中枢神经系统白血病脑脊液蛋白质、氯化物、糖定量变化分析

选取中枢神经系统白血病与非中枢神经系统白血病患者各40例,行腰椎穿刺术取得脑脊液标本检测蛋白质、氯化物、糖定量。中枢神经系统白血病组患者脑脊液蛋白质水平较非中枢神经系统白血病患者升高(P0.05),氯化物及糖定量水平较非中枢神经系统白血病患者下降(P0.05);中枢神经系统白血病组患者治疗2w后脑脊液蛋白质水平较确诊时下降(P0.05),氯化物及糖定量水平较确诊时升高(P0.05)。中枢神经系统白血病患者较非中枢神经系统白血病患者脑脊液蛋白质升高、氯化物及糖定量降低,治疗后指标逐渐恢复正常,检测脑脊液白蛋白、氯化物及糖定量对判定患者病情严重程度及治疗进展具有一定指导价值。     

再障生血片联合雄激素及环孢素治疗慢性再生障碍性贫血30例效果观察

目的 :研究再障生血片联合雄激素(安特尔)及免疫抑剂(环孢素)治疗慢性再生障碍性贫血(CAA)的临床效果。方法:慢性再生障碍性贫血60例随机分成观察组和对照组各30例,对照组用环孢素A、安特尔口服治疗,观察组在环孢素A、安特尔的基础上加用再障生血片口服治疗,比较两组用药后临床疗效及不良反应发生情况。结果:(1)总有效率:观察组为86.7%,对照组为70.0%,两组比较差异有统计学意义(P<0.05)。(2)两组治疗后白细胞、血红蛋白、血小板比较:观察组分别为(3.7±1.0)×109/L,(77.0±29.8)g/L,(67.2±25.8)×109/L。对照组分别为(2.4±0.9)×109/L,(52.6±25.1)g/L,(46.1±20.7)×109/L,两组比较差异有统计学意义(P<0.05)。结论 :再障生血片联合环孢素A、安特尔的联合治疗CAA的方案更佳。     

过表达miR-520d 通过抑制自噬蛋白Beclin1 逆转三阴性乳腺癌细胞化疗耐药性

[摘要] 目的：探讨miR-520d 通过调控自噬逆转三阴性乳腺癌（TNBC）细胞化疗耐药的作用及分子机制。方法：以人TNBC细胞系MDA-MB-231 和MDA-MB-468 为亲本株细胞构建多西他赛（Doc）耐药细胞株MDA-MB-231/Doc 和MDA-MB-468/Doc,实验分为空白组（亲本细胞）、对照组（耐药细胞组）和过表达miR-520d 组。用qPCR检测空白组和耐药细胞组细胞中miR-520d 的表达水平,MTT实验检测过表达miR-520d 的耐药细胞对Doc 的敏感性,MDC染色后荧光显微镜观察细胞中自噬小体的发生情况、共聚焦显微镜观察过表达miR-520d 的耐药细胞中自噬相关蛋白LC3 阳性的细胞数。用荧光素酶报告基因实验验证miR-520d 与Beclin1 的靶向关系。用WB实验检测过表达miR-520 对细胞中自噬相关蛋白Beclin1 和LC3Ⅰ、LC3Ⅱ表达的影响。结果：TNBC耐药细胞中miR-520d 的表达水平明显低于空白组细胞（P<0.01）。过表达miR-520d 的耐药细胞对Doc的敏感性显著提高（P<0.01）、细胞的自噬活性明显降低（P<0.01）。荧光素酶报告基因实验证明Beclin1 是miR-520d 可能的靶分子。Doc 与miR-520d mimics 联合使用可降低TNBC耐药细胞中LC3-Ⅱ/Ⅰ比值和自噬蛋白Beclin1 的表达水平（均P<0.05）。结论：通过调控miR-520d 水平可能改变自噬蛋白Beclin1 表达,从而逆转TNBC细胞Doc化疗耐药性。     

