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3 beta galactosidase/мозочен удар
Врската е зачувана во таблата со исечоци
Страница 1 од 34 резултати
Update on hereditary, autosomal dominant cathepsin-A-related arteriopathy with strokes and leukoencephalopathy (CARASAL).
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Cathepsin-A-related arteriopathy with strokes and leukoencephalopathy (CARASAL) is an acronym that describes an ultra-rare, hereditary, cerebral small vessel disease. The aim is to summarize current knowledge and recent findings concerning phenotype, genotype, pathogenesis, diagnoses, and treatment
Analysis of optic nerve stroke by retinal Bex expression.
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OBJECTIVE
Few proteins are known to be selectively expressed in retinal ganglion cells (RGCs), the neurons directly affected by optic nerve stroke and glaucoma. In addition, subsets of RGCs are reported to project to various CNS areas via the retinohypothalamic pathway in rodents and primates. Many
Inhibition of oxidative stress in rostral ventrolateral medulla improves impaired baroreflex sensitivity in stroke-prone spontaneously hypertensive rats.
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Reactive oxygen species (ROS) in rostral ventrolateral medulla (RVLM) of brainstem contribute to sympathoexcitation and are critically involved in the pathogenesis of hypertension. Baroreflex sensitivity (BRS) is a valuable prognostic parameter of the autonomic nervous system, and is impaired in
Impact of elastin-derived VGVAPG peptide on bidirectional interaction between peroxisome proliferator-activated receptor gamma (Pparγ) and beta-galactosidase (β-Gal) expression in mouse cortical astrocytes in vitro.
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The process of degradation of the elastin-rich extracellular matrix produces elastin-derived peptides (EDPs). Different types of EDPs are detectable in the cerebrospinal fluid in healthy individuals and in patients after ischemic stroke. To date, it has been demonstrated that EDPs can regulate the
Intravenously Transplanted Human Bone Marrow Endothelial Progenitor Cells Engraft Within Brain Capillaries, Preserve Mitochondrial Morphology, and Display Pinocytotic Activity Toward Blood-Brain Barrier Repair in Ischemic Stroke Rats.
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Stroke is a life-threatening disease with limited therapeutic options. Cell therapy has emerged as an experimental stroke treatment. Blood-brain barrier (BBB) impairment is a key pathological manifestation of ischemic stroke, and barrier repair is an innovative target for neurorestoration in stroke.
Cardiovascular effects of overexpression of endothelial nitric oxide synthase in the rostral ventrolateral medulla in stroke-prone spontaneously hypertensive rats.
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We have previously demonstrated that the overexpression of endothelial NO synthase (eNOS) in the rostral ventrolateral medulla (RVLM) decreases blood pressure, heart rate, and sympathetic nerve activity via an increase in gamma-amino butyric acid release in normotensive Wistar-Kyoto rats (WKY).
Serum-mediated Activation of Bone Marrow-derived Mesenchymal Stem Cells in Ischemic Stroke Patients: A Novel Preconditioning Method.
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Stroke induces complex and dynamic, local and systemic changes including inflammatory reactions, immune responses, and repair and recovery processes. Mesenchymal stem cells (MSCs) have been shown to enhance neurological recovery after stroke. We hypothesized that serum factors play a critical role
Poly(ADP-ribose) polymerase impairs early and long-term experimental stroke recovery.
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OBJECTIVE
Poly(ADP-ribose) polymerase (PARP-1; Enzyme Commission 2.4.30) is a nuclear DNA repair enzyme that mediates early neuronal ischemic injury. Using novel 3-dimensional, fast spin-echo-based diffusion-weighted imaging, we compared acute (21 hours) and long-term (3 days) ischemic volume after
Brain transplantation of immortalized human neural stem cells promotes functional recovery in mouse intracerebral hemorrhage stroke model.
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We have generated stable, immortalized cell lines of human NSCs from primary human fetal telencephalon cultures via a retroviral vector encoding v-myc. HB1.F3, one of the human NSC lines, expresses a normal human karyotype of 46, XX, and nestin, a cell type-specific marker for NSCs. F3 has the
Postacute ischemia vascular endothelial growth factor transfer by transferrin-targeted liposomes attenuates ischemic brain injury after experimental stroke in rats.
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Our objective was to achieve the enhanced delivery of vascular endothelial growth factor (VEGF) to ischemically disordered brain through transferrin-coupled liposomes (Tf-PLs) via intravenous administration, and to observe the effect of Tf-VEGF-PLs on ischemic brain neuroprotection and angiogenesis.
Attenuation of stroke size in rats using an adenoviral vector to induce overexpression of interleukin-1 receptor antagonist in brain.
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Adenoviruses have been proposed as potential vectors for gene therapy in the central nervous system, but there are no reports of their use in the treatment of a brain disease. Because central administration of interleukin-1 receptor antagonist protein (IL-1ra) reduces ischemic brain damage, we
NF-kappaB protects neurons from ischemic injury after middle cerebral artery occlusion in mice.
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Knowledge about the molecular mechanisms of neuronal survival following ischemia is crucial to the development of therapeutic interventions for victims of stroke. Previous research in our laboratory has implicated nuclear factor-kappaB (NF-kappaB) as contributing to neuronal survival in response to
Adenovirus-mediated gene transfer to cerebral circulation.
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Gene therapy may, be a promising approach for treatment of cerebrovascular disease. An adenoviral vector encoding beta-galactosidase was administered intracisternally or intraventricularly into the brain of rats. Efficient expression of the reporter gene was observed at the cerebral blood vessels
Calbindin d28k overexpression protects striatal neurons from transient focal cerebral ischemia.
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OBJECTIVE
Increased intracellular calcium accumulation is known to potentiate ischemic injury. Whether endogenous calcium-binding proteins can attenuate this injury has not been clearly established, and existing data are conflicting. Calbindin D28K (CaBP) is one such intracellular calcium buffer. We
Comparison of developmental endothelial locus-1 angiogenic factor with vascular endothelial growth factor in a porcine model of cardiac ischemia.
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BACKGROUND
This study compared the angiogenic effects of developmental endothelial locus-1 (DEL-1), vascular endothelial growth factor (VEGF), as well as the negative control, beta-galactosidase (beta-gal), in a porcine model of cardiac ischemia.
METHODS
Twenty pigs underwent left circumflex artery
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