胰管良恶性狭窄的内镜治疗

目的 探讨内镜治疗胰管狭窄的临床疗效。方法 36例影像学检查确诊的胰管狭窄患者,病因包括慢性胰腺炎、胰腺分裂症、胰头癌、胰腺假性囊肿等,分别在内镜逆行胰胆管造影基础上行内镜治疗,包括胰管支架置入、气囊扩张、探条扩张以及经内镜胰管括约肌切开术（EPS）、经内镜乳头括约肌切开术（EST）,同时观察术后症状缓解情况（如腹痛缓解率）、并发症发生率以及近期与远期疗效。结果36例分别进行了胰管支架引流术、气囊扩张、探条扩张、EPS和EST,术后腹痛症状有不同程度的改善,并发症发生率较低。随访1个月～36个月,平均15个月。术后近期（≤3个月）腹痛缓解率为72.2％（26/36）,长期（>3个月）随访显示47.2％（17/36）的患者腹痛缓解无复发,63.9％（23/36）的患者体重增加,生活质量改善。高淀粉酶血症、出血的发生率分别为13.9％（5/36）和5.6％（2/36）,均经一般内科治疗于3日内缓解。支架阻塞、支架脱落的发生率分别为12.5％（3/24）和4.2％（1/24）。结论 经内镜治疗胰管狭窄是安全而有效的方法。     

Assessment of intracellular TAP-1 and TAP-2 in conjunction with surface MHC class I in plasma cells from patients with multiple myeloma

The anti-neoplastic agent 5-fluorouracil (5-FU) in high therapeutic doses can induce angina pectoris and myocardial infarction. The pathophysiological mechanism of this side-effect has not yet been elucidated. We analysed the influence of 5-FU on blood rheology in vitro . Whole blood, blood cell suspensions and plasma were incubated with increasing concentrations of 5-FU (final concentrations 0, 0.08, 0.4, 2, 10 and 25 mg/ml 5-FU) at 37°C. Erythrocyte morphology was analysed after fixation with glutaraldehyde. Viscosity was measured at high and low shear rates (94 and 0.1 s⁻¹). Erythrocyte aggregation and the cell transit times of erythrocytes through 5 μm pores and polymorphonuclear leucocytes through 8 μm pores were determined. 5-FU induced a dose-dependent formation of echinocytes within minutes and was reversible upon removal of 5-FU, which reflected a preferential intercalation of the drug in the outer hemileaflet of the cell membrane. High shear blood viscosity was increased at the highest 5-FU concentration (148 ± 12%), and at low shear rate a dose-dependent decrease was found (0 mg/ml: 100%, 0.08 mg/ml: 87 ± 10%, 0.4 mg/ml: 80 ± 19%, 2 mg/ml: 70 ± 15%, 10 mg/ml: 40 ± 19%, 25 mg/ml: 33 ± 5%). Erythrocyte aggregation was decreased by the 5-FU-induced echinocytosis. The transit time of erythrocytes through narrow pores was increased in a dose-dependent manner by 5-FU, whereas the transit time of polymorphonuclear leucocytes was initially decreased at 10 mg/ml and returned to control after 60 min incubation. We conclude that 5-FU interacts with the cell membrane, induces echinocytosis and vesiculation and affects blood rheology in several ways which may contribute to cardiovascular complications.     

自体骨髓单个核细胞移植治疗风湿性心脏病可行性研究

目的观察自体骨髓单个核细胞（BMMNCs）心肌内移植对风湿性心脏病患者心功能的影响，探讨其临床实用性。方法选取以左室扩大为主的风湿性心脏病患者5例，瓣膜置换手术当日采取髂骨骨髓20ml，同上法获得自体BMMNCs悬液备用。瓣膜置换完毕，于特定局部心肌内注入上述细胞悬液，分别于术前、术后1周及术后3个月行门控核素心血池显像（MGBP）检查，评价患者心功能及局部心肌舒缩能力，同时监测围手术期心电图及各项实验室指标。结果患者围手术期均未发现明显不良反应，术后3＋71反映左室收缩功能的各项指标显著升高，左室8个分区局部射血分数（rEF）亦明显升高，尤以S3～S6为著。结论自体BMMNCs心肌内移植方法简便、可靠，进一步的严格对照、多中心、随机双盲的大样本临床实验可以进行。     

