Sökning: "mitochondrial permeability transition pore"
Visar resultat 1 - 5 av 6 avhandlingar innehållade orden mitochondrial permeability transition pore.
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. Mitochondrial involvement in cell death : release of pro-apoptotic proteins
Sammanfattning : In addition to the role of the mitochondria in energy metabolism, these organelles play a key role in cell death signaling. In particular, mitochondrial alterations, such as stimulation of reactive oxygen species (ROS) formation, decreased ATP synthesis, loss of membrane potential and the release of pro-apoptotic proteins from the mitochondrial intermembrane space (IMS), have been shown to be involved in, and often responsible for, various manifestations of cell death. LÄS MER
4. The role of the mitochondrion in organotin-induced T-cell apoptosis
Sammanfattning : Apoptosis plays a central role in the development and the function of the immune system. The cell death program can, however, be inappropriately activated or suppressed under pathological conditions. Several toxins have been shown to interfere with intra-thymic processes, thereby contributing to autoimmune disorders. LÄS MER
5. Apoptotic mechanisms in the neonatal brain following hypoxia-ischemia
Sammanfattning : Neonatal encephalopathy is often perinatally acquired and caused by hypoxia-ischemia (HI). Brain injury develops with a delay, over 12-48 hours, after the insult. Hypothermia, an established neuroprotective treatment, saves 1 infant in 9 from neurological deficits suggesting that there is room for further improvement. LÄS MER
