前列地尔治疗糖尿病周围神经病变58例的疗效观察

目的:观察静脉注射前列地尔对糖尿病周围神经病变(DPN)的疗效。方法:选择糖尿病周围神经病变58例给予前列地尔(10—20滋g,加入0.9%生理盐水20ml缓慢静脉注射,疗程2—4周)治疗。结果:四肢麻木、肢体自发痛、感觉减退、怕冷、怕热、双足蚁行感、脚踏海绵感与溃疡均明显改善,改善率分别是91.8%,94.4%,87.5%,91.3%,75%,88.9%,63.6%和90%。患者在治疗前MCV和SCV均有降低,经过治疗后,MCV和SCV有一定改善(P<0.05)。治疗前发现有下肢动脉内膜增厚、粗糙不光滑、斑块形成、血栓、管腔不规则狭窄甚至闭塞。治疗后发现,血管内径与血流量较治疗前明显改善(P<0.05)。结论:前列地尔可有效缓解糖尿病周围神经病变症状、改善周围神经传导速度、增加下肢血管内径和血流量,对DPN有较好疗效。     

自制苏芪合剂联合治疗Ⅲ～Ⅳ级IgA肾病的临床疗效观察

目的 探讨自制苏芪合剂对Ⅲ～Ⅳ级IgA肾病患者的疗效及患者T细胞功能的改善.方法 28例Ⅲ～Ⅳ级IgA肾病患者随机分为两组,对照组:醋酸泼尼松-日1mg,kg,隔日晨起顿服,盐酸苯那普利-日10mg;治疗组:在上述用药的基础上加用自制苏芪合剂.8周后,观察患者缓解率、T细胞功能及不良反应.结果 治疗组患者在缓解率、T细胞功能改善等方面优于对照组,且因糖皮质激素的使用而出现的不良反应少于对照组.结论 苏芪合剂联合治疗Ⅲ～Ⅳ级IgA肾病疗效显著并能有效改善T细胞功能.     

In Vivo Anergized T Cells Form Altered Immunological Synapses In Vitro

T cells contact allogeneic antigen presenting cells (APCs) and assemble, at their contact interface, a molecular platform called the immunological synapse. Synapse-based molecules provide directional signals for the T cell--either positive signals, resulting in T-cell activation, or negative signals causing T-cell inactivation or anergy. To better understand the molecular basis of in vivo T-cell anergy we analyzed the contacts made between in vivo anergized T cells and APCs, and determined which signaling molecules were included or excluded from their immunological synapses. Anergy was induced in TCR transgenic mice by the intravenous injection of semiallogeneic donor spleen cells. T cells from anergized mice were mixed with APCs, the T-cell/APC synapses imaged using deconvolution microscopy, and their molecular compositions were determined. T cells from anergic mice formed unstable immunological synapses in vitro with allogeneic APCs and failed to recruit the signaling proteins necessary to initiate T-cell activation. These findings suggest that T-cell anergy induced by exposure to semiallogeneic donor cells is associated with defects in the earliest events of T-cell activation, immunological synapse formation and recruitment of TCR-mediated signaling proteins.     

Differential Effects of Immunosuppressive Drugs on T-Cell Motility

The best-characterized mechanism of the action of immunosuppressive drugs is to prevent T-cell clonal expansion, thus containing the magnitude of the ensuing immune response. As T-cell recruitment to the inflammatory site is another key step in the development of T-cell-mediated inflammation, we analyzed and compared the effects of two commonly used immunosuppressants, cyclosporin A (CsA) and the rapamycin-related compound SDZ-RAD, on the motility of human CD4+ T cells. We show that CsA, but not SDZ-RAD, inhibits T-cell transendothelial migration in vitro. CsA selectively impaired chemokine-induced T-cell chemotaxis while integrin-mediated migration was unaffected. The inhibition of T-cell chemotaxis correlated with reduced AKT/PKB but not ERK activation following exposure to the chemokine CXCL-12/SDF-1. In addition, CsA, but not SDZ-RAD, prevents some T-cell receptor-mediated effects on T-cell motility. Finally, we show that CsA, but not SDZ-RAD inhibits tissue infiltration by T cells in vivo. Our data suggest a prominent antiinflammatory role for CsA in T-cell-mediated tissue damage, by inhibiting T-cell trafficking into tissues in addition to containing clonal expansion.     

支原体肺炎肺外损伤患儿T细胞亚群、IFNγ、TNFα的变化及意义

目的 探讨支原体肺炎肺外损伤患儿细胞免疫、细胞因子状况和胸腺肽的治疗效果。方法 采用流式细胞仪和酶标仪检测31例支原体肺炎肺外损伤组患儿急性期、恢复期血中CD3CD4、CD8、CD4／CD8干扰素γ（IFNγ）、肿瘤坏死因子α（TNFα水平，并与支原体肺炎组比较。结果 ①急性期支原体肺炎肺外损伤组和支原体肺炎组比较，CD3、CD4显著降低（P〈0．05），TNFα显著升高（P〈0．01），CD8、IFNγ无统计学意义（P〉0．05）；②支原体肺炎肺外损伤组急性期和4周后比较，CD3、CD4、IFNγ升高（P〈0．05），TNFα显著降低（P〈0．01），CD8无变化。用胸腺肽治疗患者以上指标变化更明显。结论 支原体肺炎肺外损伤患儿细胞免疫功能低于支原体肺炎患儿；细胞因子中TNFα早期升高，而IFNγ不明显；恢复期TNFα下降，而IFNγ升高明显。用胸腺肽治疗能缩短病程。     

