目的:探究奥沙利铂(L-OHP)与吴茱萸碱(EVO)联用后对L-OHP耐药的人胃癌BGC-823/L-OHP细胞增殖与凋亡能力的改变及可能机制.方法:于体外建立对L-OHP耐药的胃癌BGC-823细胞株,CCK-8法分别计算EVO及L-OHP单独使用与联合使用时BGC-823/L-OHP细胞的增殖抑制率、IC50及逆转指数;流式细胞仪检测EVO联合L-OHP作用于BGC-823/L-OHP细胞前后细胞周期分布及凋亡的变化;采用Real-time PCR、Western blot法检测细胞中MDR1、MRP1 mRNA和蛋白的表达水平.结果:2.00 μmol/L EV O处理BGC-823/L-OHP细胞48 h后,L-OHP对BGC-823/L-OHP耐药细胞株的IC,.由(18.83±0.83)μg/ml变为(12.78±1.78)μg/ml,差异有统计学意义(P＜0.05);EVO与L-OHP联用耐药细胞滞留在G2期比例升高,滞留在G1期及S期的细胞比例降低(P＜0.05);细胞凋亡率高于单独用药组(P＜0.05);MDR1、MRP1 mRNA和蛋白表达水平低于单独用药组(P＜0.05).结论:EVO和L-OHP联用能逆转BGC-823/L-OHP对L-OHP的耐药性并改变其周期分布,促进细胞凋亡.

Abstract Purpose To analyze the clinical efficacy of total laparoscopic π-shaped esophageal jejunostomy and laparoscopic assisted Roux en-Y esophago-jejunostomy for cardiac cancer and their effects on traumatic stress. Methods We collected clinical data from 72 patients with adenocarcinoma of the esophagogastric junction who were treated in our department between June 2020 and July 2022. All patients underwent laparoscopic total gastrectomy + D2 lymphadenectomy, in whom 38 patients underwent total laparoscopic total gastrectomy with π-shaped esophageal jejunostomy and 34 patients underwent laparoscopic-assisted total gastrectomy with Roux en-Y esophago-jejunostomy. The short-term therapeutic effects, safety and effects on stress response indicators of different surgical methods were analyzed. Results There were no significant differences in baseline clinical and pathological data between the two groups (P > 0.05). The mean operation duration was 201.7 ± 80.3 minutes in the total endoscopic π-shaped esophageal jejunostomy group, which was longer than 166.9 ± 26.9 minutes in the laparoscopic-assisted Roux en-Y esophago-jejunostomy group (P < 0.05). The length of the surgical incision in the total endoscopic π-shaped esophageal jejunostomy group was significantly shorter, measuring 4.6 ± 2.1 cm, compared to the Roux-en-Y anastomosis group, which had an average length of 10.4 ± 2.1 cm (P < 0.01). In terms of intraoperative bleeding, the intraoperative bleeding volume of 130.3 ± 50.3 ml in the total endoscopic π-shaped esophageal jejunostomy group was significantly lower than that of 167.2 ± 72.8 ml in the laparoscopic-assisted Roux en-Y esophago-jejunostomy group (P < 0.05). Postoperative recovery time to exhaust was 3.8 ± 1.2 days in total endoscopic π-shaped esophageal jejunostomy group, significantly lower than 5.0 ± 2.0 days in laparoscopic-assisted Roux en-Y esophago-jejunostomy group (P = 0.003). In terms of postoperative extubation time, postoperative hospital stay, postoperative complications and the number of dissected lymph nodes, there were no significant differences between the total endoscopic π-shaped esophageal jejunostomy group and the laparoscopic-assisted Roux en-Y esophago-jejunostomy group (P > 0.05). In terms of stress indicators, there were no significant differences in stress indicators between the two groups before surgery, and the serum levels of CRP, cortisol (COR) and IL-6 in the π anastomosis group were significantly lower than those in the Roux en-Y esophago-jejunostomy group on postoperative days 3 and 5 (P < 0.05). Conclusion Total laparoscopic total gastrectomy with π-shaped esophageal jejunostomy demonstrates safety and feasibility. This surgical approach effectively reduces intraoperative bleeding, accelerates patient recovery time, minimizes postoperative pain, lowers the risk of complications, and minimally impacts the body's traumatic stress response.

