蛋白质组学技术鉴定吉兰-巴雷综合征患者血清急性期反应蛋白的表达

背景：吉兰-巴雷综合征患者血液中存在与发病有关的抗体、补体和细胞因子,以蛋白质组学技术分离鉴定这些标志蛋白,可为寻找新的药物靶标提供依据。 目的：以蛋白质组技术比较吉兰-巴雷综合征患者与正常对照组血清的差异表达蛋白。 方法：采集确诊的吉兰-巴雷综合征患者和正常者血清各30例,提取血清蛋白质以固相pH梯度等电聚焦为第一向,SDS-PAGE垂直电泳为第二向进行双向电泳,图象分析软件Imagemaster 2D分析电泳图谱,MALDI-TOF/TOF串联质谱鉴定差异表达蛋白。 结果与结论：在吉兰-巴雷综合征患者与正常者中24种蛋白质的表达量显著不同,其中α-2-巨球蛋白,血浆铜蓝蛋白,血清淀粉样P物质,丛生蛋白,抗糜蛋白酶,触珠蛋白,血红素蛋白,α-1-抗胰蛋白酶,血清转铁蛋白等9种蛋白质被鉴定为急性期反应蛋白。结果说明吉兰-巴雷综合征患者血清中急性期反应蛋白表达量发生了明显变化,加深了对吉兰-巴雷综合征发病分子机制的理解。     

我国高疫情地区主动发现的肺结核患者干预前后接受治疗的意愿及影响因素分析

目的 了解我国西部肺结核高疫情地区主动筛查发现的患者接受治疗的意愿,探索健康教育对纳入治疗率的影响。 方法 采用横断面研究的方法,于2017年9—12月在全国报告发病率最高的青海、贵州、广西、西藏、新疆5个省(自治区),各选择1个乡镇,对肺结核主动筛查项目中发现的149例肺结核患者,分别于诊断后进行10min的健康教育,在健康教育干预前后进行面对面访问式问卷调查。问卷内容包括患者个人基本信息、家庭及收入情况、医疗支出情况、前往肺结核定点医院交通方式及费用,以及诊断后即刻、进行10min健康教育后纳入对象的治疗意愿情况,不愿意接受治疗的原因等。干预前后两次调查均发出149份问卷,收回149份,均为有效问卷,有效率均为100.00%。分析健康教育前后肺结核患者纳入治疗率的改变情况。采用单因素分析和多因素logistic回归分析对健康教育后影响患者纳入治疗的因素进行统计学分析。 结果 开展健康教育前,主动发现的肺结核患者纳入治疗率为78.52%(117/149),10min健康教育后提高至85.23%(127/149)。经10min健康教育后,单因素分析结果显示:与贵州(0,0/39)相比,青海(29.41%,10/34)、广西(26.09%,6/23)、新疆(15.62%,5/32)的患者纳入治疗的意愿较弱(χ ²=18.13,P<0.001);与<65岁患者(2.44%,1/41)相比,≥65岁患者(19.44%,21/108)纳入治疗的意愿较弱(χ ²=6.83,P=0.009);与往返定点医院时间≤30min的患者(8.43%,7/83)相比,往返时间>30min的患者(22.73%,15/66)纳入治疗的意愿较弱(χ ²=5.97,P=0.015)。多因素分析结果显示:年龄≥65岁的患者(OR=10.18,95%CI:1.31~79.38;Wald χ ²=4.91,P=0.030)及往返定点医院所需时间>30min的患者(OR=3.36,95%CI:1.25~9.02;Wald χ ²=5.78,P=0.020)纳入治疗的意愿较弱。 结论 健康教育对提高患者纳入治疗率有明显效果,以村医入户方式效果较为明显;应重点关注65岁及以上老年人和往返治疗点时间较长患者的纳入治疗工作。     

