腹膜后局灶性Castleman病的临床分析并文献复习

目的分析总结腹膜后局灶性Castleman病(localized Castleman’s disease,LCD)的临床特点及诊治方法,以期对该病的诊断和治疗过程提供合理指导意见。方法回顾性分析2014年12月武汉大学人民医院收治的1例腹膜后LCD病人临床资料,并针对性复习相关文献。结果病人术前检查未明确诊断,手术行腹膜后肿瘤切除,术后病理切片检查确诊,未行辅助性治疗。1年后随访复查,病人恢复可,手术效果较好。结论腹膜后LCD术前诊断较困难,手术切除预后良好,术前充分评估可以为治疗方式的选择以及手术方式提供依据,提高手术成功率,减少副损伤及并发症。     

ΔNp63上调羟甲基戊二酸单酰辅酶A还原酶表达促进食管鳞癌细胞增殖及迁移

目的：探讨肿瘤蛋白p63的转录变体ΔNp63调控食管鳞癌细胞增殖及迁移的分子机制。方法：以ECA109细胞为模型,通过慢病毒介导的转基因（LV.ΔNp63）在细胞中过表达ΔNp63,通过定量PCR及Western blot检测羟甲基戊二酸单酰辅酶A还原酶（HMG-CoA reductase,HMGCR）表达水平,通过染色质免疫沉淀(ChIP)和荧光素酶活性报告实验检测ΔNp63蛋白与HMGCR基因5’-非翻译区的结合;细胞中过表达ΔNp63同时利用RNA干扰抑制HMGCR表达,通过细胞计数试剂-8（CCK-8）检测细胞增殖情况, Annexin V-FITC/PI双染检测细胞凋亡,Transwell小室培养实验检测细胞迁移。结果：ECA109细胞中过表达ΔNp63后,HMGCR的mRNA和蛋白表达水平分别提高了241%和81%;结合ChIP及荧光素酶活性报告实验结果提示ΔNp63识别位点位于HMGCR启动子-747至-728区域。过表达ΔNp63同时抑制HMGCR表达组细胞增殖能力显著低于单纯过表达ΔNp63组(24hr,P<0.05;48/72hr,P<0.01);细胞凋亡水平为16.5±1.5%,显著高于单纯过表达ΔNp63组细胞（26.9±1.9%,P<0.01）,同时细胞的迁移率显著低于单纯过表达ΔNp63组细胞( 52.2±2.6% vs. 33.4±3.1%,P<0.01)。结论：ΔNp63通过上调HMGCR转录表达促进食管鳞癌细胞增殖及迁移能力。     

肝移植术后早期急性肾损伤预测指标的研究进展

肝移植术是治疗终末期肝病最有效的方法,术后急性肾损伤(AKI)与患者的预后及长期生存密切相关,因此肝移植术后AKI的早期识别与预防尤为关键。由于血清肌酐(SCr)水平易受肾功能损伤以外因素的影响,常在测得血清SCr升高前肾功能早已发生了损伤。近年来在肾损伤评估中比SCr更灵敏、更准确的新型生物指标不断被报道,使肝移植后AKI早期有效的干预成为可能。文章就肝移植术后早期AKI的新型预测生物指标进行综述。     

天麻素治疗梅尼埃病进展

临床认为在基础治疗上使用天麻素联合其他药物治疗梅尼埃病起协同作用,从而明显提高了疗效及安全性。特别是天麻素联合中药治疗梅尼埃病还充分体现了治未病的思想,其疗效及安全性较天麻素及其联合西药治疗梅尼埃病更高。     

大建中汤治疗胃溃疡的疗效观察

目的:观察以经方大建中汤为基础方,随症加减对脾胃阳虚、阴寒内盛型胃溃疡患者的临床疗效。方法:将60例患者随机分为对照组和治疗组各30例,对照组给予奥美拉唑治疗,幽门螺杆菌阳性加阿莫西林;治疗组在对照组的基础上,再给予大建中汤加味治疗。结果:治疗组总有效率为90%,对照组为76.67%,差异有显著性(P<0.05)。结论:观察以经方大建中汤为基础方,随症加减对脾胃阳虚、阴寒内盛型胃溃疡患者的临床疗效明显。     

川穹嗪通过调节P糖蛋白表达逆转乳腺癌多重耐药性的机制

<正>目的:肿瘤的多重耐药性是造成肿瘤化学治疗困难的因素之一。近期研究表明,川穹嗪对肿瘤的多重耐药性有逆转作用,但其机制仍不明确。因此,本文设计以下实验,通过川穹嗪对药物耐药乳腺癌细胞的作用进一步探讨多重耐药的相关机制。方法:将MCF-7细胞和P糖蛋白过表达的MCF-7/dox细胞分别培养后加入川穹嗪,用MTT法检测细胞增殖,用流式细胞术检测细胞内多柔比星积聚,用RT-PCR和Western Blotting检测P糖蛋白表达。     

瘦素和瘦素受体在食管癌中的表达及其意义

Objective To investigate the role of leptin and leptin receptor in carcinogensis and development of esophageal carcinoma. Methods The expression of leptin and leptin receptor was detected in 52 cases of esophageal carcinoma tissues and 49 cases of normal esophageal tissues by immunohistochemistry. The correlation between their expression and clinicopathological parameters was also analysized. Results The expression rate of leptin and leptin receptor in esophageal carcinoma was 78. 8% (41/52) and 82.7% (43/52) respectively, and the rate in normal esophagus was 58.3% (28/49) and 59.2% (29/49) respectively. The expression rate of leptin and leptin receptor both had statistically significantly differences between esophageal carcinoma and normal esophagus tissues (P ＜ 0. 05). The expression rate of leptin was associated with position, tumor size, differentiation, lymphatic metastasis and TNM stage (P ＜ 0. 05 ). Conclusion Leptin and leptin receptor were dually expressed in esophageal carcinoma.They played important roles in the process of carcinogensis and development of esophageal carcinoma.     

