醒脑静注射液对脑缺血再灌注损伤家兔花生四烯酸代谢的影响

目的：观察醒脑静注射液(XNJI)对脑缺血再灌注家兔花生四烯酸代谢的影响，并探讨其脑保护机制。方法：将健康家兔20只以“四管闭塞法”及再开放颈动脉建立家兔急性全脑缺血及缺血再灌注动物模型，造模后分为生理盐水组(n=10)和醒脑静组(n=10)，于缺血前和再灌注前，生理盐水组家兔静脉注射生理盐水1ml·kg~(-1)，醒脑静组静脉注射醒脑静注射液1ml·kg~(-1)。观察血浆、脑组织中血栓素B_2(TXB_2)、6-酮-前列腺素F_(1α)(6-Keto-PGF_(1α))含量与比值的变化，并观察脑超微结构变化。结果：醒脑静组与生理盐水组同时相相比血浆和脑组织TXB_2含量、TXB_2／6-Keto-PCF_(1α)比值明显降低(P＜0．05)，醒脑静组脑组织超微结构病理改变不明显。结论：XNJI通过抑制TXB_2合成、促进6-Keto-PGF_(1α)生成而下调两者比值，这可能是其减轻脑缺血再灌注损伤的又一作用机制。     

中药外用离子导入法治疗癌性疼痛30例

近年来 ,我们医院应用中药外用离子导入法治疗癌症疼痛 30例 ,经临床观察疗效满意 ,现将临床资料报告分析如下。1　临床资料　本组晚期癌症 30例 ,男 2 1例 ,女 9例 ;年龄 47岁～ 74岁 ,平均年龄 5 6 3岁 ;全部病例经Ｘ线、ＣＴ、彩超、内窥镜或手术后确诊 ;其中手术后病人 2 2例 ,未做手术 8例 ;包括食管癌 4例 ,肺癌 2例 ,胃癌 10例 ,乳腺癌 3例 ,肝癌 3例 ,大肠癌 8例 ;治疗原发病灶 9例 ,转移或复发病灶 2 1例 ;中医辨证分型阴虚热盛型 16例 ,气阴两虚型 9例 ,痰结互瘀型 5例。2　治疗方法地龙 6 0 ｇ ,露蜂房、乳香、没药、血竭各 30…     

吗啡自控镇痛对快通道不停跳冠脉搭桥患者应激反应的影响

目的 观察快通道不停跳冠脉搭桥（OPCABG）患者吗啡自控镇痛（PCA）与间断肌注镇痛对应激反应的影响。方法 30例OPCABG手术患者随机分为静脉PCA组（Ⅰ组）和间断肌注镇痛组（Ⅱ组），每组各15例。于术后12、24、36和48 h分别对患者的安静痛和咳嗽痛进行VAS评分；于麻醉前、术中90 min、术后24和48 h测定血糖、血浆胰岛素和皮质醇水平。结果 术后12、24、36和48 h Ⅰ组患者的安静痛、咳嗽痛VAS评分均显著低于Ⅱ组（P<0.01）；术后24和48 h两组患者血浆胰岛素水平明显升高（P<0.05），组间比较差异无显著性；术中90 min后与麻醉前比较，两组患者血糖及皮质醇水平均明显升高（P<0.05），Ⅰ组术后48 h恢复至麻醉前水平，Ⅱ组高水平持续至术后48 h（与麻醉前比较，P<0.05）；组间比较术后血糖、皮质醇水平Ⅰ组显著低于Ⅱ组（P<0.05）。结论 OPCABG手术患者术后吗啡PCA较本文采用的间断肌注镇痛能更有效地减轻术后疼痛及应激反应。     