目的:探究基于成果导向的教学模式在肿瘤外科学教学中的应用.方法:将2021年1月至2022年1月在蚌埠医学院第一附属医院学习的120名临床见习学生,随机分为对照组和观察组,每组60名.对照组采用常规授课方式进行教学,观察组采用基于成果导向的教学模式.对2组学生的成绩以及对教学的满意度进行分析.结果:观察组学生的理论成绩及实践成绩均高于对照组(P＜0.01);观察组学生对课程效果、知识收获和实践的满意度均高于对照组学生(P＜0.01).结论:基于成果导向的教学模式应用在肿瘤外科学临床见习学生的教学工作中,能够提高教学质量,提升学生满意度,使学生更主动地获取知识和提高成绩,值得进一步探究和推广.

BackgroundThis study aims to investigate the effects of ω-3, ω-6 polyunsaturated fatty acids (PUFAs), and their middle metabolites prostaglandin (PGE)2 and PGE3 on proliferation, invasion, and angiogenesis formation of gastric cancer cells and to explore associated mechanism.MethodsRT-PCR and ELISA were used to detect the expression of cyclooxygenase (COX)-1 and COX-2 in gastric cancer cell lines. The effect of ω-3, ω-6, PGE2, and PGE3 on the proliferation, invasion, and angiogenesis of gastric cancer cells were measured by cell proliferation, invasion, and angiogenesis assay in vitro. COX-2 small interfering RNA (siRNA) was transfected into gastric cancer cells, and the expression of COX-2 protein was detected by Western blot. COX-2 gene silencing influencing proliferation, invasion, and angiogenesis potential of gastric cancer cells was detected by WST-1, transwell chamber, and angiogenesis assay, respectively.ResultsCOX-2 was only expressed in MKN74 and MKN45 cells. In gastric cancer cell lines with positive COX-2 expression, ω-6 and PGE2 could significantly enhance the proliferation, invasion, and angiogenesis of gastric cancer cells, and after transfection with COX-2 siRNA, the effects of ω-6 and PGE2 on enhancing the proliferation, invasion, and angiogenesis of gastric cancer cells were significantly attenuated; ω-3 and PEG3 could inhibit the proliferation, invasion, and angiogenesis of gastric cancer cells. In gastric cancer cell lines with negative COX-2 expression, ω-6 and PGE2 had no significant effect on the proliferation, invasion, and angiogenesis of gastric cancer; ω-3 and PGE3 could significantly inhibit the proliferation, invasion, and angiogenesis of gastric cancer.Conclusionω-6 PUFAs reinforce the metastatic potential of gastric cancer cells via COX-2/PGE2; ω-3 PUFAs inhibit the metastatic potential of gastric cancer via COX-1/PGE3 signaling axis.

目的 探究胃癌细胞中CLDN18-ARHGAP26融合突变基因引起的耐化疗药的作用,并探究人参皂苷在治疗因CLDN18-ARHGAP26融合突变基因表达引起的耐化疗药治疗过程中的抗肿瘤作用.方法 采用免疫磁珠抗体标记胃癌细胞系BGC-823的侧群(SP)细胞和非侧群(NSP)细胞,选出NSP细胞转染过表达CLDN18-ARHGAP26融合突变基因的慢病毒载体.用qPCR检测细胞中CLDN18-ARHGAP26融合突变基因和三磷酸腺苷结合转运蛋白G超家族成员2(ABCG2)mRNA水平的表达.用Western blot检测转染上皮-间质转化(EMT)相关蛋白E-Cadherin、Vimentin的表达.用CCK-8检测转染细胞对化疗药奥沙利铂的敏感性.用CCK-8检测人参皂苷对转染细胞耐药性的影响.人参皂苷处理转染细胞后Western blot检测转染细胞的钙黏蛋白E(E-Cadherin)、波形蛋白(Vimentin)的表达.结果 qPCR检测显示转染过表达CLDN18-ARHGAP26融合突变基因慢病毒载体的NSP细胞中CLDN18-ARHGAP26融合突变基因表达高于未转染组,ABCG2 mRNA表达高于未转染组(P<0.001).Western bolt显示过表达CLDN18-ARHGAP26融合突变基因的NSP细胞中E-Cadherin蛋白表达低于未转染组(P<0.05),Vimentin蛋白表达高于未转染组(P<0.01),转染细胞对奥沙利铂的敏感性低于未转染组(P<0.05).人参皂苷和奥沙利铂同时处理转染细胞,细胞存活率低于单纯奥沙利铂处理(P<0.05).人参皂苷处理转染细胞后E-Cadherin蛋白表达高于未处理组(P<0.01),Vimentin蛋白表达低于未处理组(P<0.05).结论 人参皂苷能逆转胃癌细胞中CLDN18-ARHGAP26融合突变基因表达诱导的细胞EMT转化和奥沙利铂的耐药性.

