Publications by authors named "Revett K"

The pathogenesis of penumbral tissue infarction during acute ischemic stroke is controversial. This peri-infarct tissue may subsequently die, or survive and recuperate, and its preservation has been a prime goal of recent therapeutic trials in acute stroke. Two major hypotheses currently under consideration are that penumbral tissue is recruited into an infarct by cortical spreading depression (CSD) waves, or by a non-wave self-propagating process such as glutamate excitotoxicity (GE).

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When a cerebral infarction occurs, surrounding the core of dying tissue there usually is an ischemic penumbra of nonfunctional but still viable tissue. One current but controversial hypothesis is that this penumbra tissue often eventually dies because of the metabolic stress imposed by multiple cortical spreading depression (CSD) waves, that is, by ischemic depolarizations. We describe here a computational model of CSD developed to study the implications of this hypothesis.

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Twenty male subjects, 11 normal and 9 carbohydrate-sensitive, participated in a study in which the effect of feeding diets low in copper (1.03 mg/d) on the number and affinity of insulin receptors was determined. Since carbohydrate-sensitive subjects are hyperinsulinaemic, it was anticipated that they would demonstrate a down-regulation of insulin receptors.

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Sixty-two Asian Indian and American vegetarians participated in a 3-h glucose tolerance test after an overnight fast to study clinical indices of glucose homeostasis. The Asian Indians had a higher (p less than 0.0035) insulinogenic score than the Americans.

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Obese Zucker rats are hyperlipemic and mildly hyperglycemic. Because insulin and glucagon are involved in lipid and carbohydrate metabolism and they act via their receptors, we investigated the role of insulin and glucagon receptors in obese and lean female Zucker rats. Because dietary sucrose is more lipogenic than starch, we also studied the effect of dietary carbohydrates on the receptors.

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A catabolic and hypolipemic effect of glucagon has been described in normal animals. We therefore studied the role of glucagon in genetically obese, hyperlipemic rats. Twelve genetically obese hyperlipemic LA/N-cp/cp (corpulent) rats and 12 lean littermates were fed either 54% starch or 54% sucrose for 12 weeks.

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