抗龟壳花及赤尾鲐蛇毒血清治疗竹叶青蛇伤3例

我院 2 0 0 0年期间使用台湾产抗龟壳花及赤尾鲐蛇毒血清治疗竹叶青蛇 ( Trimercsurusstejnegeri schmidt) [1] 咬伤 3例 ,疗效较好。现报告如下。1　临床资料1 .1　一般资料　在本组 3例病人中 ,男 2例 ,女1例 ;年龄分别为 65岁 ,32岁 ,35岁 ;职业 :专业户 1例 ,农民 2例 ;其中咬伤手部 2例 ,足部 1例。1 .2　治疗方法　给予抗龟壳花蛇及赤尾鲐蛇毒血清一剂量 (含 1 0 0 0抗毒单位以上 )稀释于 30 0 ml生理盐水中 ,皮试阴性后静脉滴注。如注射后局部或全身症状仍继续恶化 ,则应每隔 30 min至 2 h再注射一剂量至全身症状改善。同时给予抗生…     

中西医结合治疗326例竹叶青蛇伤患者的疗效观察

目的观察中西医结合治疗竹叶青蛇咬伤的疗效。方法对326例竹叶青蛇伤患者采用口服蛇伤胶囊、三草汤,外用三黄散,穴位放血,结合西医治疗。结果 326例中,治愈293例（占89.88%）,显效28例（占8.59%）,有效3例（占0.92%）,无效2例（占0.61%）,总有效率99.39%。结论口服蛇伤胶囊、三草汤,外用三黄散,穴位放血,结合西医治疗能提高治愈率,是救治竹叶青蛇伤有效的方法。     

竹叶青蛇伤的治疗策略研究

目的探讨竹叶青蛇伤后的救治策略,为毒蛇咬伤程序化急诊急救方案提供依据。方法选择55例竹叶青蛇咬伤患者的资料进行分析临床及治疗措施。结果 55例竹叶青蛇咬伤患者按临床分型,血液学变化有统计学意义(P0.01),其中血小板(PLT)、白细胞(WBC)各型比较均有统计学意义(P0.05);竹叶青蛇伤致血液功能障碍主要表现为PLT、纤维蛋白原(Fg)降低,凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、D-二聚体(DD)和凝血酶时间(TT)延长,甚至出现类DIC。本组危重型患者全部出现类DIC,轻型患者在应用抗蛇毒血清与血液学恢复时间上无统计学意义(P0.05);2例患者在院外行伤口切开排毒出现出血不止,1例在院外诊为"DIC"行肝素抗凝治疗而出现消化道及伤口出血不止。经规范化治疗全部患者均治愈出院。结论按毒蛇伤程序化急诊急救方案治疗竹叶青蛇伤,禁止伤口切开排毒;对重及危重型病例应用同亚科五步蛇、蝮蛇的抗蛇毒血清治疗;对于轻型患者可暂时不用抗蛇毒血清,但应留观,动态观察血液学变化情况;出现类DIC不行抗凝治疗,而是止血、抗纤溶治疗。     

蛇伤胶囊对竹叶青蛇伤t-PA、PAI-1和AT-Ⅲ的影响

目的研究蛇伤胶囊治疗竹叶青蛇伤凝血障碍的机制。方法根据前期实验复制竹叶青蛇伤的动物及细胞模型,均设置空白组(KB),模型组(MX),低、中、高剂量蛇伤胶囊药液组(DY、ZY、GY),共5组,每组10个样本。在动物实验中,KB组经兔右后腿皮下注射0.75ml/kg生理盐水,6h后灌胃10ml/kg生理盐水。MX、DY、ZY和GY组经兔右后腿皮下注射0.75ml/kg竹叶青蛇毒液,6h后分别灌胃10ml/kg生理盐水和10ml/kg低、中、高剂量蛇伤胶囊药液。各组均每日灌胃1次,连续灌胃1周。于末次灌胃后24h经耳缘静脉采血,分离血清。在细胞实验中,KB组加入10%正常兔血清培养,MX组在KB组的基础上加入5μg/ml竹叶青蛇毒液培养,DY、ZY、GY组在MX组基础上培养6h后分别加入5%、10%、15%的含中药兔血清继续培养,各组分别培养72h后,收集细胞培养液。以酶联免疫吸附法检测兔血清及细胞培养液中组织型纤溶酶原激活剂(tissue plasminogen activator,t-PA)、纤溶酶原激活物抑制物-1(plasminogen activator inhibitor-1,PAI-1)和抗凝血酶-Ⅲ(Antithrombin-Ⅲ,AT-Ⅲ)水平。结果 MX组的AT-Ⅲ和t-PA水平相对KB组均显著升高(P0.01),PAI-1水平较KB组显著降低(细胞实验中,P0.05;动物实验中,P0.01);DY、ZY和GY组的AT-Ⅲ及t-PA水平相对MX组均明显降低(动物实验:ZY组t-PA和DY组AT-Ⅲ,均P0.05;细胞实验:ZY组AT-Ⅲ,P0.05;其余均P0.01),DY、ZY和GY组的PAI-1水平较MX组明显升高(P0.01)。结论蛇伤胶囊具有促凝和抗纤溶、改善机体凝血功能的作用,是蛇伤胶囊治疗竹叶青蛇伤凝血障碍的部分机制。     

