空气波压力治疗仪用于预防骨科卧床患者血栓形成的研究

目的:探讨空气波压力治疗仪(IPC)用于预防骨科卧床患者深静脉血栓形成(DVT)的效果。方法:将400例骨科卧床患者随机分为实验组及对照组各200例,两组均采用常规预防方法,实验组应用空气波压力治疗仪,2次/d,30min/次,10d为1疗程。对照组未使用治疗仪。对两组患者DVT发生率及肿胀、疼痛、舒适度方面进行观察比较。结果:实验组DVT的发生率明显低于对照组(P<0.01),且空气波压力治疗仪在消除肿胀、减轻疼痛及提高舒适度方面效果明显。结论:空气波压力治疗仪能有效预防骨科卧床患者下肢深静脉血栓形成,且安全舒适、经济适用。     

弥可保联合空气压力波治疗糖尿病周围神经病变临床分析

目的探讨弥可保和空气波压力治疗仪联合治疗糖尿病周围神经病变的效果。方法将96例糖尿病周围神经病变患者随机分成两组,对照组单独用弥可保治疗,治疗组弥可保联合空气波压力治疗仪治疗,观察治疗前后自觉症状、腱反射和神经传导速度。结果治疗组总有效率为91．67％,对照组为70．83％,神经传导速度较对照组有显著改善,两组差异有统计学意义（P〈0．05）。结论弥可保联合空气波压力治疗仪治疗糖尿病周围神经病变疗效显著,值得临床推广。     

空气波压力治疗仪治疗糖尿病周围神经病变的护理研究

目的通过系统的个体化糖尿病周围神经病变（DPN）护理教育方法的建立、实施与效果评价,观察使用空气波压力治疗仪治疗DPN的护理效果。方法将308例DPN患者随机分为空气波压力治疗护理教育干预组（教育干预组）和对照组各154例。教育干预组在药物治疗基础上联合空气波压力治疗,并接受DPN的护理课程教育及护理干预,一对一具体指导下肢皮肤护理的方法,对照组通过集中患者讲课进行宣教,发放教育手册供患者阅读学习。评价两组患者的足部皮肤改善情况、自觉症状、神经症状评分、10g尼龙丝试验和神经传导速度变化。结果教育干预组患者使用空气波压力治疗两个疗程并接受课程教育、护理干预,6个月时足部皮肤改善情况、MNSI评分、10g尼龙丝试验和神经传导速度较对照组有显著改善,差异有统计学意义（P〈0.05）。结论空气波压力治疗仪治疗DPN疗效显著,配合护理教育干预,能提高患者自我护理能力,避免足部损伤,促进康复。     

K-ATP channel independent effects of pinacidil on ATP production in isolated cardiomyocyte or pancreatic beta-cell mitochondria

Evidence has been presented that mitochondria contain ATP sensitive potassium channels (mK-ATP channels), which may confer tissue protection upon activation. It is, however, not known whether activation of mK-ATP channels has a direct effect on mitochondrial ATP production. This study was performed to define the effect of pinacidil (PIN) on ATP production by oxidative phosphorylation in isolated cardiomyocyte or pancreatic beta-cell mitochondria. Cardiomyocyte mitochondria produced seven times more ATP than beta-cell mitochondria in the presence of pyruvate/malate. PIN inhibited pyruvate/malate-induced mitochondrial ATP production with half maximal effect at 360 microM in both cell types. The inclusion of 5-hydroxydecanoate (5-HD) did not prevent this inhibition. Succinate induced a similar ATP production in cardiomyocyte or beta-cell mitochondria. In beta-cell mitochondria succinate-induced ATP production was inhibited by PIN with half maximal effects at 500 microM PIN. However, in cardiomyocyte mitochondria PIN stimulated succinate-induced ATP production 3-fold with half maximal effect at 100 microM and maximal effect at 200 microM. This PIN-dependent stimulation was mimicked by rotenone. The inclusion of 5-HD could not prevent these PIN effects. In conclusion, PIN may inhibit complex 1 of the respiratory chain without indications of opening mK-ATP channels. In cardiomyocytes with metabolically inhibited succinate dehydrogenase this results in a stimulation of ATP production conferring tissue protection. In beta-cells without a metabolically inhibited succinate dehydrogenase, there is no stimulation by PIN and tissue protection by PIN is not to be expected.     

中医诊疗技术在国际专利分类表中的分布

《国际专利分类表》(International Patent Classification,IPC)是目前国际通用的管理和利用专利文献的工具。中医诊疗技术专利可按照其运用于诊断或治疗过程的不同分为两大类,主要分布于IPC分类的"A部:人类生活必需的"分部:保健;救生;娱乐"下的"A61医学或兽医学;卫生学"医学部类中。尚有部分依从于其技术结合学科,分布于计算、测量等非医学部类中。对中医诊疗技术专利的IPC分类号进行分析研究,可了解其主题分布与技术布局。     

New role of Notch-mediated signaling pathway in myocardial ischemic preconditioning

Ischemic preconditioning (IPC) is the strongest endogenous myocardial protective mechanism, but up to now, its specific mechanisms have not been completely understood. The Notch network regulates multiple cellular processes, including cell fate determination, development, differentiation, proliferation, apoptosis, and regeneration. Recent loss-of-function studies have shown that the Notch1 receptor controls the response to injury in the adult heart by limiting myocyte hypertrophy, enhancing myocyte survival, promoting precursor proliferation and reducing interstitial fibrosis. Notch signaling also plays a regulatory role in adult cardiac injury and in protection of myocardial function after ischemia. The Notch pathway cross-talks with the PI3K/Akt and NF-κB signaling pathways, both of which are well-known factors involved in IPC-induced myocardial protection. We therefore hypothesize that Notch signaling may play a regulatory role in myocardial protection during ischemic preconditioning and hope to find new drug targets to attain the same beneficial effects of Notch signaling without ischemic insults.