哈乐在良性前列腺增生伴急性尿潴留中的应用

目的 :探讨α1A肾上腺素能受体阻滞剂哈乐 (tamsulosin)对良性前列腺增生 (BPH)伴急性尿潴留病人的治疗作用。方法 :对 72例BPH伴急性尿潴留病人采用随机、对照研究 ,分为治疗组和对照组。病人均行保留导尿 ,口服抗生素治疗。治疗组加用哈乐 0 .4mg ,1次 /d ,连续服用 3次。 72h后拔除导尿管。　结果 :拔除导尿管后 4 4 % (32 / 72 )的病人能自行排尿。有效率治疗组为 6 1% (2 2 / 36 ) ,对照组为 2 8% (10 / 36 ) ,两组比较差异有显著性 (P <0 .0 1)。　结论 :对BPH伴急性尿潴留应用哈乐治疗 ,可提高早期拔除导尿管后病人自行排尿的成功率 ,且疗效与前列腺体积大小无关。     

原发性输尿管癌31例临床分析

目的：提高原发性输尿管癌的术前诊断水平。方法：对南京医科大学第一附属医院1989-2002年间收治的31例原发性输尿管癌的临床资料进行回顾性分析。结果：31例中，肉眼血尿22例(71．0％)，腰痛11例(35，5％)。B超、静脉肾盂造影(IVU)、CT和逆行造影检查的阳性率分别为输尿管腔内占位4例(13．0％)、输尿管腔内占位3例(11．5％)、膀胱或合并膀胱占位8例(36．4％)，输尿管充盈缺损6例(40．0％)。29例患者经手术治疗，其中13例行患侧肾、输尿管、膀胱袖状切除。结论：老年患者反复发作的腰痛及血尿应考虑原发性输尿管癌的可能，造影诊断对本病有较高价值，应作CT及MRU无创检查。     

无张力性吊带术治疗女性压力性尿失禁

目的探讨无张力阴道吊带术(tension-free vaginal tape，TVT)治疗女性压力性尿失禁的疗效。方法13例经尿动力学检查证实为压力性尿失禁在连续硬膜外麻醉下经阴道前壁行无张力阴道吊带术，低平截石位，经阴道前壁向上穿刺尿道两侧间隙，从耻骨上腹壁引出TVT吊带，调整张力，关闭切口。结果手术时间15～45min，平均35min。13例随访6～24个月，平均13个月，12例治愈，1例改善，无尿失禁复发或排尿困难。结论TVT操作简单，创伤小，手术时间短，术后恢复快，治疗压力性尿失禁疗效好。     

腔镜下甲状旁腺腺瘤切除1例

原发性甲状旁腺功能亢进是一种严重的内分泌代谢疾病,临床较少见,欧美国家报道其年发病率7.8/10万[1].主要导致代谢紊乱,其中以泌尿系统结石最常见,骨病、消化性溃疡及胰腺炎次之,治疗首选手术切除.我们应用微创腹腔镜技术治疗1例甲状旁腺腺癌,效果良好,现报道如下.     

α1A受体阻滞剂在前列腺癌中的应用

目的：探讨α1A受体阻滞剂坦素罗辛对改善前列腺癌患者下尿路梗阻症状的作用。方法：对存在有下尿路梗阻症状的26例前列腺癌患者,在进行联合雄激素阻断治疗的同时,加用α1A受体阻滞剂坦素罗辛。结果：治疗后2周和4周,治疗组的最大尿流率（Qmax）、国际前列腺症状评分（I－PSS）、残余尿量（PVR）均比 对照组有显著性改善（P＜0.05）。结论：α1A受体阻滞剂坦素罗辛可有效地改善前列腺癌患者下尿路梗阻症状。     

