孕妇血小板α-颗粒膜蛋白-140的表达

目的　观察正常妊娠、妊娠高血压综合征、妊娠期糖尿病妇女血小板 α-颗粒膜蛋白 - 14 0( CD6 2 P)的表达 ,了解孕妇血小板活性。　方法　选择正常妊娠中期 2 0例、正常晚期妊娠 2 0例、孕晚期中度妊高征 2 1例 ,孕晚期糖尿病 2 3例 ,并与正常非孕妇女 2 0例对照 ,用流式细胞仪分别测定其血小板 CD6 2 P的表达。　结果　正常妊娠中期、正常妊娠晚期、中度妊高征、妊娠期糖尿病组CD6 2 P分别为 ( 18.71± 3.36 ) %、 ( 2 6 .2 1± 7.0 9) %、 ( 4 1.82± 12 .95 ) %、 ( 4 1.76± 14 .2 3) % ,均较正常非孕组 ( 11.38± 3.85 ) %明显升高 ;中度妊高征组 ,妊娠期糖尿病组分别与正常妊娠晚期组比较 ,差异有显著性 ( P<0 .0 0 1,P<0 .0 5 )。　结论　随着孕期进展血小板活性增强 ,而妊高征及妊娠期糖尿病与同期正常妊娠相比 ,血小板活化更加明显     

ADP和CPA诱导的高血压病人血小板胞浆游离钙的变化

[目的]探讨高血压病人血小板胞浆游离钙浓度(cytoplasmicfreeCa2 concentration,[Ca2 ]i)的变化.[方法]采用Fura-2/Am荧光双波长测定[Ca2 ]i技术,动态观察激动剂二磷酸腺苷(adenosinediphosphate,ADP)和环匹阿尼酸(cyclopiazonicacid,CPA)对高血压病人血小板[Ca2 ]i的影响.[结果]高血压病人静息血小板[Ca2 ]i与正常人比较明显增高(P<0.05);ADP和CPA激动的高血压病人的血小板平台钙与静息钙比较有统计学意义(P<0.05);峰位钙-平台钙的差(既钙释放)与正常人比较明显增高(P分别<0.05和<0.01);平台钙-静息钙的差(既钙内流)与正常人比较无明显差异(P>0.05).[结论]高血压病人静息血小板[Ca2 ]i增高,平台钙水平明显增高,血小板呈高反应状态;高血压病人的血小板被ADP和CPA激活不能恢复至静息动状态;ADP和CPA激动的高血压病人的血小板钙释放增多,钙内流正常.     

氯通道阻断剂对血小板胞浆游离钙和血小板聚集的影响

目的　探讨氯通道在血小板胞浆游离钙和血小板聚集功能调节中的作用。方法　新鲜分离人血小板,以凝血酶为诱导剂,观察氯通道阻断剂DIDS、NFA和钙通道阻断剂SK&F96365、Nife dipine对血小板胞浆游离钙和血小板聚集的单独作用和相互作用。结果　氯通道阻断剂DIDS、NFA可以浓度依赖性地抑制凝血酶 ( 1U/ml)诱导的血小板聚集,对静息血小板胞浆游离钙无明显影响;DIDS、SK&F96365、Nifedipine可以明显降低凝血酶诱导的血小板聚集、钙释放和钙内流,与对照组比较,P<0. 05;DIDS与SK&F96365联合,对凝血酶诱导的血小板聚集、钙释放和钙内流的抑制比各自单独抑制作用明显增高(P<0. 05),两者的作用相互增强;DIDS与Nifedipine联合,对凝血酶诱导的血小板钙释放的抑制比各自单独抑制作用明显增高 (P<0. 05 ),两者可相互增强;NFA与SK&F96365联合,对凝血酶诱导的血小板钙释放的抑制比各自的单独作用明显降低 (P<0. 05 ),两者可相互减弱;NFA与Nifedipine联合,对凝血酶诱导的血小板聚集、钙释放和钙内流的抑制比各自的单独作用明显降低(P<0. 05),两者可相互减弱。结论　氯通道阻断剂DIDS、NFA对人静息血小板胞浆钙浓度无影响;DIDS可抑制凝血酶诱导的血小板聚集、钙释放和钙内流,NFA仅抑制凝血酶诱导的钙释放;氯通道阻断剂和     

强化免疫抑制治疗重型再生障碍性贫血18例

目的:探讨强化免疫抑制治疗重型再生障碍性贫血(SAA)的临床效果.方法:以抗胸腺细胞球蛋白(ATG)为主的强化免疫抑制治疗SAA患者18例,并随访远期疗效.结果:18例患者总有效率为72.2%,治疗前中性粒细胞、血小板、网织红细胞计数的高低及病程长短与疗效无相关.结论:以ATG为主的强化免疫抑制治疗可显著提高SAA的疗效.     

三七皂甙单体2A-1-1对人血小板聚集和钙内流的作用

目的观察三七皂甙单体2A-1-1对人血小板聚集和钙内流的影响,并探讨其对受体操纵性钙通道的作用.方法比浊法测定血小板聚集;Fura-2/Am荧光探针双波长测定细胞胞浆游离钙浓度,观察2A-1-1、硝苯地平、SK＆F96365对二磷酸腺苷(ADP)、环匹阿尼酸(CPA)介导的人血小板钙内流的变化.结果硝苯地平(20μmol/L)不能抑制ADP诱导的血小板聚集,不能抑制ADP或CPA介导的血小板钙内流;SK＆F96365(20μmol/L)可以抑制ADP诱导的血小板聚集,抑制率为59.83%;SK＆F96365(15μmol/L)可以抑制CPA和ADP介导的钙内流;2A-1-1(5,10,20,μmol/L)可抑制ADP诱导的血小板聚集,抑制率分别为47.06%,53.47%,71.52%;2A-1-1(10,20 μmol/L)可抑制CPA和ADP介导的钙内流.结论三七皂甙单体2A-1-1能抑制人血小板聚集,抑制血小板受体操纵性钙通道,从而抑制钙内流,有抗血小板作用.     

