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Biomedical subjects

R G Bell

Publications and source records attributed to R G Bell.

At least 91 records · Page 5Linked to original sources
PubMed1984

A single gene determines rapid expulsion of Trichinella spiralis in mice.

In rats and some inbred mouse strains, one immune response, rapid expulsion, confers up to 95% protection against a challenge infection with Trichinella spiralis. Strain analysis in mice has shown that only three inbred strains, all originating from Swiss-line mice at the National Institutes of Health, Bethesda, Md., express rapid expulsion. Crosses between responder strain mice (NFR/N) and nonresponders (C3H/HeJ or B10 X BR) have indicated that rapid expulsion is dominant and autosomal (Bell et al., Exp. Parasitol. 53:301-314, 1982). In this study a segregation analysis of rapid expulsion in the F2 and backcross conformed to the Mendelian ratios expected of a single gene. This gene was not linked to the major histocompatibility complex (MHC) (chromosome 17) or the gene for albinism (c/c locus on chromosome 7). This locus has not previously been identified as conferring resistance to any infectious agent, and we have therefore designated the gene Ihe-1 (intestinal helminth expulsion 1).

Animals↗
PubMed1983

Vitamin K dependent carboxylation of glutamate residues to gamma-carboxyglutamate in microsomes from spleen and testes: comparison with liver, lung, and kidney.

Vitamin K dependent carboxylation of glutamate residues to gamma-carboxyglutamate was demonstrated in proteins of spleen and testes microsomes. The rate of carboxylation in spleen microsomes was 0.9% and testes 3% of that in liver microsomes per milligram of microsomal protein. For comparison the rates of carboxylation in lung and kidney microsomes were 17 and 8%, respectively, of the rate in liver microsomes. The high rate in liver microsomes may be due to a high carboxylase level as indicated by the high rate of peptide carboxylation in liver microsomes. Protein carboxylation in liver microsomes was linear for only 15 min while carboxylation in microsomes from extrahepatic tissue persisted much longer so that the total protein carboxylation in lung microsomes was 60%, kidney 18%, testes 12%, and spleen 9% of that occurring in liver microsomes. Protein carboxylation was higher in microsomes from extrahepatic tissues of rats fed a vitamin K deficient diet as compared to animals fed a vitamin K sufficient diet. Protein carboxylation in microsomes from extrahepatic tissues was greatly stimulated by manganese ions and was dependent upon the addition of dithioerythritol. NADH could partially replace the dithiol in spleen, testes, and lung, but NADH-dependent carboxylation was relatively low in kidney and liver microsomes. Dithiol-dependent carboxylation was completely blocked by 10 microM warfarin, but NADH-dependent carboxylation was only slightly inhibited by 100 microM warfarin. Menaquinone-3 was much more active than vitamin K1 in driving carboxylation. Solubilized microsomes catalyzed the carboxylation of glutamate residues to gamma-carboxyglutamate in a pentapeptide Phe-Leu-Glu-Glu-Leu. The rate of carboxylation in lung microsomes was 22%, testes 3.3%, kidney 1.9%, and spleen 1.6% of the rate in liver microsomes.

1-Carboxyglutamic Acid↗
PubMed1983

Trichinella spiralis: selective intestinal immune deviation in the rat.

In rats, infections with 100-2000 Trichinella spiralis muscle larvae lead to a prompt immunity that is expressed in parasite expulsion within 14 days. Rats infected with more than 2000 larvae display impaired immunity with rejection delayed by 50% (7 days) or more. Suppression is selective for expulsive immunity as the antifecundity response of rats is directly proportional to dose and is expressed sooner in heavily infected subjects. Suppression of intestinal expulsive immunity was suggested by the fact that, with low doses (2000 larvae or less), worm rejection was inhibited by cortisone, whereas cortisone inhibited antifecundity but had no discernable effect on worm rejection in high-dose infections. Evidence for local immune deviation as opposed to systemic immunosuppression was obtained in experiments using parabiotic rats. When one partner was infected with 6000 worms and the other with 200, the rat infected with 200 parasites showed earlier rejection than was seen in single controls infected with 200 worms. The prolonged survival of high-dose adults was not accompanied by a change in the site of worm residence in the gut. Immunological parameters such as serum antibody levels, the number of activated cells or specific anti-T. spiralis lymphocytes in thoracic duct lymph were all increased in a dose-dependent manner. These experiments therefore demonstrate a novel autoprotective mechanism by which adult T. spiralis selectively reduce the expression of expulsive immunity in the gut.

Animals↗
PubMed1983

A note on the microbial spoilage of undercooked chub-packed luncheon meat.

Contrary to expectations slight undercooking 968.5 degrees C instead of 70 degrees C for 90 min) dramatically increased the shelf-life of chub-packed luncheon meat stored at 25 degrees C. The pH of undercooked chubs fell rapidly to below 5.0 as a result of the growth of enterococci. The accumulated acid prevented the growth of Bacillus spores and gave the luncheon meat a not unpleasant tangy flavour. Degradative changes associated with the spoilage of commercially cooked chub-packed luncheon meat did not occur, even after 42 d storage. Apparently, post-cooking fermentation by enterococci can effectively convert a perishable product into a 'shelf stable' one by lowering the pH below 5.0.

Bacillus↗
PubMed1983

Nitrite loss and spoilage microflora development in chub-packed luncheon meat.