血清总胆红素对老年女性ST段抬高型心肌梗死患者介入术后造影剂肾病的预测价值

目的探究血清总胆红素(TBIL)对老年女性ST段抬高型心肌梗死(STEMI)患者接受直接PCI后造影剂肾病(CIN)的预测价值。方法回顾性分析我院心脏内科接受直接PCI的老年女性STEMI患者579例,分为CIN组48例和非CIN组531例;收集患者一般临床资料,计算估算的肾小球滤过率(eGFR),检测TBIL水平。结果与非CIN组比较,CIN组年龄、高血压、糖尿病、肌酐、尿素、空腹血糖、白细胞计数、血小板计数明显升高,eGFR、TBIL、血红蛋白水平明显降低,差异有统计学意义(P<0.05,P<0.01)。logistic回归分析模型结果显示,低TBIL是CIN的独立危险因素(OR=1.430,95%CI:1.217~1.834,P=0.024);年龄、糖尿病、基线肌酐、基线eGFR也均为CIN的独立危险因素(P<0.05,P<0.01)。结论低TBIL是老年女性STEMI患者PCI术后CIN的独立危险因素,TBIL可能有助于及早且准确地识别CIN高危患者,为临床治疗决策的制定提供一定的依据。     

急性心肌梗死早期QRS波群终末变形对预后判断的价值

为探讨急性心肌梗死早期QRS波群终末变形对判断预后的价值,回顾分析67例发病12h内的急性心肌梗死患者的临床和心电图资料。结果显示:QRS波群终末变形组和不变形组在年龄、性别、糖尿病史、原发性高血压史以及心肌梗死部位等方面差异并无显著意义,但变形组患者心绞痛病史少见(27.5％对52.6％,P<0.05),平均每例ST段抬高的导联数(4.24±1.10对3.11±1.22,P<0.01)、平均每个导联ST段抬高的程度(0.45±0.07对0.36±0.09mV,P<0.01)、肌酸磷酸激酶峰值(1275.86±323.97对1107.05±278.06U/L,P<0.05)和严重并发症(65.5％对36.8％,P<0.05)等方面明显高于不变形组,死亡率也趋于升高。提示QRS波群终末变形对于急性心肌梗死的预后判断有一定的价值。     

血管紧张素Ⅱ拮抗剂在大鼠应激性溃疡中的作用

目的:探讨血管紧张素Ⅱ拮抗剂在大鼠应激性溃疡(SU)中的作用.方法:水浸束缚应激后,肉眼计算胃黏膜溃疡指数(UI);取动脉血和胃液做血气分析计算胃黏膜内pH值;采用放射免疫方法检测血栓素B2(TXB2)和6-酮前列腺素F1α(6-K);观察胃组织病理形态学变化.结果:管紧张素Ⅱ拮抗剂组与阴性对照组比较,pH值、6-K水平显著升高(4.82±0.31vs4.53±0.11,P=0.026;974.95±109.11ng/Lvs654.50±221.31ng/L,P<0.01),而TXB2,UI显著降低(48.53±8.26ng/Lvs98.18±39.24ng/L,P<0.01;36.13±6.49vs69.00±33.27,P<0.01).病理形态学观察,血栓形成减少.血管紧张素Ⅱ拮抗剂组与奥美拉唑组比较,除6-K(974.95±109.11ng/Lvs737.61±96.10ng/L,P<0.05)外,其他数据无统计学差异.结论:血管紧张素Ⅱ拮抗剂通过舒张血管,增加胃黏膜血流量起到保护胃黏膜的作用,其机制可能是减轻肾上腺髓质对应激的反应,抑制由应激引起的儿茶酚胺的合成和释放,促进前列腺素的分泌.     

