西洛他唑与银杏叶提取物治疗糖尿病周围神经病变对比临床观察

[目的]对比西洛他唑(培达)与银杏叶提取物治疗糖尿病周围神经病变(DNP)的临床疗效。[方法]将46例DNP患者随机分为培达组23例,银杏叶组23例。两组均经糖尿病教育、饮食控制、合理运动、降糖药物及胰岛素强化治疗,血糖基本平稳后,两组均予甲钴胺注射液500μg肌肉注射,每日1次,银杏叶组加用银杏叶提取物87.5mg加入生理盐水250mL内静滴每日1次;培达组加用西洛他唑0.2g加入生理盐水250mL内静滴每日1次,分别治疗15天。观察治疗后两组症状、体征并监测感觉神经和运动神经传导速度。[结果]治疗后两组症状均有改善,但培达组的效果更明显,两组间比较差异有显著性(P<0.05)。[结论]培达与银杏叶提取物治疗糖尿病周围神经病变均有临床疗效,但培达组优于银杏叶提取物组。     

益气通络方联合西药治疗糖尿病周围神经病变52例

目的：观察益气通络方联合西药治疗糖尿病周围神经病变的临床效果。方法：将104例患者随机分为治疗组和对照组各52例，2组均予西药降糖治疗，空腹血糖控制在7mmol／L以下，糖化血红蛋白〈7％，口服弥可保、维生素B1，治疗组加服中药益气通络方，每日l荆，两个月为1疗程。结果：治疗组治愈26例，好转22例，无效4例，总有效率为92．3％（95％CI=80．9％-97．8％）；对照组治愈12例，好转20例，无效20例，总有效率为61．5％（95％CI=48．3％～74．7％）；两组综合疗效比较（u=3．5539，P=0．0006），差异有显著性意义。结论：益气通络方联合西药治疗糖尿病周围神经病变的临床效果优于单纯西药治疗，其收益为OR=0．13（95％CI=0．04～0．43），NNT=3（95％CI=2．13，6．86）。     

红花黄色素前列地尔和甲钴胺联合治疗糖尿病周围神经病变的疗效观察

目的：观察红花黄色素、前列地尔和甲钴胺联合治疗糖尿病周围神经病变的疗效。方法：将60例2型糖尿病合并周围神经病变患者随机分为2组,对照组30例,治疗组30例。治疗组用注射用红花黄色素150mg加入生理盐水250mL中静脉滴注,1日1次,前列地尔注射液20μg加入生理盐水100mL中静脉滴注,1日1次,甲钴胺注射液0.5mg肌肉注射,1日1次,对照组单纯用甲钴胺0.5mg肌肉注射,1日1次,两组疗程均为14天。观察两组临床疗效及其神经传导速度的改变。结果：治疗组临床疗效总有效率为80.0%,对照组总有效率为53.3%,两组差别有统计学意义,治疗组优于对照组（P〈0.05）。两组治疗后神经传导速度比治疗前均有显著提高,治疗组优于对照组（P〈0.05）。结论：红花黄色素、前列地尔和甲钴胺联合是治疗糖尿病周围神经病变的有效方法。     

通脉足浴方治疗糖尿病周围神经病变的疗效观察及护理

[目的]观察通脉足浴方治疗糖尿病周围神经病变的疗效。[方法]将60例患者随机分成两组各30例,两组均保持原来的饮食、运动控制和口服降糖药及胰岛素的用法和用量。治疗组应用通脉足浴方足浴治疗,对照组应用温水足浴治疗。[结果]治疗组总有效率90.0%,对照组为73.3%,两组比较有显著性差异(P<0.05)。[结论]通脉足浴方治疗糖尿病周围神经病变操作简单,疗效好,易被患者接受,值得推广应用。     

Lesions outside the CNS in Parkinson's disease

Parkinson's disease (PD) is not a simple movement disorder induced just by loss of dopaminergic neurons in the substantia nigra pars compacta. Apparently, the substantia nigra is not the only or the first brain region damaged in PD. Moreover, older and recent studies have shown that the degenerative process in PD is much more extensive and affects not only the central nervous system (CNS) but also the peripheral autonomic nervous system and the organs outside the brain that the latter innervates. These include mainly the gastrointestinal tract, the heart, kidneys, urogenital system, and skin. Additional extra‐CNS organs that are involved in PD include the eye and the adrenal gland. This article reviews the anatomical, physiological, and clinical features of extracerebral manifestations of PD, and describes their relevance to the etiology and pathogenesis of the disease. It establishes this illness as a systemic CNS and peripheral disorder that warrants new hypotheses regarding its causation and progression. © 2009 Movement Disorder Society     

Inhibition of a secondary human alloimmune response via the soluble active component of CD154 (CD40L) in severe combined immune-deficient mice engrafted with human lymphocytes

BACKGROUND: Alloimmunization requires a process known as co-stimulation. An important co-stimulatory pathway for most immune responses is mediated by the interaction of CD40 on antigen-presenting cells with CD154 (CD40L) on host T cells. Blockade of this co-stimulatory pathway simultaneous with exposure to challenge with HLA-incompatible cells is hypothesized to inhibit alloimmunization. STUDY DESIGN AND METHODS: Severe combined immune-deficient (SCID) mice were reconstituted with human peripheral blood lymphocytes (Hu-PBL-SCID mice) from a subject primed to HLA antigens and challenged with HLA-incompatible lymphocytes. Mice were challenged in the presence or absence of an 18-kDa soluble recombinant active form of human CD154 (18-kDa CD154). Human IgG production, alloimmunization, and in vitro T-cell responsiveness were assessed. RESULTS: There was no significant effect of 18-kDa CD154 on human IgG levels in these mice, but it inhibited the development of HLA-specific alloantibody in this model to five subsequent untreated white cell challenges. In vitro T-cell proliferation in a mixed lymphocyte culture was also prevented by 18-kDa CD154. CONCLUSION: The recombinant protein 18-kDa CD154 inhibited the ability of the Hu-PBL-SCID mice to mount a secondary immune response to allostimulation. This implies that transfusion-induced alloimmunization utilizes CD40-CD154 co-stimulation and that blockade of this pathway can inhibit T-cell function and interfere with the development of alloimmunization.