布地萘德、特布他林雾化治疗小儿哮喘临床观察

目的探讨布地萘德、特布他林雾化吸入治疗小儿哮喘急性发作的疗效。方法将本院收治的小儿哮喘急性发作患者56例，分为治疗组28例，对照组28例，两组的年龄、性别、病程等差别无显著性。对照组仅给予传统治疗；治疗组在对照组的基础上，加用布地萘德0．5—1mg／次，2次／d，特布他林2．5～5mg／次，2～3次／d雾化吸入；比较两组平喘效果。结果治疗组总有效率94．14％，对照组56．17％，两组有非常显著性差异（疋。=12．72，P〈0．01）。结论布地萘德、特布他林雾化治疗小儿哮喘急性发作疗效良好。     

克山病胰腺腺泡的病理改变及其意义

以往文献曾提到克山病时可有胰腺腺泡的萎缩性改变。已知某些胰腺病变有腺泡萎缩,可伴有大片心肌坏死,某些方面类似克山病的心肌病变。为了探讨克山病患者胰腺腺泡的病理改变以及胰腺腺泡萎缩和心肌坏死及克山病的关系,我们进一步对云     

深低温选择性脑灌注技术在主动脉夹层动脉瘤DeBekeyⅠ型手术中的应用

目的总结32例主动脉瘤行深低温停循环选择性脑灌注技术,为以后的体外配合提供临床经验。方法体外循环中行股动脉右心房插管,全身降温至深低温,停循环经腋动脉行脑部灌注。结果 CPB时间为187-402（212±110）min,主动脉阻断时间为96-217（152±30）min,术后死亡5例,1例术后低心排低血压病重自动出院,26例病人经积极治疗治愈出院。结论主动脉瘤手术技术复杂费时,根据手术需要选择适当的体外循环方法及管理是确保手术成功减少脑、脊髓、肾等重要器管并发症的关键。     

化疗加非常规用药治疗结核病性胸膜炎40例

以往认为结核性胸膜炎的发病机罅是主要是机体对结核菌的迟发性高过敏反应 ,而经国外学者多方证实 ,目前认为除此之外 ,结核杆菌直接感染胸膜是结核性胸膜炎的最主要发病机制 ,其发生率可达 5 0 %～ 80 %。结核菌侵入胸膜的途径主要为淋巴 ,血行及肺部结核病变的直接蔓延。非常规药物微卡菌苗 ,6 5 4 - 2加基础全身化疗 ,治疗结核性胸膜炎具有较大价值 ,治疗肺部结核取得令人满意的疗效。临床资料1.一般资料2 0 0 0年 1月至 2 0 0 1年 1月收治初治结核性渗出性胸膜炎4 0例。随机分为试验组和对照组进行临床治疗。各病例依据胸部 X线 ,胸腔…     

升主动脉替换联合三分支支架血管术中置入治疗急性A型主动脉夹层

目的 总结升主动脉人工血管替换联合三分支支架血管术中置入治疗急性Stanford A型主动脉夹层的初步经验.方法 2008年6月至2009年9月20例急性A型主动脉夹层病人接受了升主动脉人工血管替换和三分支支架血管置入术.体外循环鼻咽温度降至20℃时,停止下半身灌注,经无名动脉近端升主动脉横断切口,将三分支支架血管置入主动脉弓和近端胸降主动脉真腔内,并将其分支支架血管依次置入左锁骨下动脉、左颈总动脉和无名动脉.将主干支架血管的近端与无名动脉近端的升主动脉切口重建后与替换近端升主动脉的人工血管端端吻合.结果 所有病人术中均顺利地置入三分支支架血管,平均体外循环(163.2±19.2)min,主动脉阻断(89.4±10.0)min,低流量选择性脑灌注和下半身缺血(32.7±6.6)min.术后出现短暂性神智障碍1例,急性肾功能衰竭1例.20例均治愈出院.术后3个月电子束CT检查结果示,主干支架血管及分支支架血管通畅、无扭曲;支架血管置入部位夹层假腔闭合;16例远端胸降主动脉夹层假腔闭合.结论 三分支支架血管术中置入是简化急性主动脉夹层者主动脉弓重建、提高手术安全性的一种有效方法.主要适应证为弓内内膜无破口而需主动脉弓重建的急性A型主动脉夹层病人.支架血管大小、分支支架血管间的距离选择和放置过程中避免内膜损伤是术中三分支支架血管成功放置的关键.