目的:探讨白细胞介素-1受体2型(interleukin-1 receptor 2,IL1R2)与原癌基因c-Fos的相互作用,及其影响结肠癌细胞增殖、侵袭和血管新生的机制.方法:采用Western blot法检测结肠癌组织及癌旁组织中IL1R2和c-Fos的表达.通过双重荧光素酶测定IL1R2和c-Fos之间的相互作用关系.通过RT-PCR法检测IL1R2不同转染组IL1R2和c-Fos的mRNA表达.通过CCK8和Transwell法检测人结肠癌细胞SW620的增殖和侵袭作用.使用ELISA法测定SW620培养上清液中VEGF、VEGFR2、HIF-1α和bFGF的表达水平.结果:结肠癌组织较癌旁组织IL1R2和c-Fos的表达升高(P＜0.05).双重荧光素酶测定结果证实了c-Fos是IL1R2的真正靶点.与对照组比较,IL1R2 mimic组IL1R2和c-Fos mRNA表达升高(P＜0.05),而IL1R2 inhibitor组IL1R2和c-Fos mRNA表达降低(P＜0.05);IL1R2 mimic组细胞增殖和侵袭升高(P＜0.05),而IL1R2 inhibitor组细胞增殖和侵袭降低(P＜0.05);IL1R2 mimic组VEGF、VEGFR2、HIF-1α和bFGF表达水平升高(P＜0.05),而IL1R2 inhibitor组VEGF、VEGFR2、HIF-1α和bFGF表达水平降低(P＜0.05).结论:IL1R2与c-Fos的相互作用可以进一步影响结肠癌细胞的增殖、侵袭和血管新生.

In this study, we aimed to compare clinical efficacy of laparoscopic surgery and open surgery for colorectal cancer in the Huaihe River Basin in China. A total of 92 patients with colorectal cancer were selected as subjects. Patients were divided into control group (open surgery, n = 27 cases) and test group (laparoscopic surgery, n = 28 cases). Our results showed that the duration of operation (122.54 +/- 14.85) min and length of incision (4.51 +/- 1.065) cm were shorter in the experimental group than those in the control group. The intraoperative blood loss of the experimental group was (161.12 +/- 10.694) ml, which was less than that of the control group (218.53 +/- 15.369) ml (P < 0.05). Patients in the experimental group have higher Five-year survival rate and lower incidence of postoperative complications than those in the control group (all P < 0.05). In conclusion, in the treatment of colorectal cancer, laparoscopic surgery has a better clinical effect than open surgery, which is worthy of clinical application.

Certain progress has been made in the therapeutic method against gastric cancer such as surgical operation combined with chemotherapy and radiation therapy in recent years. But the therapeutic efficacy and prognosis on gastric cancer was still not satisfactory. The function of exosome of miR-328–3p secreted by bone marrow stromal cells (BMSCs) on restraining the gastric cancer was studied in the present study. The BMSCs with highly-expressed miR-328-3p was established. The exosome in cell supernatant was collected. The exosome of BMSCs and MSCs with highlyexpressed miR-328-3p was added into SGC-7901 cells followed by analysis of miR-328-3p level by Real-time PCR and TFF3 (Trefoil Factor 3) level in exosome by Western blot, cell proliferation, expression of E-cadherin, Vimentin and Caspase-3. miR-328-39 expression was reduced and TFF3 was elevated in gastric cancer tissue ( P < 0.05). miR-328-3p was upregulated and TFF3 was downregulated after addition of BMSCs exosomes along with increased cell proliferation and reduced E-cadherin and Caspase3 expression ( P < 0.05). In conclusion, exosome of BMSCs could be regulated by miR-328-3p and TFF3 expression is restrained so as to regulate the biological behaviors of gastric cancer cell.

