通过SLC19A1 80G>A遗传变异增加了非综合征性裂唇的易感性,有或没有裂 palates
Archana Patel1, Nisha Sahu1, Henu Kumar Verma2
1Department of Zoology, Guru Ghasidas Vishwavidyalaya, Bilaspur, India.
Journal of the World federation of orthodontists
|February 23, 2024
概括
该SLC19A1 80G>A遗传变异与非综合征裂唇与或没有裂 palates (NSCL/P) 的风险增加有关. 这一元分析证实了这种特定基因变异与NSCL/P发展之间的关联.
科学领域:
- 遗传学 遗传学 是一个
- 发展生物学 发展生物学
- 公共卫生 公共卫生
背景情况:
- 带有或没有口腔裂纹的非综合性裂纹唇 (NSCL/P) 是由于胚胎面发育的障碍引起的.
- 孕产妇的孕期营养,特别是叶酸水平,与NSCL/P病因学有关.
- 在NSCL/P风险中SLC19A1基因变异,特别是80G>A (rs1051266) 的作用需要进一步澄清.
研究的目的:
- 调查SLC19A1 80G>A (rs1051266) 基因变异与NSCL/P.风险之间的关联.
- 通过元分析来巩固现有证据,以确定这种变种的整体影响.
主要方法:
- 在遵循PRISMA指南的10项研究中进行了元分析.
- 分析数据使用等位基因,衰退基因和主导基因模型来评估NSCL/P风险.
- 使用MetaGenyo软件与Bonferroni校正计算了聚合赔率比率 (ORs) 和95%置信区间 (CI).
主要成果:
- 这种SLC19A1 80G>A变异与NSCL/P的风险增加有显著的关联.
- 这种增加的风险在等位基因 (OR 1.39) 后退性 (OR 1.37) 和主导性 (OR 1.7) 遗传模型中观察到.
- 在元分析中没有发现显著的出版偏差.
结论:
- 遗传变异SLC19A1 80G>A是非综合征裂唇与或没有裂 palates (NSCL/P) 的风险因素.
- 这一发现支持了对NSCL/P发展的遗传贡献,可能受到叶酸代谢途径的影响.
关键词:
基因变异是一种基因变异.进行元分析分析.在NSCL/P没有综合症的裂口唇.RFC1 80G>A RFC1 80G>A 80G>A RFC1 80G>A 80G>A RFC1 80G>A 80G>A RFC1 80G>A 80G>A更多相关视频
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