Helicobacter pylori induces epithelial-mesenchymal transition in gastric carcinogenesis via the AKT/GSK3β signaling pathway

Helicobacter pylori (H. pylori) is a main risk factor for gastric cancer (GC). Epithelial-mesenchymal transition (EMT) is involved in the development and progression of H. pylori-associated GC. However, the exact molecular mechanism of this process remains unclear. The AKT/GSK3β signaling pathway has been demonstrated to promote EMT in several types of cancer. The present study investigated whether H. pylori infection induced EMT, and promoted the development and metastasis of cancer in the normal gastric mucosa, and whether this process was dependent on AKT activation. The expression levels of the EMT-associated proteins, including E-cadherin and N-cadherin, were determined in 165 gastric mucosal samples of different disease stages by immunohistochemical analysis. The expression levels of E-cadherin, N-cadherin, AKT, phosphorylated (p-)AKT (Ser473), GSK3β and p-GSK3β (Ser9) were further determined in H. pylori-infected Mongolian gerbil gastric tissues and cells co-cultured with H. pylori by immunohistochemical analysis and western blotting. The results indicated that the expression levels of the epithelial marker E-cadherin were decreased, whereas the expression levels of the mesenchymal marker N-cadherin were increased during gastric carcinogenesis. Their expression levels were associated with H. pylori infection. Furthermore, H. pylori infection resulted in downregulation of E-cadherin expression and upregulation of N-cadherin expression in Mongolian gerbils and GES-1 cells. In addition, an investigation of the associated mechanism of action revealed that p-AKT (Ser473) and p-GSK3β (Ser9) were activated in GES-1 cells following co-culture with H. pylori. Furthermore, following pretreatment of the cells with the AKT inhibitor VIII, the expression levels of E-cadherin, N-cadherin, p-AKT and p-GSK3β did not show significant differences between GES-1 cells that were co-cultured with or without H. pylori. The levels of p-AKT and p-GSK3β were increased in H. pylori-infected Mongolian gerbils. In conclusion, the present study demonstrated that H. pylori infection activated AKT and resulted in the phosphorylation and inactivation of GSK3β, which in turn promoted early stage EMT. These effects were AKT-dependent. This mechanism may serve as a prerequisite for GC development.     

经皮微波消融联合经皮穿刺椎体成形术治疗腰椎转移瘤的疗效

目的 观察微波消融（microwave ablation，MWA）联合经皮穿刺椎体成形术（percutaneous vertebroplasty，PVP）治疗腰椎转移瘤的临床疗效。方法 回顾性分析2016年6月至2019年6月广西医科大学附属肿瘤医院收治的50例腰椎转移瘤患者的临床资料，其中行经皮椎体成形术26例（PVP 组），经皮微波消融联合经皮椎体成形术24例（PVP+MWA组）。观察两组患者疼痛、功能状态以及骨水泥外渗情况和术后肿瘤复发率。结果 随访6～36个月，PVP组VAS评分从术前的（7.58±1.06） 分降至术后1个月的（3.27±1.40） 分和术后6个月的（3.08±1.60） 分；PVP+MWA组从术前的（7.67±1.05） 分降至术后1个月的（3.04±1.20） 分和术后6个月的（2.96±1.46） 分，两组术后 1个月及6个月的VAS评分低于术前（均P<0.05）,但重复测量方差显示，组间效应差异无统计学意义（F=0.223，P=0.801）。术后1个月，PVP组的KPS评分较术前提升（21.50±11.32） 分，PVP+MWA组较术前提升（19.92±13.19） 分，两者差异无统计学意义（t=0.457，P=0.650）。PVP+MWA 组的骨水泥外渗率（12.5% vs 38.5%，P=0.037）和肿瘤复发率（8.3% vs 30.8%，P=0.048）均低于PVP 组。结论 经皮穿刺椎体成形术单独或联合微波消融治疗腰椎转移瘤均可取得较好临床疗效，两者联合在减少骨水泥外渗及局部肿瘤控制中更有优势。      

脊柱化脓性感染动物模型的建立及应用进展

手术部位感染是脊柱手术后常见且非常严重的并发症,严重影响患者的身体健康。尽管手术操作无菌细致,及时给予适当的全身抗生素,但手术部位感染率仍然很高[1-2]。据报道,我国脊柱手术感染的风险从0.5%~7.8%不等[3-4]。糖尿病、肥胖、高血压等疾病显著增加脊柱术后感染,感染后治疗的费用可达10多万美元[5],大大增加了患者的经济负担。     

Characterization of membrane occupation and recognition nexus repeat containing 3, meiosis expressed gene 1 binding partner,in mouse male germ cells

Mammalian spermatogenesis is a well-organized process of cell development and differentiation. Meiosis expressed gene 1 (MEIG1) plays an essential role in the regulation of spermiogenesis. To explore potential mechanisms of MEIG1''s action, a yeast two-hybrid screen was conducted, and several potential binding partners were identified; one of them was membrane occupation and recognition nexus repeat containing 3 (MORN3). MORN3 mRNA is only abundant in mouse testis. In the testis, Morn3 mRNA is highly expressed in the spermiogenesis stage. Specific anti-MORN3 polyclonal antibody was generated against N-terminus of the full-length MORN3 protein, and MORN3 expression and localization was examined in vitro and in vivo. In transfected Chinese hamster ovary cells, the antibody specifically crossed-reacted the full-length MORN3 protein, and immunofluorescence staining revealed that MORN3 was localized throughout the cytoplasm. Among multiple mouse tissues, about 25 kDa protein, was identified only in the testis. The protein was highly expressed after day 20 of birth. Immunofluorescence staining on mixed testicular cells isolated from adult wild-type mice demonstrated that MORN3 was expressed in the acrosome in germ cells throughout spermiogenesis. The protein was also present in the manchette of elongating spermatids. The total MORN3 expression and acrosome localization were not changed in the Meig 1-deficient mice. However, its expression in manchette was dramatically reduced in the mutant mice. Our studies suggest that MORN3 is another regulator for spermatogenesis, probably together with MEIG1.     

借力医院文化环境探索传染病专科医院研究生医德培养的方法及途径

新医改环境下，临床医学人才的医德培养愈发重要，也越来越引起管理层重视。而医院文化环境对研究生医德培养可以起着潜移默化的引领作用，优秀的医院文化，能塑造并铸就研究生良好信念，强化研究生医德养成。结合传染病专科医院自身文化环境特点，探索传染病学研究生医德培养方式，对于传染病专科医院研究生医德培养具有一定理论指导意义。     

关节镜下TightRope治疗后交叉韧带撕脱骨折

目的探讨关节镜下使用TightRope治疗后交叉韧带(PCL)撕脱骨折的技术应用和临床疗效。方法 12例膝关节PCL撕脱骨折患者在关节镜下使用TightRope固定PCL撕脱骨块。术后1周开始在支具保护下被动活动膝关节,术后10个月评估膝关节功能恢复情况。结果 12例患者均获随访,时间10～14个月,平均12.6个月,骨折均Ⅰ期愈合。1例屈膝受限15°,无伸膝受限;2例后抽屉试验(+)。Lysholm膝关节功能评分术前(45.6±6.3)分,术后10个月(87.8±4.8)分,差异有统计学意义(P 0.05)。结论关节镜下使用TightRope治疗PCL撕脱骨折固定可靠,操作相对简单,疗效满意。