首页> 外国专利> A SIMULATION OF INTERSTITIAL CELLS OF CAJAL IN THE SMALL INTESTINE

A SIMULATION OF INTERSTITIAL CELLS OF CAJAL IN THE SMALL INTESTINE

机译:小肠中日惹间质细胞的模拟

摘要

Rhythmic contractions of the gastrointestinal tract, including the small intestine is associated with pacemaker activity that occurs in the muscle. This activity is occurring less frequently without outside stimulation. The pacemaker activities have been known to occur by the ICC (interstitial cells of Cajal) distributed in the gastrointestinal tract near the interlayer region. Pacemaker activity has spread to the muscle through the gap junction (gap junction) causes the contraction of the entire gastrointestinal tract. The invention can describe or predict the various changes, such as a slow wave characteristics that are repeated automatically by simulating the pacemaker activity by the ICC as part of the small intestine and the mathematical model of intracellular calcium. Pathogenesis of slow wave described in the present invention are as follows. Calcium influx into cells is to cause the incoming SR calcium release mediated by IP 3 (inositol 1,4,5-trisphosphate) . Increase in cytosolic calcium induced by the influx of calcium into the mitochondria largely lowers the calcium concentration of the non-selective cation channel region. Activation of these passages will cause a pacemaker current. Pacemaker current depolarization of the cells and makjeonap, this depolarization will cause a change in the IP 3 metabolism (inositol 1,4,5-trisphosphate) that increases the amount of zoom. Increase in IP 3 is given continuous increase in the intracellular calcium calcium-dependent Cl - to activate a pathway, non-selective cation channel, and thus the cells maintain the plateau voltage. When the internal calcium gradually reduced by the calcium pump, cells should recover a stable membrane potential.
机译:胃肠道(包括小肠)的节律性收缩与肌肉中发生的起搏器活动有关。没有外界刺激,这种活动的发生频率降低。已知起搏器活动是通过分布在靠近中间层区域的胃肠道中的ICC(Cajal的间质细胞)发生的。起搏器的活动已通过间隙连接(间隙连接)扩散到肌肉,引起整个胃肠道的收缩。本发明可以描述或预测各种变化,例如通过模拟作为小肠一部分的ICC的起搏器活动和细胞内钙的数学模型自动重复的慢波特性。本发明中描述的慢波的发病机理如下。钙流入细胞会导致由 IP 3(肌醇1,4,5-三磷酸)介导的SR钙释放。钙流入线粒体引起的胞质钙增加大大降低了非选择性阳离子通道区域的钙浓度。这些通道的激活将引起起搏器电流。心脏起搏器电流使细胞和麦哲那氏菌去极化,这种去极化将引起IP 3 代谢(肌醇1,4,5-三磷酸)的变化,从而增加放大倍数。 IP 3 的增加被赋予了细胞内钙依赖的Cl -的持续增加,从而激活了一条非选择性阳离子通道,因此细胞维持了平台电压。当内部钙通过钙泵逐渐减少时,细胞应恢复稳定的膜电位。

著录项

相似文献

  • 专利
  • 外文文献
  • 中文文献
获取专利

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号