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Biomedical subjects

Y Dror

Publications and source records attributed to Y Dror.

At least 37 records · Page 2Linked to original sources
PubMed1982

Dietary factors affecting experimental models of nutritional encephalomalacia.

Various factors affecting the experimental development of nutritional encephalomalacia (NE) were studied in young chicks. The effects of these factors were evaluated by calculation of the age at which one-half were affected (T1/2). The incidence of ataxia and mortality and statistical analysis of the intensity of the disease were also calculated. No differences were found among the safflower oil samples oxidized for periods ranging from 12 to 48 hr in their potency to induce NE, while oil oxidized for 72 hr was less effective. No difference was observed between the effects of oxidized safflower oil and freshly distilled methyl esters of safflower oil on the development of NE. This disorder was more severe in chicks fed a fat-free diet deficient in vitamin E for the first week and then the NE-inducing diet than in chicks fed the NE-inducing diet from hatching. Feeding chicks vitamin E for the first week delayed the development of encephalomalacia but did not prevent it. In order to prevent NE in young chicks fed oxidized safflower oil, a ratio of .3 mg alpha-tocopherol per gram oil was required.

Animals↗
PubMed1980

Lysosomal acid phosphatase decrease in nutritional encephalopathy in chicks.

Encephalopathy was induced in 14-day-old chicks by a vitamin E-deficient diet containing 15% thermally oxidized safflower oil. Bound acid phosphatase activity in the cerebellum was markedly lower in affected chicks than in vitamin E-supplied control chicks. Free activity also tended to be lower in the deficient group. There were no differences in enzyme activities of cerebrum and liver between deficient and control chicks.

Acid Phosphatase↗
PubMed1979

Lipid oxidation products and chick nutritional encephalopathy.

Safflower oil and its distilled methyl esters were thermally oxidized and fed to young chicks in a vitamin E deficient diet. At a dietary level of 10%, the oxidized lipids caused more severe nutritional encephalopathy (NE) than the unoxidized methyl esters, indicating that factors other than dietary linoleic acid and vitamin E affect the development of NE. A polar lipid extract from oxidized methyl esters accelerated the induction of NE, as did the synthetic methyl esters of keto-octadecenoic and keto-octadecadienoic acids. Dicumarol exerted a protective action against NE. The possibility is discussed that conjugated keto-polyenoic fatty acids, provided by oxidized oils or formed endogenously in vitamin E deficiency, may play a role in causing NE.

Aging↗
PubMed1978

Mineralized cells: neurons, glia or macrophages? Ultrastructure of cerebellum in chick nutritional encephalopathy.

Mineralized dead cells were found in infarcted areas in the cerebella of three chicks killed in the healing stage of nutritional encephalopathy. The mineral depostis were found in vacuoles and consisted of radially packed threads and spicules, concentric laminated structures and centrally located amorphous masses. The cells in which these deposits were found were positively identified as astrocytes and macrophages. The presence of such deposits in neurons was suspected but not proven.

Animals↗
PubMed1978

Influence of overfeeding on growth, obesity and intestinal tract in young chicks of light and heavy breeds.

1. Heavy-breed (HB) chicks differed from light-breed (LB) ones in their propensity to be overfed. Whereas in the LB chicks the amount by which they could be overfed reached 70% more than the food consumed daily by the ad lib.-fed chicks, in the HB chicks the maximal excess was only 13%. 2. Overfeeding caused a slight but statistically significant increase in the linear growth rate (shank length) of the LB chicks, with an opposite effect in the HB chicks. 3. Overfeeding increased the weight of the crop, proventriculus, small intestine, pancreas, liver and adipose tissue but had no such effect on the heart, cerebrum or cerebellum. 4. Overfeeding had no effect on the specific activities of the pancreatic digestive enzymes, liver xanthine dehydrogenase, or tryptophan oxygenase (EC 1.13.1.12). The increase in the total activities was due entirely to organ hypertrophy. 5. Obesity induced in young chicks had no residual effects on the adult LB chicks, but reduced the linear growth of the adult HB chicks. 6. An explanation for the difference between breeds in response to overfeeding at an early age is discussed.

Adipose Tissue↗
PubMed1977

The relative growth of internal organs in light and heavy breeds.

The relative weights of the gastro-intestinal segments and of some other internal organs from light and heavy breed chicks from hatching to 21 days of age were compared. 2. The relative weight of the duodenum and jejunum was higher in the light breed than in the heavy one, the reverse relationship was found for the ileum and caecum. 3. The relative growth of the pancreas, heart, cerebrum and cerebellum was greater in the light breed.

Animals↗
PubMed1976

Effect of dietary fat on pancreatic lipase activity in chicken.

Pancreatic lipase activity was measured in young chicks receiving experimental diets for 18 to 24 days. The addition of 15% soybean oil to a commercial-type diet, without changing the calorie-protein ratio, produced a slight but significant increase in lipase activity. No differences in lipolytic activity were found when chicks received a semipurified diet with or without the addition of 10% partially hydrogenated soybean oil, nor did fasting and fasting-refeeding affect the activity. Pancreatic lipase activity in chicks appears to depend on factors other than the amount or type of fat consumed.

Animals↗