الفهرس 
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Abstract
Congenital heart disease occurs in approximately 8 for 1.000 live births. The incidence is higher among stillborns (2%), abortuses (10¬25%), and premature infant (2%; Dennis et a!., 1981). The aetiology of most specific congenital heart defects is still unknown. However, recent advances in molecular genetics may soon permit the identification of specific chromosomal abnormalities associated with many of these defects. Approximately 30/0 of patients with congenital heart diseases have an identifiable single gene defects, such as Marfan or Noonan syndrome. 5-80/0 of patients with congenital heart disease have an associated chromosomal abnormality (Hoffman et a!., 1990). DiGeorge anomaly and velocardiofacial syndrome are frequently associated with monosomy of chromosomal sub-band 22q11 (Hou et a!., 1997). The ability to alter gene expression at any point during embryonic development and then study the effects on subsequent development provides a new and powerful tool for studying cardiogenesis that may provide new insights into treatment of congenital heart disease. It is now possible to isolate genes together with, their flanking regions which contain at least some of the important regulatory sequences (Joseph et a!., 1997). The replacement of defective genes, or forms of corrective manipulation of genetic defects, must be a major goal in the application of genetic engineering, technology to human disease (Weatherall et