健康教育对ARN并视网膜脱离术后疗效的影响

目的 :研究健康教育对急性视网膜坏死综合征 (acuteretinalnecrosissyndromo ,ARN)并视网膜脱离术后疗效的影响。方法 :随机将 32例 (4 2眼 )ARN并视网膜脱离病人分为A ,B两组。A组 ,2 2例 (2 9眼 )作为观察组 ,术后按制订的健康教育方案进行护理。B组 ,10例 (13眼 )作为对照组 ,常规护理 ,不进行健康教育。对比观察两组术后疗效及并发症。结果 :AB两组对照比较 ,A组手术成功率明显增加 ,术后并发症如视网膜脱离复发、角膜水肿、继发性青光眼等发生率明显降低 (P <0 .0 5 )。结论 :健康教育有助于提高ARN并视网膜脱离病人手术疗效 ,减少术后并发症。     

咪达普利与氯沙坦对糖尿病大鼠心肌间质重构的对比研究

目的:研究在不同水平阻断肾素-血管紧张素系统(RAS)对糖尿病大鼠心肌间质重塑过程的影响及保护机制。方法:50只健康雄性SD大鼠随机分为空白对照组(10只)和糖尿病组(40只),糖尿病组用链脲佐菌素(STZ)50 mg/kg腹腔注射建立实验性糖尿病大鼠模型,将建模成功的39只大鼠随机分为咪达普利组10只、氯沙坦组10只、联合用药组10只及模型对照组9只,给药9周后麻醉处死,免疫组化SP法检测肿瘤坏死因子-α(TNF-α)、核因子-κB(NF-κB)、基质金属蛋白酶-9(MMP-9)的蛋白表达,RT-PCR法测NF-κB、MMP-9和TNF-α的mR-NA表达。VG染色观察心肌胶原容积分数(CVF)变化。结果:与空白对照组相比,糖尿病组大鼠心脏指数、左心室指数、心肌CVF明显升高,心肌间质发生重构,TNF-α、MMP-9、NF-κB含量和TNF-αmRNA、MMP-9 mRNA和NF-κB mRNA的表达均增高。咪达普利、氯沙坦及联合用药干预后,上述指标表达均明显降低,但咪达普利和氯沙坦的改善程度无明显差异,联合用药明显优于单独用药。结论:咪达普利和氯沙坦可能通过影响TNF-α、MMP-9的表达来改善糖尿病心肌间质重构,NF-κB参与了这一过程。     

乳腺癌根治术后两种不同负压引流效果的对比分析

目的探讨乳腺癌根治术后两种负压引流方法的效果。方法我科在1999年1月至2005年12月对359例乳腺癌根治术后不同引流方法下皮瓣坏死及皮瓣下积液的发生率进行回顾性分析。结果两组间皮瓣坏死和皮下积液的发生率比较有显著性差异。结论乳腺癌根治术后单纯低负压瓶Y型管引流效果非常可靠,值得临床推广。     

髋关节腔、股骨颈髓腔自体骨髓移植药液灌注并中医药治疗在股骨头坏死术后的临床应用(附17例报告)

目的:髋关节腔、股骨颈髓腔自体骨髓移植药液灌注并中医药治疗在股骨头坏死术后的临床应用,探索力学刺激的影响。方法:自2005年~2011年采用开放和微创术式治疗股骨头缺血性坏死患者17例(23髋),年龄19~60岁,平均22.4岁,ARCO分期为ⅠA期3例,ⅡA期8例,ⅡC期3例,ⅢA期3例。全部病例均行自体骨髓移植并药液局部灌注在血管束植入、骨移植及微创术后的应用,术后随访1~7年,根据手术前后Harris评分变化,X线影像学表现随访观察。结果:术后患者Harris评分变化均提高35.71分(平均术前56.29分,术后92分),影像学表现17例保持稳定。结论:自体骨髓移植药液局部灌注并中药治疗在股骨头缺血性坏死术后的应用,操作简单,取材方便,无排异反应。术后恢复快,力学刺激对成骨、成软骨、新生血管形成有一定促进作用。     

干细胞移植改善股骨头坏死缺血状态122例临床观察

目的探讨经动脉自体骨髓干细胞（BMSC）和外周血干细胞（PBSC）移植改善股骨头坏死缺血状态的临床疗效。方法2004年7月至2006年12月对122例（211髋）成人缺血性股骨头坏死（ANFH）患者施行自体BMSC或PBSC移植治疗,按国际分期标准（ARCO）分期,设自身前后对照方法进行疗效观察。BMSC组90例和PBSC组32例在DSA下行股骨头供血动脉干细胞移植术,移植后第3、6、12、24个月进行髋关节Harris评分做疗效评价,6个月复查股骨头供血动脉造影观察血管新生情况。每间隔6个月复查影像学变化。结果122例患者随访3～24个月（平均10．2个月）,髋关节疼痛缓解104例（85．1％）,关节功能改善76例（62．0％）,90例（73．9％）行走间距延长。干细胞移植术后6个月,15例患者股骨头供血动脉造影检查见供血动脉较移植前明显增多、增粗,血流速度增快;12～24个月20例股骨头区可见骨质病变获得改善。结论经动脉自体BMSC和PBSC移植方法简便,安全有效,对缺血性股骨头无再次损伤,患者依从性好,是治疗缺血性股骨头坏死的一种新途径。     

