CPU86017及其旋光异构体对L-甲状腺素致大鼠心肌病异常的calcineurin和NFκB基因表达的抑制作用

目的研究CPU86017及其旋光异构体对L-甲状腺素致大鼠心肌病异常的calcineurin和 NFκB基因改变,并比较CPU86017及其旋光异构体对它们的作用.方法大鼠随机分成7组,每日给予L-甲状腺素(0.2 mg·kg-1, sc) 共 10 d 造成心肌病模型,CPU86017及其旋光异构体(SR、SS、RS、RR)(4 mg·kg-1, sc)在 d 6 连续给药 5 d.动物处死后测定心脏指数,取大鼠心脏测定心肌组织中氧化应激指标,NO和iNOS的活力,大鼠左心室心肌Calcineurin、NF-κB的基因表达由半定量逆转录酶PCR方法测定.结果L-甲状腺素致大鼠心肌病模型组心肌明显肥大,氧化应激增强,NO含量减少,iNOS活力增强,Calcineurin和NF-κB基因表达上调.给予CPU86017及其旋光异构体能不同程度地改善心肌中NO含量及iNOS活力,减轻氧化应激,可以下调这些基因的表达,其中SR比其它旋光异构体疗效好.结论Calcineurin 和NF-κB可能对L-甲状腺素所致大鼠心肌病中细胞内钙调节起着重要的作用,CPU86017及其旋光异构体SR对L-甲状腺素所致大鼠心肌病具有保护作用,该作用与抑制心肌Calcineurin、NF-κB基因的表达、抑制NOS及抗氧化有关.     

CPU86017及其旋光异构体对抗异丙肾上腺素对小鼠心肌的损害作用*

目的:比较口服给CPU86017(对氯卞基四氢小檗碱)及其C-13a旋光异构体(SR和SS)对抗异丙肾上腺亲(ISO)所致小鼠心肌损害作用。方法:连续皮下注射ISO(1 mg·kg~(-1))10 d建立心肌肥厚模型,在d5～d10各治疗组分别灌胃给予普萘洛尔(5 mg·kg~(-1))、CPU 86017(40 mg·kg~(-1)),SR+SS(40 mg·kg~(-1))和SS(40 mg·kg~(-1))。末次给药24 h后取血处死小鼠。测定心重指数(全心重量/体重)和左心室重量指数(左心室重量/体重);左心室匀浆中丙二醛(MDA)和超氧化物歧化酶(SOD)活力;血清中谷草转氨酶(AST)、肌酸激酶(CK)、乳酸脱氢酶(LDH)活力。结果:CPU86017及SR,SS异构体均可显著逆转ISO模型组升高的心重指数,心肌中过度增加的MDA水平及降低的SOD活力,并显著降低血清中升高的AST,CK和LDH水平,其治疗效果与普奈洛尔相当。结论: CPU86017及其旋光异构体均明显对抗ISO所致的心肌肥大性损害作用。     

Abrupt changes in FKBP12.6 and SERCA2a expression contribute to sudden occurrence of ventricular fibrillation on reperfusion and are prevented by CPU86017

Aim： The occurrence of ventricular fibrillation （VF） is dependent on the deterioration of channelopathy in the myocardium. It is interesting to investigate molecular changes in relation to abrupt appearance of VF on reperfusion. We aimed to study whether changes in the expression of FKBP12.6 and SERCA2a and the endothelin （ET） system on reperfusion against ischemia were related to the rapid occurrence of VF and whether CPU86017, a class III antiarrhythmic agent which blocks Ikr.IKs. and ICa.L, suppressed VF by correcting the molecular changes on reperfusion. Methods： Cardiomyopathy （CM） was produced by 0.4 mg/kg sc L-thyroxin for 10 d in rats, and subjected to 10 min coronary artery ligation/reperfusion on d 11. Expressions of the Ca^2＋ handling and ET system and calcium transients were conducted and CPU86017 was injected （4 mg/kg, sc） on d 6-10. Results： A high incidence of VF was found on reperfusion of the rat CM hearts, but there was no VF before reperfusion. The elevation of diastolic calcium was significant in the CM myocytes and exhibited abnormality of the Ca^2＋ handling system. The rapid downregulation of mRNA and the protein expression of FKBP12.6 and SERCA2a were found on reperfusion in association with the upregulation of the expression of the endothelin-converting enzyme 0ECE） and protein kinase A （PKA）, in contrast, no change in the ryanodine type 2 receptor （RyR2）, phospholamban （PLB）, endothelin A receptor （ETAR）, and iNOS was found. CPU86017 removed these changes and suppressed VE Conclusion： Abrupt changes in the expression of FKBP12.6, SERCA2a, PKA, and ECE on reperfusion against ischemia, which are responsible for the rapid occurrence of VF, have been observed. These changes are effectively prevented by CPU86017.     

