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Using microarray technology, we investigated whether the gene expression profile in white blood cells could be used as a fingerprint of different disease states. Adult rats were subjected to ischemic strokes, hemorrhagic strokes, sham surgeries, kainate-induced seizures, hypoxia, or insulin-induced
The Goal: The aim of the study was to investigate whether stroke volume or the presence of ischemic stroke lesion on follow-up computed tomography 1 day after admission had association with sleep apnea among ischemic stroke patients undergoing Stroke-prone spontaneously hypertensive rats (SHRSP) is a valuable animal model to investigate human strokes. SHRSP Izumo strain (Izm) neurons are highly sensitive to blood supply changes. Furthermore, SHRSP/Izm astrocytes show various abnormalities upon hypoxic stimulation compared to control
The myocardium is well protected against chronic hypoxia. In chronic hypoxia stroke volume falls both at rest and on exercise. The fall in stroke volume is associated with reduction in left ventricular dimensions and filling pressure. An obvious explanation for this is the reduction in plasma volume
OBJECTIVE
Patients who have had a stroke are at risk of hypoxia through alterations in the central regulation of respiration, through aspiration, and through respiratory muscle weakness. Sleep-related breathing disorders are common and may lead to episodes of nocturnal hypoxia even when daytime
BACKGROUND
Sleep disorders and nocturnal hypoxia are common in patients with cerebrovascular disease. Sleep-disordered breathing is associated with a poor functional outcome in stroke patients.
OBJECTIVE
We investigated the relationship between nocturnal hypoxia and functional outcome in the
We studied the level of blood oxygen saturation (SpO2) in the brain in newborn rats in the pre- and post-stroke periods, as well as the changes in cerebral blood flow and beta-arrestin-1 as a marker of hypoxic stress. Our results show that mild hypoxia precedes the stroke development and is
The role of generalized hypoxia-ischemia in the genesis of perinatal focal arterial stroke remains puzzling. Animal studies have demonstrated that hypoxia-ischemia may alter blood flow through the ductus venosus, thereby increasing the risk for placental emboli entering the cerebral circulation. A
Hypoxia produced by intravenous infusion of gaseous carbon dioxide was associated in conscious rabbits with decreases in cardiac output and stroke volume. At the same time the arterial blood pressure, oxygen uptake and blood pH decreased, whereas carbon dioxide pressure and lactate level in the
Collateral density variations are a major determinant of stroke outcome. Here, we explored the association of missense variants in hypoxia-induced VEGFA/VEGFR2 signaling and stroke outcome. We recruited 683 large artery atherosclerotic (LAA) stroke patients as the training set from Nanjing Stroke
To reduce side effects due to non-specific expression, the heme oxygenase-1 (HO-1) gene under control of a hypoxia-inducible erythropoietin (Epo) enhancer (pEpo-SV-HO-1) was developed for site-specific gene therapy of ischemic stroke.
pEpo-SV-HO-1 was constructed by insertion of the Epo enhancer
Pial collaterals provide protection in stroke. Evidence suggests their formation late during gestation (collaterogenesis) is driven by reduced oxygen levels in the cerebral watersheds. The purpose of this study was to determine if collaterogenesis can be re-activated in the adult to induce formation
Purpose: The hemodynamic consequences of exercise in hypoxia have not been completely investigated. The present investigation aimed at studying the hemodynamic effects of contemporary normobaric hypoxia and metaboreflex
The effects of lytic stroke therapy in patients with sickle cell anemia are unknown, although a recent study suggested that coexistent sickle cell anemia does not increase the risk of cerebral hemorrhage. This finding calls for systemic analysis of the effects of thrombolytic stroke therapy, first
Stroke is a leading cause of death, disability, and socioeconomic loss worldwide. All attempts at pharmacological reduction of the complications of stroke (e.g. post-stroke seizure, and brain׳s vulnerability to hypoxic/ischemic injury) have failed. Endogenous opioids and nitric oxide (NO)