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121.
OKT3在肾移植术后急性排斥反应防治中的应用 总被引:4,自引:0,他引:4
目的 探讨应用抗淋巴细胞单克隆抗体OKT3预防及治疗肾移植术后急性排斥反应(AR)的效果和安全性、副反应等.方法 对照组128例肾移植患者,术后常规应用甲基泼尼松龙(MP)、强的松(Pred)、硫唑嘌呤(Aza)、骁悉/布累迪宁和环孢素A(CsA)、普乐可复(FK506);实验组36例在上述用药的基础上,术后前10d连续应用OKT3 10mg,使用前以MP 200mg诱导.结果 实验组AR发生时间较对照组明显推迟,其AR发生率明显降低(χ^2=4.725,P<0.05).6例耐激素性急性排斥反应(SR-AR)应用OKT3治疗,4例逆转,逆转率为66.7%.结论 OKT3作为肾移植术后的预防用药,能减少AR的发生率,并能降低排斥反应的强度,可提高移植肾长期存活率.OKT3作为肾移植AR的治疗用药,能较好的逆转SR-AR反应,可使一部分患者避免因AR丧失移植肾,OKT3进入人体能引起首剂综合症等很多副反应,应当引起重视. 相似文献
122.
郭华林 《南阳理工学院学报》2010,2(2):102-106
目的:研究地塞米松对百草枯所致家兔急性肺损伤的保护作用,为临床防治急性肺损伤提供治疗依据。方法:将40只家兔随机分为3组。家兔按百草枯50mg/kg一次性腹腔注射染毒。百草枯中毒组:不予抢救。观察中毒后兔生存情况、死亡时间。地塞米松组:在染毒后,给予地塞米松5mg/kg注射。对照组,呋塞米5mg/kg注射。两组均每30分钟注射一次。持续监护呼吸变化及中毒表现。3小时为实验终点。采集死亡兔的肺作病理切片。取静脉血做心肌酶检测。结果:地塞米松冲击治疗百草枯急性中毒,生存期超过3小时。地塞米松可明显降低肺系数,纠正中毒心肌缺血。结论:地塞米松能在较短时间内降低百草枯急性中毒所致的家兔肺水肿症状,减轻肺损伤。对家兔中毒后有明显的心肌保护作用。 相似文献
123.
本研究以蟾蜍为实验对象,采用机械损伤心肌的方法,获得心电图S—T段形态的典型改变。这种S—T段的改变与人的心肌梗塞的急性损伤型的改变极为相似,可作为急性心肌损伤的模型。 相似文献
124.
P. A. Bernabei V. Santini O. Dal Pozzo R. Bezzini V. Gattei R. Saccardi G. Rombolà P. Rossi Ferrini 《Cellular and molecular life sciences : CMLS》1988,44(10):903-906
Summary We devised a serum-free medium for growth of leukemic colony-forming units (CFU-L), enriched with albumin, transferrin, lipids, insulin, hydrocortisone and oligoelements. Blast cells from 15 patients affected by acute non-lymphocytic leukemia were grown in this medium in the presence of human placental conditioned medium obtained under serum-free conditions (sfHPCM). Their clonogenic growth was comparable with that obtained in a serum-containing system. Furthermore, when serum-free cultures were carried out in absence of sfHPCM, either CFU-L growth was prevented or, if clones were obtained, the cultures showed a marked decrease in clonogenicity, indicating their strict dependence on growth factors. 相似文献
125.
老年急性胆囊炎腹腔镜胆囊切除术后并发症的防治 总被引:1,自引:0,他引:1
分析37例老年急性胆囊炎(包括慢性胆囊炎急性发作)腹腔镜胆囊切除术后并发症的发生情况,并提出对术后并发症防治应注意的事项。 相似文献
126.
A complete sequence and comparative analysis of a SARS-associated virus (Isolate BJO1) 总被引:16,自引:0,他引:16
QINE'de ZHUQingyu YUMan FANBaochang CHANGGuohui SIBingyin YANGBao'an PENGWenming JIANGTao LIUBohua DENGYongqiang LIUHong ZHANGYu WANGCui'e LIYuquan GANYonghua LIXiaoyu LUFushuang TANGang CAOWuchun YANGRuifu WANGJian LIWei XUZuyuan LIYan WUQingfa LINWei CHENWeijun TANGLin DENGYajun HANYujun LIChangfeng LEIMeng LIGuoqing LIWenjie LUHong SHIJianping TONGZongzhong ZHANGFeng LISonggang LIUBin LIUSiqi DONGWei WANGJun GaneK-SWong YUJun YANGHuanming 《科学通报(英文版)》2003,48(10):941-948
The genome sequence of the Severe Acute Respiratory Syndrome (SARS)-assoclated virus provides essential information for the identification of pathogen(s), exploration of etiology and evolution, interpretation of transmission and pathogenesis, development of diagnostics, prevention by future vaccination, and treatment by developing new drugs.We report the complete genome sequence and comparative analysis of an isolate (B J01) of the coronavirus that has been recognized as a pathogen for SARS. The genome is 29725 nt in size and has 11 ORFs (Open Reading Frames). It is composed of a stable region encoding an RNA-dependent RNA polymerase (composed of 20RFs) and a variable region representing 4 CDSs (coding sequences) for viral structural genes (the S, E, M, N proteins) and 5 PUPs (putative uncharacterized proteins). Its gene order is identical to that of other known coronaviruses. The sequence alignment with all known RNA viruses places this virus as a member in the family of Coronaviridae. Thirty putative substitutions have been identified by comparative analysis of the 5 SARS-associated virus genome sequences in GenBank. Fifteen of them lead to possible amino acid changes (non-synonymous mutations) in the proteins. Three amino acid changes, with predicted alteration of physical and chemical features, have been detected in the S protein that is postulated to be involved in the immunoreactions between the virus and its host.Two amino acid changes have been detected in the M protein,which could be related to viral envelope formation. Phylogenetic analysis suggests the possibility of non-human origin of the SARS-associated viruses but provides no evidence that they are man-made. Further efforts should focus on identifying the etiology of the SARS-associated virus and ruling out conclusively the existence of other possible SARS-related pathogen(s). 相似文献