Vascular dysfunction in a murine model of severe hemolysis. - Wikidata - awgldk - TriplyDB

Vascular dysfunction in a murine model of severe hemolysis.

Vascular dysfunction in a murine model of severe hemolysis.

http://www.wikidata.org/entity/Q36742507

about

Erythrocyte hemolysis and hemoglobin oxidation promote ferric chloride-induced vascular injury NO reactions with sol-gel and solution phase samples of the ferric nitrite derivative of HbA Vascular endothelial dysfunction in β-thalassemia occurs despite increased eNOS expression and preserved vascular smooth muscle cell reactivity to NO Anion exchange HPLC isolation of high-density lipoprotein (HDL) and on-line estimation of proinflammatory HDL Increased risk of venous thromboembolism is associated with genetic variation in heme oxygenase-1 in Blacks.NT-pro brain natriuretic peptide levels and the risk of death in the cooperative study of sickle cell disease.Effects of a single sickling event on the mechanical fragility of sickle cell trait erythrocytes Circulating membrane-derived microvesicles in redox biology.Hemoglobin-driven pathophysiology is an in vivo consequence of the red blood cell storage lesion that can be attenuated in guinea pigs by haptoglobin therapy.The Mechanism of Proinflammatory HDL Generation in Sickle Cell Disease Is Linked to Cell-Free Hemoglobin via Haptoglobin.A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia.C560Rβ3 caused platelet integrin αII b β3 to bind fibrinogen continuously, but resulted in a severe bleeding syndrome and increased murine mortality Pulmonary vascular and ventricular dysfunction in the susceptible patient (2015 Grover Conference series).Pulmonary hypertension associated with chronic hemolytic anemia and other blood disorders.Prothrombotic mechanisms and anticoagulant therapy in dogs with immune-mediated hemolytic anemia.Nitric oxide transport in blood: a third gas in the respiratory cycle.Intravascular hemolysis and the pathophysiology of sickle cell disease.Peroxisome Proliferator-Activated Receptor γ Regulates the V-Ets Avian Erythroblastosis Virus E26 Oncogene Homolog 1/microRNA-27a Axis to Reduce Endothelin-1 and Endothelial Dysfunction in the Sickle Cell Mouse Lung.Rapid conditional targeted ablation model for hemolytic anemia in the rat Pulmonary hypertension and NO in sickle cell.Dose-related differences in the pharmacodynamic and toxicologic response to a novel hyperglycosylated analog of recombinant human erythropoietin in Sprague-Dawley rats with similarly high hematocrit.

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Vascular dysfunction in a murine model of severe hemolysis.

http://www.wikidata.org/entity/Q36742507

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Vascular dysfunction in a murine model of severe hemolysis.

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Vascular dysfunction in a murine model of severe hemolysis.

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Vascular dysfunction in a murine model of severe hemolysis.

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Vascular dysfunction in a murine model of severe hemolysis.

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Vascular dysfunction in a murine model of severe hemolysis.

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Vascular dysfunction in a murine model of severe hemolysis.

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Vascular dysfunction in a murine model of severe hemolysis.

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Anne C Frei

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Deron W Jones

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Karen A Fagan

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Kirkwood A Pritchard

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Nancy J Wandersee

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Neil Hogg

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YiHe Guo

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P2860

Red blood cell membrane disorders

Hemopexin: structure, function, and regulation

Thrombosis and secondary hemochromatosis play major roles in the pathogenesis of jaundiced and spherocytic mice, murine models for hereditary spherocytosis

Pulmonary prostacyclin synthase overexpression in transgenic mice protects against development of hypoxic pulmonary hypertension

Spectrin deficient inherited hemolytic anemias in the mouse: characterization by spectrin synthesis and mRNA activity in reticulocytes

Murine recessive hereditary spherocytosis, sph/sph, is caused by a mutation in the erythroid alpha-spectrin gene

Possible evidence of endothelial cell activation and disturbance in thalassemia: an in vitro study.

Markers of endothelial cell activation and injury in childhood haemolytic uraemic syndrome.

Differential expression of E- and P-selectin in the microvasculature of sickle cell transgenic mice.

Soluble circulating cell adhesion molecules in haemolytic uraemic syndrome.

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