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.     

PEA3蛋白在乳腺癌组织中的表达及其与Her-2/neu的关系

背景与目的:Ets转录因子家族成员多瘤病毒增强子激活因子3基因(polyomavirus enhancer activator 3,PEA3)与肿瘤的侵袭和转移密切相关,其在乳腺癌发生、发展中的作用有待探讨.本研究旨在探讨PEA3蛋白在乳腺癌组织中的表达及其与Her-2/neu和乳腺癌临床病理因素的关系.方法:采用免疫组化法检测80例乳腺癌组织中PEA3及Her-2/neu的表达,对Her-2/neu(++)的病例采用显色原位杂交(coloration in situ hybridization,CISH)检测Her-2基因扩增情况.结果:80例乳腺癌组织中PEA3的阳性率57.5％(46/80),高于正常乳腺组织及乳腺纤维腺瘤,与肿瘤大小、组织学分级及腋淋巴结转移均有一定的相关性,且与Her-2/neu的表达呈正相关.PEA3蛋白的阳性表达与乳腺癌患者5年生存率呈负相关.结论:PEA3与乳腺癌浸润转移及预后密切相关,有望作为乳腺癌预后的一个参考指标,其作用机制可能与Her-2/neu相关.     

扩散加权成像对不同病理类型乳腺癌的鉴别诊断价值

目的：探讨扩散加权成像（DWI）及ADC值（ADC）测量对不同病理类型乳腺癌的鉴别诊断价值。方法：回顾分析50例经病理证实的乳腺癌患者的MRI资料,DWI检查采用EPI技术,分别测量乳腺病灶及正常乳腺ADC值,对不同病理类型乳腺癌的ADC值进行单因素方差分析并进行两两比较。结果：50例中浸润性导管癌34例,黏液腺癌6例,乳头状癌4例,浸润性筛状癌4例和髓样癌2例。乳腺癌和正常组织的ADC值分别为（1.31±0.06）×10-3及（2.06±0.04）×10-3mm2/s。浸润性导管癌、黏液腺癌、乳头状癌及筛状癌之间ADC值差异有统计学意义（F=9.406,P〈0.05）,黏液腺癌与浸润性导管癌、乳头状癌及筛状癌之间ADC值差异有统计学意义（P〈0.01）,浸润性导管癌与乳头状癌及筛状癌间的ADC值差异无统计学意义（P值分别为0.671和0.333）。结论：不同类型乳腺癌因病理基础不同,ADC值变化存在一定差异,ADC值测量有助于部分病理类型乳腺癌的鉴别诊断。     

单采血小板采集2个治疗单位献血者筛选指标探讨

目的:探讨机采血小板采集2个治疗量献血者筛选指标。方法:对78例献血者分析其体重、体表面积和采前血小板(PLT)计数对血小板减少量的影响。结果:体重(W)≥55kg,体表面积(S)≥1.7,采前血PLT计数≥200×109/L者采集后血小板计数均≥100×109/L。对男性献血者来说W≥70或S≥1.9采集后血小板降低较少;对55≤W<65,1.7≤S积<1.8献血者来说,采后血小板降低较多。结论:机采血小板采集2个治疗单位献血者筛选时要求W≥55kg,S≥1.7,采前血PLT计数≥200×109/L。     

CD105和VEGF、TGF-β1在结直肠癌的表达及其与浸润、转移和血管生成的关系

目的 探讨结直肠癌中CD105和VEGF、TGF-β1的表达及与血管生成的关系.方法 应用免疫组化方法检测60例结直肠癌中CD105标记的微血管密度(MVD)和VEGF、TGF-β1的表达.结果 60例结直肠癌中CD105表达的MVD为36.50±9.43.VEGF、TGF-β1表达的阳性率为68.3%,75.0%.MVD和VEGF、TGF-β1表达与肿瘤浸润深度、淋巴结转移和Dukes分期密切相关(P＜0.05).VEGF、TGF-β1表达均与MVD呈正相关(P＜0.01),TGF-β1与VEGF也呈正相关(P＜0.05).结论 CD105、VEGF、TGF-β1关系密切,三者联合检测可作为结直肠癌新生血管和浸润转移的有价值的标志物.     

非酒精性脂肪肝大鼠肝组织FGF21mRNA表达与脂质沉积、胰岛素抵抗的关系

目的观察非酒精性脂肪肝(NAFLD)大鼠肝组织成纤维细胞生长因子21(FGF21)mRNA表达,并探讨其与脂质沉积、胰岛素抵抗的关系。方法选择SD大鼠40只,随机分为对照组10只、高脂组30只。对照组给予基础饲料喂养,高脂组给予高脂饲料喂养。喂养8周,两组均取10只,评价NAFLD模型建立情况。高脂组剩余大鼠继续高脂饲料喂养,分别于12、24周各取10只,腹主动脉取血,检测血清空腹血糖(FPG)、空腹胰岛素(FINS)、ALT、AST、TC、TG、FGF21、FFA水平,计算胰岛素抵抗指数(HOMA-IR);处死大鼠取肝组织,制备石蜡切片,行HE染色,观察肝细胞形态学变化;制备肝组织匀浆液,检测TG含量;采用RT-PCR法检测肝组织FGF21 mRNA表达。结果喂养8周时,高脂组体质量、肝湿重及血清TG、TC水平均高于对照组(P均<0.05),肝组织呈大泡性脂肪变性并出现炎症细胞浸润及点状坏死,提示NAFLD模型建立成功。高脂组喂养12、24周时,血清FFA水平、肝组织TG含量、HOMA-IR明显高于喂养8周时,且喂养24周时均高于喂养12周时(P均<0.05);而血清FGF21水平、肝组织FGF21 mRNA表达则呈先升高再下降趋势(P均<0.05)。结论 NAFLD大鼠肝组织FGF21 mRNA表达、血清FGF21水平与肝组织TG含量有关,在NAFLD早期二者变化一致,胰岛素抵抗可间接抑制其表达。     