Gastric cancer (GC) remains a major public health problem. Ursolic acid (UA) is reported to be effective in inhibiting GC; however, its low solubility and poor biocompatibility have greatly hindered its clinical application. Herein, an innovative reactive oxygen species (ROS)-sensitive UA dimeric prodrug is developed by coupling two UA molecules via a ROS-cleavable linkage, which can self-assemble into stable nanoparticles in the presence of surfactant. This new UA-based delivery system comprises the following major components: (I) dimeric prodrug inner core that can achieve high drug-loading (55%, w/w) and undergo rapid and selective conversion into intact drug molecules in response to ROS; (II) a polyethylene glycol (PEG) shell to improve colloid stability and extend blood circulation, and (III) surface-modified internalizing RGD (iRGD) to increase tumor targeting. Enhancement of the antitumor effect of this delivery system was demonstrated against GC tumors in vitro and in vivo. This novel approach offers the potential for clinical applications of UA.

Abstract Background: The aim of this study was to investigate the co-operative role of CXCR4/ CXCL12 axis and IL-1Ra in metastatic processes mechanism by interactions between colorectal cancer cells and stromal cells in their microenvironment. Methods: Expression of IL-1a, CXCL12 and CXCR4 mRNA and proteins were determined by RT-PCR and Western blot. The effect of secreted level of CXCL12 by IL-1Ra on fibroblasts was measured by ELISA. CXCL12 regulate metastatic potential of colorectal cancer was evaluated by proliferation, invasion and angiogenesis assays, respectively, in which invasion and angiogenesis assays used an in vitro system consisting of co-cultured colorectal cells and stromal cells. Results: IL-1a was expressed in high liver metastatic colorectal cancer cell lines (HT-29 and WiDr). The colorectal cancer cell-derived IL-1a and rIL-1a significantly promoted CXCL12 expression by fibroblasts, and this enhancing effect can be significantly inhibited by IL-1Ra (P<0.01). CXCL12 not only enhanced the migration and proliferation of human umbilical vein endothelial cells (HUVECs), but also significantly enhanced angiogenesis (P<0.01). Furthermore, the high liver-metastatic colorectal cancer cell line (HT-29), which secretes IL-1a, significantly enhanced angiogenesis compared to the low liver-metastatic cell line (CaCo-2), which does not produce IL-1a (P<0.01). On the contrary, IL-1Ra can significantly inhibit migration, proliferation and angiogenesis (P<0.01). Conclusion: Autocrine IL-1a and paracrine CXCL12 co-enhances the metastatic potential of colorectal cancer cells; IL-1Ra can inhibit the metastatic potential of colorectal cancer cells via decrease IL-1a/CXCR4/CXCL12 signaling pathways.

目的:探讨胃癌病人全胃切除术后早期经口肠内营养的安全性与可行性.方法:选择行腹腔镜辅助根治性全胃切除术的胃癌病人,依照肠内营养方式不同分为早期经口营养(无营养管组,25例)和经空肠营养管肠内营养(有营养管组,23例).分析比较2组病人术后并发症发生情况、术后应激反应指标、术后营养指标、术后肠道屏障功能指标、术后排气时间及术后住院时间.结果:2组病人在术后营养指标、术后排气时间及住院时间方面差异均无统计学意义,在术后咽喉疼痛、腹泻发生率方面,无营养管组明显优于有营养管组(P<0.01和P<0.05),且术后C反应蛋白水平、血D-乳酸和I-FABP水平,无营养管组均低于有营养管组(P<0.05～P<0.01).结论:对于全胃切除的胃癌病人,与经鼻空肠营养管肠内营养相比,早期经口营养是安全的,并能减少病人咽部不适、腹泻的发生率,减轻机体应激反应,促进机体肠道屏障功能修复.

