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phospholipid/atrofi
Länken sparas på Urklipp
Sida 1 från 920 resultat
Deterioration of membrane morphology, phospholipids, and cytoskeletal protein in rat erythrocytes exposed to tert-butyl hydroperoxide: protection by exogenous glutathione fails in selenium deficiency.
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Here we report scanning electron microscopy, phospholipid and fatty acid composition and cytoskeleton proteins of erythrocytes from Se-adequate and Se-deficient rats, showing protection by glutathione (GSH) against tert-butyl hydroperoxide (t-BuOOH)-induced hemolysis of erythrocytes from
Proteomics-based identification and validation of novel plasma biomarkers phospholipid transfer protein and mannan-binding lectin serine protease-1 in age-related macular degeneration.
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Age-related macular degeneration (AMD) is a major cause of severe, progressive visual loss among the elderly. There are currently no established serological markers for the diagnosis of AMD. In this study, we carried out a large-scale quantitative proteomics analysis to identify plasma proteins that
Brain phospholipids and fatty acids in Friedreich's ataxia and spinocerebellar atrophy type-1.
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Previous studies of patients with spinocerebellar atrophy type 1 (SCA-1) and Friedreich's ataxia (FA) have suggested the occurrence of membrane disturbances in both disorders. We measured concentrations of phosphatidylcholine (PC), diacyl and plasmalogen phosphatidylethanolamine (PE), and
Review: pharmacological manipulation of docosahexaenoic-phospholipid biosynthesis in photoreceptor cells: implications in retinal degeneration.
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Docosahexaenoic acid (22:6n-3, DHA) is derived in vertebrate animals from n-3 fatty acids present in the diet (i.e., alpha-linolenic acid, 18:3n-3 and/or other n-3-long chain polyunsaturated fatty acids) and is found in very high concentrations in phospholipids from membranes of the central nervous
Mass spectrometric analyses of phospholipids in the S334ter-3 rat model of retinal degeneration.
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OBJECTIVE
The purpose of this study was to profile the endogenous phospholipid species in the retinal tissue of the S334ter-3 rat model of retinal degeneration. Retinal tissue was collected from S334ter-3 rats at postnatal day (P) 20, P30, and P60, while control retinal samples were collected from
Specific phospholipid scramblases are involved in exposure of phosphatidylserine, an "eat-me" signal for phagocytes, on degenerating axons.
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Axonal degeneration is a key pathological feature of several neurological disorders. Emerging evidence has suggested a pathological connection between axonal degeneration and autophagy, a lysosomal degradation pathway. We recently reported that GSK3B-mediated phosphorylation of MCL1 regulates axonal
[Incorporation of plasma radiophosphate into the inorganic, organic acid-soluble and phospholipid phosphate fractions of the normal rabbit sciatic nerve and during Wallerian degeneration].
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Inorganic phosphate exchanges between plasma and sciatic nerve have been measured in the rabbit using a 32PO4 tracer technique. Inorganic phosphate is taken up at the rate of 0.13 microng per hour and per 100 mg fresh weight. Incorporation of plasma radiophosphate is markedly increased into the
Metabolic labeling of rod outer segment phospholipids in miniature poodles with progressive rod-cone degeneration (prcd).
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The recessive genetic defect in miniature poodles which results in progressive rod-cone degeneration (prcd) has been investigated in an attempt to determine the biochemical abnormality involved. In the present study, the rod outer segments of young prcd affected miniature poodles and normal dogs
Phospholipid metabolite levels are altered in cerebral cortex of patients with dominantly inherited olivopontocerebellar atrophy.
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We measured metabolic precursors and breakdown products of phosphatidylcholine (choline, glycerophosphocholine (GPC) and phosphatidylethanolamine (ethanolamine, glycerophosphoethanolamine (GPE)) as well as the amino acid serine, a precursor of phosphatidylserine, in four morphologically unaffected
A novel nontoxic alkyl-phospholipid with selective antitumor activity, plasmanyl-(N-acyl)-ethanolamine (PNAE), isolated from degenerating chick embryonal tissues and from an anticancer biopreparation cACPL.
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A novel alkyl-phospholipid with selective antitumor activity was isolated from an anticancer biopreparation cACPL (crude anticancer phospholipids) and from tissues of degenerating chick embryos. The alkyl-phospholipid was isolated and purified by chromatographic methods using silicic acid column
Mechanical effects of the intraarticular administration of high molecular weight hyaluronic acid plus phospholipid on synovial joint lubrication and prevention of articular cartilage degeneration in experimental osteoarthritis.
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OBJECTIVE
To examine in vivo the effects of a mixture of high molecular weight hyaluronic acid (HA) plus phospholipids on joint lubrication and articular cartilage degeneration.
METHODS
Experimental osteoarthritis (OA) of the right knee was induced by anterior cruciate and medial collateral ligament
Oxidized phospholipids in the macula increase with age and in eyes with age-related macular degeneration.
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OBJECTIVE
There is good evidence that oxidative stress is involved in the pathogenesis of age-related macular degeneration (AMD). Because AMD has risk factors and histopathology similar to with atherosclerosis, we hypothesized that oxidized phospholipids, which contribute to the pathogenesis of
Differential Sphingolipid and Phospholipid Profiles in Alcohol and Nicotine-Derived Nitrosamine Ketone-Associated White Matter Degeneration.
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BACKGROUND
Alcohol-mediated neurodegeneration is associated with white matter (WM) atrophy due to targeting of myelin and oligodendrocytes. However, variability in disease severity suggests cofactors contribute to WM degeneration. We examined the potential cofactor role of the tobacco-specific
Complement factor H genotypes impact risk of age-related macular degeneration by interaction with oxidized phospholipids.
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The rs1061170T/C variant encoding the Y402H change in complement factor H (CFH) has been identified by genome-wide association studies as being significantly associated with age-related macular degeneration (AMD). However, the precise mechanism by which this CFH variant impacts the risk of AMD
Abnormal activity of membrane phospholipid synthetic enzymes in the brain of patients with Friedreich's ataxia and spinocerebellar atrophy type-1.
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Much evidence, derived from biochemical studies of both blood and autopsied brain, has suggested that phospholipid metabolism is abnormal in patients with Friedreich's ataxia (FA), a disorder characterized by severe neuronal loss in the spinal cord and lower brain stem with no, or only modest,
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