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Functional deficits after spinal cord injury have originated not only from the direct physical damage itself, but from the secondary biochemical and pathological changes. Apoptotic cell death has been seen around the periphery of an injured site and has been known to ultimately progress to necrosis and infarction. We have initiated the present study(More)
Feeding and housing conditions that induce gastric lesions were investigated. Rats were housed in activity wheels or in hanging cages and exposed to food deprivation, ad lib cellulose or 6 g of cellulose per day for 5 days. Food-deprived rats in both housing conditions had ulcers in the rumen but many rats also had mucosal ulcers. Cellulose prevented(More)
Rats were housed in activity wheels (n = 32) or in hanging cages (n = 32) for 2 weeks. Food intake of rats in hanging cages was curtailed to match body weight to that of the activity group. All rats then received 6 g of food at one of four different times of day (n = 8, each mealtime) for 4 consecutive days and were sacrificed 24 h after the last meal.(More)
The purpose of this experiment was to explicitly test the hypothesis that the depletion of fat reserves is a critical factor in the generation of ulcers in the glandular stomach. Fat reserves were systematically manipulated by using chow vs. high-fat diets and by using rats of different ages (3, 7, and 17 months). The ulcerogenic procedure consisted of(More)
Rats housed in activity wheels (A-W) or hanging cages (H-C) received food restriction to 4 h/day for 15 days. Food was given at fixed times to entrain the feeding entrainable oscillator or at irregular times to prevent entrainment. One half of the rats received food in the light phase, the other half in the dark phase of the light-dark cycle. Food was then(More)
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