Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine - Wikidata - awgldk - TriplyDB

Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine

Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine

http://www.wikidata.org/entity/Q34374197

about

Cognitive dysfunction and diabetes mellitus Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans Neuroprotection in cerebral ischemia by neutralization of 3-aminopropanal.Caloric restriction mimetics: metabolic interventions.Extracellular spermine exacerbates ischemic neuronal injury through sensitization of ASIC1a channels to extracellular acidosis Decreased cerebrovascular brain-derived neurotrophic factor-mediated neuroprotection in the diabetic brain.The interleukin-8 (IL-8/CXCL8) receptor inhibitor reparixin improves neurological deficits and reduces long-term inflammation in permanent and transient cerebral ischemia in rats.The HMGB1 receptor RAGE mediates ischemic brain damage.Advanced glycation and lipoxidation end products--amplifiers of inflammation: the role of food.Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke.Erythropoietin crosses the blood-brain barrier to protect against experimental brain injury.Preventive aspects in peripheral artery disease.Methylglyoxal in diabetes: link to treatment, glycaemic control and biomarkers of complications.Cerebral ischemia enhances polyamine oxidation: identification of enzymatically formed 3-aminopropanal as an endogenous mediator of neuronal and glial cell death.Loss of NF-kappaB activity during cerebral ischemia and TNF cytotoxicity.Expression of TNF and TNF receptors (p55 and p75) in the rat brain after focal cerebral ischemia Delayed treatment with aminoguanidine decreases focal cerebral ischemic damage and enhances neurologic recovery in rats.Biochemical and Clinical Impact of Organic Uremic Retention Solutes: A Comprehensive Update.Reduced functional deficits, neuroinflammation, and secondary tissue damage after treatment of stroke by nonerythropoietic erythropoietin derivatives.Effect of transient cerebral ischemia on the expression of receptor for advanced glycation end products (RAGE) in the gerbil hippocampus proper.Advanced glycation end products in myocardial reperfusion injury.

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Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine

http://www.wikidata.org/entity/Q34374197

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1995 nî lūn-bûn

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1995 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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1995 թվականի ապրիլին հրատարակված գիտական հոդված

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1995年の論文

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1995年論文

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1995年論文

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1995年論文

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1995年論文

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1995年論文

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1995年论文

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Proceedings of the National Academy of Sciences of the United States of America

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Neurotoxicity of advanced glyc ...... tive effects of aminoguanidine

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A Cerami

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D Risucci

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G A Zimmerman

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P2860

The L-arginine-nitric oxide pathway

Apparent hydroxyl radical production by peroxynitrite: implications for endothelial injury from nitric oxide and superoxide

Oxidative damage to brain proteins, loss of glutamine synthetase activity, and production of free radicals during ischemia/reperfusion-induced injury to gerbil brain.

Advanced protein glycosylation induces transendothelial human monocyte chemotaxis and secretion of platelet-derived growth factor: role in vascular disease of diabetes and aging.

Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications.

Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.

Role of tumor necrosis factor-alpha in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat.

Role of NO production in NMDA receptor-mediated neurotransmitter release in cerebral cortex.

Excitatory amino acids as a final common pathway for neurologic disorders.

Hydrogen ions kill brain at concentrations reached in ischemia.

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3744-3748

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