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oxidase/accident vascular cerebral
L'enllaç es desa al porta-retalls
Pàgina 1 des de 730 resultats
NADPH oxidase in stroke and cerebrovascular disease.
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Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) was originally identified in immune cells as playing an important microbicidal role. In stroke and cerebrovascular disease, inflammation is increasingly being recognized as contributing negatively to neurological outcome, with NOX as
NADPH oxidases as therapeutic targets in ischemic stroke.
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Reactive oxygen species (ROS) act physiologically as signaling molecules. In pathological conditions, such as ischemic stroke, ROS are released in excessive amounts and upon reperfusion exceed the body's antioxidant detoxifying capacity. This process leads to brain tissue damage during
Possible therapeutic effect of T-794, a novel reversible inhibitor of monoamine oxidase-A, on post-stroke emotional disturbances, assessed in animal models of depression.
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Emotional disturbances, such as lack of motivation or depression, are common after stroke. The drugs mainly used to treat these syndromes in Japan are the cerebral metabolic enhancers whose biochemical and pharmacological profiles are similar to those of antidepressant drugs. In order to examine the
[State of serotonin--monoamine oxidase and histamine--diamine oxidase systems in circulating blood in ischemic strokes].
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The serotonin-monoamine oxidase and histamine-diamine oxidase systems in the arteria and venous blood of the brain were examined in 65 patients with ischemic cerebral stroke. The examinations have shown that in the acute period of the disease the metabolism of serotonin and histamine is disturbed,
[Role of semicarbazide-sensitive amine oxidase in disturbances of endogenic detoxication in ischemic stroke patients].
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Oxidative stress is a pathogenetic factor of ischemic stroke. Enhancement in the activity of one of xenobiotic transformation enzymes and biogenic amines (serum semicarbazide-sensitive amine oxidase (SSAO)) leads to the higher production of secondary toxins stimulating oxidative stress. We studied
Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic stroke.
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Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multisubunit enzyme complex that utilizes nicotinamide adenine dinucleotide phosphate to produce superoxide anions and other reactive oxygen species. Under normal circumstances, reactive oxygen species mediate a number of important
High Expression Levels of NADPH Oxidase 3 in the Cerebrum of Ten-Week-Old Stroke-Prone Spontaneously Hypertensive Rats.
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We previously demonstrated that the high levels of oxidative stress in the brains of ten-week-old stroke-prone hypertensive rats (SHRSP) were attributable to intrinsic, not extrinsic factors (Biol. Pharm. Bull., 33, 2010, Michihara et al.). The aim of the present study was to determine whether
The 1027th target candidate in stroke: Will NADPH oxidase hold up?
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As recently reviewed, 1026 neuroprotective drug candidates in stroke research have all failed on their road towards validation and clinical translation, reasons being quality issues in preclinical research and publication bias. Quality control guidelines for preclinical stroke studies have now been
Decreased monoamine oxidase activity in stroke-prone spontaneously hypertensive rat kidneys.
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The present study was undertaken to measure kidney monoamine oxidase activity (MAO) isolated from three different rat groups: Wistar Kyoto rats (WKY), stroke-free cases of stroke-prone spontaneously hypertensive rats (SHRSP-control) and SHRSP-stroke cases (SHRSP-stroke). The SHRSP group was found to
Stroke-like episodes in autosomal recessive cytochrome oxidase deficiency.
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Stroke-like episodes, defined as periods of acute localized neurological dysfunction during which brain imagery suggests cerebral ischemia but vascular anatomy is normal, occurred in 3 patients with autosomal recessive Saguenay-Lac St-Jean (SLSJ) cytochrome oxidase (COX) deficiency. The patients
Change in platelet monoamine oxidase activity in the acutest period of ischemic stroke is associated with the degree of neurological recovery.
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We studied monoamine oxidase activity (MAO) in platelets of patients in the acute period of ischemic stroke. Neurological deficit was evaluated by the data of clinical examinations and scales. In 80% patients MAO activity was considerably increased on 3-5 day after stroke. We found a correlation
Retraction statement: Dynamics of Cytochrome C Oxidase Activity in Acute Ischemic Stroke' by Selaković, V.M., Jovanović, M.D., Mihajlović, R.R. and Radenović, L.L.J.
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The above article from Acta Neurologica Scandinavica, published online on 7 April 2005 in Wiley Online Library (wileyonlinelibrary.com) and in Volume 111, pp. 329-332, has been retracted by agreement between the journal Editor in Chief, Professor Elinor Ben-Menachem, and John Wiley & Sons Ltd. The
Metabolic stroke in a late-onset form of isolated sulfite oxidase deficiency.
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We report the first case of late-onset isolated sulfite oxidase deficiency (ISOD) presenting with a stroke-like episode. Clinical, biochemical and neuroradiological features at diagnosis and during follow-up after dietary treatment intervention are described. Furthermore, pathogenic mechanisms
Lysyl oxidase polymorphisms and ischemic stroke--a case control study.
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Ischemic stroke is a common neurological disease and causes severe disability and death worldwide. Lysyl oxidase (LOX) plays a crucial role in the maintenance of extracellular matrix stability and may participate in vascular remodeling in the development of ischemic stroke. The objective of this
Xanthine oxidase inhibition for the improvement of long-term outcomes following ischaemic stroke and transient ischaemic attack (XILO-FIST) - Protocol for a randomised double blind placebo-controlled clinical trial.
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UNASSIGNED
Allopurinol, a xanthine oxidase inhibitor, reduced progression of carotid-intima media thickness and lowered blood pressure in a small clinical trial in people with ischaemic stroke. Xanthine oxidase inhibition for improvement of long-term outcomes following ischaemic stroke and transient
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