武警哨兵国产CPU 芯片集成多生理参数及环境信息智能监测系统的设计与应用研究

 目的 利用信息化途径构建起武警哨位与执勤监控站点,以及上级管理站点间武警哨兵生理信号参数、环境信息参数监测信息初筛,为武警监管站点提供直观的哨兵的生理状态及环境状况预警。方法 应用大数据和人工智能,设计一套基于国产CPU芯片的武警哨兵集成多生理参数及环境信息的智能监测系统,对在一个集成融合的监控中心实现对武警哨兵的生理信号参数和哨位环境信息参数进行实时监测分析。结果 通过该系统的建设最大限度地依托国产CPU芯片进行开发,极大地优化了信息安全手段,提高对武警哨兵的多途径实时有效看护,武警监管站点能及时根据参数的改变和预警判断哨兵身体突发状况,及时给出处置方案,严防武警哨兵在执勤过程中的意外事件发生。结论 实现对武警哨兵的生理信号参数和哨位环境信息参数进行实时监测分析 ,为执勤监控站点及上级管理站点预警。     

Oracle中两种数据同步技术的性能测试与评价

目的：掌握oracle的两种数据同步技术高级复制和流技术。方法：设计一个通用的层次管理结构,分别用0racle的两种数据同步技术实现数据同步的原型系统,并对此进行测试和评价。结果：进一步掌握了Oracle的数据同步技术。结论：应Oracle的数据同步技术实现数据同步是可行的,并为设计基于OracIe的数据同步方案提供了参考。     

CPU86017-RS attenuate hypoxia-induced testicular dysfunction in mice by normalizing androgen biosynthesis genes and pro-inflammatory cytokines

Aim:

Downregulation of androgen biosynthesis genes StAR (steroidogenic acute regulatory) and 3β-HSD (3β-hydroxysteroid dehydrogenase) contributes to low testosterone levels in hypoxic mice and is possibly related to increased expression of pro-inflammatory cytokines in the testis. The aim of this study is to investigate the effects of {"type":"entrez-protein","attrs":{"text":"CPU86017","term_id":"899077019","term_text":"CPU86017"}}CPU86017-RS that block Ca²⁺ influx on hypoxia-induced testis insult in mice.

Methods:

Male ICR mice were divided into 5 groups: control group, hypoxia group, hypoxia group treated with nifedipine (10 mg/kg), hypoxia groups treated with {"type":"entrez-protein","attrs":{"text":"CPU86017","term_id":"899077019","term_text":"CPU86017"}}CPU86017-RS (60 or 80 mg/kg). Hypoxia was induced by placing the mice in a chamber under 10%±0.5% O2 for 28 d (8 h per day). The mice were orally administered with drug in the last 14 d. At the end of experiment the testes of the mice were harvested. The mRNA and protein levels of StAR, 3β-HSD, connexin 43 (Cx43), matrix metalloprotease 9 (MMP9), endothelin receptor A (ET_AR) and leptin receptor (OBRb) were analyzed using RT-PCR and Western blotting, respectively. The malondialdehyde (MDA), lactate dehydrogenase (LDH), succinate dehydrogenase (SDH) and acid phosphatase (ACP) levels were measured using biochemical kits. Serum testosterone concentration was measured with radioimmunoassay.

Results:

Hypoxia significantly increased the MDA level, and decreased the LDH, ACP and SDH activities in testes. Meanwhile, hypoxia induced significant downregulation of StAR and 3β-HSD in testes responsible for reduced testosterone biosynthesis. It decreased the expression of Cx43, and increased the expression of MMP9, ETAR and OBRb, leading to abnormal testis function and structure. These changes were effectively diminished by {"type":"entrez-protein","attrs":{"text":"CPU86017","term_id":"899077019","term_text":"CPU86017"}}CPU86017-RS (80 mg/kg) or nifedipine (10 mg/kg).

Conclusion:

Low plasma testosterone level caused by hypoxia was due to downregulation of StAR and 3β-HSD genes, in association with an increased expression of pro-inflammatory cytokines. These changes can be alleviated by {"type":"entrez-protein","attrs":{"text":"CPU86017","term_id":"899077019","term_text":"CPU86017"}}CPU86017-RS or nifedipine.     

L-甲状腺素增强氧化应激及四氢小檗碱衍生物CPU86017的对抗作用

目的探讨L-甲状腺素对氧化应激状态的诱导作用及四氢小檗碱衍生物CPU86017的抗氧化应激作用。方法将实验大鼠分为正常组、L-甲状腺素组(L-甲状腺素0.4mg/kg,ip,连续10天)和CPU86017治疗组(L-甲状腺素0.4mg/kg,ip,连续10天。第8~10天时,加用CPU8601780mg/kg,po),至第11天时,取其肾脏制匀浆和线粒体液,测定匀浆中谷胱甘肽过氧化物酶(GSH-PX)、黄嘌呤氧化酶(XOD)和过氧化氢酶(CAT)的活性,判别L-甲状腺素是否能造成模型动物的氧化应激状态。在各组肾线粒体液中分别加入Fenton’s试剂,测定肾线粒体液中的MDA含量,判断Fenton’s试剂对不同组肾线粒体的氧化应激损伤程度。结果甲亢大鼠肾脏组织中氧化应激呈明显增强状态,其MDA和XOD活性增强;GSH-PX和CAT活性降低。CPU86017可明显改善氧化应激,并且在体外能部分对抗Fenton’s试剂对大鼠肾线粒体的脂质过氧化反应。结论L-甲状腺素能明显增强氧化应激;而CPU86017具有良好的体内、外抗氧化应激作用。     

F52-8C北京万东程控500mA X线机ERR11故障成因分析

目的：CPU控制的普放设备在本世纪之初早就已经进入到基层医疗组织,如何能够利用故障代码进行分析,最快尽短时间的查出故障,减少损失,是本文最大的目标。方法：分析ERR11故障的所有可能成因,并讲解相关检测方法。结果：从多个方面分析该故障的成因,避免遗漏。结论：掌握原理分析可以为维修节省大量的时间,不可忽视实践的重要性但是也不能忽视理论分析的作用,维修结束做好维修总结是一个良好的维修习惯。