[Abstract] Objective: To investigate the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) in colorectal cancer tissues and cells and its effect on the invasion and migration of colorectal cancer cells and the underlying mechanism. Methods: From January 2018 to December 2019, 78 pairs of colorectal cancer tissue and para-cancerous tissues from the patients who had radical colorectal cancer resection in Henan Provincial People's Hospital were collected. Quantitative PCR (qPCR) was performed to quantify the levels of lncRNA SNHG10 and miR-532-3p in colorectal cancer tissues, colorectal cancer cell lines (SW480, SW620, HT-29 and LoVo) and human normal colorectal mucosal FHC cells; and their correlations with the clinicopathological features of colorectal cancer patients were further analyzed. Dual-luciferase reporter gene assay was used to validate the targeted relationship between lncRNA SNHG10 and miR-532-3p. After transfection with si-SNHG10 or miR-532-3p mimic or co-transfection of si-SNHG10 and miR-532-3p inhibitor, the invasion and migration of SW620 cells were detected by Transwell assay, and the protein expression of E-cadherin, N-cadherin and vimentin were detected by WB. Results: SNHG10 was highly expressed in colorectal cancer tissues and cells (all P<0.05), and its expression was related to TNM stage and distant metastasis (all P<0.05). miR-532-3p was lowly expressed in colorectal cancer tissues and cells, and its expression was correlated with TNM stage, lymphonode metastasis and distant metastasis (all P<0.05). The expression of SNHG10 and miR-532-3p in colorectal cancer tissues was negatively correlated (r=-0.225, P=0.048). Dual-luciferase reporter gene assay confirmed that SNHG10 targetedly regulated miR-532-3p. Both down-regulation of SNHG10 and up-regulation of miR-532-3p significantly inhibited the invasion and migration of SW620 cells (all P<0.05), up-regulated the expression of E-cadherin (P<0.05), while down-regulated the expression of N-cadherin and vimentin (all P<0.05). After transfection with miR-532-3p inhibitor, the inhibitory effect of knocking down the expression of lncRNA SNHG10 on the invasion and migration of colorectal cancer cells was reversed (all P<0.05). Conclusions: LncRNA SNHG10 is highly expressed in colorectal cancer and is associated with TNM stage and distant metastasis. LncRNA SNHG10 affects the invasion and metastasis of colorectal cancer cells by targeting miR-532-3p and regulating EMT.

[摘 要] 目的：探究连翘苷（Phi）通过调控Hippo/YAP信号通路对结肠癌LS180细胞增殖、迁移和侵袭的影响。方法：用不同浓度（0、5、10、20、40、80 µmol/L）的Phi处理人结肠癌LS180细胞，MTT法检测24、48 和72 h时的细胞活力。将LS180细胞分为对照组、Phi-L（5 µmol/L Phi）组、Phi-M（10 µmol/L Phi）组、Phi-H（20 µmol/L Phi）组、Phi-H+YAP抑制剂维替泊芬（VP）组（20 µmol/L Phi+5 µmol/L VP），各组均处理24 h。EdU法检测Phi对各组细胞增殖的影响，划痕愈合实验、Transwell小室法分别检测Phi对细胞迁移和侵袭的影响，免疫荧光法和WB法检测Phi对细胞Ki-67表达率和LATS1、YAP和p-YAP、MMP-2、MMP-9、E-cadherin、N-cadherin表达的影响。构建LS180细胞移植瘤裸鼠模型，观察Phi对移植瘤体积和质量的影响，免疫荧光法和WB法检测移植瘤组织中Ki-67表达率和LATS1、YAP和p-YAP蛋白的表达水平。结果：与对照组比较，Phi-L、Phi-M和Phi-H组LS180细胞EdU阳性率、划痕愈合率、侵袭细胞数、Ki-67阳性率、MMP-2、MMP-9、N-cadherin表达均显著降低（均P<0.05），E-cadherin、LATS1和p-YAP/YAP表达均显著升高（均P<0.05）；同时使用VP则部分逆转了Phi对LS180细胞增殖、迁移与侵袭的抑制作用（均P<0.05）。Phi显著抑制裸鼠移植瘤生长，与对照组比较，Phi组裸鼠移植瘤体积、质量和Ki-67阳性率均显著降低（均P<0.05），LATS1和p-YAP/YAP水平均显著升高（均P<0.05）。结论：Phi可能通过激活Hippo/YAP信号通路抑制结肠癌LS180细胞的恶性生物学行为。