Abstract：

Objective To report the primary experience of open placement of triple-branched stent graft for acute Stanford type A aortic dissection. Methods Between June 2008 and September 2009, 20 well-selected patients with acute Stanford type A aortic dissection underwent open placement of triple-branched stent graft for total arch reconstruction. When core cooling to a 20℃ nasophageal temperature, perfusion to the lower body was discontinued and the ascending aorta was transected at the base of the innominate artery. Through a transverse incision, the triple-branched stent graft was inserted into the true lumen of the arch and descending aorta, and each side arm of the stent graft was positioned one by one into the arch branches.The transected stump of the ascending aorta was reconstructed by inner proximal stent-free dacron tube of the main graft and outer teflon felt, and subsequently continuous anastomosis to the 1-branched dacron tube graft was made. Results Open placement of triple-branched stent graft was technically successful in all patients. The mean cardiopulmonary bypass time, aortic cross-clamp time and lower body arrest time were (163.2 ±19.2) min, (89.4 ±10.0) min and (32. 7 ±6. 6)min, respectively. Transient postoperative neurological dysfunction was observed in 1 patient and acute renal failure in 1 patient. All patients were discharged from the hospital. Their computed tomographic scans at 3 months postoperatively showed that all stent grafts were fully opened without distortion. In the vascular stent implantation site the dissected false lumen was eliminated. The false lumen of the descending aorta distal to the stent graft was closed with thrombus in 16 cases. Conclusion Open placement of triple-branched stent graft is a new effective technique for total arch reconstruction in acute type A aortic dissection. Patients have the indications of the extensive primary repair of the thoracic aorta without primary intimal tears in the arch may be the best candidates for this new technique. The size of the stent graft, the distances between two neighboring side arm grafts and the prevention of the intimal trauma during the placement are crucial for successful open placement of triple-branched stent graft.     

皮质基底节变性患者的蛋白质组研究

目的 探讨皮质基底节变性的分子机制并寻找诊断治疗该疾病的蛋白质标记物.方法 尸检来自解放军总医院死亡24 h内、经病理证实的男性皮质基底节变性患者(4例)脑及无神经系统疾患的正常老年男性(4例)脑组织,额叶、颞叶和纹状体部位取材,应用HE染色、Gallyas-Braak银染色和Tau蛋白免疫组织化学染色观察皮质基底节变性患者的脑组织学改变;额叶部位取材,以固相pH梯度等电聚焦为第一向,SDS-聚丙烯酰胺凝胶电泳(SDS-PAGE)电泳为第二向进行双向电泳,分析电泳图谱后采用MALDI-TOFTOF串联质谱仪进行蛋白质的鉴定.结果 HE染色显示皮质基底节变性患者额叶神经元明显脱失,伴胶质细胞大量增生,Gallyas-Braak和Tau免疫组化染色结果显示纹状体中大量球形团样缠结;与正常老年人脑组织比较,皮质基底节变性患者脑组织9个蛋白表达增加(经鉴定为coflin、尿嘧啶DNA糖苷水解酶、Cu-Zn超氧化物歧化酶、异柠檬酸脱氢酶亚单位、突触结合蛋白Ⅰ、硫氧还蛋白过氧化物酶1、胶质纤维酸性蛋白、P25alpha、Peroxircdoxin 5),5个蛋白表达下降(经鉴定为碳酰还原酶[NADPH]1、铁蛋白H链、肽基脯氨酸顺反异构酶A、血清白蛋白前体、二氢嘧啶酶相关蛋白2),差异有统计学意义(P＜0.05).结论 上述差异蛋白有助于探讨皮质基底节变性的分子机制及其早期诊断和新药开发.