原发性甲状腺功能减退症合并原发性干燥综合征肾小管酸中毒及肾性骨病四例报道

目的提高原发性甲状腺功能减退症(原发性甲减)合并原发性干燥综合征(Pss)的认识。方法报道4例确诊为原发性甲减合并pSS的临床特点．结果4例患者均为女性．病程1一8年．原发性甲减诊断明确，也符合pSS同际诊断标准，并伴有低钾血症、低钙血症等临床表现．结论原发性甲减和pSS常共存，二者可能有共同的免疫学发病机制．     

γδ T cells affect IL-4 production and B-cell tolerance

γδ T cells can influence specific antibody responses. Here, we report that mice deficient in individual γδ T-cell subsets have altered levels of serum antibodies, including all major subclasses, sometimes regardless of the presence of αβ T cells. One strain with a partial γδ deficiency that increases IgE antibodies also displayed increases in IL-4–producing T cells (both residual γδ T cells and αβ T cells) and in systemic IL-4 levels. Its B cells expressed IL-4–regulated inhibitory receptors (CD5, CD22, and CD32) at diminished levels, whereas IL-4–inducible IL-4 receptor α and MHCII were increased. They also showed signs of activation and spontaneously formed germinal centers. These mice displayed IgE-dependent features found in hyper-IgE syndrome and developed antichromatin, antinuclear, and anticytoplasmic autoantibodies. In contrast, mice deficient in all γδ T cells had nearly unchanged Ig levels and did not develop autoantibodies. Removing IL-4 abrogated the increases in IgE, antichromatin antibodies, and autoantibodies in the partially γδ-deficient mice. Our data suggest that γδ T cells, controlled by their own cross-talk, affect IL-4 production, B-cell activation, and B-cell tolerance.The role of γδ T cells within the vertebrate immune system is not yet fully understood, but it has become clear that they exert a strong influence on the immune responses. These cells represent a system of specialized subsets with different developmental kinetics, tissue distributions, and functional roles (1). Moreover, at least some of the subsets appear to balance each other’s influence on the immune system (2). Like αβ T cells and B cells, γδ T cells express antigen receptors encoded by rearranging genes (3, 4), which enable adaptive responses to antigenic challenge. Following such stimulation in the course of diseases, γδ T-cell populations can undergo large changes in size and subset composition (5). The γδ T-cell populations also change during ontogeny and due to interindividual genetic differences (6, 7). Conceivably, such changes might alter γδ T-cell balance and, with it, γδ T-cell influence on other immune cells.In mice and humans, it was found that functional attributes of γδ T cells segregate with expressed γδ T-cell receptors (TCRs) (8, 9), although functional differentiation has also been observed within or across TCR-defined subsets and correlated with other markers, such as CD27 and CD8 (10, 11). The murine TCR-γ locus contains seven Vγ genes, six of which are functional and expressed on the cell surface (3, 12). In the normal mouse spleen, the largest γδ T-cell population expresses Vγ1, followed by Vγ4^pos cells and smaller populations expressing Vγ2 and Vγ7 (13). Vγ5^pos and Vγ6^pos cells are not present in substantial numbers. In earlier studies relying on cell transfer and targeted inactivation with antibodies, we and others (8, 10, 14, 15) found that splenic Vγ1^pos and Vγ4^pos cells exert opposite influences on host responses to infection, allergic sensitization, and malignancy. The data suggested that these two γδ T-cell subsets balance each other in their influence on the immune responses (2).In the current study, we further tested this idea by examining antibody levels and B cells in nonimmunized mice genetically deficient either in individual γδ T-cell subsets or in all γδ T cells. The focus on antibodies derives from our earlier observation that mutant mice selectively deficient in Vγ4 and Vγ6 (B6.TCR-Vγ4^−/−/6^−/−) produce substantially more IgE antibody than WT controls or mice deficient in all γδ T cells (B6.TCR-δ^−/−) (10). Here, we report that deficiency in individual γδ T-cell subsets (16, 17) can change antibody production and B-cell activation in nonimmunized mice to a degree that jeopardizes self-tolerance. However, the effect cannot simply be ascribed to an altered γδ T-cell balance. Instead, it correlates with functional changes that occur within the remaining γδ T cells themselves, when they are no longer restrained by normal γδ cross-talk. Our data show that this cross-talk controls the amount of IL-4 produced by a subset of γδ T cells and other T cells, resulting in downstream effects on antibodies, B cells, and self-tolerance.