[Abstract] Objective: To investigate the effects of forkhead box transcription factor (FOXK2) overexpression on the proliferation, migration, invasion and adhesion of human ovarian cancer SK-OV-3 cells and its related molecular mechanism. Methods: The open reading frame (ORF) of FOXK2 was cloned into lentivirus expression vector, which was then enveloped in HEK293T cells and transfected into human ovarian cancerSK-OV-3cells.TheoverexpressionefficiencywasdetectedbyqPCRandWesternblotting.Theproliferation, migration, invasion and adhesion of SK-OV-3 cells were detected by CCK-8, Scratch-healing, Transwell and Cell adhesion assays respectively, and the expressions of epithelial-mesenchymal transition (EMT) markers were detected by qPCR. Results: The FOXK2 overexpression vector was constructed successfully and packaged into lentivirus, which was then transfected into SK-OV-3 cells. After transfection, the expression of FOXK2 was significantly increased (P<0.01); the proliferation, migration and invasion of SK-OV-3 cells were significantly reduced while the adhesion ability was significantly increased (P<0.05 or P<0.01); and the expression levels of E-cadherin and β-catenin were significantly increased while that of vimentin and fibronection were significantly decreased (all P<0.01). Conclusion: Overexpression of FOXK2 in SK-OV-3 cells leads to a significant decrease in proliferation, migration and invasion but increase in adhesion. The molecular mechanism may be related to the reversion of the EMT process in tumor cells, suggesting that FOXK2 may be a potential target for the diagnosis and treatment of ovarian cancer.

<b>Objective:b> To analyze the relationship between medication taken during pregnancy and congenital heart disease of the newborns. <b>Methods:b> A large cross-sectional survey was conducted between August and November 2013. A questionnaire survey was conducted among the childbearing aged women, selected through multistage stratified random sampling in Shaanxi from 2010 to 2013. All of the childbearing aged women under study were in pregnancy and with definite pregnancy outcomes. Multivariable Poisson regression was conducted for data analyses. <b>Results:b> A total of 28 680 cases were included in this study. The proportion of medication taken at any time during pregnancy was 16.0%, and the prevalence of congenital heart disease among the newborns was 67.9/10 000. After adjustment for factors as general demographic characteristic, history of heart disease and drug allergy and the situation of disease during pregnancy of these women, results from the multivariable Poisson regression showed that, factors as taking drugs (RR=1.95, 95%CI: 1.42- 2.68), cold medicine (RR=1.68, 95%CI: 1.07-2.64), antibiotics (RR=1.90, 95%CI: 1.25-2.90), salicylates (RR=5.01, 95%CI: 1.84-13.64) and antifungal drugs (RR=10.22, 95%CI: 3.25-32.19) during pregnancy were all related to congenital heart disease, and with the history of taking cold medicine (RR=1.90, 95%CI: 1.01-3.61), antibiotics (RR=2.18, 95%CI: 1.17-4.06), salicylates (RR=6.07, 95%CI: 1.45-25.41), antifungal drugs (RR=21.01, 95%CI: 4.17-105.87) and other drugs (RR=2.31, 95%CI: 1.19-4.47) during early pregnancy. These factors were with higher risks for congenital heart disease. <b>Conclusion:b> Women of childbearing age who took cold medicine, antibiotics, salicylic acid drugs, antifungal drugs and other drugs during early pregnancy would increase the risks related to congenital heart diseases.
Adult ; Cross-Sectional Studies ; Drug Therapy ; Drug-Related Side Effects and Adverse Reactions ; Female ; Heart Diseases/epidemiology* ; Humans ; Infant, Newborn ; Pregnancy ; Pregnancy Outcome ; Prevalence ; Surveys and Questionnaires

