PBL及mini-CEX量表运用于八年制血液科见习带教的探索

目的　为进一步提高八年制医学生血液内科见习教学水平、完善测评与反馈机制,探讨PBL教学及mini-CEX量表测评法在血液内科见习带教中运用的可行性。方法　选取参与血液内科临床见习的５４名八年制医学生平均分为两组,将PBL教学法与传统见习带教进行对比,同时采用mini-CEX量表对学生的进行临床能力评估。应用SPSS 20.0统计软件进行数据分析。结果　问诊技巧、临床诊断、治疗计划方面的测试,PBL教学组均优于传统教学组（P＜0.05）;人文关怀的测试,PBL教学组成绩优于传统教学组（P=0.03）。在理论知识,体格检查及操作能力方面,PBL教学组与传统教学组比较无差异。PBL教学组从全神贯注于小组讨论、及时与正面反馈、适时及正确引导、适时纠正学生错误、协助实现学习目标5个方面对教师进行评价,满意度均≥85%。结论　PBL与传统的教学方法相比,在血液内科见习带教中具有一定的优势,mini-CEX量表在见习生中的运用具有可操作性。     

急性白血病FLAG方案化疗后肺孢子菌病6例临床分析

目的明确化疗后患者发生肺孢子菌病(PCP)的危险因素;为急性白血病FLAG方案[氟达拉滨30 mg/(m2.d),第1～5天;阿糖胞苷1～2 g/(m2.d),第1～5天;粒细胞刺激因子5μg/(kg.d),d1～d5)]化疗后肺孢子菌病的预防和治疗提供依据。方法回顾性分析6例白血病化疗后发生肺孢子菌病患者的临床特点,分析发生肺孢子菌病患者的临床特点。结果 6例患者中急性淋巴细胞白血病2例,急性非淋巴细胞白血病4例;患者年龄14～19岁、体质量指数14～18 kg/m2,发生PCP前3个化疗方案中均至少包含2个FLAG方案;PCP起病时均出现明显呼吸困难和血氧饱和度降低,PCP发病时间大约在患者外周血中性粒细胞数恢复后3 d,发病时淋巴细胞和CD4+T淋巴细胞数量和比例明显减少,6例患者均采用复方磺胺甲基异恶唑+棘白霉素类药物联合治疗,症状于1周内好转。结论急性白血病患者应用FLAG方案化疗后,当患者年龄14～19岁、体型偏瘦时,在中性粒细胞恢复后,需监测CD4+T淋巴细胞数量,出现CD4+T细胞数量明显减低时,需密切留意肺孢子菌病的防治。     

获得性血友病甲2例报告并文献复习

目的: 探讨获得性血友病甲的临床特点,以提高对该病的认识.方法: 分析2例获得性血友病甲患者的临床资料,包括其临床表现、实验室检查及治疗经过,并结合相关文献进行复习.结果与结论: 2例患者均为老年男性,表现为自发性广泛皮下出血及软组织血肿,活化部分凝血活酶时间(activated partial thromboplastin time,APTT)明显延长且不能被正常血浆纠正,血浆凝血因子Ⅷ凝血活性部分(factor Ⅷ coagulant activity,FⅧ :C)活性下降,抗FⅧ:C抗体滴度升高,予输注FⅧ浓缩制剂及肾上腺皮质激素、人血丙种球蛋白后出血控制.获得性血友病甲可致严重出血,及早诊断、及早控制出血、及时补充缺乏的凝血因子,清除抗FⅧ:C抗体是成功治疗的关键.     

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.     

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.     

三七皂苷单体对高血压病人血小板功能的影响

目的:以硝苯地平及1{β[3-4-甲基苯丙氧基-甲氧苯]-1-H-盐酸咪唑}(SK&F96365)为对照,探讨三七皂苷单体人参皂苷-2A对血小板聚集功能的作用。方法:肘静脉采高血压病人血标本30份,正常人血标本30份,常规制备富含血小板血浆,分别用不同浓度的硝苯地平、SK&F96365、人参皂苷-2A孵育,以2μmol/L二磷腺苷为诱聚药,连续5次测定5分钟血小板的聚集率,以血小板最大聚集率(maximal platelet aggregation,PAGmax)为观察指标。结果:①高血压病人PAGmax为0.89±0.06,与正常人PAGmax0.68±0.07比较,差异有统计学意义(P<0.01);②两种浓度(10 μmol/L、20 μmol/L)的硝笨地平时正常人和高血压病人PAGmax均无影响;③4种浓度(2.5 μmol/L、5μmol/L、10μmol/L、20μmol/L)的SK&F96365对高血压病组的PAGmax均有抑制作用(均为P<0.05);④4种浓度(2.5μmol/L、5μmol/L、10μ,mol/L、20 μmol/L)的人参皂苷-2A对高血压病组的PAGmax均有抑制作用(均为P<0.05);3种浓度(5 μmol/L、10 μmol/L、20 μmol/L)的人参皂苷-2A对正常组的PAGmax均有抑制作用(均为P<0.05)。结论:高血压病人血小板聚集功能明显高于正常人,血小板呈高反应状态,是血栓形成的重要因素之一;硝苯地平不能抑制血小板聚集;SK&F96365能抑制血小板的聚集功能;人参皂     