双黄蛇伤散治疗竹叶青蛇咬伤96例体会

目的探讨双黄蛇伤散对竹叶青蛇咬伤的临床疗效．方法将96倒竹叶青蛇咬伤患者随机分为治疗组和对照组各48侧,均给予常规治疗,治疗组加外敷双黄蛇伤散．结果两组息肢肿胀开始消退时间、肿胀完全消退时间、疼痛缓解时间和住院时间比较均有极显著性差异（P〈0．01）．治疗组局部坏死和功能受限发生事与对照组比较均有极显著性差异（P〈0．01）．结论双黄蛇伤散外敷治疗竹叶青蛇咬伤有显著疗效．     

竹叶青蛇咬伤中毒抗蛇毒血清的选用与优化探讨

目的 探讨竹叶青蛇咬伤治疗中抗蛇毒血清选用策略与优化.方法 收集我院157例竹叶青蛇咬伤住院患者的临床资料,依据抗蛇毒血清的使用情况分为抗五步蛇毒血清单用组(A组)、抗蝮蛇毒血清单用组(B组)、两种抗蛇毒血清联用组(C组),分析比较各组的抗蛇毒血清使用量、治疗效果及不良反应发生情况.结果 157例患者中共应用229支抗...     

蛇伤胶囊对竹叶青蛇伤患者t-PA、PAI-1、TAT及SFMC的影响

目的研究中药蛇伤胶囊治疗竹叶青蛇伤患者凝血障碍的机制。方法将40例竹叶青蛇咬伤患者随机分为两组,均给予常规治疗,如伤口消毒清创处理,肌注破伤风抗毒素1500u,常规使用抗生素,给予地塞米松10mg、奥美拉唑40mg。对照组在常规治疗的基础上给予口服季德胜蛇药10片,每天3次;治疗组在常规治疗的基础上给予口服蛇伤胶囊5片,每天3次。检测治疗前及治疗后1周各组患者血浆中t-PA、PAI-1、TAT及SFMC水平。结果两组患者治疗前t-PA、PAI-1、SFMC、TAT值无明显差异(P0.05)。治疗后两组患者t-PA、SFMC值均降低,差异均无统计学意义(P0.05);PAI、TAT值均升高,差异均具有统计学意义(P0.05)。治疗前后两组患者的t-PA、PAI、SFMC、TAT差值比较无统计学意义(P0.05)。结论蛇伤胶囊和季德胜蛇药对竹叶青蛇咬伤均有显著疗效,两种蛇药可能通过促进凝血酶的生成、增强凝血酶的活性,同时抑制纤溶系统而发挥止血作用。     