Residual nitrite was lost from chub-packed luncheon meat during storage through both chemical breakdown and microbial consumption. The relative importance of these mechanisms in this pasteurized product was determined by the speed of development of the spoilage microflora, which is influenced by storage conditions. The nitrite half-life due to chemical loss was 13 d at 25 degrees C and 36 d at 10 degrees C. When microbial growth occurred these half-lives were reduced to 2.6 d and 21 d, respectively. Qualitative differences in the microflora that developed at these two temperatures (denitrifying Bacillus spp. at 25 degrees C and non-denitrifying Streptococcus spp. at 10 degrees C) account for the large temperature effect. Growth of Streptococcus spp. increased the rate of chemical nitrite loss in chubs by reducing the pH value. Nitrite did not inhibit the aerobic growth of either Bacillus or Streptococcus species associated with spoilage but did inhibit the anaerobic growth of Bacillus spp. This bacteriostatic effect of residual nitrite in anaerobic conditions will decrease during storage as nitrite level falls and oxygen penetrates the chub pack. Nitrite-mediated bacteriostasis does not obviate the need for refrigerated storage but does afford a real, if ephemeral, safeguard against spoilage occurring during short periods of temperature abuse.

Animals↗
PubMed1983

The effect of variation of thermal processing on the microbial spoilage of chub-packed luncheon meat.

Process pasteurization values for reference temperature 70 degrees C (P70) were calculated from the temperature profiles of 250 g luncheon meat chubs cooked under experimental conditions. A simple equation relating Process P70-value and the time and temperature of cooking was derived. With minimal cooking (P70 = 40) the surviving microflora (10(3)/g) wad dominated by species of Lactobacillus, Brochothrix and Micrococcus. These organisms were destroyed by more intensive cooking (P70 = 105), leaving a flora (10(2)/g) composed of Bacillus and Micrococcus species. The spoilage that developed after 14 d storage at 25 degrees C reflected the severity of the heat treatment received by each chub: with P70 between 40 and 90, a Streptococcus spoilage sequence occurred; with P70 between 105 and 120, a Bacillus/Streptococcus spoilage sequence occurred; with P70 of 135 and above, a Bacillus spoilage sequence occurred. Cooking to a P70 = 75 was adequate to reduce the surviving microflora to the 10(2)/g level associated with current good manufacturing practice.

Bacillus↗
PubMed1983

A note on the identity and properties of the spoilage microflora of chub-packed luncheon meat stored at ambient temperature.

The principal spoilage bacteria isolated from chub-packed luncheon meat stored at 25 degrees C have been identified as strains of Bacillus licheniformis and Streptococcus faecium. Bacillus licheniformis alone is responsible for those degradative changes (surface softening and discolouration, gas production and eventual product liquefaction) regarded as overt product spoilage. Streptococcus faecium metabolizes carbohydrate homofermentatively, and the resultant accumulation of lactic acid causes souring of the luncheon meat.

Bacillus↗
PubMed1982

Vitamin K activity and metabolism of vitamin K-1 epoxide-1,4-diol.

Vitamin K-1 epoxide, the major metabolite of vitamin k-1, has similar activity to vitamin K-1 in inducing prothrombin synthesis and protein carboxylation. The high activity of K-1 epoxide could be due to its conversion to vitamin K-1 hydroquinone without going through vitamin K-1. A logical intermediate in this conversion would be vitamin K-1 epoxide-1,4-diol. The epoxide diol was synthesized and clearly stimulated prothrombin synthesis in vitamin K deficient rats at a minimum dose of 100 micrograms/kg body weight. Since vitamin K-1 produced a similar response at a minimum dose of 1 microgram/kg, the epoxide diol had about 1% of the activity of vitamin K-1. [3H]K-1 or [3H]epoxide could not be detected as metabolites of [3H]epoxide diol indicating that the activity of epoxide diol was probably not due to its conversion to K-1 hydroquinone, since any [3H]hydroquinone formed would be oxidized in air to [3H]K-1 during analysis. Vitamin K-1 epoxide diol represents a new type of structure possessing vitamin K activity. It is probably not active itself but has to be converted to an active compound since there is a delay in the response to the diol and the activity is completely blocked by Warfarin.

Animals↗
PubMed1982

Studies on the inhibition of rapid expulsion of Trichinella spiralis in rats.

A variety of inhibitors was examined for their ability to interfere with the expression of rapid expulsion (RE) of challenge Trichinella spiralis infections in rats. Inhibitors of immediate hypersensitivity, prostaglandin release, peristalsis, or complement function, did not impair RE when administered to immune rats. Induction of intestinal anaphylaxis against T. spiralis or ovalbumin by passive serum transfer to intestinally primed rats (prior infection with Heligmosomoides polygyrus) or administration of the histamine liberator 48/80 also failed to stimulate RE. In contrast, irradiation or cortisone treatment 1, 3 or 5 days before challenge inhibited RE. We conclude that immediate hypersensitivity is not the terminal mediator of RE and plays a minor role or none at all. The effects of cortisone and irradiation suggest a major involvement by lymphoid cells in the RE reaction.

Anaphylaxis↗
PubMed1981

Corrosion of mild and stainless steel by four tropical Desulfovibrio desulfuricans strains.

The corrosion potential of four tropical Desulfovibrio desulfuricans isolates was determined using a semicontinuous batch culture technique in a 56-day test incubated at 37 degrees C. The corrosion potentials for mild and stainless steel of marine or brackish water isolates (0.55 and 0.0026 mg cm-2 day-1) were observed to be approximately twice those of freshwater isolates (0.23 and 0.0014 mg cm-2 day-1). Under comparable experimental conditions of severe anaerobic corrosion, stainless steel was found to be over 200 times more resistant than mild steel.

Alloys↗