认知行为干预对青少年脊柱侧凸矫形术后的影响

目的 探讨认知行为干预在缓解青少年脊柱侧凸矫形术后焦虑和疼痛中的作用,以及年龄和性别对缓解程度的影响.方法 选择2005年1月～2008年12月我该科接受后路矫形手术的青少年特发性脊柱侧凸患者43例,根据入院时间的先后顺序分为两组.A组患者22例(男9例,女13例),年龄10～18岁,平均(13.95±1.86)岁,同时接受脊柱外科常规护理和认知行为干预;B组患者21例(男10例,女11例),年龄10～18岁,平均(14.00±2.15)岁,仅接受脊柱外科常规护理.所有患者分别在术前和术后2d接受焦虑状态评估(Speilberger's量表,STAI,1983),并在术后2、4d进行VAS视觉疼痛评分,对结果进行统计学分析.结果 接受了认知行为干预的A组患者,术后2d焦虑状态评分和2、4d进行VAS评分分别为(31.14±4.33)、(6.91±0.92)和(6.00±1.27),均明显低于B组患者(P＝0.010,0.009和0.003).A组患者组内比较,年龄14岁以下患儿的术后焦虑状态评分和2、4d VAS评分,明显低于14岁以上儿童组(P＝0.002、0.008和0.003).A组中男性患者的术后STAI和VAS评分均要低于女性患者,其中术后2d的STAI和术后4d VAS评分差异具显著性(P＝0.019,0.032).结论 认知行为干预能够减轻青少年脊柱侧凸患者矫形术后焦虑和疼痛的程度,尤其对14岁以下的男性儿童缓解效果好,临床具体实施时要采取个体化的治疗方案.     

介入病房进修医师的培养浅谈

在介入进修医师的培养中,充分认识其来源的差异性及临床知识与技能的参差不齐,合理利用其专长,理论联系实际,循序渐进地带教,重视临床工作,同时兼顾科研方法的传授,半年至1年后,进修生就可以达到相当的水平。     

乳腺癌小鼠动物模型中白细胞介素-17的表达及其意义

目的 探讨小鼠乳腺癌动物模型中白细胞介素-17(IL-17)的表达及意义.方法 以MA782/5S28102及4T1细胞株建立两种乳腺癌动物模型.分别于接种后1周和4周采用Western blot检测肿瘤组织中IL-17的表达.使用PMA+CD3单抗+CD28单抗刺激后,采用酶联免疫吸附试验(ELISA)检测肿瘤细胞和淋巴细胞培养体系上清中IL-17的含量.同时观察IL-17对培养体系及4T1荷瘤小鼠中肿瘤细胞生长的影响.结果 乳腺癌模型中晚期肿瘤组织中IL-17的表达水平均明显较早期有所升高.分离的肿瘤细胞接受刺激后,几乎不分泌IL-17,淋巴细胞分泌大量IL-17(P＜0.01).IL-17不能促进4T1细胞的生长(增长率分别为1.11±0.11和1.28 ±0.21,P＞0.05);将IL-17输注至4T1荷瘤小鼠的体内,可见肿瘤生长速度明显加快(P＜0.05).输注IL-17的荷瘤小鼠肿瘤组织中微血管密度(MVD)明显增加(MVD分别为:35.79±9.49,13.52±3.55,P＜0.01).结论 IL-17在晚期肿瘤组织中明显升高,IL-17可能通过促进肿瘤组织内微血管形成加快肿瘤的生长.

Abstract：

Objective To explore the impact of interleukin (IL) -17 expression on tumor growth in experimental models of murine mammary carcinoma and potential mechanisms. Methods Two murine cell lines, MA782/5S28102 and 4T1 were used to establish experimental models of murine mammary carcinoma. The IL-17 expression in tumor tissues derived from MA782-bearing mice or 4T1-bearing mice was detected in early and late stages of the tumor by Western blotting. The tumor cells and tumor-infiltrated-lymphocytes were separated from tumor tissues and cultured for 5 days with stimulation of PMA, anti-CD3 antibody and anti-CD28 antibody. The supernatants of culture media of stimulated tumor cells or tumor-infiltrated-lymphocytes were harvested and tested for IL-17 concentration by enzyme linked immunosorbent assay (ELISA). To evaluate the effect of IL-17 on the proliferation of tumor cells, 4T1 cells were culture in media with or without IL-17 and the cell number was counted on the day 5. For ire vivo assay, 4T1-bearing mice were injected with IL-17 or culture media via tail vein, and the tumor volume was measured. To assay the angiogenesis, the tumor tissues from 4T1-bearing mice with or without injection of IL-17 were stained with anti-CD31 antibody by immunohistochemistry. Results The IL-17 expression was significantly higher in late stage than in early stage of tumor in two experimental models. The tumor expression of IL-17 was secreted by tumor infiltrated lymphocytes (P ＜0.01). IL-17 could not increase the generation of tumor cells in vitro (1. 11 ±0. 11, 1. 28 ±0. 21 ,P ＞0. 05). But IL-17, injected into 4T1 -bearing mice, markedly enhanced in vivo tumor growth and significantly increased tumor vascularity (35. 79 ±9. 49, 13. 52 ±3. 55,P ＜0.01). Conclusion IL-17 in tumor tissue probably promotes tumor growth through enhancing angiogenesis.