tetralogy of fallot/tyrosine

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Decreased expression of neurotrophic tyrosine receptor kinase 3 is associated with the outflow tract defect of human tetralogy of Fallot.

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BACKGROUND The molecular mechanism of human tetralogy of Fallot (TOF) is incompletely defined. Animal models have suggested that neurotrophic tyrosine receptor kinase 3 (NTRK3) might be associated with the outflow tract defect, similar to that seen in human TOF, however, the expression pattern of

Polymorphism C242T of the gene of the p22phox subunit for nicotinamide adenine dinucleotide phosphate oxidase, and erythrocytic antioxidant enzymes, in patients with tetralogy of Fallot.

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BACKGROUND Nicotinamide adenine dinucleotide phosphate oxidase of the vascular cell membrane is an important source of reactive oxygen species. The aim of our study was to evaluate the possible influence of the p22phox C242T gene polymorphism on blood pressure and some markers of oxidative stress in

Ratio between fms-like tyrosine kinase 1 and placental growth factor in children with congenital heart disease.

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Serum levels of soluble fms-like tyrosine kinase 1 (sFlt-1), an antiangiogenic factor, and its binding protein, placental growth factor (PlGF), are altered in women with preeclampsia. Recently, the sFlt-1/PlGF ratio has been shown to predict acute coronary syndrome in adults. However, few reports

Gastrointestinal bleeding in tetralogy of fallot.

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This article reports an uncommon cause of gastrointestinal bleeding in a young male with uncorrected Tetralogy of Fallot (TOF). This is the first reported instance of gastrointestinal stromal tumor (GIST) causing bleeding in a patient with uncorrected TOF. A 32-year-old Caucasian male with severe

Conditional deletion of focal adhesion kinase leads to defects in ventricular septation and outflow tract alignment.

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To examine a role for focal adhesion kinase (FAK) in cardiac morphogenesis, we generated a line of mice with a conditional deletion of FAK in nkx2-5-expressing cells (herein termed FAKnk mice). FAKnk mice died shortly after birth, likely resulting from a profound subaortic ventricular septal defect

Identification of an essential nonneuronal function of neurotrophin 3 in mammalian cardiac development.

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Neurotrophin 3 (Nt3) is one of five neurotrophin growth factors which shape the development of the nervous system by regulating neuronal survival and differentiation. Peripheral neuronal subpopulations expressing the TrkC receptor tyrosine kinase respond to Nt3 with enhanced survival, mitogenesis or

The expanding phenotypes of cohesinopathies: one ring to rule them all!

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Preservation and development of life depend on the adequate segregation of sister chromatids during mitosis and meiosis. This process is ensured by the cohesin multi-subunit complex. Mutations in this complex have been associated with an increasing number of diseases, termed cohesinopathies. The

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