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Pagina 1 a partire dal 1697 risultati
Microglial NADPH oxidase activation mediates rod cell death in the retinal degeneration in rd mice.
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Accumulating evidence supports that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase contributes to microglia-mediated neurotoxicity in the CNS neurodegenerative diseases. Several studies, including ours, suggest that microglial activation is involved in the retinal degeneration in the
Whole blood monoamine oxidase activity in Parkinson's disease and multiple system atrophy patients.
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Monoamine oxidase type B (MAO-B), which catalyses the breakdown of dopamine (DA) in human brain, is said to be involved in the pathophysiology of Parkinson's disease (PD). Activity of MAO-B in PD has been measured in platelets isolated from blood samples in different studies, with contradictory
Degeneration of dopaminergic neurons induced by thrombin injection in the substantia nigra of the rat is enhanced by dexamethasone: role of monoamine oxidase enzyme.
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Anti-inflammatory strategies receive growing attention for their potential to prevent pathological deterioration in disorders such as Parkinson's disease, which is accompanied by inflammatory reactions that might play a critical role in the degeneration of nigral dopaminergic neurons. We
Increased expression of monoamine oxidase-B results in enhanced neurite degeneration in methamphetamine-treated PC12 cells.
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In vivo administration of methamphetamine (MA) produces selective damage to dopaminergic nerve terminals, which is hypothesized to be due to release of dopamine from synaptic vesicles within the terminals, allowing the generation of reactive oxygen species (ROS) via dopamine metabolism. Hydrogen
NADPH Oxidase Contributes to Photoreceptor Degeneration in Constitutively Active RAC1 Mice.
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The active form of small GTPase RAC1 is required for activation of NADPH oxidase (NOX), which in turn generates reactive oxygen species (ROS) in nonphagocytic cells. We explored whether NOX-induced oxidative stress contributes to rod degeneration in retinas expressing constitutively active (CA)
Ectopic expression of ecdysone oxidase impairs tissue degeneration in Bombyx mori.
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Metamorphosis in insects includes a series of programmed tissue histolysis and remolding processes that are controlled by two major classes of hormones, juvenile hormones and ecdysteroids. Precise pulses of ecdysteroids (the most active ecdysteroid is 20-hydroxyecdysone, 20E), are regulated by both
Delayed onset of neurologic deterioration following anoxia/ischemia coincides with appearance of impaired brain mitochondrial respiration and decreased cytochrome oxidase activity.
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We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of
Progressive hair loss and myocardial degeneration in rough coat mice: reduced lysyl oxidase-like (LOXL) in the skin and heart.
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The rough coat (rc) is a spontaneous recessive mutation in mice. To identify the mutated gene, we have characterized the rc phenotype and initiated linkage mapping. The rc mice show growth retardation, cyclic and progressive hair loss, hyperplastic epidermis, abnormal hair follicles, cardiac muscle
Neuronal degeneration in the brain of the brindled mouse. Histochemical demonstration of decreased cytochrome oxidase activity in the cerebellum and brain stem.
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In order to investigate the levels of cytochrome oxidase activity in neuronal mitochondria in the brain of the brindled mouse hemizygote (BM), the cerebella and brain stems from 12 pairs of brindled and normal littermates aged 13-16 days were examined. The diaminobenzidine method for light- and
Cytochrome c oxidase subunit Vb interacts with human androgen receptor: a potential mechanism for neurotoxicity in spinobulbar muscular atrophy.
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Spinobulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by the expansion of the polyglutamine (polyGln) tract in the human androgen receptor (hAR). One mechanism by which polyGln-expanded proteins are believed to cause neuronotoxicity is through aberrant interaction(s) with, and
Modular organization of human extrastriate visual cortex: evidence from cytochrome oxidase pattern in normal and macular degeneration cases.
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The human extrastriate occipital cortex contains several visual areas that are probably analogues of macaque areas V2, V3, VP, V4 and V5. Tracing of callosal connections has led to the anatomical identification of these areas and to the characterization of some of them by cyto- and myeloarchitecture
Cytochrome c oxidase inhibition by N-retinyl-N-retinylidene ethanolamine, a compound suspected to cause age-related macula degeneration.
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The endogenous lipophilic and cationic compound N-retinyl-N-retinylidene ethanolamine (A2E) is suspected to cause age-related macula degeneration. It inhibits cytochrome c oxidase, detaches proapoptotic proteins from mitochondria, and induces apoptosis in mammalian retinal pigment epithelial cells
Postheparin plasma diamine oxidase in subjects with small bowel mucosal atrophy.
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Diamine oxidase (DAO) is an enzyme whose low plasma values are enhanced by an intravenous injection of heparin, which releases the enzyme from the enterocytes of the villous tips. In 20 normal controls and 15 untreated subjects affected with an overt malabsorption syndrome and subtotal atrophy shown
NADPH oxidase hyperactivity induces plantaris atrophy in heart failure rats.
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BACKGROUND
Skeletal muscle wasting is associated with poor prognosis and increased mortality in heart failure (HF) patients. Glycolytic muscles are more susceptible to catabolic wasting than oxidative ones. This is particularly important in HF since glycolytic muscle wasting is associated with
Progressive cerebral degeneration of childhood with liver disease (Alpers Huttenlocher disease) with cytochrome oxidase deficiency presenting with epilepsia partialis continua as the first clinical manifestation.
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A previously healthy and normally developed 17-year-old young female presented with a sudden onset of focal motor seizure status that proved to be refractory to anticonvulsive treatment. Severe encephalopathy with visual impairment leading to blindness, mental deterioration, and predominantly left
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