改良Sigma直肠膀胱术14例临床分析

目的：介绍并评价改良Sigma后术的可控性尿流改道临床疗效。方法：14例膀胱、前列腺肿瘤患者接受该手术。取25cm左右乙状结肠折叠后全层切开,再缝合成低袋,低压袋顶端固定在骶岬处,两输尿管末端合并吻合并外翻形成乳头,从低压袋上方引入再植。结果：术后发生直肠阴道瘘1例,经横结肠造口过渡后自愈;1例左肾积水伴上尿路感染,经输尿管顺行扩张后恢复正常,该患者术后3个月发生严重低血钾,经补充枸橼酸钾后治愈。平均随访22.5个月,本组未见尿失禁、上尿路感染。3例肿瘤复发,2例肉瘤复发患者于术后6个月后死亡。结论：改良Sigma 手术费时短,对肠管扰动小,操作简便,术后尿控满意,无上尿路积水、感染及明显酸碱电解质紊乱,明显提高了患者生活质量。     

急性上尿路梗阻无尿80例诊治分析

目的：分析急性上尿路梗阻性无尿80例的诊断和治疗方法,以尽早诊断,及时治疗。方法：报告1989-1999年收治的急性上尿路梗阻性无尿患者80例,诊断依据为少尿以致无尿、水肿、血尿素氮和肌酐进行性增高,初步诊断首选腹部平片（KUB）和B超及肾图检查。结果：10例患者术前行血液透析,手术治疗53例,包括输尿管切开取石术18例,肾造瘘术20例,狭窄段输尿管切除膀胱再植8例,输尿管腹壁皮肤造口术7例,双“J”管内引流术27例,结论：本病病因,病情复杂多变,应采取不同的治疗措施。     

老年患者肾移植（附10例报告）

为探讨老年患者肾移植的临床疗效,分析自１９９０年６月至１９９７年６月期间１０例６０ｙ以上肾移植受者的临床资料。结果表明：术后发生急性排斥反应２例。发生各种并发症７例。４例死亡,分别死于肺部感染、脑出血、脑梗死和急性坏死性胰腺炎。术后１、３、５ａ的人／肾存活率分别为９０％／９０％、８０％／８０％、６０％／６０％。认为年龄已不再是老年尿毒症患者选择手术的障碍,老年患者同样可以安全地接受肾移植并获得满意的疗效。并发症所致的患者带肾死亡是移植失败的主要原因。严格选择手术适应证,移植前原发疾病和合并症的积极治疗,免疫抑制剂的合理应用以及术后并发症的积极防治对提高老年肾移植的长期存活率具有重要的意义。     

曲尼司特对环孢素A诱导的人肾小管上皮细胞向间充质转变的抑制作用

目的 研究曲尼司特(Tran)对环孢素A(CsA)诱导的人肾小管上皮细胞(HK-2)向间充质转变的影响,并探讨该药抗纤维化的机制.方法 所有用于实验的HK-2细胞株均为8～12代细胞,分为4组:(1)空白对照组,收获细胞,不做任何处理;(2)CsA组,加入4.2μmol/LCsA;(3)CsA+Tran组,预先加入100μmol/L Tran,作用2 h后再加入4.2 μmol/L CsA;(4)Tran组,仅加入100μmol/L Tran.72 h后于共聚焦显微镜下观察各组细胞形态学变化;用免疫荧光法以及免疫印迹法检测各组钙黏蛋白(E-cadherin)、平滑肌肌动蛋白α(α-SMA)和骨桥蛋白(OPN)的表达.结果 HK-2细胞在正常情况下表现为典型的"鹅卵石"样形态,细胞圆钝,且与邻近的细胞连接较为紧密;空白对照组和Tran组细胞表现为典型的HK-2细胞形态;CsA组细胞变狭长,甚至向周边伸出"伪足"样改变,细胞间连接较为稀疏;CsA+Tran组的细胞形态学改变有明显改善.CsA组细胞E-cadherin荧光表达强度明显弱于对照组,α-SMA、OPN荧光表达强于对照组;CsA+Tran组细胞E-cadherin荧光表达强于CsA组,α-SMA、OPN荧光表达弱于CsA组.免疫印迹检查中,CsA组细胞E-cadherin 的表达明显低于对照组,而α-SMA、OPN的表达明显高于对照组,CsA+Tran组细胞E-cadherin的表达高于CsA组,而α-SMA、OPN的表达低于CsA组.结论 曲尼司特能抑制CsA诱导的HK-2细胞由肾小管上皮向间充质细胞转化的过程,其机制可能与抑制OPN的表达有关.

