toluidine/infarction

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Glyceraldehyde-3-phosphate dehydrogenase versus toluidine blue as a marker for infarct volume estimation following permanent middle cerebral artery occlusion in mice.

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Infarct size is a good predictor of the neurological outcome following stroke. Estimation of infarct size in the early phase following experimental stroke depends on the availability of reliable techniques that can distinguish ischemic from nonischemic tissue. The objective of this study was to

Systemic mast cell disease with splenic infarction: a case report.

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An autopsy case of systemic mast cell disease (SMCD) without primary skin lesions in a 57-year-old Japanese male is described. Initially the patient was suspected of having liver cirrhosis or malignant lymphoma because of hepatomegaly and lymph node enlargement on admission. However, a lymph node

Effects of ketamine-midazolam anesthesia on the expression of NMDA and AMPA receptor subunit in the peri-infarction of rat brain.

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BACKGROUND Activation of N-methyl-D-aspartate (NMDA) receptors and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors play an important role in the neurons death induced by ischemia. The mitigating effect of intravenous anesthetics on ischemic neuron injury is related to

PKCβII inhibition attenuates myocardial infarction induced heart failure and is associated with a reduction of fibrosis and pro-inflammatory responses.

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Protein kinase C βII (PKCβII) levels increase in the myocardium of patients with end-stage heart failure (HF). Also targeted overexpression of PKCβII in the myocardium of mice leads to dilated cardiomyopathy associated with inflammation, fibrosis and myocardial dysfunction. These reports suggest a

Identification of mast cells in the cellular response to myocardial infarction.

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Myocardial infarction is associated with an acute inflammatory response, leading to replacement of injured cardiomyocytes with granulation tissue. Mast cells are actively involved in postinfarction inflammation by releasing histamine and tumor necrosis factor-alpha, triggering a cytokine cascade.

An ultrastructural study of cardiac myocytes in postmyocardial infarction ventricular aneurysm representative of chronic ischemic myocardium using semiquantitative and quantitative assessment.

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To elucidate the characteristic myocytic changes in chronic ischemic myocardium, an electronmicroscopic (EM) study was carried out in surgically excised postmyocardial infarction left ventricular aneurysm (LVAN) (n = 15) using semiquantitative (in all 15 cases) and quantitative assessment methods

An assessment of the extent and distribution of experimentally induced cerebral atheroembolic vascular occlusions and infarcts.

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Certain types of stroke, TIAs and Amaurosis Fugax can result from atheroembolism from the Carotid bifurcation. This study was undertaken to establish qualitative and quantitative baseline criteria in an animal model for future studies evaluating the effectiveness of thrombolytic and cholesterol

Participation of mast cells in angiogenesis in the border zone of myocardial infarction in rats.

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BACKGROUND We hypothesized that mast cells may participate in coronary angiogenesis in acute myocardial infarction, contributing to myocardial salvage. METHODS The left coronary artery was occluded in control (n = 30) and Ws rats (n = 30), which genetically lacked c-kit, resulting in a mast cell

Influence of EGF/bFGF treatment on proliferation, early neurogenesis and infarct volume after transient focal ischemia.

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The persistence of neurogenesis in the adult mammalian forebrain suggests that endogenous precursors may be a potential source for neuronal replacement after injury or neurodegeneration. On the other hand basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) can facilitate neural

Human embryonic neural stem cell transplantation increases subventricular zone cell proliferation and promotes peri-infarct angiogenesis after focal cerebral ischemia.

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Neurogenesis and angiogenesis are two important processes that may contribute to the repair of brain injury after stroke. This study was designed to investigate whether transplantation of human embryonic neural stem cells (NSCs) into cortical peri-infarction 24h after ischemia effects cell

[Cerebrospinal fluid glucose, lactate and pyruvate concentration in patients with cerebral infarction after intravenous glucose loading test].

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The determinations of the above substances were done in the blood and CSF of 27 patients with cerebral infarction and 10 controls. The glucose level was determined in the blood and CSF and lactate and pyruvate levels in the CSF before and in the 8th and 16th minutes after a glucose load. The

Transmural changes in mast cell density in rat heart after infarct induction in vivo.

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The cardiac distribution of mast cells was investigated after the induction of acute myocardial infarction in the rat. The left anterior descending coronary artery (LAD) was occluded by ligation in the infarct group, whereas in sham rats only a superficial ligature was placed beside the LAD. Rats of

Detection of secondary thalamic degeneration after cortical infarction using cis-4-18F-fluoro-D-proline.

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The amino acid cis-4-(18)F-fluoro-D-proline (D-cis-(18)F-FPro) exhibits preferential uptake in the brain compared with its L-isomer, but the clinical potential of the tracer is as yet unknown. In this study we explored the cerebral uptake of D-cis-(18)F-FPro in rats with focal cortical

Alterations in the spinal cord and ventral root after cerebral infarction in non-human primates.

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BACKGROUND Cerebral infarction does not only cause focal injury in the ischemic site, but also secondary non-ischemic damage at the remote areas of nervous system associated with the primary focus. OBJECTIVE This study investigated the changes in the spinal cord and ventral root after middle

Effects of prolonged administration of oxprenolol on severity of ischaemic arrhythmias, enzyme leakage, infarct size, and intracellular cardiac muscle action potentials.

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We examined the effects of prolonged oral administration of oxprenolol (twice daily for 6 weeks) to male Sprague-Dawley rats. At two times (1 or 16-18 h) after the last oral dose, the rats were anaesthetised and subjected to acute coronary artery ligation, and the severity of the resulting

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