microflora and fiber content of the diet. They suggested an association linking colon cancer to dietary fat and fecal acids and neutral sterols.

Animals↗

Immunoprophylaxis and therapy of grafted rat colonic carcinoma.

Two independent lines of chemically-induced colonic carcinoma, serially graftable in syngeneic rats, have been used to investigate the effects of immunoprophylaxis and immunotherapy. Rats were immunised by various procedures, including BCG, irradiated tumour grafts, and cancer cells treated by mitomycin and neuraminidase. A partial inhibition of tumour growth was observed in one of the four protocols. On the other hand, a significant enhancement of tumour growth was obtained in two other experiments.

Adenocarcinoma↗

Effects of oral and rectal BCG administration on chemically-induced rat intestinal carcinoma.

Intestinal carcinomas were induced by repeated subcutaneous injections of 1,2-dimethylhydrazine in syngereic BD-IX strain rats for 12 weeks. At the end of the treatment, one group received 2 doses of 50 mg BCG by a gastric tube, then a dose of 50 mg BCG by rectal instillation. The other group received no BCG. There was no significant difference in survival time, total number of cancers per rat, or cancer localization between the treated or untreated groups. Disseminated peritoneal metastases were more frequently found in BCG-treated animals. These results do not support the use of orally administered BCG in the treatment of human colorectal cancer.

Administration, Oral↗

Resurgence of two fetal aldolases in rat duodenal adenocarcinomas.

We have shown, by kinetic, electrophoretical and immunological methods, the resurgence of two intestine fetal aldolases (A and C) in well-differentiated rat duodenal adenocarcinomas. Our findings demonstrate that the resurgence of fetal isozymes in cancer is a general phenomenon, occurring in intestine, as in liver and other tissues.

Adenocarcinoma↗

Antigens associated with chemically induced intestinal carcinomas of rats.

Rabbits were immunized with extracts of primary or grafted intestinal adeno-carcinomas induced by carcinogenic drugs in inbred rats. After absorption with normal tissue extracts, the antisera were able to recognize three tumor-associated antigens. Two of them were glycoproteins, present in cancer cells but also, in trace amounts, in mucous cells of the normal digestive tract. The third antigen is not detectable in the normal digestive system, but present in normal spleen; on im-unofluorescence, it is not located in the cancer cells, but in polymorphonuclear cells infiltrating the tumor. None of the three antigens cross-reacts with human carcinoembryonic antigen, or human or rat alphafetoprotein. On the other hand, one of the glycoprotein antigens is immunologically related to the human blood group A substance.

Adenocarcinoma↗