肿瘤坏死因子-α基因启动子-308位多态性与慢性非细菌性前列腺炎／慢性骨盆疼痛综合征中医证型相关性研究

目的探讨肿瘤坏死因子—α（TNF-α）基因启动子-308位多态性与慢性非细菌性前列腺炎,慢性骨盆疼痛综合征中医证型的相关性。方法采用PCR-R FLP技术结合ELISA法。对115例CPPS患者和21例非CPPS健康人群前列腺液TNF-α水平及启动子-308位基因多态性进行检测。并对其与中医证型的相关性进行了分析。结果CPPS组TNF-α2等位基因型频率显著高于健康对照组,OR=6．286（95％CI1．471-26．850,P〈0．01）。中医证型中。湿热蕴阻证、湿热挟瘀证与TNF—α基因启动子308-2基因型相关。与气滞血瘀证及健康对照组比较差异显著（P〈0．05）。结论TNF-α2等位基因可能与CPPS的易感性相关,并可能是CPPS中医证型中湿热蕴阻证、湿热挟瘀证的易感基因。     

墨西哥仙人掌多糖对人乳腺癌MCF-7细胞凋亡坏死诱导作用的研究

目的观察墨西哥仙人掌多糖对人乳腺癌MCF-7细胞凋亡及坏死的诱导作用。方法将浓度为20μg／mL的墨西哥仙人掌多糖作用于体外培养的人乳腺癌MCF-7细胞,分别培养24h和48h,然后利用流式细胞仪检测人乳腺癌MCF-7细胞的凋亡及坏死情况。结果不同作用时间的墨西哥仙人掌多糖均能够诱导人乳腺癌MCF-7细胞凋亡,并促进该肿瘤细胞发生坏死,与阴性对照组比较差异显著（P〈0．01）,尤以48h作用明显,凋亡及坏死肿瘤细胞占培养细胞总数的84．11％。结论墨西哥仙人掌多糖能够诱导人乳腺癌MCF-7细胞的凋亡及坏死。     

Removal of dying cells and systemic lupus erythematosus

Abstract

Systemic lupus erythematosus (SLE) is a very heterogeneous systemic autoimmune disease, in which autoantibody synthesis against nuclear constituents is the main immunological characteristic. These autoantibodies underwent affinity maturation and isotype switching. Additionally, T-cell tolerance against nuclear autoantigens should be affected in these autoimmune patients. Nuclear material derived from apoptotic and/or necrotic cells may serve as an important source of autoantigens. However, dead and dying cells as well as cellular debris are rapidly removed from tissues by phagocytes without eliciting inflammation or immune responses under healthy conditions. During apoptosis nuclear components are strongly modified through enzymatic reactions. If these cells are not timely cleared, those autoantigens may be released, taken up, and presented by dendritic cells in tissues or presented by follicular dendritic cells in lymph nodes to T and B cells, respectively. This could be a mechanism for breaking the peripheral self-tolerance. In this article we focus on the deficient clearance of apoptotic cells in SLE patients and its importance in development of this autoimmune disease.     

Amelioration of Endotoxin-Induced Uveitis in Rabbit by Topical Administration of Tacrolimus Proglycosome Nano-Vesicles

This work was aimed to improve the efficacy of tacrolimus in the treatment of endotoxin-induced uveitis (EIU) using propylene glycol modified lipid vesicles termed as proglycosome nano-vesicles (PNVs). PNVs were prepared by modified film hydration method. Experimental uveitis in rabbit eye was induced by an intravitreal injection of 20 μL of the endotoxin solution containing 100 ng of lipopolysaccharide endotoxin. In vivo efficacy of PNVs was determined by studying clinical symptoms of uveitis using slit lamp examination and by quantitatively measuring levels of tumor necrosis factor-alpha, interleukin-6, leukocytes and total proteins in aqueous humor, 24 h after intravitreal injection of endotoxin. Comparison was made with healthy, untreated and tacrolimus solution treated eyes. PNVs developed were nano-sized, deformable and showed sustained release of tacrolimus over period of 12 h. In vivo results indicated statistically significant difference between the effects of PNVs in the treatment of EIU compared to tacrolimus. PNV treatment not only subsides clinical symptoms of uveitis but also prevented breakdown of blood aqueous barrier. Tacrolimus loaded PNVs are potential new topical treatment for uveitis.     

Liver and kidney damage induced by 4-aminopyridine in a repeated dose (28 days) oral toxicity study in rats: Gene expression profile of hybrid cell death

4-Aminopyridine (4-AP) is an orphan drug indicated for the treatment of neuromuscular disorders. There is a great controversy around the use of this drug because of its narrow safety index and because a large number of adverse effects have been reported. Moreover, it was shown to induce cell death in different cell lines, being reported mainly apoptosis and necrosis as the principal pathways of cell death mediated by blockage of K channels or the Na, K-ATPase, but until now it was not described in vivo cell death induced by 4-aminipyridine. To provide new subchronic toxicity data and specifically, evaluate if 4-AP is able to induce in vivo cell death process and the main pathways related to it, a repeated dose (28 days) oral toxicity study, at therapeutic range of doses, was conducted in rats. The anatomical pathology, the biochemical and hematological parameters were analyzed and a real-time PCR array analysis was developed with an Ingenuity Pathway Analysis (IPA). The leucocytes number, the lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) enzymatic activity were increased at all dose but the erythrocytes number, the hemoglobin concentration, the alkaline phosphatase (FAL) and alanine aminotransferase (ALT) enzymatic activity were increased only at highest dose studied. However, glucose levels decreased at all doses. The biochemical results are indicative of hepatic damage. The anatomy pathology studies showed cell death only on liver and kidney, and the real-time PCR array on liver tissue expressed a gene expression profile of necrotic and apoptotic induced cell death. The present work shows for the first time in vivo cell death on liver and kidney with features of apoptosis and necrosis induced by 4-AP and the gene expression profile shows that the cell death is mediated by necrotic and apoptotic pathways that support this finding.