1.The changes of electrophysiology of the rat with cathartic colon and reaction to acetylcholine
Xiankai HUANG ; Jitai XU ; Weidong TONG ;
Journal of Third Military Medical University 2003;0(11):-
Objective To explore the etiopathology of slow transit constipation(STC). Methods The model of rat with cathartic colon was established and the changes of colonic electromyography and reaction to acetylcholine(Ach) were examined. Result The frequency, amplitude of slow wave and colon reaction to Ach of rats with cathartic colon decreased markedly. Conclusion Long term abuse of stimulant laxatives could damage enteric nervous system(ENS) and accelerate the pathological changes of STC.
2.Correlation of insulin-like growth factor 1 expression in placenta with DNA methylation and fetal macrosomia.
Jitai ZHANG ; Kele WU ; Xinyun XU ; Ziwei LIU ; Chong LIN ; Yuhuan WANG ; Hongtao YAN ; Xinyun YANG
Chinese Journal of Medical Genetics 2015;32(1):36-39
OBJECTIVETo explore the correlation between methylation of insulin-like growth factor 1 (IGF-1) gene promoter and its placenta-specific expression and fetal macrosoma.
METHODSOne hundred twenty nine healthy pregnant women were recruited between April 2011 and March 2012. Baseline data were collected with self-report questionnaires. Real-time quantitative PCR was used to determine the expression of IGF-1 mRNA in the placenta. Methylation level of the IGF 1 gene was determined with matrix-assisted laser desorption/ionization-time of flight mass spectrometry.
RESULTSThe expression of IGF-1 in placenta and its methylation level showed no significant difference between macrosomic fetuses and controls. No linear correlation was found between IGF-1 mRNA expression and methylation level of IGF-1 promoter (r=0.128, P=0.295). IGF-1 promoter region in placenta showed a hypomethylation status. However, a positive correlation was found between IGF-1 expression and birth weight below 4260 g (r=0.264, P=0.022). The expression of IGF-1 mRNA was significantly higher in those with a birth weight below 4260 g, which suggested that placental IGF-1 expression may contribute to increased birth weight. In regard to fetal overgrowth, however, there seemed to be a negative correlation in which placental IGF-1 expression was downregulated to limit fetal overgrowth.
CONCLUSIONNo linear correlation was found between placental IGF-1 expression and methylation level of IGF-1 promoter with a hypomethylation status. The contribution of placental IGF-1 expression to birth weight is bidirectional. Increased expression seems to promote fetal growth, while decreased expressions may curb overgrowth, therefore control fetal growth in a relatively normal range.
Birth Weight ; DNA Methylation ; Female ; Fetal Macrosomia ; genetics ; Humans ; Infant, Newborn ; Insulin-Like Growth Factor I ; genetics ; Placenta ; metabolism ; Pregnancy ; Promoter Regions, Genetic ; RNA, Messenger ; analysis