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Maj-Lis Smith

Researcher at Lund University

Publications -  69
Citations -  6675

Maj-Lis Smith is an academic researcher from Lund University. The author has contributed to research in topics: Ischemia & Brain damage. The author has an hindex of 38, co-authored 69 publications receiving 6582 citations.

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Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model

TL;DR: By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long‐term recovery studies.
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Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma.

TL;DR: In situ hybridization was used to study expression of mRNAs for members of the nerve growth factor (NGF) family in the rat brain after 2 and 10 min of forebrain ischemia and 1 and 30 min of insulin-induced hypoglycemic coma to influence functional outcome and neuronal necrosis following ischemic and hypogly diabetic insults.
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The effect of mild hyperthermia and hypothermia on brain damage following 5, 10, and 15 minutes of forebrain ischemia.

TL;DR: The results confirm previous findings showing that a decrease in temperature of only 2°C significantly reduces damage to several selectively vulnerable neuronal populations, and show that an increase in temperature significantly enhances brain damage.
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The influence of mild body and brain hypothermia on ischemic brain damage.

TL;DR: The results suggest that whatever biochemical events are responsible for selective neuronal vulnerability, they are temperature sensitive; however, since there are differences in sensitivity between different parts of the brain, more than one mechanism may be involved.
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Increased production of the TrkB protein tyrosine kinase receptor after brain insults

TL;DR: It is shown that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus, suggesting that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.