内镜下乳头括约肌小切开联合气囊扩张术对胆总管结石患者的疗效观察

目的 观察乳头括约肌小切开联合气囊扩张术对胆总管结石( CDS)患者的疗效.方法 将我院2010年1月至2011年9月间的161例CDS患者分为3组,54例行内镜下乳头括约肌切开术(EST组),54例行内镜下乳头气囊扩张术(EPBD组),53例行内镜下乳头括约肌小切开联合气囊扩张术(sEST+EPBD组),均根据实际情况在乳头治疗后行取石篮取石和(或)气囊取石,部分患者以碎石篮碎石后取石.结果 与EST组比较,sEST+EPBD组术后并发症的发生率显著降低,出血发生减少,较EPBD组提高了一次取石的成功率,明显降低了术后高淀粉酶血症的发生率.结论 应用乳头括约肌小切开联合气囊扩张术治疗胆总管结石,术后并发症减少,在胆总管结石取石治疗中更为有效、安全.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

目的 探讨水通道蛋白1(AQP1)在急性坏死性胰腺炎(ANP)大鼠胰腺的表达及其意义.方法 将48只雄性SD大鼠随机分为对照组和ANP组,制模后3、6、12、18 h各时间点分别处死6只.记录腹水量,测定血清淀粉酶;采用酶联免疫吸附试验(ELISA)检测血清AQP1含量;苏木素-伊红(HE)染色观察胰腺组织病理改变;伊文思兰染料(EB)血管外渗法检测胰腺组织毛细血管通透性;免疫组织化学和Westem blot法检测胰腺组织AQP1蛋白表达;荧光定量聚合酶链反应(PCR)检测AQP1基因mRNA表达.结果 (1)对照组3、6、12、18 h血清淀粉酶水平分别为(1308±759)、(1077±508)、(1325±761)、(1328±762)U/L,ANP组分别为(9102±2199)、(8799±1634)、(9398±1473)、(9484±862)U/L;对照组胰腺组织EB含量分别为(205.61±32.99)、(141.46±27.18)、(96.94±26.79)、(61.43±24.82)mg/L;ANP组分别为(273.59±23.47)、(253.51±31.68)、(221.15±73.68)、(185.28±42.35)mg/L;血清AQP1含量对照组为(74.08±11.80)、(78.49±9.06)、(75.77±7.37)、(72.75±13.87)mg/L,ANP组为(73.29±9.61)、(62.85±7.28)、(62.07±4.39)、(46.33±11.91)mg/L,两组比较差异均有统计学意义(P<0.01).(2)对照组3、6、12、18 h免疫组织化学灰度值分别为114.13±7.92、122.39±7.99、145.98±6.48、113.98±6.48,ANP组分别为80.07±14.89、110.54±4.45、103.77±10.48、99.18±6.95;对照组Western blot蛋白含量分别为1.19±0.33、1.02±0.25、0.90±0.33、1.06±0.20,ANP组分别为0.83±0.11、0.96±0.21、0.58±0.28、0.72±0.14.结果 均显示ANP组胰腺AQP1蛋白表达低于对照组(P<0.05);(3)对照组3、6、12、18 h荧光定量PCR检测ANP组胰腺AQP1基因mR-NA表达分别为2.13±0.63、2.02±1.40、2.07±0.86、2.49±2.47,ANP组为0.91±0.22、1.01±0.83、0.48±0.23、0.61±0.51,ANP组较对照组减弱(P<0.01).结论 ANP大鼠胰腺组织AQP1表达明显减弱,这可能在毛细血管渗漏综合征的发生中起重要作用.     

直肠腺瘤合并原发性肝脏神经内分泌癌一例

原发性肝脏神经内分泌癌(PHNEC)较罕见,临床症状、体征、超声及影像学检查均不具特异性,病理表现和免疫表型是确诊的主要依据。本例患者因直肠和肝脏特殊的影像学表现,入院初考虑直肠癌伴肝转移,后经病理和免疫组化确诊PHNEC。该病例提示我们临床工作中应警惕因经验主义引起的误诊,应重视病理学诊断结果。     