目的 探究糖酵解抑制剂WZB117通过下调Yes相关蛋白(YAP)影响病人来源的胃癌细胞干性和糖酵解的机制.方法 胰蛋白酶消化临床获取的胃癌组织,培养制备胃癌细胞;细胞分为正常组、低糖对照组和WZB117处理组,qRT-PCR检测细胞干性相关基因(Nanog、oct-4、sox-2)、基质金属蛋白酶-2 (MMP-2)、基质金属蛋白酶-9(MMP-9)和凋亡相关基因(Bcl-2、bax和Cyt-C)的表达;Western blot测定细胞中YAP和代谢相关蛋白己糖激酶2(HK2)、丙酮酸激酶M2亚型(PKM2)和活化的含半胱氨酸的天冬氨酸蛋白水解酶3(Cleaved Caspase-3)的表达;MTT测定细胞增殖活性;平板克隆实验测定细胞克隆形成能力;划痕试验观察细胞迁移能力;Transwell实验观察细胞的侵袭能力;试剂盒测定细胞中三磷酸腺苷(ATP)及培养液上清液中的乳酸含量.结果 WZB117培养细胞后,YAP表达水平较正常组及低糖对照组显著降低(P＜0.05);Nanog、BMil、c-Myc的表达以及细胞增殖活性、克隆形成率、侵袭能力、迁移能力降低(P＜0.05);Cleaved Caspase-3水平及细胞凋亡率升高(P＜0.05);Bcl-2表达随WZB117浓度增高而降低(P＜0.05);Bax和Cyt-C表达随WZB117浓度增高而升高(P＜0.05);ATP、上清液中乳酸含量以及HK2、PKM2蛋白水平降低(P＜0.05).结论 抑制剂WZB117可通过下调胃癌细胞中YAP表达,干扰糖酵解关键酶HK2、PKM2的表达,抑制胃癌细胞糖酵解,降低细胞ATP水平.

目的:探究糖酵解抑制剂WZB117通过抑制糖酵解和促进线粒体调节的凋亡途径诱导人胃癌细胞系MGC-803的凋亡的机制.方法:处于对数生长期的胃癌MGC-803细胞用于实验.根据实验要求,将培养的细胞分为2组:对照组(正常培养的胃癌细胞),WZB117组(用20μg/mL的葡萄糖运转蛋白抑制剂处理的胃癌细胞).通过MTS测定试剂盒检测细胞的增殖能力;通过CCK-8测定细胞活力,TUNEL分析细胞细胞凋亡;通过测定ATP含量检测线粒体功能;通过免疫印迹分析Bcl-2、Bax、caspase-3和Cyt-c蛋白和糖酵解相关酶己糖激酶(HK)和磷酸果糖激酶(PFK)蛋白的表达.结果:24 h时和48 h时WZB117组较对照组细胞增殖降低(P<0.01).WZB117组较对照组细胞凋亡率升高(P<0.01),WZB117组较对照组细胞活力降低(P<0.01).12 h时和24 h时WZB117组较对照组ATP含量均降低(P<0.01).WZB117组较对照组Bcl-2蛋白表达降低(P<0.01),WZB117组较对照组Bax、caspase-3和Cyt-c的蛋白表达升高(P<0.01).WZB117组较对照组HK和PFK表达降低(P<0.01).结论:WZB117通过抑制糖酵解途径和减少线粒体的ATP产能诱导胃癌细胞系MGC-803的凋亡.

同源盒基因Six1是一多基因家族的转录调节因子,与恶性肿瘤的发生发展相关. 异常表达的Six1基因可以通过多种信号通路导致正常细胞的凋亡与增殖失衡,上游调控因子的异常表达可以导致Six1的功能失调,而异常表达的Six1可以作用于其靶基因CyclinA1、TGF-β等,从而促进肿瘤的发生发展.

