317-321-GNAS2 Polymorphisms in Children with Arrhythmia

al4 showed that immunity in newborn children was weak, making these children susceptible to diseases, such as arrhythmia. Arrhythmia in newborn children has become one of the most important factors affecting their lives. Otterbach et al5 observed that roughly 1.3% of children in China presently are afflicted with arrhythmias of varying degree, and the number is increasing annually. At present, the pathogenesis of child arrhythmia remains unclear, and there are no therapeutic drugs or accurate detection methods to treat children with arrhythmias6. Yamawake et al7 showed that the GNAS2 (human GS protein alpha subunit) gene on chromosome 12q13.2-13.3, is 1926 Kb in length and consists of 13 exons and 12 introns. Also, Mao et al8 showed that a T393C mutation within the fifth exon of GNAS2 led to changes of GS protein function. They further demonstrated that the C-containing genotype was more frequent in the normal population than the TT genotype and correlated with changes in systolic blood pressure and left ventricular ejection fraction, which indicated that the function of the GS protein changed after the GNAS2 gene underwent T to C substitution. The result of the substitution was an enhancement of adenylate cyclase (AC) activity, an important factor9 in maintaining a stable heart rate. Adenine nucleotides play an important role in the release of thyroid hormone, which affects the sympathetic nerves that regulate the heart. In the present study, we evaluated GNAS2 gene polymorphisms in patients between the control group (without arrhythmia) and the observation group (with arrhythmia) to provide a basis for the diagnosis and treatment of children with arrhythmia.