血小板膜糖蛋白Ⅱb/Ⅲa受体拮抗剂RGDS对血小板释放反应的影响

【目的】观察血小板膜糖蛋白Ⅱb/Ⅲa（GPⅡb/Ⅲa）拮抗剂——四肽Arg-Gly-Asp-Ser（RGDS）对血小板聚集和CD62p表达的作用,探讨RGDS对血小板聚集和释放反应的影响。【方法】检测二磷酸腺苷（ADP;终浓度5μmol/L,下同）诱导血小板聚集的最大聚集率（rPA,max）、静息血小板和ADP诱导的血小板CD62p表达,检测不同浓度RGDS对ADP诱导的rPA,max的抑制率和血小板CD62p表达的抑制率,进行回归分析。【结果】5种浓度（50、100、200、400、800μmol/L）的RGDS对rPA,max均有显著抑制作用。正常人静息血小板CD62p表达率为（3.5±0.6）%;ADP激动的血小板CD62p表达率为（65.6±13.8）%,两组比较有显著性差异（P〈0.01）;50、100μmol/L的RGDS对血小板CD62p表达无抑制作用;当RGDS浓度≥200μmol/L时（200、400、800μmol/L）,其可抑制血小板CD62p的表达;RGDS对rPA,max的抑制作用和其对血小板CD62p表达的抑制作用相关。【结论】RGDS浓度〈200μmol／L时，对ADP诱导的血小板释放反应无影响；RGDS浓度≥200μmol/L时，可抑制ADP诱导的血小板释放反应；与RGDS显著的抗聚集效应相比，其对血小板释放反应的影响比较小：RGDS抑制血小板释放反应的作用与其抗血小板聚集有关。     

血小板膜糖蛋白Ⅱb/Ⅲa受体拮抗剂RGDS对血小板释放反应的影响

 【目的】观察血小板膜糖蛋白Ⅱb/Ⅲa（GPⅡb/Ⅲa）拮抗剂——四肽Arg-Gly-Asp-Ser（RGDS）对血小板聚集和CD62p表达的作用,探讨RGDS对血小板聚集和释放反应的影响。【方法】检测二磷酸腺苷（ADP;终浓度5μmol/L,下同）诱导血小板聚集的最大聚集率（rPA,max）、静息血小板和ADP诱导的血小板CD62p表达,检测不同浓度RGDS对ADP诱导的rPA,max的抑制率和血小板CD62p表达的抑制率,进行回归分析。【结果】5种浓度（50、100、200、400、800μmol/L）的RGDS对rPA,max均有显著抑制作用。正常人静息血小板CD62p表达率为（3.5±0.6）%;ADP激动的血小板CD62p表达率为（65.6±13.8）%,两组比较有显著性差异（P〈0.01）;50、100μmol/L的RGDS对血小板CD62p表达无抑制作用;当RGDS浓度≥200μmol/L时（200、400、800μmol/L）,其可抑制血小板CD62p的表达;RGDS对rPA,max的抑制作用和其对血小板CD62p表达的抑制作用相关。【结论】RGDS浓度〈200μmol／L时，对ADP诱导的血小板释放反应无影响；RGDS浓度≥200μmol/L时，可抑制ADP诱导的血小板释放反应；与RGDS显著的抗聚集效应相比，其对血小板释放反应的影响比较小：RGDS抑制血小板释放反应的作用与其抗血小板聚集有关。     

二次异体造血干细胞移植成功治疗慢性髓系白血病1例

1病例报告 患者为男性,22岁,确诊慢性粒细胞性白血病慢性期(CML-CP)1年,Ph染色体100%阳性.供体为患者胞姐,HLA配型结果:血清学完全相合,基因分型(PCR-SSO)HLA-A位点亚型不合.于2003年7月9日入层流病房行异体造血干细胞移植术,第一次移植失败且自身造血未能恢复,而于9月2日(第一次移植后46 d)行第二次移植(同一供体),随访17个月,结果报告如下.     

骨髓瘤RPMI 8226细胞体外逃逸NK细胞免疫杀伤机制的初步研究

目的:探讨骨髓瘤细胞RPMI 8266逃逸NK细胞免疫杀伤的机制。方法:流式细胞仪检测K562和8266细胞表面MICA/B、ULBP1～3和HLA-Ⅰ类分子的表达。4hLDH释放法测定效靶比20∶1时阻断前后NK细胞对2种细胞杀伤活性变化。观察效靶比20∶1时NK细胞对药物处理后RPMI 8226细胞杀伤活性变化、RPMI 8226细胞表面NKG2D配体和HLA-Ⅰ类分子的表达及NK细胞对RPMI 8266细胞的克隆形成率的影响。结果:K562细胞高表达MICA/B和ULBP 1～3分子;RPMI 8266细胞表达HLA-Ⅰ类分子,2株细胞NKG2D配体表达差异有统计学意义,P<0.001。单抗分别阻断MICA/B、ULBP 1～3分子后,效靶比为20∶1时NK细胞对K562细胞的杀伤活性明显降低,P值均<0.05;对RPMI 8266细胞的杀伤活性基本无变化,P值均>0.05。抗W6/32单抗封闭8266细胞表面HLA-Ⅰ类分子后,NK细胞对K562细胞的杀伤活性无上升(P=0.721),而对RPMI 8266细胞的杀伤活性上升,P=0.000。1/2IC50的三氧化二砷处理后RPMI8226细胞ULBP...