To better explore the underlying mechanism of liver metastatic formation by placenta-specific protein 1 (PLAC1) in human colorectal cancer, we investigated the proliferation, invasion and angiogenic capabilities of human colorectal cancer cells with different liver metastatic potentials as well as the mechanism of action of PLAC1 in the metastatic process. The expression of PLAC1 was detected by reverse transcriptase PCR, western blot, and real-time PCR. The effect of PLAC1 on metastatic potential was determined by proliferation, invasion, and angiogenesis assays, including an in-vitro coculture system consisting of cancer cells and vascular endothelial cells that were used to detect the relationship between cancer cells and angiogenesis. In addition, we also determined PLAC1 downstream targets that preferentially contribute to the metastatic process. PLAC1 was expressed in HT-29, WiDr, and CaCo-2 colorectal cancer cells but not in Colo320 colorectal cancer cells. PLAC1 not only enhanced significantly the proliferation of CoLo320 and human umbilical vein endothelial cells (HUVECs) but also promoted the invasion of CoLo320 cells. The angiogenesis of HUVECs was enhanced by PLAC1 in a dose-dependent manner. In cocultured systems, angiogenesis was significantly increased by coculture with HT-29 cells. In addition, PLAC1 could promote angiogenesis in coculture with HT-29 cells. Furthermore, PLAC1-enhanced metastatic potential of colorectal cancer cells was dependent on the activation of the PI3K/Akt/NF-κB pathway. The activation of PI3K/Akt/NF-κB signaling by PLAC1 may be critical for metastasis of colorectal cancer cells. According to our results, we suggest that modification of PLAC1 function might be a promising new therapeutic approach to inhibit the aggressive spread of colorectal cancer.

目的:分析老年进展期胃癌病人行全腹腔镜与腹腔镜辅助胃癌根治术的临床效果及安全性,为老年胃癌病人的手术治疗提供依据.方法:选取54例老年进展期胃癌病人,随机数字法分为全腹腔镜胃癌根治术组24例和腹腔镜辅助胃癌根治术组30例,比较2组病人的术中出血量、淋巴结清扫数量、术后疼痛评分、术后排气时间、术后进食时间、术后住院时间、术后并发症发生率、术后C-反应蛋白、CD4/CD8及病人满意度.结果:全腹腔镜组在术后疼痛评分、排气时间、术后住院时间较腹腔镜辅助组有统计学差异(P<0.01),CRP在术后3 d、7 d明显低于腹腔镜辅助组(P<0.01),CD4/CD8在术后1 d、7 d明显高于腹腔镜辅助组(P<0.01和P<0.05);全腹腔镜组术后1 d明显高于术前(P<0.01).结论:对于老年进展期胃癌病人,全腹腔镜胃癌根治术有较明显的近期疗效优势.

目的:探讨具有乳头状核特征的非浸润性甲状腺滤泡性肿瘤(non-invasive follicular thyroid neoplasm with papillary-like nu-clear features,NIFTP)的临床病理学特征.方法:回顾性分析2012年1月至2017年12月蚌埠医学院第一附属医院7例NIFTP患者的临床表现、组织形态学、免疫组织化学、分子遗传和预后特征,并复习相关文献.结果:7例NIFTP患者中,男性3例,女性4例,年龄36～54岁,中位年龄50岁;肿瘤直径0.2～3.0 cm,中位直径1.2 cm.单发结节4例,双发结节2例,多发结节1例.7例形态学表现为包膜完整、边界清晰,无血管和包膜浸润;肿瘤细胞核大、拥挤,部分可见核沟、核内假包涵体及毛玻璃样核,具有甲状腺乳头状癌(papillary thyroid carcinoma,PTC)的核特征.免疫组织化学缺乏特异性表达,诊断价值有限,Ki-67增殖指数低.荧光定量PCR检测KRAS和NRAS基因突变2例,均无BRAF V600E突变.5例随访21～74个月,无复发和转移,2例失访.结论:NIFTP是一种极低度恶性潜能的甲状腺交界性肿瘤,具有特定形态学表现和惰性生物学行为,RAS基因突变检测有助于诊断.