蛇伤胶囊对竹叶青蛇伤血管内皮细胞IL-8、VCAM-1、MIP-1α表达的影响

目的观察蛇伤胶囊对竹叶青蛇伤血管内皮细胞IL-8、VCAM-1、MIP-1α表达的影响。方法根据课题组前期实验方法制备蛇伤胶囊兔含药血清及复制竹叶青蛇伤细胞模型,设空白组(KB组)、模型组(MX组)和低、中、高浓度蛇伤胶囊药液治疗组(DY组、ZY组、GY组)5组,每组10个样本。在细胞实验中,KB组加入10%正常兔血清培养,MX组在KB组的基础上加入5μg/ml竹叶青蛇毒液培养,DY组、ZY组和GY组在MX组基础上培养6h后分别加入5%、10%和15%的含中药兔血清继续培养。各组分别培养72h后,收集细胞培养液,以酶联免疫吸附法检测细胞培养液中的IL-8、VCAM-1、MIP-1α含量。结果MX组的IL-8、VCAM-1及MIP-1α水平相对KB组均显著升高(均P0.01),蛇伤胶囊药液治疗组IL-8、VCAM-1及MIP-1α水平相对MX组均不同程度降低,其中ZY组变化有统计学意义(P0.01或P0.05)。结论蛇伤胶囊可通过降低IL-8、VCAM-1及MIP-1α表达治疗竹叶青蛇伤所致血管内皮炎症反应。     

竹叶青蛇毒血小板聚集剂的分离纯化及生化特性

经ＳｅｐｈａｄｅｘＧ－７５凝胶过滤和ＦＰＬＣＭｏｎｏＱ阴离子交换柱层析及Ｓｕｐｅｒｏｓｅ－１２凝胶过滤,从竹叶青蛇的蛇毒中纯化到一个能诱导人血小板聚集的均一组分．经ＳＤＳ－聚丙烯酰胺凝胶电泳测定其分子量为６８０００左右．等电点为４．３．测定了它的氨基酸组成,对它活化血小板的作用机理进行了初步研究,结果表明它是一种强的血小板激动剂．     

Enantioselective synthesis of (R)-(+)- and (S)-(-)-higenamine and their analogues with effects on platelet aggregation and experimental animal model of disseminated intravascular coagulation

Optically active tetrahydroisoquinoline alkaloids, (R)-(+)-higenamine (1R) and (S)-(−)-higenamine (1 S), and their optically active 1-naphthylmethyl analogues (2 and 3), were synthesized by enantioselective hydrogenation of the corresponding dihydroisoquinoline intermediates 7 as a key step. The evaluation of the platelet anti-aggregation effect demonstrated clearly that the (S)-(−)-enantiomers, 1S, 2S, and 3S, had higher inhibitory potency than the corresponding (R)-(+)-antipodes, 1R, 2R, and 3R, respectively, to platelet aggregation induced by epinephrine. 1S enantiomer was superior to the corresponding 1R enantiomer in attenuating all of the disseminated intravascular coagulation (DIC) and multiple organ failure (MOF) parameters tested, while the S enantiomers 2S and 3S ameliorated some of the DIC and MOF parameters more effectively than the corresponding antipodes 2R and 3R.     

A novel big protein TPRBK possessing 25 units of TPR motif is essential for the progress of mitosis and cytokinesis

Through the comprehensive analysis of the genomic DNA sequence of human chromosome 22, we identified a novel gene of 702 kb encoding a big protein of 2481 amino acid residues, and named it as TPRBK (TPR containing big gene cloned at Keio). A novel protein TPRBK possesses 25 units of the TPR motif, which has been known to associate with a diverse range of biological functions. Orthologous genes of human TPRBK were found widely in animal species, from insecta to mammal, but not found in plants, fungi and nematoda. Northern blotting and RT-PCR analyses revealed that TPRBK gene is expressed ubiquitously in the human and mouse fetal tissues and various cell lines of human, monkey and mouse. Immunofluorescent staining of the synchronized monkey COS-7 cells with several relevant antibodies indicated that TPRBK changes its subcellular localization during the cell cycle: at interphase TPRBK locates on the centrosomes, during mitosis it translocates from spindle poles to mitotic spindles then to spindle midzone, and through a period of cytokinesis it stays on the midbody. Co-immunoprecipitation assay and immunofluorescent staining with adequate antibodies revealed that TPRBK binds to Aurora B, and those proteins together translocate throughout mitosis and cytokinesis. Treatments of cells with two drugs (Blebbistatin and Y-27632), that are known to inhibit the contractility of actin–myosin, disturbed the proper intracellular localization of TPRBK. Moreover, the knockdown of TPRBK expression by small interfering RNA (siRNA) suppressed the bundling of spindle midzone microtubules and disrupted the midbody formation, arresting the cells at G₂ + M phase. These observations indicated that a novel big protein TPRBK is essential for the formation and integrity of the midbody, hence we postulated that TPRBK plays a critical role in the progress of mitosis and cytokinesis during mammalian cell cycle.