نتایج جستجو برای: Conotruncal Defects

تعداد نتایج: 134160  

Journal: :Indonesian Journal of Cardiology 2016

Journal: :American journal of epidemiology 2003
Gary M Shaw Huiping Zhu Edward J Lammer Wei Yang Richard H Finnell

How folate reduces the risks of congenital anomalies is unknown. The authors focused on a gene involved in folate transport-reduced folate carrier-1 gene (RFC1). Using data from a California case-control study (1987-1989 births), the authors investigated whether the risks of orofacial clefts or conotruncal heart defects were influenced by a polymorphism of infant RFC1 or by an interaction betwe...

Journal: :Cell 2001
Sandra Merscher Birgit Funke Jonathan A. Epstein Joerg Heyer Anne Puech Min Min Lu Ramnik J. Xavier Marie B. Demay Robert G. Russell Stephen Factor Kazuhito Tokooya Bruno St. Jore Melissa Lopez Raj K. Pandita Marie Lia Danaise Carrion Hui Xu Hubert Schorle James B. Kobler Peter Scambler Anthony Wynshaw-Boris Arthur I. Skoultchi Bernice E. Morrow Raju Kucherlapati

Velo-cardio-facial syndrome (VCFS)/DiGeorge syndrome (DGS) is a human disorder characterized by a number of phenotypic features including cardiovascular defects. Most VCFS/DGS patients are hemizygous for a 1.5-3.0 Mb region of 22q11. To investigate the etiology of this disorder, we used a cre-loxP strategy to generate mice that are hemizygous for a 1.5 Mb deletion corresponding to that on 22q11...

Journal: :Journal of the American College of Cardiology 1998
E Goldmuntz B J Clark L E Mitchell A F Jawad B F Cuneo L Reed D McDonald-McGinn P Chien J Feuer E H Zackai B S Emanuel D A Driscoll

OBJECTIVES This study was designed to determine the frequency of 22q11 deletions in a large, prospectively ascertained sample of patients with conotruncal defects and to evaluate the deletion frequency when additional cardiac findings are also considered. BACKGROUND Chromosome 22q11 deletions are present in the majority of patients with DiGeorge, velocardiofacial and conotruncal anomaly face ...

Journal: :Annals of clinical and laboratory science 1987
I T Thomas J L Frias

The application of new knowledge on the pathogenesis of congenital heart defects has increased our understanding of associated, non-cardiac malformations seen in certain syndromes. Defects in the proliferation and migration of neural crest cells are thought to contribute to conotruncal defects. These are seen in association with conditions such as DiGeorge syndrome. CHARGE association, hemifaci...

Journal: :Journal of the American College of Cardiology 1999
M C Digilio B Marino A Giannotti R Mingarelli B Dallapiccola

Goldmuntz et al. (1) have reported the frequency of 22q11 deletions in a prospectively ascertained sample of 251 patients with conotruncal defects. Deletions were found in 17.9% of the patients, including 50% with interrupted aortic arch (IAA), 34.3% with truncus arteriosus (TA), and 15.9% with tetralogy of Fallot (TOF). Although this study was designed to determine the frequency of deletions i...

Journal: :Journal of medical genetics 1993
E Goldmuntz D Driscoll M L Budarf E H Zackai D M McDonald-McGinn J A Biegel B S Emanuel

Congenital conotruncal cardiac defects occur with increased frequency in patients with DiGeorge syndrome (DGS). Previous studies have shown that the majority of patients with DGS or velocardiofacial syndrome (VCFS) have a microdeletion within chromosomal region 22q11. We hypothesised that patients with conotruncal defects who were not diagnosed with DGS or VCFS would also have 22q11 deletions. ...

Journal: :Molecular medicine reports 2014
Xike Wang Wei Ji Jian Wang Pengjun Zhao Ying Guo Rang Xu Sun Chen Kun Sun

GATA binding protein 6 (GATA6) encodes a zinc‑finger transcription factor that is essential for normal heart development. Mutations in this gene lead to conotruncal heart defects associated with cyanotic congenital heart disease; however, it remains unclear whether the mutations in GATA6 are also responsible for the development of the nonsyndromic conotruncal heart defects. The coding region exo...

2010
Anna Wozniak Danuta Wolnik-Brzozowska Marzena Wisniewska Renata Glazar Anna Materna-Kiryluk Tomasz Moszura Magdalena Badura-Stronka Joanna Skolozdrzy Maciej R Krawczynski Joanna Zeyland Waldemar Bobkowski Ryszard Slomski Anna Latos-Bielenska Aldona Siwinska

BACKGROUND The 22q11.2 microdeletion syndrome (22q11.2 deletion syndrome -22q11.2DS) refers to congenital abnormalities, including primarily heart defects and facial dysmorphy, thymic hypoplasia, cleft palate and hypocalcaemia. Microdeletion within chromosomal region 22q11.2 constitutes the molecular basis of this syndrome. The 22q11.2 microdeletion syndrome occurs in 1/4000 births. The aim of ...

Journal: :Journal of Cardiovascular and Thoracic Research 2018

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