多房棘球绦虫重组BCG-EmⅡ/3疫苗诱导小鼠脾细胞因子变化的研究

目的 探讨多房棘球绦虫(Em)重组BCG-EmⅡ/3疫苗免疫和Em原头节攻击后小鼠脾细胞因子的变化.方法 将Balb/c小鼠按体质量随机分为3组:疫苗皮下注射组、疫苗鼻腔内接种组、对照组.免疫后8周用Em原头节进行攻击感染,感染后18周杀鼠取脾,分离脾细胞,分别用原液、Em抗原(EmAg)、刀豆蛋白A(ConA)或植物血凝素(PHA)培养,酶联免疫吸附(ELISA)法检测脾细胞培养上清液中白细胞介素2(IL-2)、γ干扰素(IFN-γ)、肿瘤坏死因子α(TNF-β)、白细胞介素4(IL-4)水平.结果 疫苗皮下注射组原液培养条件下IL-2、IFN-γ、TNF-α和IL-4水平分别为(34.6±2.7)、(34.5±2.8)、(265.0±0.0)、(9.8±2.6)ng/L,与对照组[(25.0±1.9)、(30.0±0.0)、(10.0±0.0)、(12.5±2.7)ng/L]比较差异均有统计学意义(P＜0.01或＜0.05);疫苗鼻腔内接种组原液培养条件下上述4种指标分别为(32.5±2.2)、(33.6±2.7)、(130.0±0.0)、(10.4±2.7)ng/L.与对照组比较差异均有统计学意义(P＜0.01或＜0.05);疫苗皮下注射组原液培养条件下TNF-α水平明显高于疫苗鼻腔内接种组(P＜0.01).EmAg、ConA(或PHA)刺激培养条件下,上述4种指标明显高于相同组别的原液培养(P＜0.01),且ConA(或PHA)刺激培养条件下,上述4种指标明显高于相同组别的EmAg刺激培养条件(P＜0.01).结论 多房棘球绦虫重组BCG-EmⅡ/3疫苗诱导小鼠产生辅助T淋巴细胞(Th)1型免疫反应,从而对抗Em原头节攻击感染.     

Amifostine (WR-2721) shortens the engraftment period of 4- hydroperoxycyclophosphamide-purged bone marrow in breast cancer patients receiving high-dose chemotherapy with autologous bone marrow support

4-Hydroperoxycyclophosphamide (4-HC), a commonly used marrow-purging agent, is active against many tumors, but is also toxic to normal marrow progenitors. Amifostine (WR-2721) is a sulfhydryl compound with chemoprotectant activity. Preclinical studies using suspensions of bone marrow and breast cancer cells demonstrated that ex vivo treatment with amifostine followed by 4-HC resulted in protection of marrow progenitors, with no compromise in the antitumor effect of 4-HC. This fact stimulated the development of a clinical trial. Bone marrow was harvested from 15 poor-prognosis breast cancer patients and randomly assigned to ex vivo treatment with amifostine followed by 4-HC (amifostine + 4-HC), or treatment with 4-HC alone. High-dose chemotherapy was then administered followed by infusion of the purged autologous bone marrow support (ABMS). Leukocyte engraftment, defined as a white blood cell count > or = 1 x 10(9)/L, was achieved in an average of 26 days for patients whose marrow was purged with amifostine + 4-HC versus 36 days for patients whose marrow was purged with 4-HC alone (P = .032). The average number of platelet transfusions (12 v 29; P = .017) and days of antibiotic therapy (28 v 40; P = .012) were significantly less for patients whose marrow was exposed to amifostine + 4-HC, compared with 4-HC alone. Unpurged backup marrow fractions were infused into three patients whose marrow was purged with 4-HC alone, because of inadequate marrow recovery. None of the patients who received amifostine + 4-HC-purged marrow required a backup marrow fraction. Complete remissions were achieved in 83% of patients with measurable disease, with no difference between the two cohorts. Forty- three percent of patients remained alive and progression-free at a mean of 13 months posttransplant. There was no significant difference in the rate or pattern of relapse for patients whose marrow was purged with amifostine + 4-HC compared with those whose marrow was purged with 4-HC alone. Ex vivo treatment of marrow with amifostine significantly shortens the time to marrow recovery, thereby reducing the risk of myelosuppressive complications in breast cancer patients receiving high- dose chemotherapy and 4-HC-purged ABMS. Since supportive care requirements are also significantly decreased, amifostine may reduce the cost of such therapy.     

社会主义核心价值体系融入医学生医德教育的伦理诉求

医德修养和医德品质是医务人员必备的思想品质,是和谐医患关系的道德前提。以社会主义核心价值体系为指导,把社会主义核心价值体系融入医德教育中,是帮助医学生树立崇高的医德理想、明确医德追求、继承医德传统、锤炼医德品质和提升医德修养的重要途径和方法。     

动脉化疗栓塞术联合微波消融及静脉化疗治疗消化道肿瘤肝转移临床观察

目的：探讨动脉化疗栓塞术（transcatheter arterial chemoembolization ,TACE）联合微波消融及静脉化疗治疗消化道肿瘤肝转移的临床价值。方法不能或不愿手术的消化道肿瘤肝转移患者72例,随机分为2组。联合治疗组37例,序贯行TACE、替加氟1g连续静脉化疗4d、肝内转移瘤微波消融术;对照组35例,仅行XELOX或FOLFOX6方案静脉化疗。以患者缓解率、生存期作为评价指标。结果联合治疗组病情缓解率为64.9％,显著高于对照组28.6％,且联合组治疗后6个月、12个月、18个月、24个月生存率分别为100％、78.4％、48.7％、24.3％,较对照组明显延长。结论 TACE联合微波消融及静脉化疗治疗消化道肿瘤肝转移,是一种较安全有效的治疗方法。     

Inactivation of factor XIa in human plasma assessed by measuring factor XIa-protease inhibitor complexes: major role for C1-inhibitor

From experiments with purified proteins, it has been concluded that factor XIa (FXIa) is inhibited in plasma mainly by alpha 1-antitrypsin (a1AT), followed by antithrombin III (ATIII), C1-inhibitor (C1Inh), and alpha 2-antiplasmin (a2AP). However, the validity of this concept has never been studied in plasma. We established the relative contribution of different inhibitors to the inactivation of FXIa in human plasma, using enzyme-linked immunosorbent assays (ELISAs) for the quantification of complexes of FXIa with a1AT, C1Inh, a2AP, and ATIII. We found that 47% of FXIa added to plasma formed complexes with C1Inh, 24.5% with a2AP, 23.5% with a1AT, and 5% with ATIII. The distribution of FXIa between these inhibitors in plasma was independent of whether FXIa was added to plasma, or was activated endogenously by kaolin, celite, or glass. However, in the presence of heparin (1 or 50 U/mL), C1Inh appeared to be the major inhibitor of FXIa, followed by ATIII. Furthermore, at lower temperatures, less FXIa-C1Inh and FXIa-a1AT complexes but more FXIa-a2AP complexes were formed. These data demonstrate that the contribution of the different inhibitors to inactivation of FXIa in plasma may vary, but C1Inh is the principal inhibitor under most conditions.