CAG方案治疗骨髓增生异常综合征疗效观察

 目的 观察CAG方案治疗骨髓增生异常综合征（MDS）疗效。方法 经FAB标准确诊的MDS患者接受CAG方案（阿糖胞苷+阿柔比星+粒细胞集落刺激因子）诱导治疗。结果 15例患者经过1个疗程后,10例骨髓获得完全缓解（CR）,5例获得部分缓解（PR）,PR者经两个疗程治疗后1例达CR,余改用其他方案治疗。结论 CAG方案疗效较好,毒副作用相对较少,为MDS患者延长生存期、改善生活质量提供了一种可行的方案。     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

水通道蛋白1在急性坏死性胰腺炎大鼠胰腺组织的表达及其意义

Objective To study the expression of aquaporin 1 ( AQP1 ) in pancreas and its pathogenic role in rats with experimental acute necrotizing pancreatitis (ANP). Methods Forty-eight male Sprague-Dawley rats were randomly divided into two groups : control group ( n = 24 ) and ANP group ( n = 24). Six rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models. Quantity of ascites and levels of serum amylases were measured at each time point. Serum AQPI was determined by ELISA. Pathological changes of pancreatic tissues were examined. Capillary permeability in pancreatic tissues was tested by Evans Blue (EB) extravasation method. AQPI expression in pancreatic tissues was detected by immunohistochemieal staining, Western blot and fluorescence quantitative polymerase chain reaction (FQ-PCR). Results (1) Serum amylase level at 3,6,12, and 18 h in control group was (1308±759) ,(1077±508), (1325±761),(1328±762) U/L,and that in ANP group was (9102± 2199), (8799±1634), (9398±1473), (9484±862) U/L respectively. The concentration of EB in pancreatic tissues at each time point in control group was (205.61±32.99), (141.46±27.18 ), (96.94± 26.79), (61.43±24.82) mg/L, and that in ANP group was ( 273.59±23.47 ), ( 253.51±31.68 ), (221.15±73.68 ), (185.28±42.35) ,respectively. There was significandy difference between two groups. Serum AQP1 level in control group at each point was ( 74.08±11.80), (78.49±9.06 ), (75.77± 7.37 ), ( 72.75±13.87 ) mg/L, and that in AN P group was (73.29±9.61 ), ( 62.85±7.28 ), (62.07± 4.39 ), (46.33±11.91 ) mg/L, respectively ( P < 0.01 ). ( 2 ) Protein expression of AQPI in pancreatic tissues detected by immunohistochemical staining in control group at each time point was 114.13±7.92, 122.39±7.99,145.98±6.48,113.98±6.48, and that in ANP group was 80.07±14.89,110.54± 4.45,103.77±10.48,99.18±6.95;Protein expression of AQP1 in pancreatic tissues detected by Western blot in control group at each time point was 1.19±0.33,1.02±0.25,0.90±0.33,1.06±0.20,and that in ANP group was 0.83±0.11,0.96±0.21,0. 58±0.28,0.72±0.14, respectively ( P < 0.05 ). ( 3 ) The mRNA level of AQP1 gene expressed in pancreas in control group at each time point was 0.91±0.22,1.01±0.83,0.48±0.23,0.61±0.51,and that in ANP group was 2.13±0.63,2.02±1.40, 2.07±0.86,2.49±2.47,respectively (P<0.01).Condusion The expression of AQP1 wasdown-reg-ulated in pancreas in rats with ANP,which might could play an important role in the pathogenesis of capil-lary leak syndrome.     

转化生长因子-β1/Smads信号在增生性瘢痕形成中的作用研究进展

病理性的创面愈合常导致增生性瘢痕的形成,并伴随疼痛、瘙痒和挛缩,给患者带来生理和心理上的巨大痛苦。肌成纤维细胞的过度增殖及细胞外基质的过度沉积是增生性瘢痕的重要特征,其中TGF(转化生长因子)-β1/Smads信号的调节发挥了重要作用。抑制TGF-β1/Smads可抑制细胞的过度增殖,减少细胞外基质的沉积。目前针对该信号通路抗增生性瘢痕形成的研究日益增多,为减少瘢痕的形成及减轻瘢痕提供了重要的依据。本文就肌成纤维细胞及细胞外基质在增生性瘢痕中的作用及TGF-β1/Smads在增生性瘢痕形成调节中发挥的重要作用作一综述。