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目的　观察节律基因Ｐｅｒｉｏｄ1和Ｐｅｒｉｏｄ2在胃癌组织中的表达变化，并探讨其临床意义。方法　选择138 例胃癌患者，术中留取胃癌及癌旁组织，采用免疫组化法检测胃癌及癌旁组织中的Ｐｅｒｉｏｄ1和Ｐｅｒｉｏｄ2，实时荧光定量 ＰＣＲ法检测胃癌及癌旁组织中的Ｐｅｒｉｏｄ1和Ｐｅｒｉｏｄ2ｍＲＮＡ。结果　胃癌组织中Ｐｅｒｉｏｄ1和Ｐｅｒｉｏｄ2阳性表达率分别为 23.2％、31.2％，均低于癌旁组织中的44.9％、64.5％（Ｐ均＜0.01）；胃癌组织中Ｐｅｒｉｏｄ1ｍＲＮＡ和Ｐｅｒｉｏｄ2ｍＲＮＡ相对 表达量分别为1.05±0.10、1.09±0.12，均低于癌旁组织中的1.31±0.13、1.47±0.16（Ｐ均＜0.01）；Ｐｅｒｉｏｄ1ｍＲＮＡ表 达与胃癌组织分化程度、浸润深度、淋巴结转移和Ｌａｕｒｅｎ分型有关（Ｐ均＜0.05），Ｐｅｒｉｏｄ2ｍＲＮＡ表达与胃癌组织分化 程度、浸润深度、ＴＮＭ分期、淋巴结转移和Ｌａｕｒｅｎ分型均有关（Ｐ均＜0.05）；相关性分析显示，胃癌组织中Ｐｅｒｉｏｄ1与 Ｐｅｒｉｏｄ2表达呈正相关（ｒ＝0.285，Ｐ＜0.05），Ｐｅｒｉｏｄ1ｍＲＮＡ与Ｐｅｒｉｏｄ2ｍＲＮＡ表达呈正相关（ｒ＝0.379，Ｐ＜0.05）。结论 　胃癌组织中节律基因Ｐｅｒｉｏｄ1和Ｐｅｒｉｏｄ2呈低表达，可能在胃癌的发生、发展中起重要作用。 [ABSTRACT FROM AUTHOR]

Objective To observe the effects of miR-128 and ZEB1 on the migration, invasion and epithelial mesen‐ chymal transition( EMT) of endometrial carcinoma( EC) cells and to verify the targeted relationship between them. Meth⁃ ods The qRT-PCR and Western blotting were used to detect the relative expression levels of miR-128 and ZEB1 in three EC cell lines( HEC-1A, Ishikawa, and KLE) and one endometrial epithelial cell line hEEC, respectively. Ishikawa cell line with the lowest expression level of miR-128 was taken as the follow-up study object. Ishikawa cells were divided into the negative control group and miR-128 overexpression group, and were transfected with miRNA-NC and miR-128 mim‐ ics, respectively. After 48 h, the cells were collected for follow-up experiments. Cell Scratch test and Transwell test were used to detect the migration and invasion abilities of cells in each group after transfection. Western blotting was used to de‐ tect ZEB1, E-cadherin, Fibronectin and Vimentin protein of cells in each group after transfection. Double luciferase re‐ porter gene experiment was used to verify the targeted regulatory relationship between miR-128 and ZEB1. Results Com‐ pared with hEEC, the expression of miR-128 in EC cell lines HEC-1A, Ishikawa and KLE decreased( all P<0. 05), and the expression of ZEB1 protein increased( P<0. 05) . After transfection, the expression of miR-128 increased significantly in Ishikawa cells( P<0. 05), the number of transmembrane cells and scratch healing rate decreased( all P<0. 05), the rel‐ ative expression levels of ZEB1, Fibronectin and Vimentin decreased( all P<0. 05), and the expression of E-cadherin protein increased( P<0. 05). The results of double luciferase reporter gene experiment showed that miR-128 could target and regulate ZEB1 gene( P<0. 05). Conclusions MiR-128 can inhibit the migration, invasion and EMT of Ishikawa cells. ZEB1 can promote the migration, invasion and EMT of Ishikawa cells. MiR-128 and ZEB1 have a targeted regulatory rela‐ tionship. [ABSTRACT FROM AUTHOR]