复合神经营养因子的神经导管研究进展

目前周围神经的组织工程研究热点之一就是研制具有生物活性的神经导管,主要方法是神经导管与雪旺细胞或者神经营养因子相结合来促进周围神经的再生。就复合神经营养因子的神经导管的相关研究进展作一综述。     

肝动脉结扎在重度肝外伤中的临床应用

目的探讨严重肝外伤的治疗和疗效。方法总结分析10年间收治的81例严重肝外伤,按AAST分级法。Ⅲ级30例,Ⅳ级36例,Ⅴ级15例,分别以不同的方法治疗对比。结果治愈71例,10例死于术后胆瘘并发感染及多器官衰竭,为能忽视Ⅲ级肝外的肝动脉结扎及T管引流术。结论肝动脉结扎加网膜及纱布带填塞、不规则的肝叶切除、T管引流、肝血回输,是提高严重肝外伤抢救成功率的重要措施。     

Role of Integrin CD103 in Promoting Destruction of Renal Allografts by CD8+ T Cells

Infiltration of CD8(+)TCRalphabeta(+) T-effector populations (CD8 effectors) into graft epithelial compartments has long been recognized as a key lesion in progression of clinical renal allograft rejection. While the afferent phase of allograft immunity is increasingly well-defined, the efferent pathways by which donor-reactive CD8-effector populations access and ultimately destroy the graft renal tubules (rejection per se) have received remarkably little attention. This is an important gap in our knowledge of transplantation immunology, because epithelial compartments comprise the functional elements of most commonly transplanted organs including not only kidney, but also liver, lung, pancreas, and intestine. Furthermore, there is increasing evidence that attack of graft epithelial elements by CD8-effector populations not only causes short-term graft dysfunction but is also a major contributor to development of chronic allograft nephropathy and late graft loss, which now represent the salient clinical problems. Recent studies of the T-cell integrin, alpha(E)beta(7) (CD103), have provided insight into the mechanisms that promote interaction of CD8 effectors with graft epithelial compartments. The purpose of this communication is to review the known properties of the CD103 molecule and its postulated role in the efferent phase of renal allograft rejection.     

Hypoxia‐inducible factor 1α may be a marker for vasculitic neuropathy

Neuromuscular biopsy is still an essential method for diagnosing vasculitic neuropathy, although its diagnostic sensitivity is at most 60%. Our objective was to examine the expression of hypoxia‐inducible factor 1α (HIF‐1α) in peripheral nerves and to evaluate its usefulness in diagnosing vasculitic neuropathy, especially for discrimination from other axonal neuropathies. Forty‐one patients with vasculitic neuropathy consisting of 20 definite, 14 probable and seven possible diagnoses, 15 patients with metabolic neuropathy, five with motor neuron disease and six with chronic inflammatory demyelinating polyneuropathy were included. Nerve biopsy specimens were immunohistochemically examined for HIF‐1α and various cell markers. Distinct immunoreactivity (IR) was observed in nuclei of endoneurial cells in 54% (22/41) of vasculitic patients, while specimens from metabolic neuropathies showed less nuclear IR and the difference of mean density of HIF‐1α‐positive nuclei was significant. Two patients with possible vasculitis who showed HIF‐1α‐positive nuclei in endoneurium, were later confirmed to have vasculitis by skin biopsies. Most of the cells expressing HIF were demonstrated to be Schwann cells. There was a trend in the vasculitic patients with early phase nerve damage to display higher endoneurial HIF‐1α‐IR. HIF‐1α may be an immunohistochemical marker for vasculitic neuropathy, especially when the observed section contains no vasculitic lesions.     

胸腔镜辅助小切口手术诊治肺周围型结节

目的探讨胸腔镜辅助小切口手术在诊断和治疗肺周围型结节病变中的临床应用价值。方法胸腔镜辅助小切口手术诊治肺周围型结节55例，其中单发结节54例，多发结节1例。肺楔形切除术23例；肺叶切除联合淋巴结清扫治疗原发性肺癌32例，采用常规开胸手术器械及胸腔镜用器械切除肺叶，自制淋巴结摘除钳完成淋巴结清扫。结果55例均在胸腔镜下完成手术。手术时间35～180min，平均109min，术中出血量50～400ml，平均122min。均未输血，1例术后漏气术后32d出院，1例切口延迟愈合，术后19d出院，余53例术后住院4～11d，平均8．3d。无严重并发症。术后病理：良性病变15例，原发性肺癌38例，非典型性腺瘤样增生1例，转移性肺癌1例。良性病变行肺楔形切除术，32例原发性肺癌行解剖学肺叶切除联合淋巴结清扫，4例肺癌胸膜广泛播散未手术处理，2例肺癌因肺功能差行姑息性肺楔形切除。结论胸腔镜辅助小切口手术有助于明确诊断肺周围型结节病变，治疗临床早期原发性肺癌的长期疗效有待随访观察。