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Страница 1 од 2777 резултати
Rapid loss of motor nerve terminals following hypoxia-reperfusion injury occurs via mechanisms distinct from classic Wallerian degeneration.
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Motor nerve terminals are known to be vulnerable to a wide range of pathological stimuli. To further characterize this vulnerability, we have developed a novel model system to examine the response of mouse motor nerve terminals in ex vivo nerve/muscle preparations to 2 h hypoxia followed by 2 h
Neuronal degeneration and microglial reaction in the fetal and postnatal rat brain after transient maternal hypoxia.
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This study examined the neuropathological changes in different areas of the brain of fetal and postnatal rats after transient maternal hypoxia. At different time intervals following hypoxia, reactive microglia as determined immunohistochemically with the antibody OX-42 that recognizes complement
Perinatal hypoxia induces subsequent retinal degeneration in the offspring of ovoviviparous fish, Xiphophorous maculates.
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OBJECTIVE
This experiment evaluated the perinatal hypoxic effect on the retina of offspring of the ovoviviparous fish.
METHODS
The ovoviviparous fish Xiphophorous maculates was used for the experiment.
METHODS
The mothers were kept in a hypoxic environment of 3.5% oxygen for 6 h, starting 30 h
[The relationship between hypoxia-inducible factor-1α and cartilage degeneration in osteoarthritis: a review].
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Osteoarthritis is one of the most common diseases seen in clinical practice. Cartilage survives in the hypoxic microenvironment. Hypoxia-inducible factor-1α (HIF-1α) is a key nuclear transcription factor which mediates the hypoxic response of cells. HIF-1α gene is an important regulator for the
Selective degeneration of interneurons in the motor cortex of infant monkeys following controlled hypoxia: a possible cause of epilepsy.
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Infant monkeys have been subjected to hypoxia with an arterial pO2 of 20-22 Torr for 30 min. Following perfusion 1-2 weeks later electron microscopy of the motor cortex shows a selective degeneration of axon terminals making symmetrical synapses and which probably arise from inhibitory GABAergic
Astrocytes protect cultured neurons from degeneration induced by anoxia.
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Neurons grown in cultures of dissociated brain cells degenerate when exposed to anoxia and deprived of glucose. We have developed culture systems in which neurons can be grown in the presence or absence of astrocytes and have used them to study the influence of astrocytes on the neuronal
The role of autophagy in Nmnat-mediated protection against hypoxia-induced dendrite degeneration.
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The selective degeneration of dendrites precedes neuronal cell death in hypoxia-ischemia (HI) and is a neuropathological hallmark of stroke. While it is clear that a number of different molecular pathways likely contribute to neuronal cell death in HI, the mechanisms that govern HI-induced dendrite
Isoform-specific effects of transforming growth factors-beta on degeneration of primary neuronal cultures induced by cytotoxic hypoxia or glutamate.
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The transforming growth factors-beta (TGFs-beta) are multifunctional peptide growth factors that have been localized in neuronal and glial cells of the CNS of mice, rats, and chick embryos. We tested the TGF-beta isoforms 1, 2, and 3 for their protective effects against neuronal degeneration caused
Autophagy-associated atrophy and metabolic remodeling of the mouse diaphragm after short-term intermittent hypoxia.
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BACKGROUND
Short-term intermittent hypoxia (IH) is common in patients with acute respiratory disorders. Although prolonged exposure to hypoxia induces atrophy and increased fatigability of skeletal muscle, the response to short-term IH is less well known. We hypothesized that the diaphragm and limb
Atrophy, hypertrophy, and hypoxemia induce transcriptional regulators of the ubiquitin proteasome system in the rat heart.
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BACKGROUND
In skeletal muscle, transcript levels of proteins regulating the ubiquitin proteasome system (UPS) increase with atrophy and decrease with hypertrophy. Whether the same is true for heart muscle is not known.
OBJECTIVE
We set out to characterize the transcriptional profile of regulators of
The effect of systemic hyperoxia and hypoxia on scotopic thresholds in people with early and intermediate age-related macular degeneration.
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PurposeMorphological retinal changes combined with functional evidence implicate hypoxia in the pathogenesis of age-related macular degeneration (AMD). However, the role of hypoxia in the scotopic threshold deficit reported in AMD has not been investigated. This study compared scotopic thresholds in
Attenuation of heart rate control and neural degeneration in nucleus ambiguus following chronic intermittent hypoxia in young adult Fischer 344 rats.
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Chronic intermittent hypoxia (CIH) attenuates baroreflex control of heart rate (HR). In this study, we assessed whether CIH exposure reduced nucleus ambiguus (NA) control of HR and induced neural degeneration in the NA. Fischer 344 (age: 3-4 months) rats were exposed to either room air (RA:
Delayed neurologic deterioration following anoxia: brain mitochondrial and metabolic correlates.
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Hyper- but not normoglycemic cats exposed to 8 min of anoxia show neurologic signs (fasciculations, myoclonic jerks, seizures) that develop after a symptom-free period. We examined brain mitochondrial function and metabolite concentrations at 0, 1, 3, and 5 h following exposure to anoxia, to
Immobilization-induced cartilage degeneration mediated through expression of hypoxia-inducible factor-1alpha, vascular endothelial growth factor, and chondromodulin-I.
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Immobilization results in thinning of the articular cartilage and cartilage degeneration, although the exact mechanisms are not clear yet. Hypoxia is thought to contribute to the degeneration of articular cartilage. We investigated the roles of hypoxia inducible factor (HIF)-1alpha, vascular
Prostatic atrophy: immunohistochemical study of hypoxia induced factors.
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BACKGROUND
There is evidence that chronic local ischemia may be one possible etiology of prostatic atrophy (PA). Our aim was to study the expression of hypoxia induced factors in areas of PA.
METHODS
The immunohistochemical expression of hypoxia-inducible factor-1 alpha (HIF-1) and vascular
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