Sökning: "mitochondrial permeability transition"
Visar resultat 1 - 5 av 13 avhandlingar innehållade orden mitochondrial permeability transition.
1. Ischemic and Hypoglycemic Brain Damage, Involvement of the Mitochondrial Permeability Transition Pore
Sammanfattning : Brain damage from ischemia-reperfusion and hypoglycemia are major causes of morbidity and mortality. Therapeutic strategies include hypothermia, glutamate-receptor blockade, immunosuppression and lately treatment aiming at preserving mitochondrial integrity and function. LÄS MER
2. Calcium-induced mitochondrial permeability transition in CNS-derived mitochondria - Pharmacological aspects of specificity and toxicity in neuroprotection
Sammanfattning : Mitochondria are the main site for energy conversion in the cell. Under certain circumstances, such as excess calcium retention or production of reactive oxygen species, a pore forms at contact sites between the outer and the normally impermeable inner mitochondrial membrane. LÄS MER
3. Mechanisms of Mitochondria-Induced Brain Damage Following Ischemia and Hypoglycemia
Sammanfattning : Mechanisms of Mitochondria-Induced Brain Damage Following Ischemia and Hypoglycemia Following prolonged disruption of blood flow to the central nervous system (CNS), or energy deprivation by other means, such as hypoglycemia, some cells will inevitably degenerate. It has been, and still is, the subject of considerable debate and intense research on brain ischemia, as to the mode of cell death, i. LÄS MER
4. Experimental Traumatic Brain Injury and Cell Death - in vivo and in vitro aspects
Sammanfattning : Traumatic and ischemic brain damage are major causes of disability and death. While much effort has been spent on developing pharmacological treatments for these conditions, no neuroprotective drugs are in clinical use. LÄS MER
5. Cellular and molecular mechanisms of ischemic brain damage in hyperglycemic rats
Sammanfattning : The present study is centered on mechanisms of ischemic brain damage in hyperglycemic animals, and in those in which exaggerated intraischemic acidosis was induced by superimposed hypercapnia in normoglycemic animals. The initial experiments were focussed on the pathophysiology of postischemic seizures. LÄS MER