嘌呤类似物单用或联合环磷酰胺治疗慢性淋巴细胞白血病安全性的Meta分析

目的系统评价嘌呤类似物联合环磷酰胺与单用嘌呤类似物治疗慢性淋巴细胞白血病（CLL）的安全性。方法检索PubMed数据库、ISI数据库、Embase数据库、Cochrane图书馆临床对照试验数据库、OVID数据库嘌呤类似物联合环磷酰胺、单用嘌呤类似物治疗CLL的随机对照试验,按Cochrance协作网推荐的方法进行质量评价、资料提取,采用Revman4．3．2软件进行Meta分析。结果共纳入4个随机对照试验,包括1358例患者。Meta分析结果显示,嘌呤类似物联合环磷酰胺与单用嘌呤类似物比较,严重白细胞减少（Ⅲ-Ⅳ级）发生率增加,差异有统计学意义[RR=1．47,95％置信区间（CI）1．10—1．98,P=0．011;严重贫血（Ⅲ—Ⅳ级）（RR=1．03,95％C10．74—1．43,P=0．87）、血小板减少（Ⅲ～Ⅳ级）（RR=1．28,95％CIO．99～1．65,P=0．06）发生率差异无统计学意义。结论与单用嘌呤类似物治疗CLL比较,嘌呤类似物联合环磷酰胺严重贫血、血小板减少发生率无明显增加,但严重白细胞减少发生率增加,临床使用时应引起重视。     

低分子肝素治疗弥散性血管内凝血疗效观察

目的　观察低分子肝素治疗弥散性血管内凝血(disseminatedintravascularcoagulation ,DIC)的疗效。方法　对2 0例确诊的DIC患者在积极治疗基础疾病的同时,予低分子肝素0 3ml皮下注射,2次/d ,隔12h 1次,观察出血状况及凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(Fbg)、D -二聚体、纤维蛋白(原)降解产物(FDP)、3P试验、血小板(Plt)等指标。结果　治愈12例,显效3例,无效5例,总有效率75 % ;PT、Fbg、Plt、D-二聚体、FDP和3P试验治疗后较治疗前有明显改善(P <0 0 5 ) ,无一例应用低分子肝素后出血表现加重。结论　低分子肝素治疗DIC安全有效,副作用小。     

替罗非班在体外对P-选择素、白介素-6、白介素-1β的影响

目的：探讨血小板膜糖蛋白（GP）Ⅱb/Ⅲa受体拮抗剂替罗非班在体外对血浆炎症因子的影响,为合理应用血小板GPⅡb/Ⅲa受体拮抗剂提供理论依据。方法：以二磷酸腺苷（ADP）或凝血酶为诱聚剂在体外激活血小板,同时加入20%、50%和80%抑制浓度的替罗非班,37℃共同孵育30min,标本离心,取上清液用ELISA法检测P-选择素和IL-6、IL-1β等炎症因子的改变。结果：ADP（终浓度为10μmol/L）可诱导P-选择素增多;此效应能被31.25μmol/L（IC20）以上浓度的替罗非班抑制;ADP对IL-6、IL-1β的产生无影响。凝血酶（终浓度0.03U/L）可诱导P-选择素、IL-6、IL-1β产生增多;此效应能被156.25μmol/L（IC50）以上浓度的替罗非班抑制。各浓度替罗非班单独应用对P-选择素、IL-6、IL-1β均无影响。结论：替罗非班浓度在IC50以上时可抑制凝血酶诱导的P-选择素和炎症因子增多。充足剂量的替罗非班在体外有抑制血小板活化和炎症反应的双重效应。     

白血病K562细胞XIAP表达RNAi下调对凋亡及化疗敏感性影响的研究

目的:通过RNAi下调K562细胞X染色体连锁的凋亡抑制蛋白(XIAP)的表达,观察XIAP下调后细胞凋亡及对化疗药物敏感性的变化情况。方法:K562细胞分为3组,实验组和阴性对照组分别用XIAP siRNA及阴性对照siR-NA转染,空白对照组不做任何转染处理。用实时荧光定量PCR和蛋白质印迹法检测转染后各组细胞XIAP mRNA及蛋白的表达,CCK-8法检测各组细胞对阿糖胞苷和依托泊苷敏感性的变化,流式细胞仪和Hochest染色法检测各组细胞加入不同化疗药物后细胞的凋亡情况。结果:转染后48h,实验组XIAP mRNA及蛋白表达量较阴性对照组分别下降约70.0%和60.0%,P<0.05;实验组细胞对依托泊苷和阿糖胞苷的敏感性分别提高2.77和2.28倍,P<0.05;转染siR-NA 48h后,实验组与阴性对照组、空白对照组间凋亡率差异无统计学意义,P>0.05;转染siRNA 6h后加入依托泊苷孵育48h,实验组凋亡率(41.3±1.6)%较阴性对照组(34.3±1.9)%和空白对照组(30.6±1.7)%明显增加;加入阿糖胞苷孵育48h,实验组凋亡率(47.4±1.1)%较阴性对照组(37.0±1.8)%和空白对照组(35.5±1.7)%明显增加,P<0.05。结论:XIAP siRNA能特异性下调K562细胞的XIAP mRNA和蛋白质水平的表达,提高K562细胞对依托泊苷和阿糖胞苷的敏感性,同时伴化疗药物诱导的细胞凋亡增强。     

家兔动脉粥样硬化与血小板源内皮型氧化氮合酶表达的相关性

Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.