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1 congenital malformations (eg, spina bifida, cardiac anomalies).
2 The patient had no additional cardiac anomaly.
3 patients in whom this defect is the primary cardiac anomaly.
4 rget for the treatment to obesity-associated cardiac anomalies.
5 viving cardiac surgery, and many do not have cardiac anomalies.
6 coma, as well as craniofacial, skeletal, and cardiac anomalies.
7 epsin K protects against diabetes-associated cardiac anomalies.
8 ues results in murine aortic arch artery and cardiac anomalies.
9 tumours, aortic arch disease and other rare cardiac anomalies.
10 ement of neural crest perturbations in these cardiac anomalies.
11 varying degrees of alopecia, but no apparent cardiac anomalies.
12 us, right pulmonary isomerism and a range of cardiac anomalies.
13 alves, ventricular septal defects, and other cardiac anomalies.
14 evelopment and in the etiology of congenital cardiac anomalies.
15 e demonstrated highly penetrant, pleiotropic cardiac anomalies.
16 etermine the diagnostic value of DSCT in the cardiac anomalies.
17 itional mutations in groups of probands with cardiac anomalies and first-degree AV block, idiopathic
18 Mutations in human NKX2.5 cause a variety of cardiac anomalies and may account for a clinically signi
19 arizes the prenatal and postnatal outcome of cardiac anomalies and sustained arrhythmias diagnosed du
20 to evaluate the role of MIF in aging-induced cardiac anomalies and the underlying mechanism involved.
22 polydactyly, cognitive impairment, renal and cardiac anomalies as well as hypertension and diabetes.
23 polydactyly, cognitive impairment, renal and cardiac anomalies, as well as hypertension and diabetes.
27 osage to modulate the severity of cranial or cardiac anomalies in DiGeorge/22q1 deletion syndrome (22
28 tems, encompassing severe failure to thrive, cardiac anomalies including hypertrophic cardiomyopathy
29 so called noncompaction, along with diverse cardiac anomalies, including atrioventricular septal def
32 he second heart field revealed a spectrum of cardiac anomalies resembling forms of human congenital h
33 luding Tbx5, Tbx20 and Nkx2-5, causes severe cardiac anomalies, revealing an essential allelic balanc
34 ncodes a Pbx DNA-binding partner, results in cardiac anomalies that resemble those caused by Pbx muta
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