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Biomedical subjects

B E Sheffy

Publications and source records attributed to B E Sheffy.

At least 19 recordsLinked to original sources
PubMed1985

Nutrition and metabolism of the geriatric dog.

Sixteen 10-12-year-old and eight 1-year-old dogs were studied over a two year period to determine comparative differences in physiological response to 4 diets varying in protein content and percentages of energy contributed by protein. The ability of old dogs to utilize nutrients as supplied by these foods was not significantly different from that of young adult dogs. Except for indices of mitogenic stimulation and serum urea nitrogen (SUN) other physiological parameters studied were not affected by the diet fed. Regardless of diet, old dogs had significantly higher serum levels of cholesterol, phosphorus and alkaline phosphatase and had lower indices of mitogenic stimulation than did young dogs.

Aging↗
PubMed1983

Effect of antioxidants on the proliferative response of canine lymphocytes in serum from dogs with vitamin E deficiency.

The in vitro effect of vitamin E and 3 other antioxidants--ethoxyquin, 2-mercaptoethanol, and ascorbic acid--on proliferation of canine lymphocytes was examined. Lymphocytes from 2 groups of dogs given a vitamin E-deficient diet or whelped from a bitch fed such a diet were cultured with pooled samples of serum from dogs fed a vitamin E-deficient diet or whelped from a bitch fed such a diet, or normal canine serum, and stimulated with phytohemagglutinin. Added vitamin E enhanced the responsiveness in serum from the dogs with vitamin E deficiency, but not in normal canine serum. A similar effect was noted with added ethoxyquin and 2-mercaptoethanol. Ascorbic acid had no effect on proliferation in either serum pool. These results indicated that depressed lymphocyte responsiveness seen with serum from vitamin E-deficient dogs may, at least in part, be due to a loss of antioxidant activity in this serum.

Animals↗
PubMed1981

Nutrition and the aging animal.

The surge in current thinking and research on aging, replete with causes and/or effects, has greatly stimulated serious biologists concerned with giving counsel for the feeding and management of animals to reevaluate present practices. This is particularly true for the feeding of dogs. If we are indeed concerned with the feeding of the geriatric dog, we must begin to emphasize changes in nutritional practices that go back to the period preceding birth. Unrestricted caloric intake of dogs during periods of growth and development, even when in proper balance with intake of essential nutrients, has been shown to accelerate somatic processes, resulting in delayed maturation of cartilage and excessive bone apposition. This was followed by reduced bone resorption and remodeling. These processes were associated with the development of either earlier or more severe degenerative diseases of the skeletal system. Studies with rodents have demonstrated damaging effects of unrestricted dietary intake on longevity itself. Most damaging have been the decreasing efficiency of cellular immunity and corresponding increases in autoimmune responses during later life. Judicious caloric restriction beginning even in adult life can have a rejuvenating effect on immune response capacity. Regardless of age, a controlled nutrient intake seems the order of the day. Returning to Lucretius, the graves are indeed being dug with teeth.

Aging↗
PubMed1981

Vitamin E deficiency retinopathy in dogs.

Dogs fed purified diets developed retinopathy consistently when the nutrition was deficient in vitamin E. Deleting DL-methionine along with vitamin E and selenium (groups 3 dogs) varied the development minimally. Supplementation of vitamin E to a selenium-deficient diet (group 1 dogs) protected the retina from changes. Ethoxyquin added to a diet deficient in vitamin E, but supplemented with National Research Council levels of selenium or 10 times the National Research Council levels, induced no beneficial recognizable changes in the retinopathy. the characteristic retinopathy was ophthalmoscopically visible as early as 3 months (group 2 to 9 dogs). Typical lesions developed first in the central, outer layers and progressed slowly toward the periphery. The tapetal retina was more extensively involved, showing a color change and mottling. Microscopically, a yellow autofluorescent pigment accumulated in large amounts within the retinal epithelium. Later stages of retinopathy showed this pigment was present in migrating cells in all the retinal layers. The early disappearance of a recordable electroretinogram, night blindness, and eventual severe day visual impairment makes this retinopathy similar to some aspects of degenerations described for persons and pure breed dogs.

Animals↗
PubMed1981

Effect of vitamin E deficiency on the proliferative response of canine lymphocytes.