双重杂合性突变Arg304Gln和Arg304Trp导致的遗传性凝血因子Ⅶ缺陷症

目的 探讨1例遗传性凝血因子Ⅶ(coagulation factorⅦ，FⅦ)缺陷症及其家系基因突变的类型。方法 检测凝血指标以明确诊断；用DNA直接测序法对先证者及其家庭成员FⅦ基因的全部外显子和其侧翼以及启动子进行分析，寻找基因突变；将含突变序列克隆人pGEM T—easy质粒载体中，对所得两条染色体相应序列分别测序，以确定不同突变在染色体上的分布。应用限制性内切酶Msp Ⅰ对先证者及家系成员相应基因片段进行酶切分析，证实测序所发现的突变。结果 先证者在第8外显子上有两种基因突变：11348位C→T突变和11349位G→A突变。pGEM T—easy质粒克隆测序结果显示上述两种突变位于不同的染色体上。为不同染色体同一编码区Arg(CGG)304Trp(TGG)和Arg(CGG)304Gln(CAG)双重杂合性突变。其父亲、母亲分别为11349位G→A和11348位C→T杂合突变；其弟弟FⅦ基因为正常野生型；其哥哥和先证者的3个子女均为杂合性突变。聚合酶链反应辅助限制性酶切证实了先证者及其家系成员的基因突变。结论 先证者FⅦ基因突变为不同染色体同一编码区Arg304Trp和Arg304Gln双重杂合性突变，此种突变类型的组合尚属首例。     

带血管蒂上臂后侧筋膜瓣肘关节成形术的解剖和临床应用

目的：为肘关节成形术提供一个新的带血供的筋膜瓣供区。方法：通过解剖学观察,设计了以桡侧副动脉背侧支或尺侧上、下副动脉背侧分支为蒂的上臂后侧筋膜瓣,该筋膜瓣向肘关节内移位,包绕肱骨远端、尺骨切迹及桡骨小头。结果：临床应用６例,筋膜瓣面积６～８ｃｍ×１０～１２ｃｍ,血运良好,术后经１～４．５年,平均２年随访,肘关节功能明显改善。结论：带血管蒂的上臂后侧筋膜瓣转位适合于肘关节成形术,该手术可明显改善肘关节功能。     

IVS J-4delGTTG和c.1325del导致的凝血因子Ⅺ缺陷症

目的:对一个遗传性凝血因子Ⅺ(coagulation factor Ⅺ,FⅪ)缺陷症家系进行调查和基因测序分析,探讨其分子机制。方法:检测先证者及其家系成员血浆的活化部分凝血活酶时间(activated partial thromboplatin time,APTT)、凝血酶原时间(prothrombin time,P...     

一个遗传性凝血因子Ⅻ缺陷症家系凝血因子Ⅻ基因分析

目的 对一个遗传性FⅫ缺陷症家系进行 FⅫ基因突变检测,探讨其参与的分子发病机制.方法 通过活化aPTT、FⅫ:C和FⅫ:Ag等测定进行表型诊断;用PCR技术对先证者及其家系成员FⅫ基因的14个外显子及其侧翼序列进行扩增,PCR产物纯化后,由DNA测序仪进行测序,发现突变位点则反向测序以证实.选择100名健康体检者作对照.结果 先证者及胞弟aPTT明显延长,分别为aPTT79.1s/35 s、aPTT 84.6 s/35 s,大儿子aPTT稍高,为42.1 s/35 s,家系其他成员aPTT正常范围.先证者及胞弟FⅫ:C极度降低,分别为2%、3%,其FⅫ:Ag水平均<1%;胞兄、大儿子和小儿子FⅫ:C明显下降,分别为39%、29%、34%,FⅫ:Ag水平分别为32%、30%、37%.先证者及胞弟FⅫ 1号外显子启动子区46位表现为46T/T型;5号外显子发现5741delc,5742delA,读码框移位,导致Set400Pro;10号外显子发现7142insertC,使得Lys346Gln终止密码子提前出现,产生截短蛋白.此外,家系其他成员:胞兄、大儿子及小儿子发现46T/T和7142insertC;小孙女发现46T/T;侄女、大孙女、二孙女发现46C/T.结论 在该遗传性FⅫ缺陷症家系发现常见的46C/T多态性及exon5区5741delC,5742delA与exon10区7142insertC.5741delC,5742delA及7142insertC与FⅫ水平的降低有关.     

Changes of Tumor Necrosis Factor-α and the Effects of Ulinastatin Injection during Cardiopulmonary Cerebral Resuscitation

The changes of tumor necrosis factor-α (TNF-α) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-α were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-α among different time points (P>0.05). In resuscitation group, the level of TNF-α was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-α showed in UTI group. There were no differences in TNF-α among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-α was expressed rapidly and kept increasing. It indicated that TNF-α might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-α and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.