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Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia
TLDR
It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia. Expand
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia.
TLDR
It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia. Expand
Serial echocardiographic assessment of left ventricular geometry and function after large myocardial infarction in the rat.
TLDR
Postinfarction LV remodeling in the rat is characterized by progressive cavity dilatation, inadequate hypertrophy of the surviving myocardium, the gradual development of regional contractile dysfunction in noninfarcted segments, and marked abnormalities of diastolic filling. Expand
Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure.
TLDR
These experiments provide the first direct evidence from actively contracting human myocardium that intracellular Ca2+ handling is abnormal and may cause systolic and diastolic dysfunction in heart failure. Expand
Mice mutant for Egfr and Shp2 have defective cardiac semilunar valvulogenesis
TLDR
The results identify the Egfr and Shp2 as components of a growth-factor signalling pathway required specifically for semilunar valvulogenesis, support the hypothesis that Shp 2 is required for Egfr signalling in vivo, and provide an animal model for aortic valve disease. Expand
Gait dynamics in mouse models of Parkinson's disease and Huntington's disease
TLDR
The distinct characteristics of gait and gait variability in the MPTP model of Parkinson's disease and the 3NP model of Huntington's disease may reflect impairment of specific neural pathways involved. Expand
Suppression of voltage-gated L-type Ca2+ currents by polyunsaturated fatty acids in adult and neonatal rat ventricular myocytes.
TLDR
It is concluded that PUFAs may act as antiarrhythmic agents in vivo in normal and Ca2-overloaded cells principally because they reduce Ca2+ entry by blocking I(Ca,L). Expand
Deficient production of cyclic AMP: pharmacologic evidence of an important cause of contractile dysfunction in patients with end-stage heart failure.
TLDR
An abnormality in cyclic AMP production may be a fundamental defect present in patients with end-stage heart failure that can markedly diminish the effectiveness of agents that depend on generation of this nucleotide for production of a positive inotropic effect. Expand
VEGF, flk-1, and flt-1 expression in a rat myocardial infarction model of angiogenesis.
TLDR
Acute myocardial infarction is accompanied by rapid and prolonged increase in expression of VEGF and its receptors with characteristic spatial and temporal kinetic, and these findings suggest that the V EGF/VEGF receptor system plays an important role in the angiogenesis and stromal deposition associated with myocardIAL infarctions. Expand
Transplantation of embryonic stem cells improves cardiac function in postinfarcted rats.
TLDR
The present data demonstrate that ES cell transplantation is a feasible and novel approach to improve ventricular function in infarcted failing hearts. Expand
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