Abstract：

Objective To investigate the molecular mechanism of corticobasal degeneration and search the protein markers ofdiagnoseis and treatment of this disease. Methods The brains of subjects died without clinical or pathological involvement of nervous system (n=4) and brains of patients with corticobasal degeneration (n=4) were obtained at autopsy. Tissues samples were cut from the frontal and temporal lobes, and the striatum. Histological changes of the tissue samples were observed by HE staining, Gallyas-Braak silver staining and Tau protein immunohistochemistry. The samples extracted from the frontal lobe were performed dimensional electrophoresis with immobilized pH gradient (IPG)isoelectric focusing electrophoresis as the first dimension and with vertical sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) as the second dimension; the maps were visualized by Coomassie brilliant blue staining and analyzed with ImageMaster 2D Elite software; the protein profiles were in-gel digested and identified by mass spectrometry (MALDI-TOFTOF). Results Significant neuron loss in the temporal lobe of patients with corticobasal degeneration was noted by HE staining, with mass proliferation of gliocyte in the temporal lobe; sphere-like entanglement in the striatum was noted by Gallyas-Braak silver staining and Tau immunohistochemistry. Fourteen protein spots in the brains of patients with corticobasal degeneration were differentially expressed as compared with those in age-matched nondemented control brains; the expression of 9 proteins (cofilin, uracil DNA glycosylase,Cu-Zn superoxide dismutase, isocitrate dehydrogenase subunit, synaptotagmin Ⅰ, thioredoxin peroxidase 1, glial fibrillary acidic protein, P25 alpha and peroxiredoxin 5) in brains of patients with corticobasal degeneration was up-regulated as compared with that in the normal brain tissue (P＜0.05); the expression of 5 proteins (carbonyl reductase [NADPH] 1, ferritin heavy chain, peptidyl-prolyl cis-trans isomerase A,serum albumin precursor and dihydropyrimidinase-related protein 2) in brains of patients with corticobasal degeneration was down-regulated as compared with that in the normal brain tissues (P＜0.05).Conclusion We get a number of related-proteins of corticobasal degeneration. Some proteins are quite useful in discovering the molecular mechanisms of corticobasal degeneration and may be helpful in the ealry diagnosis and treatment of corticobasal degeneration and in the development of new medicine.     

糖尿病前期患者血浆纤维蛋白原水平检测

目的 探讨空腹血糖受损和糖耐量减低患者血浆纤维蛋白原水平变化.方法 采用全自动血生化分析仪检测空腹及餐后2小时血糖,全自动血凝分析仪检测血浆纤维蛋白原,比较组间差异.结果 空腹血糖受损和糖耐量减低患者血浆纤维蛋白原水平明显升高(P<0.01).结论 血浆纤维蛋白原可作为空腹血糖受损和糖耐量减低患者病情发展变化的有临床意义重要指标.     

急性运动轴索型神经病患者血清对大鼠脊髓运动神经元凋亡相关蛋白表达的影响

目的 采用蛋白质组学技术研究急性运动轴索型神经病(AMAN)患者血清对大鼠脊髓运动神经元凋亡相关蛋白表达的影响.方法 分别以16例AMAN患者和16名健康献血者的血清对原代培养大鼠脊髓运动神经元进行干预,24 h后行双向凝胶电泳,MALDI-TOF/TOF串联质谱鉴定神经元发生变化的蛋白,表达水平上升或下降超过30%的点判定为差异蛋白质点.结果 AMAN患者血清干预与健康献血者血清干预的大鼠脊髓运动神经元比较,有21种差异表达蛋白,其中内质网蛋白29、不均一核糖核蛋白H、蛋白酶体α亚基1、3-磷酸甘油醛脱氢酶、电压门控阴离子选择性通道蛋白1为凋亡相关蛋白.结论 在AMAN患者血清作用下,大鼠脊髓运动神经元的细胞凋亡相关蛋白表达发生了变化.