Objective To investigate the therapeutic effect and mechanism of Caveolin-1 (Cav1) mutant to F92ACav1 modified rat bone marrow mesenchymal stem cells (rBMSCs/F92A-Cav1) on rats with pulmonary hypertension (PAH). Methods PAH was induced by intraperitoneal injection of 1% monocrotaline (MCT, 60 mg/kg) in adult male Wistar rats. The PAH rats were randomly divided into four groups( 10 rats/group) after 2 weeks of MCT injection:PAH group (only MCT), Cav1 group( transduced with LV-Cav1 modified r BMSCs), F92A-Cav1 group (transduced with LV-F92A-Cav1 modified r BMSCs),and the control group. Gene modified r BMSCs (1 × 106/ml) were transplanted into PAH rats in each group by tail vein injection. After 3 weeks of transplantation,the percentage of media wall thickness (MT%) and right ventricular hypertrophy index( RVHI) were evaluated by Image-Pro Plus 6 software,serum NO concentration was checked by Griess method, and the expression of phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) was detected by Western blotting. Results MT%, RVHI, PI3K and AKT was all increased but NO was decreased in the PAH group as compared with that of the control group (P < 0. 05 or P < 0. 01). Compared with the PAH group, MT%, RVHI, PI3K and AKT was decreased but NO was increased in the Cav1 and F92A-Cav1 groups, especially in the F92A-Cav1 group (P < 0. 01). Conclusion F92A-Cav1 can abrogate the inhibitory effect of wild-type Cav1 on e NOS and promote the release of NO, then inhibit the activation of PI3K/Akt signaling pathway and thus exert its therapeutic effect on PAH rats. [ABSTRACT FROM AUTHOR]

目的观察缺血后预处理对缺血再灌注大鼠肝内胆管细胞损伤的影响并探讨其机制。方法取健康雄性SD大鼠24只,随机分为假手术组、缺血再灌注组、缺血后处理组,每组8只。假手术组:大鼠麻醉后于上腹部正中取一长3.5 cm纵切口,将腹壁各层依次切开,肝脏显露后进一步游离出肝十二指肠韧带,关腹,无其他干预。缺血再灌注组:在假手术组基础上,游离肝十二指肠韧带,用无损伤动脉夹将肝门区域夹闭,缺血30 min后取下血管夹,使血管开放,对肝脏持续再灌注,最后关腹。缺血后处理组:在缺血再灌注组基础上,血供完全恢复之前再灌注10 s,夹闭10 s,如此反复6个循环(共2 min)后完全恢复血供。比色法测定血清γ-GT、SOD活力,免疫组化法测定胆管组织中Bcl-2和Bax蛋白表达,采用原位缺口末端标记法测算胆管细胞凋亡指数(AI),HE染色后光镜下观察胆管上皮细胞基本形态学变化。结果 IR组、IPO组、SO组血清γ-GT值分别为(34.64±3.28)、(26.30±3.32)、(17.33±2.08)U/L,三组间两两比较,P均<0.05。SO组、IR组、IPO组大鼠血清SOD活力值分别为(58.26±3.00)、(60.28±3.73)、(61.53±7.99)U/m L,各组间比较,P均>0.05。IR组、IPO组、SO组胆管组织中Bcl-2蛋白阳性表达率分别为(42.67±3.73)%、(77.94±5.25)%、(18.21±4.16)%,三组间两两比较,P均<0.05。 IR组、IPO组、SO组胆管组织中Bax蛋白阳性表达率分别为(90.17±2.12)%、(70.10±4.27)%、(30.63±3.00)%,三组间两两比较,P均<0.05。IR组、SO组、IPO组AI分别为79.31±1.12、26.06±2.27、58.90±2.75,三组间两两比较,P均<0.05。IPO组病理改变较IR组明显减轻,肝小叶结构较完整,肝细胞变性程度减轻,汇管区胆管上皮连续完整,炎细胞浸润少。结论缺血后预处理通过促进肝内胆管组织中Bcl-2蛋白表达、抑制Bax蛋白表达,抑制SD大鼠肝脏缺血再灌注过程中肝内胆管细胞凋亡,从而减轻肝脏缺血再灌注过程中肝内胆管细胞的损伤。 [ABSTRACT FROM AUTHOR]