Abstract：

Objective To study the effect of tranilast on cyclosporine A (CsA)-induced epithelial-to-mesenchymal transition in human renal tubular epithelial cells, and investigate the mechanism of its antifibrotic effect. Methods Cultured HK-2 cells were divided into four groups: (1)In the control group, cells were treated without any medicine; (2) The cell were treated with CsA (4. 2μmol/L) for 72 h; (3) The cells were treated with a combination of CsA (4. 2 μmol/L) and tranilast (100μmol/L); (4) The cells were treated with tranilast (100 μmol/L) alone for 72 h.Morphological changes of the cells were assessed by phase-contrast microscopy. The immunofluorescence and Western blotting were adopted to detect the expression of E-cadherin, α-SMA and OPN mRNA and proteins respectively. Results Tranilast could markedly ameliorate the morphological changes of HK-2 cells stimulated by CsA. The irmmunofluorescence staining revealed the expression of E-cadherin was markedly decreased in HK-2 cells stimulated with CsA for 72 as compared with the control group, while the expression of α-SMA and OPN was significantly higher in CsA group than the control group. The expression of E-cadherin in the CsA + Tranilast group was higher than the CsA group, while the expression of α-SMA and OPN in the CsA + Tranilast group was lower than the CsA group. Western blotting showed that protein expression level of E-cadherin in CsA group was dramatically lower than that in the control group (P＜0. 05), while that of α-SMA and OPN in CsA group was significantly higher than in the control group (P＜0.05). The protein expression level of E-cadherin in HK-2 cells in the CsA + Tranilast group was markedly higher than in the CsA group (P＜0.05), and that of α-SMA and OPN in CsA + Tranilast group was significantly lower than in the CsA group (P＜0. 05). Conclusion Tranilast can block the CsA-induced epithelialto-mesenchymal transition in HK-2 cells probably by suppressing the expression of OPN.     

曲尼司特对环孢素A诱导的人肾小管上皮细胞向间充质转变的抑制作用

Objective To study the effect of tranilast on cyclosporine A (CsA)-induced epithelial-to-mesenchymal transition in human renal tubular epithelial cells, and investigate the mechanism of its antifibrotic effect. Methods Cultured HK-2 cells were divided into four groups: (1)In the control group, cells were treated without any medicine; (2) The cell were treated with CsA (4. 2μmol/L) for 72 h; (3) The cells were treated with a combination of CsA (4. 2 μmol/L) and tranilast (100μmol/L); (4) The cells were treated with tranilast (100 μmol/L) alone for 72 h.Morphological changes of the cells were assessed by phase-contrast microscopy. The immunofluorescence and Western blotting were adopted to detect the expression of E-cadherin, α-SMA and OPN mRNA and proteins respectively. Results Tranilast could markedly ameliorate the morphological changes of HK-2 cells stimulated by CsA. The irmmunofluorescence staining revealed the expression of E-cadherin was markedly decreased in HK-2 cells stimulated with CsA for 72 as compared with the control group, while the expression of α-SMA and OPN was significantly higher in CsA group than the control group. The expression of E-cadherin in the CsA + Tranilast group was higher than the CsA group, while the expression of α-SMA and OPN in the CsA + Tranilast group was lower than the CsA group. Western blotting showed that protein expression level of E-cadherin in CsA group was dramatically lower than that in the control group (P＜0. 05), while that of α-SMA and OPN in CsA group was significantly higher than in the control group (P＜0.05). The protein expression level of E-cadherin in HK-2 cells in the CsA + Tranilast group was markedly higher than in the CsA group (P＜0.05), and that of α-SMA and OPN in CsA + Tranilast group was significantly lower than in the CsA group (P＜0. 05). Conclusion Tranilast can block the CsA-induced epithelialto-mesenchymal transition in HK-2 cells probably by suppressing the expression of OPN.