Pathogenic mechanisms in ischemic damage: a computational study.

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).

Spreading depression in focal ischemia: a computational study.

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.

Increased insulin receptors in carbohydrate-sensitive subjects: a mechanism for hyperlipaemia in these subjects?

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.