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Cardioprotective effect of diazoxide and its interaction with mitochondrial ATP-sensitive K+ channels. Possible mechanism of cardioprotection.
TLDR
The profile of activity of diazoxide (and perhaps KATP openers in general) suggests that they protect ischemic hearts in a manner that is consistent with an interaction with mitochondrial KatP. Expand
Iron accumulation in Alzheimer disease is a source of redox-generated free radicals.
TLDR
It is found, using a modified histochemical technique that relies on the formation of mixed valence iron complexes, that redox-active iron is associated with the senile plaques and neurofibrillary tangles-the pathological hallmark lesions of Alzheimer disease. Expand
Advanced Maillard reaction end products are associated with Alzheimer disease pathology.
TLDR
Evidence is presented that antibodies against two Maillard end products, pyrraline and pentosidine, immunocytochemically label neurofibrillary tangles and senile plaques in brain tissue from patients with Alzheimer disease contain modifications typical of advanced Maillard reaction end products. Expand
Glycoxidation and oxidative stress in Parkinson disease and diffuse Lewy body disease
TLDR
Immunolocalization of advanced glycation end-products and a marker of oxidative stress response induction provides evidence that glycoxidation and oxidative stress may be an important pathogenic factor in diseases characterized by Lewy body formation, and furthers the evidence that cytoskeletal proteins and their inclusions are susceptible to oxidative stress. Expand
All fatty acids are not equal: discrimination in plant membrane lipids.
TLDR
Recent research that has given new insights into how plants prevent the accumulation of unusual fatty acids in membrane lipids are discussed, and how strict this censorship of membrane composition is is described. Expand
Chemistry and biochemistry of oxidative stress in neurodegenerative disease.
TLDR
Delineation of the profile of oxidative damage in each disease will provide clues to how the specific neuronal populations are differentially affected by the individual disease conditions. Expand
Causes of oxidative stress in Alzheimer disease
TLDR
An overview of the potential causes of oxidative stress in AD appears to be multi-faceted, with interactions between abnormal mitochondria, redox transition metals, and other factors. Expand
Activation and redistribution of c‐Jun N‐terminal kinase/stress activated protein kinase in degenerating neurons in Alzheimer's disease
TLDR
Findings suggest that JNK/SAPK dysregulation, probably resulting from oxidative stress, plays an important role in the increased phosphorylation of cytoskeletal proteins found in AD. Expand
Amyloid‐β Deposition in Alzheimer Transgenic Mice Is Associated with Oxidative Stress
TLDR
Evidence that amyloid‐β and oxidative damage are inextricably linked in vivo is provided, and the use of transgenic animals for the development of antioxidant therapeutic strategies is supported. Expand
Evidence of oxidative stress and in vivo neurotoxicity of beta-amyloid in a transgenic mouse model of Alzheimer's disease: a chronic oxidative paradigm for testing antioxidant therapies in vivo.
TLDR
The results provide strong support for the hypothesis that Abeta is neurotoxic in vivo and that such toxicity is mediated by free radicals and validate the transgenic approach for the study of oxidative stress in AD and for the evaluation of antioxidant therapies in vivo. Expand
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