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作 者:颜建英[1] 廖秋萍[1] 刘青闽[1] 徐榕莉[1] 黄晓燕[1] 林顺和[1] 陈文祯[1] 罗美瑜[1]
机构地区:[1]福建医科大学福建省妇幼保健院教学医院,福建福州350001
出 处:《中国实用妇科与产科杂志》2014年第2期113-117,共5页Chinese Journal of Practical Gynecology and Obstetrics
基 金:福建省科技计划重点项目(2009Y0008);福建省医学创新课题(2009-CXB-32)
摘 要:目的探讨产妇子宫平滑肌大电导钙激活钾通道(BKCa)α、β亚基表达变化在宫缩乏力性产后出血发病中的作用。方法 2009年10月至2011年2月福建省妇幼保健院产科,采用肌条等长张力实验测定30例宫缩乏力性产后出血产妇(病例组)和30例宫缩正常无产后出血产妇(对照组)子宫平滑肌收缩频率、幅度及收缩活动力;应用蛋白印迹法(Western blot)测定两组产妇子宫平滑肌BKCa通道α、β亚基蛋白表达水平;应用实时荧光定量聚合酶链反应(real-time RT-PCR)测定两组产妇子宫平滑肌BKCa通道α、β亚基mRNA表达水平。结果 (1)病例组子宫平滑肌自发宫缩收缩频率、幅度、收缩活动力均低于对照组,分别比较差异均有统计学意义(P<0.05)。(2)病例组子宫平滑肌BKCa通道α、β亚基蛋白表达水平及其mRNA表达水平均高于对照组,分别比较,差异均有统计学意义(P<0.05)。(3)两组产妇子宫平滑肌收缩活动力与BKCa通道α、β亚基蛋白表达水平及BKCa通道α、β亚基mRNA表达水平均呈明显负相关(病例组:r分别为-0.401、-0.727及-0.723、-0.895;对照组:r分别为-0.541、-0.378及-0.703、-0.625;P均<0.05)。结论宫缩乏力性产后出血产妇子宫平滑肌BKCa通道α、β亚基表达水平升高可能是发病的重要因素之一。Objective To detect the expression of large conductance Ca2+ activated K + channel(BKCa) in myometrium in patients with postpartum hemorrhage(PPH). Methods The levels of contractile frequency, amplitude and contraction of myometrium were detected by RM6240 biological experimental system ; the BKCa ( α,β subunit) protein expression levels in myometrium were detected by Western blot; the BKCa( α,β subunit) mRNA expression levels in myometrium were detected by real-time fluorescent quantitative reverse transcription-polymerase chain reaction for women with PPH caused by uterine atony( study group, n = 30) and normal uterine smooth muscle contraction( control group, n = 30). Resuits ( 1 ) In study group, the levels of myometrium contractile frequency, amplitude and contraction were lower than that of the controls(P 〈 O. 05). (2) In study group, BKCa (α,β subunit) protein and mRNA expression in myometri- um were significantly higher than that of control group( P 〈 0. 05 ). ( 3 ) Both groups, the level of myometrium contraction was negatively related to BKCa (α,β subunit) protein, BKCa ( α,β subunit) mRNA level in myometrium. Conclusion Increased BKCa expression in myometrium may be involved in the pathogenesis of PPH caused by uterine atony.
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