embolism/tyrosine

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Inhibition of nitric oxide production and protein tyrosine nitration contribute to neuroprotection by a novel calmodulin antagonist, DY-9760e, in the rat microsphere embolism.

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Microsphere embolism (ME)-induced ischemia model in rat resembles to multiple brain embolism in human with several clinical features. We here tested whether nitric oxide (NO) production contributes to the neuronal injury in the ME model. A novel calmodulin antagonist, DY-9760e, having a potent

Effect of cerebrospinal fluid removal on cerebral blood flow and metabolism in the baboon: influence of tyrosine infusion and cerebral embolism on cerebrospinal fluid pressure autoregulation.

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Cerebral blood flow (CBF) and metabolism were measured before and after withdrawal of 5 to 6 ml of cerebrospinal fluid (CSF) in 17 baboons. The measurements were made before and after infusion of tyrosine, the precursor amino acid of the putative neurotransmitters, dopamine and norepinephrine, in

Accumulation of beta-amyloid in the brain microvessels accompanies increased hyperphosphorylated tau proteins following microsphere embolism in aged rats.

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To define mechanisms underlying neurovascular injury following brain embolism-induced neurodegeneration, we investigated temporal and spatial pathological changes in brain microvessels up to 12 weeks after microsphere embolism (ME) induction in aged male rats. Mild ME upregulated endothelial nitric

Effects of delayed treatment with nafronyl oxalate on microsphere embolism-induced changes in monoamine levels of rat brain regions.

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1. The present study was undertaken to examine the effects of delayed treatment with nafronyl oxalate (nafronyl), a cerebral vasodilator, on monoamine neurotransmitters of brain regions in the microsphere-embolized rat. 2. Microsphere embolism was induced by injecting 900 microspheres with a

Microsphere embolism-induced endothelial nitric oxide synthase expression mediates disruption of the blood-brain barrier in rat brain.

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Microsphere embolism (ME)-induced up-regulation of endothelial nitric oxide synthase (eNOS) in endothelial cells of brain microvessels was observed 2-48 h after ischemia. eNOS induction preceded disruption of the blood-brain barrier (BBB) observed 6-72 h after ischemia. In vascular endothelial

Pulmonary embolism with haemorrhagic pericardial effusion and tamponade: a clinical dilemma.

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The synchronous presentation of a patient with pulmonary embolism (PE) and haemorrhagic cardiac tamponade is uncommon and presents a therapeutic dilemma. Both conditions can be life-threatening and require opposing management strategies. The authors report a 50-year-old woman who presented with

Potential role of sympathetic activity on the pathogenesis of massive pulmonary embolism with circulatory shock in rabbits.

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We recently showed that intravenous sodium nitroprusside treatment (SNP) could relieve the pulmonary vasospasm of pulmonary embolism (PE) and non-pulmonary embolism (non-PE) regions in a rabbit massive pulmonary embolism (MPE) model associated with shock. The present study explored the

Is there truly an increase in risk of cardiovascular and hematological adverse events with vascular endothelial growth factor receptor tyrosine kinase inhibitors?

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Objectives: Recent studies have shown an increase risk of cardiovascular and hematological adverse events associated with vascular endothelial growth factor tyrosine kinase inhibitors (VEGF-TKIs). The authors hypothesize that the original studies may have produced exaggerated results because

[Brain embolism-induced injury of vascular endothelial cells and a novel vasoprotective drug].

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Microsphere embolism-induced up-regulation of endothelial nitric oxide synthase (eNOS) in endothelial cells of brain microvessels was found after brain ischemia. The eNOS induction preceded disruption of the blood-brain barrier following ischemia. In vascular endothelial cells, microsphere

Cerebral ischemia enhances tyrosine phosphorylation of occludin in brain capillaries.

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Cerebral ischemia induces disruption of the blood-brain barrier (BBB), and this disruption can initiate the development of brain injuries. Although the molecular structure of tight junctional complexes in the BBB has been identified, little is known about alterations of tight junctional proteins

Src tyrosine kinase inhibition prevents pulmonary ischemia-reperfusion-induced acute lung injury.

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OBJECTIVE Pulmonary ischemia-reperfusion is a pathological process seen in several clinical conditions, including lung transplantation, cardiopulmonary bypass, resuscitation for circulatory arrest, atherosclerosis, and pulmonary embolism. A better understanding of its molecular mechanisms is very

Changes in striatal dopamine metabolism after microsphere embolism in rats.

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OBJECTIVE Dopamine plays an important role in striatal function. The present study was undertaken to elucidate the pathophysiological changes in striatal dopamine metabolism after microsphere embolism. METHODS Microspheres (48 microns) were injected into the right internal carotid artery of rats.

Chronic Embolic Pulmonary Hypertension Caused by Pulmonary Embolism and Vascular Endothelial Growth Factor Inhibition.

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Our understanding of the pathophysiological basis of chronic thromboembolic pulmonary hypertension (CTEPH) will be accelerated by an animal model that replicates the phenotype of human CTEPH. Sprague-Dawley rats were administered a combination of a single dose each of plastic microspheres and

Risk of fatal pulmonary events in patients with advanced non-small-cell lung cancer treated with EGF receptor tyrosine kinase inhibitors: a comparative meta-analysis.

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We performed a meta-analysis of fatal pulmonary events associated with erlotinib, gefitinib or afatinib in patients with non-small-cell lung cancer (NSCLC). Eligible studies included randomized trials of patients with NSCLC on the three drugs describing events of high-grade pulmonary events. The

Second-line dovitinib (TKI258) in patients with FGFR2-mutated or FGFR2-non-mutated advanced or metastatic endometrial cancer: a non-randomised, open-label, two-group, two-stage, phase 2 study.

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BACKGROUND Activating FGFR2 mutations are found in 10-16% of primary endometrial cancers and provide an opportunity for targeted therapy. We assessed the safety and activity of dovitinib, a potent tyrosine-kinase inhibitor of fibroblast growth factor receptors, VEGF receptors, PDGFR-β, and c-KIT, as

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