phosphorylase/stroke

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New biomarker for acute ischaemic stroke: plasma glycogen phosphorylase isoenzyme BB.

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BACKGROUND Glycogen phosphorylase is the key enzyme that breaks down glycogen to yield glucose-1-phosphate in order to restore depleted energy stores during cerebral ischaemia. We sought to determine whether plasma levels of glycogen phosphorylase BB (GPBB) isoform increased in patients with acute

Stroke in purine nucleoside phosphorylase deficiency.

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The first documented case of cerebrovascular disease occurring in a 13-year-old girl with purine nucleoside phosphorylase deficiency is reported. This patient, the oldest known survivor with purine nucleoside phosphorylase deficiency, had previously experienced multiple sequential neurologic

[Electron histochemical study of phosphorylase in the retina and choroid of stroke-prone spontaneously hypertensive rats (SHRSP) (author's transl)].

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MTAP gene is associated with ischemic stroke in Chinese Hans.

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Common pathogenic mechanisms may be involved in the prevalence of ischemic stroke and coronary heart disease. Recently, genome-wide association (GWA) studies identified a chromosome region (9p21) that confers the risk of coronary heart disease. In a hospital-based case-control study conducted in

Thymidine phosphorylase: A potential new target for treating cardiovascular disease.

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We recently found that thymidine phosphorylase (TYMP), also known as platelet-derived endothelial cell growth factor, plays an important role in platelet activation in vitro and thrombosis in vivo by participating in multiple signaling pathways. Platelets are a major source of TYMP. Since

Gene expression in blood changes rapidly in neutrophils and monocytes after ischemic stroke in humans: a microarray study.

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Ischemic brain and peripheral white blood cells release cytokines, chemokines and other molecules that activate the peripheral white blood cells after stroke. To assess gene expression in these peripheral white blood cells, whole blood was examined using oligonucleotide microarrays in 15 patients at

Molecular basis of impaired glycogen metabolism during ischemic stroke and hypoxia.

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BACKGROUND Ischemic stroke is the combinatorial effect of many pathological processes including the loss of energy supplies, excessive intracellular calcium accumulation, oxidative stress, and inflammatory responses. The brain's ability to maintain energy demand through this process involves

Glycogenolysis Is Crucial for Astrocytic Glycogen Accumulation and Brain Damage after Reperfusion in Ischemic Stroke

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Astrocytic glycogen is an important energy reserve in the brain and is believed to supply fuel during energy crisis. However, the pattern of glycogen metabolism in ischemic stroke and its potential therapeutic impact on neurological outcomes are still unknown. Here, we found extensive brain glycogen

Role of cardiac work in regulating myocardial biochemical characteristics.

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The purpose of this study was to determine the extent to which functional demand regulates the biochemical character and enzyme capacities of the rat myocardium. Hearts from donor rats were heterotopically transplanted onto the abdominal aorta and inferior vena cava of isogenic recipients. The

[Clinical and biochemical analysis of 27 patients with myoglobinuria of unknown causes].

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We examined the clinical and biochemical features of 27 cases with acute myoglobinuria who had been suspected of having metabolic myopathies. The systematic biochemical studies included the measurements of 13 glycolytic enzymes, mitochondrial respiratory chain enzymes, carnitine palmitoyltransferase

Mitochondrial syndromes with leukoencephalopathies.

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White matter involvement has recently been recognized as a common feature in patients with multisystem mitochondrial disorders that may be caused by molecular defects in either the mitochondrial genome or the nuclear genes. It was first realized in classical mitochondrial syndromes associated with

Paralytic ileus in MELAS with phenotypic features of MNGIE.

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This report describes a child having the syndrome of overlapping phenotypic features of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) and mitochondrial neurogastrointestinal encephalopathy syndrome (MNGIE). Mitochondrial DNA analysis revealed a point

Purine uptake and release in rat C6 glioma cells: nucleoside transport and purine metabolism under ATP-depleting conditions.

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Adenosine, through activation of membrane-bound receptors, has been reported to have neuroprotective properties during strokes or seizures. The role of astrocytes in regulating brain interstitial adenosine levels has not been clearly defined. We have determined the nucleoside transporters present in

Catalpol Enhances Neurogenesis And Inhibits Apoptosis Of New Neurons Via BDNF, But Not The BDNF/Trkb Pathway.

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The role of catalpol in brain neurogenesis and newborn neuron survival has not been previously determined in permanent middle cerebral artery occlusion (pMCAO).Fifty-four rats were divided into 6 groups: pMCAO (model, n=9); sham operation (NS, n=9);

Adenosine produced by neurons is metabolized to hypoxanthine by astrocytes.

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Adenosine (ADO) is an important neuromodulator in brain. During pathophysiological events such as stroke or brain trauma, ADO levels can increase up to 100-fold. We tested the hypothesis that astrocytes are important for the removal of ADO produced by neurons and for the metabolism of ADO to inosine

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