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Heat shock protein 70 protects PC12 cells against ischemia-hypoxia/reoxygenation by maintaining intracellular Ca(2+) homeostasis.
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Heat shock protein 70 (HSP70) maintains Ca(2+) homeostasis in PC12 cells, which may protect against apoptosis; however, the mechanisms of neuroprotection are unclear. Therefore, in this study, we examined Ca(2+) levels in PC12 cells transfected with an exogenous lentiviral HSP70 gene expression
Heterogeneities of regional cerebral blood flow during hypoxia-ischemia in the rat.
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The distribution of regional cerebral blood flow (rCBF) within the cerebral hemispheres of rats was investigated following an hypoxic-ischemic insult consisting of a 30-minute exposure to 6.5% to 7% inspired oxygen coupled with unilateral ligation of the common carotid artery and maintenance of
DRAM is Involved in Hypoxia/Ischemia-Induced Autophagic Apoptosis in Hepatocytes.
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Liver hypoxia/ischemia injury leads to acute liver injury, delayed graft dysfunction, and failure during liver transplantation. Previous studies showed that autophagy is involved in liver hypoxia/ischemia injury. Our and others' studies have found that the damage-regulated autophagy modulator (DRAM)
Altered astrocyte-neuronal interactions after hypoxia-ischemia in the neonatal brain in female and male rats.
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OBJECTIVE
Increased susceptibility to excitotoxicity of the neonatal brain after hypoxia-ischemia (HI) may be caused by limited capacity of astrocytes for glutamate uptake, and mitochondrial failure probably plays a key role in the delayed injury cascade. Male infants have poorer outcome than
Galantamine administration reduces reactive astrogliosis and upregulates the anti-oxidant enzyme catalase in rats submitted to neonatal hypoxia ischemia.
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Neonatal hypoxia ischemia (HI) plays a role in the etiology of several neurological pathologies and causes severe sequelae. Acetylcholine is a neurotransmitter in the central nervous system and cholinesterase inhibitors have demonstrated a positive action over HI induced deficits. In order to
Glucose and Intermediary Metabolism and Astrocyte-Neuron Interactions Following Neonatal Hypoxia-Ischemia in Rat.
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Neonatal hypoxia-ischemia (HI) and the delayed injury cascade that follows involve excitotoxicity, oxidative stress and mitochondrial failure. The susceptibility to excitotoxicity of the neonatal brain may be related to the capacity of astrocytes for glutamate uptake. Furthermore, the neonatal brain
Early biochemical effects after unilateral hypoxia-ischemia in the immature rat brain.
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Perinatal hypoxia-ischemia (HI) gives rise to inadequate substrate supply to the brain tissue, resulting in damage to neural cells. Previous studies at different time points of development, and with different animal species, suggest that the HI insult causes oxidative damage and changes Na+,
Connexin 43 and ATP-sensitive potassium channels crosstalk: a missing link in hypoxia/ischemia stress.
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Connexin 43 (Cx43) is a gap junction protein expressed in various tissues and organs of vertebrates. Besides functioning as a gap junction, Cx43 also regulates diverse cellular processes like cell growth and differentiation, cell migration, cell survival, etc. Cx43 is critical for normal cardiac
Hypoxia-ischaemia is involved in the pathogenesis of vulvar lichen sclerosus.
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BACKGROUND
Lichen sclerosus (LS) is a chronic inflammatory skin disease, the pathogenesis of which is poorly understood.
OBJECTIVE
To evaluate the role of hypoxia-ischaemia (HI) in vulvar LS.
METHODS
Samples from five patients with vulvar LS and five control subjects were collected for analysis by
Micro-electrode measurement of skin pH in humans during ischaemia, hypoxia and local hypothermia.
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1. The extracellular pH value in the dermis of human skin (skin pH) was measured in vivo using glass micro-electrodes. They were found to be both reliable and accurate. 2. The mean value of skin pH measured in the legs of forty different volunteers was found to be pH 7.54 +/- 0.09 (S.D.). No
[Changes of hypothalamus and peripheral orphanin in fetal rats with intrauterine ischemia and hypoxia].
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OBJECTIVE
To evaluate the role of orphanin in the perinatal ischemia-hypoxia.
METHODS
The concentration of hypothalamus and peripheral orphanin were measured by radioimmunoassay. Animal model of perinatal ischemia-hypoxia was set up by ligating uterine vessels. All the rats were delivered by
[Early expression of hypoxia-inducible factor-1 alpha after acute myocardial ischemia in rats].
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OBJECTIVE
To observe the changes of hypoxia-inducible factor-1 alpha (HIF-1alpha), the expression in the early stage (within 6 h) of acute myocardial ischemia and to explore the potential forensic application.
METHODS
SD rats were randomly divided into one control group, one sham operation group and
Hypoxia-ischemia-induced apoptotic cell death correlates with IGF-I mRNA decrease in neonatal rat brain.
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Hypoxia-ischemia induces apoptotic and necrotic cell death, which results partially from persistent alterations in cellular energy homeostasis. Insulin-like growth factor I (IGF-I) is an anabolic pleiotrophic factor required by developing neurons for their optimal proliferation, differentiation, and
Glial fibrillary acidic protein immunohistochemistry of spinal cord astrocytes after induction of ischemia or anoxia in culture.
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The effects of ischemia (removal of oxygen and glucose for 4 h) and anoxia (removal of oxygen alone) on astrocytes were studied in dissociated cultures of E14 spinal cord containing both neurons and astrocytes. In addition, a group of cultures was treated with a low Na+, low Ca2+, and high K+ medium
Functional integrity of proximal tubule cells. Effects of hypoxia and ischemia.
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Effects of warm hypoxia and ischemia on electrophysiologic properties of isolated perfused mouse proximal straight tubules were studied. Oxyrase (5 to 10 microliters/mL) was added to the hypoxic and ischemic solutions to lower the oxygen tension to 5 mm Hg. The ischemic solution also simulated
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