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tetralogy of fallot/phosphatase
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6 risultati
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
Long-term administration of prostaglandin E1: report of two cases with tetralogy of Fallot and esophageal atresia.
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The authors continuously administered prostaglandin E1 (PGE1) iv to 2 infants with tetralogy of Fallot (TOF) and esophageal atresia with tracheoesophageal fistula (TEF) for more than 30 days, and observed side effects which could be attributed to the long-term administration of PGE1. After division
Peritoneal dialysis in an adult patient with tetralogy of Fallot diagnosed with incomplete Alagille syndrome
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Background: Alagille syndrome is an autosomal dominant disorder usually caused by pathogenic variants of the JAG1 gene. In the past, cholestasis was a condition sine qua non for diagnosis of the syndrome. However, recent advancements in
Ca²+-regulatory proteins in cardiomyocytes from the right ventricle in children with congenital heart disease.
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BACKGROUND
Hypoxia and hypertrophy are the most frequent pathophysiological consequence of congenital heart disease (CHD) which can induce the alteration of Ca2+-regulatory proteins and inhibit cardiac contractility. Few studies have been performed to examine Ca2+-regulatory proteins in human
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
Dullard-mediated Smad1/5/8 inhibition controls mouse cardiac neural crest cells condensation and outflow tract septation.
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The establishment of separated pulmonary and systemic circulation in vertebrates, via the cardiac outflow tract (OFT) septation is a sensitive developmental process accounting for 10% of all congenital anomalies. Neural Crest Cells (NCC) colonising the heart condensate along the primitive
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