结直肠癌组织中CD151表达及其临床意义

目的 探讨结直肠癌组织中CD151的表达及其与结直肠癌发生、发展和转移的关系.方法 采用实时荧光定量PCR技术检测22例肠癌组织及癌旁组织中CD151mRNA的表达,采用免疫组化SP法检测此22例及另67例石蜡包埋肠癌组织及癌旁组织中CD151蛋白的表达,并分析其与肠癌临床病理因素之间的关系.结果 CD151mRNA和蛋白在结直肠癌中的表达明显高于癌旁组织,其蛋白的表达与结直肠癌浸润深度、淋巴结转移和TNM分期密切相关,差异具有统计学意义(P<0.05).结论 CD151可望成为与结直肠癌浸润、转移有关并提示预后不良的指标.     

CD151及整合素α6在肠癌中的表达及其与上皮间质转化的关系

目的:研究结直肠癌组织中CD151及整合素α6的表达,探讨他们与结直肠癌临床病理因素及上皮间质转化(epithelial-mesenchymal transition,EMT)的关系.方法:132例结直肠癌制成2张组织芯片,以30例癌旁组织作对照,采用免疫组织化学检测其中CD151、整合素α6及E-钙黏蛋白(E-cadherin)、波形蛋白(Vimentin)的表达,分析比较前两种蛋白与结直肠癌临床病理因素之间的关系及其与上皮间质表达标志物之间的关系.结果:结直肠癌组织中CD151及整合素α6表达阳性率分别为65.9%和75.7%,均高于癌旁组织;CD151和整合素α6的表达均与肿瘤浸润深度及淋巴结转移密切相关;CD151在结直肠癌中表达还与E-cadherin的低表达、Vimentin的高表达密切相关.结论:CD151和整合素α6通过促进EMT促进结直肠癌浸润转移,为研究结直肠癌EMT发生机制提供新的思路,同时为CD151作为肠癌的靶向治疗指标提供理论依据.     

索拉非尼联合树突状细胞与细胞因子诱导的杀伤细胞对肝癌生长与侵袭转移的作用

目的探讨索拉非尼联合树突状细胞（DC）与细胞因子诱导的杀伤细胞（CIK）对肝癌生长与侵袭转移的作用。方法采集健康自愿者外周血50mL,体外培养健康成人细胞因子诱导的DC和CIK。160只雄性ICR小鼠建立H22肝癌细胞小鼠原位肝癌模型,采用随机数字表法分为4组：（1）生理盐水组：仅经胃灌注与索拉非尼组同等的生理盐水;（2）索拉非尼组：经胃灌注索拉非尼100μg/g,1次/d;（3）DC—CIK细胞组：经腹腔注射DC—CIK共培养细胞,1×10^7／只,1次／3d;（4）索拉非尼联合DC—CIK细胞组：经胃灌注索拉非尼,同时腹腔注射DC—CIK共培养细胞,剂量同前。每组40只,治疗3周。各组取20只处死,获取外周血和肝脏肿瘤组织。采用ELISA法检测AFP水平,HE染色检测肿瘤坏死程度,免疫组织化学染色分别检测肿瘤组织Ki-67和CD34表达。各组余下20只小鼠,观察生存时间。多组比较采用单因素方差分析,组问比较采用LSD检验。结果DC和CIK诱导、培养成功。生理盐水组、索拉非尼组、DC—CIK组和索拉非尼联合DC—CIK组AFP分别为（0．675±0．177）ng／L、（0．379±0．052）ng／L、（0．415±0．028）ng／L和（0．288±0．012）ng／L,4组比较,差异有统计学意义（F=0．415,P〈0．05）。生理盐水组肝内和腹腔转移数目分别为（21．2±1．3）个和（29．7±7．6）个,索拉非尼组分别为（16．4±1．6）个和（17．4±1．8）个,DC—CIK组分别为（20．2±1．7）个和（26．4±1．7）个,索拉非尼联合DC—CIK组分别为（15．2±1．3）个和（15．2±1．3）个,4组比较,差异有统计学意义（F=2．137,3．271,（P〈0．05）。生理盐水组、索拉非尼组、DC—CIK组和索拉非尼联合DC—CIK组抑瘤率分别为0、21％±3％、9％4-3％和24％±5％,4组比较,差异有统计学意义（F=3．715,P〈0．05）。生理盐水组、索拉非尼组、DC—CIK组和索拉非尼联合DC—CIK组生存时间分别为（18．2±2．5）d、（21．6±2．1）d、（24．3±2．8）d和（25．4±1．4）d,4组比较,差异有统计学意义（F=6．247,P〈0．05）。结论索拉非尼联合DC与CIK免疫治疗能够显著延长肝癌荷瘤小鼠生存时间,抑制肝肿瘤生长和转移。