The effect of vitamin E deficiency on the proliferative response of canine lymphocytes was examined, using the lymphocyte blastogenesis assay, with phytohemagglutinin, concanavalin A, and pokeweed as mitogenic stimulants. A litter (4 pups; group 3) from a bitch fed a complete diet was given a complete diet from the time of weaning (6 weeks) until termination of the experiment, and served as a control group. A litter (4 pups; group 1) from a bitch fed a vitamin E-deficient diet was given a vitamin E-deficient diet from the time of weaning (6 weeks) until termination of the experiment. A litter (6 pups; group 2) from a bitch fed a complete diet was weaned onto a complete diet and then changed to a deficient diet until termination of the experiment. Lymphocytes from group 1 and 2 pups (fed deficient diets) were poorly responsive to mitogen-induced blastogenesis, compared with the lymphocytic response seen in the controls. Washing the lymphocytes from the pups fed vitamin E-deficient diet resulted in enhanced responsiveness to mitogen stimulation. Lymphocytes from controls which had good responses when cultured in bovine fetal serum or normal canine serum were poorly responsive when cultured in serum from groups 1 and 2 pups (fed vitamin E-deficient diet). Reducing the concentration of group 1 and 2 pup sera in the culture medium restored the responsiveness of lymphocytes from control pups. Supplementation of group 1 and 2 pup sera with bovine fetal serum did not result in enhancement of the responses of lymphocytes from controls. The capability of sera from vitamin E-deficient pups (groups 1 and 2) to support blastogenesis of lymphocytes from control dogs was restored following dietary supplementation with vitamin E. It was concluded that the depressed lymphocyte responsiveness in pups fed vitamin E-deficient diet was due to the presense of a suppressive factor in the serum.

Animals↗
PubMed1979

Influence of vitamin E and selenium on immune response mechanisms.

Vitamin E and selenium have both been shown to have immunostimulatory effects in a variety of species when administered in quantities in excess of established deitary requirements. Responses to each nutrient appeared to be independent of the nutrition of the other. Deficiencies of vitamin E and selenium conversely caused suppression of the immune response system, particularly, cell mediated mechanisms. Suppression was shown to be associated with serum factors coating lymphocytes from dogs deficient in vitamin E and selenium. Oral supplementation with vitamin E transformed or removed the suppressive factors, dietary selenium had no effect. In vitro peripheral lymphocyte blast transformation tests corroborated observations of in vivo studies. Reducing agents and synthetic anti-oxidants eliminated suppressive effects in vitro. Suppression was most marked in dogs fed diets highest in polyunsaturated fatty acid (PUFA) content, providing conditions most conductive to lipid peroxidation in vivo. The essential fatty acids linoleic and arachidonic have been shown to similarly influence immunoregulatory mechanisms in vivo. The effect may be a direct one since plasma membrane fluidity of lymphoid cells increases the probability of modification of cell--antigen interactions by PUFA. However, their effect may also be an indirect one. PUFA are known precursor substances of E anf F type prostaglandins which have been shown to affect immediate and delayed hypersensitivity by stimulating synthesis of cyclic AMP. More definitive studies are needed to resolve this question.

Animals↗
PubMed1978

Nutrition and the immune response.

Vitamin E--selenium deficiency in dogs resulted in complete suppression of lymphocyte responsiveness to stimulation with mitogens. Depressing effects on neutralizing antibody synthesis were also noted. A serum factor associated with the inability of lymphocytes to respond has been isolated and partially purified. The suppressor factor can be removed or transformed by both in vivo and in vitro vitamin E supplementation.

Animal Nutritional Physiological Phenomena↗
PubMed1978

An improved procedure for genetic selection against hip dysplasia in dogs.

Rapid weight gain can educe hip dysplasia of dogs with normal hip joints. It is proposed that progeny whose parents have "excellent genotypes" would not be susceptible to this stress and would develop normal hip joints. The method for reducing the incidence of hip dysplasia in dogs would be to use stress to identify carriers (parents) and potential carriers (progeny), and select for breeding only dogs with proved genotypic value and those progeny with the best hip joint conformation.

Animals↗
PubMed1975

Experimental in utero infection of fetal pigs with a porcine parvovirus.

In utero infection of fetuses of six specific-pathogen-free large white sows at 35, 48, 55, 72, 99, and 105 days was studied. The fetuses were infected by direct inoculation of porcine parvovirus into the amniotic sac. The inoculation consisted of 0.25 ml of tissue culture fluid containing 10(5.5) mean tissue culture infective doses per ml of porcine parvovirus strain G10/1. Fetuses of one uterus horn were infected, whereas fetuses in the opposite horn were given 0.25 ml of noninfected cell culture material. No clinical signs of infection were observed; however, all sows developed antibodies 7 to 9 days postinfection. A total of 24 virus-inoculated fetuses and 20 control fetuses were studied. Fetuses infected at 35, 48, and 55 days of gestation died between about 5 and 22 days after infection. Virus was isolated from their organs and fetal blood. Virus spread to control fetuses but did not cause death and mummification or stimulate antibody production. Fetuses from sows infected at 72, 99, and 105 days of gestation survived. They developed high antibody titer in utero. Control piglets remained antibody free.

Amnion↗