Vascular factors are critical in selective neuronal loss in an animal model of impaired oxidative metabolism.
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Silver nanoparticle induced blood-brain barrier inflammation and increased permeability in primary rat brain microvessel endothelial cells.High-dose thiamine prevents brain lesions and prolongs survival of Slc19a3-deficient mice.Neuronal MCP-1 mediates microglia recruitment and neurodegeneration induced by the mild impairment of oxidative metabolism.Glucose loading precipitates focal lactic acidosis in the vulnerable medial thalamus of thiamine-deficient rats.A rat model for chronic spinal nerve root compression.Vitamin B1 (thiamine) and dementiaThiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse model.ICRP publication 118: ICRP statement on tissue reactions and early and late effects of radiation in normal tissues and organs--threshold doses for tissue reactions in a radiation protection context.Porcine brain microvessel endothelial cells show pro-inflammatory response to the size and composition of metallic nanoparticles.Gene expression changes in thalamus and inferior colliculus associated with inflammation, cellular stress, metabolism and structural damage in thiamine deficiency.Surface decoration by Spirulina polysaccharide enhances the cellular uptake and anticancer efficacy of selenium nanoparticles.Serotonin as a putative scavenger of hypohalous acid in the brain.Inhibition of the alpha-ketoglutarate dehydrogenase complex by the myeloperoxidase products, hypochlorous acid and mono-N-chloramine.Translocation of amyloid precursor protein C-terminal fragment(s) to the nucleus precedes neuronal death due to thiamine deficiency-induced mild impairment of oxidative metabolism.Responses of the mitochondrial alpha-ketoglutarate dehydrogenase complex to thiamine deficiency may contribute to regional selective vulnerability.Changes in inflammatory processes associated with selective vulnerability following mild impairment of oxidative metabolismThiamine and oxidants interact to modify cellular calcium stores.PKR downregulation prevents neurodegeneration and β-amyloid production in a thiamine-deficient model.eNOS gene deletion restores blood-brain barrier integrity and attenuates neurodegeneration in the thiamine-deficient mouse brain.Reversal of thiamine deficiency-induced neurodegeneration.
P2860
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P2860
Vascular factors are critical in selective neuronal loss in an animal model of impaired oxidative metabolism.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年学术文章
@wuu
2000年学术文章
@zh
2000年学术文章
@zh-cn
2000年学术文章
@zh-hans
2000年学术文章
@zh-my
2000年学术文章
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2000年學術文章
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2000年學術文章
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name
Vascular factors are critical ...... impaired oxidative metabolism.
@en
Vascular factors are critical ...... impaired oxidative metabolism.
@nl
type
label
Vascular factors are critical ...... impaired oxidative metabolism.
@en
Vascular factors are critical ...... impaired oxidative metabolism.
@nl
prefLabel
Vascular factors are critical ...... impaired oxidative metabolism.
@en
Vascular factors are critical ...... impaired oxidative metabolism.
@nl
P2093
P2860
P356
P1476
Vascular factors are critical ...... impaired oxidative metabolism
@en
P2093
G E Gibson
N Y Calingasan
P2860
P304
P356
10.1093/JNEN/59.3.207
P50
P577
2000-03-01T00:00:00Z