目的： 第6组淋巴结所在区域涉及众多血管，是胃癌手术淋巴结清扫的难点，因此本研究探讨胃系膜与横结肠系膜平面的正确解剖在胃癌第6组淋巴结清扫中的意义。 方法： 采用回顾性队列研究的方法，分析2016年1月至2017年12月间于蚌埠医学院第一附属医院接受胃切除D(2)根治术的69例胃癌患者临床资料。根据对第6组淋巴结清扫方式不同，分为系膜平面解剖组（39例）和传统清扫组（30例）。比较两组患者第6组淋巴结清扫观察指标（手术时间、术中出血量、第6组淋巴结清扫数目以及术后胰漏和十二指肠漏发生率等）。 结果： 系膜平面解剖组与传统清扫组基线资料的差异均无统计学意义（均P>0.05）。两组患者均顺利完成胃切除+D(2)淋巴结清扫术。与传统清扫组比较，系膜平面解剖组清扫第6组淋巴结手术时间较短[（16.0±2.2）min比（23.8±2.2）min，t=-8.650，P<0.001]，术中出血量较少[（4.9±1.1）ml比（10.5±3.0）ml，t=-6.440，P<0.001]，第6组淋巴结清扫数目较多[（3.7±2.3）枚比（1.8±1.2）枚，t=-2.467，P=0.015]，差异均有统计学意义（均P<0.05）。两组术后均无十二指肠漏和胰漏的发生。 结论： 在行胃癌根治术时，正确解剖胃系膜与横结肠系膜之间平面有利于彻底清扫第6组淋巴结，同时可以减少术中出血量和手术时间。.

The purpose of paper is to investigate the depression and anxiety as well as independent influential factors between patients who underwent Da Vinci robot-assisted radical gastrectomy and radical gastrectomy. This study is a partially randomized patient preference trial. A total of 98 patients with gastric cancer were divided into the Da Vinci robot-assisted radical gastrectomy group (46 patients, observation group) and open radical gastrectomy group (52 patients, control group). They were also postoperatively and preoperatively measured with Self-Rating Depression Scale (SDS) and Self-Rating Anxiety Scale (SAS). The postoperative and preoperative data of each group were compared. The postoperative and preoperative standard scores of SDS and SAS in patients with the observation group were NS differences (P > 0.05). In the conventional control group, the postoperative mean scores of SDS and SAS were significantly higher than those in the preoperative mean scores and the postoperative mean scores of the observation group, respectively (P < 0.01). The multivariate logistic regression analysis indicated that the independent influential factors of depression and anxiety in patients with radical gastrectomy included tumor, node, metastases stage, pain grading, other postoperative complications and postoperative insomnia (P < 0.05). Robot-assisted radical gastrectomy for gastric carcinoma is conductive to relieving patients' anxiety and depression and improving their quality of life due to the advantages of relatively low incidence of pain, reduced complications and relatively good sleep.

Background: To better explore the underlying mechanism of liver metastatic formation by placenta-specific protein 1 (PLAC1) in human colorectal cancer, we investigated the proliferation, invasion and angiogenic capabilities of human colorectal cancer cell lines with different liver metastatic potentials as well as the mechanism of action of PLAC1 in the metastatic process. Methods: The expression of PLAC1 was detected by reverse transcriptase PCR, western blot and real-time PCR. The effect of PLAC1 on metastatic potential was determined by proliferation, invasion, and angiogenesis assays, including an in vitro coculture system consisting of cancer cells and vascular endothelial cells that were used to detect the relationship between cancer cells and angiogenesis. In addition, we also determined PLAC1 downstream targets that preferentially contribute to the metastatic process. Results: PLAC1 was expressed in HT-29, WiDr and CaCo-2 colorectal cancer cells but not in Colo320 colorectal cancer cells. PLAC1 could not only significantly enhance the proliferation of CoLo320 and human umbilical vein endothelial cells (HUVECs) but could also promote the invasion of CoLo320 cells. The angiogenesis of HUVECs was enhanced by PLAC1 in a dose-dependent manner. In cocultured systems, angiogenesis was significantly increased by coculture with HT-29 cells. In addition, PLAC1 could promote angiogenesis in coculture with HT-29 cells. Furthermore, PLAC1-enhanced metastatic potential of colorectal cancer cells was dependent on activation of the PI3K/Akt/NF-κB pathway. Conclusions: The activation of PI3K/Akt/NF-κB signaling by PLAC1 may be critical for the metastasis of colorectal cancer cells. According to our results, we suggest that modification of PLAC1 function might be a promising new therapeutic approach to inhibit the aggressive spread of colorectal cancer.