[摘 要] 目的：探讨1, 25-二羟维生素D3（VD3）对人乳腺癌MCF-7细胞凋亡的影响及其作用机制。方法：取体外培养的人乳腺癌MCF-7细胞，随机分为6组：对照组、2-脱氧葡萄糖（2-DG，葡萄糖抑制剂）组、1 µmol/L VD3组、10 µmol/L VD3组、2-DG+1 µmol/L VD3组和2-DG+10 µmol/L VD3组。药物干预6组细胞48 h后，以葡萄糖摄取测定试剂盒检测细胞的葡萄糖摄取量、ATP试剂盒检测细胞中ATP含量和乳酸试剂盒检测细胞的乳酸水平，WB法检测MCF-7细胞中细胞色素C（Cyt c）和凋亡相关蛋白（Bcl-2、BAX、PARP1、caspase9和caspase3）的表达水平。结果：与对照组比较，VD3干预后，MCF-7细胞的凋亡率明显增加（P<0.05或P<0.01），同时细胞的葡萄糖摄取量、ATP含量及乳酸水平均明显降低（P<0.05或P<0.01），Cyt c、BAX、PARP1、caspase9及caspase3蛋白表达量明显升高（均P<0.05），Bcl-2蛋白表达量降低（P<0.05或P<0.01）；VD3联合2-DG干预后，各组细胞检测指标的变化更为明显（P<0.05或P<0.01）。结论：VD3可通过抑制人乳腺癌MCF-7细胞的糖酵解过程并以线粒体的Cyt c途径促进细胞凋亡。

Competency-Based Education ; Curriculum ; Education, Medical, Graduate ; methods ; Emergency Medicine ; education ; Humans ; Internship and Residency ; methods ; Singapore

[摘 要] 目的：探讨低密度脂蛋白受体相关蛋白11（LRP11）在结直肠癌（CRC）组织中的表达及其对结肠癌SW480细胞增殖与凋亡的影响。方法：利用生物信息学方法分析TCGA数据库中LRP11在CRC组织中的表达水平。用慢病毒感染技术分别将sh-LRP11及sh-NC质粒转染至SW480细胞，采用qPCR、WB法检测感染后各组细胞中LRP11的mRNA和蛋白的表达，CCK-8法、流式细胞术分别检测细胞的增殖活力、凋亡率及细胞周期分布情况，WB法检测SW480细胞中cyclin D1、BAX、Bcl-2、β-catenin、活化β-catenin等蛋白的表达水平。结果：TCGA数据库数据分析显示，LRP11 mRNA在CRC组织中的表达水平显著高于正常组织（P<0.05）。与sh-NC组比较，sh-LRP11组SW480细胞的增殖活力明显降低、细胞凋亡率显著升高（均P<0.01），细胞中BAX表达显著升高、Bcl-2表达显著降低（均P<0.01）；G0/G1期细胞增多、S期细胞明显减少（均P<0.01），cyclin D1的蛋白表达显著降低（P<0.01）；Wnt/β-catenin信号通路中β-catenin和活化β-catenin的蛋白表达均显著下降（均P<0.01）。结论：LRP11 mRNA在CRC组织中呈高表达，干扰LRP11表达可抑制结肠癌SW480细胞增殖并促进其凋亡，为CRC提供了一种潜在的治疗靶点。

Objective To systematically review the research progress of sensory integration therapy in the rehabilitation of children with cerebral palsy. Methods The literatures related to the application of sensory integration therapy in the rehabilitation of children with cerebral palsy was retrieved from Web of Sciences, PubMed, CNKI, Wanfang data, and VIP databases until November 27, 2021, using subject search. And the contents of the literatures were extracted to review the implementation plan of sensory integration therapy and the effectiveness of its application in the rehabilitation of children with cerebral palsy. Results Six literatures were included. The main focus was on the research of sensory integration therapy on postural control, gross motor function, intelligence level and cognitive function, and treatment modalities in children with cerebral palsy. Conclusion Sensory integration therapy is effective on motor function, posture control and intelligence in children with cerebral palsy. To maximize the effect of sensory integration therapy, a suitable rehabilitation treatment plan should be formulated according to the degree of sensory integration disorder and the age, gender and tolerance of children.

[摘 要] 目的：通过生物信息学手段筛选乳腺癌中差异表达的关键miRNA及其靶基因，干预其在乳腺癌细胞中的表达并观察对乳腺癌细胞功能的影响。方法：利用GEO数据库筛选在乳腺癌中差异表达的miRNA，ENCORI数据库验证差异miRNA的表达，以选定最显著的差异表达miRNA为研究对象；利用Starbase、miRDB和miRWalk数据库预测miR-32-5p的靶基因，利用DAVID数据库对靶基因进行GO分析和KEGG分析，利用String数据库联合Cytoscape3.6.2软件进行PPI网络分析及核心基因的筛选，从核心基因中选择相互联系紧密“度值”最显著的Dickkopf相关蛋白3（DDK3）基因进行后续实验。qPCR检测miR-32-5p在人正常乳腺细胞 MCF10A和人乳腺癌细胞MCF7、MDA-MB-231、MDA-MB-453细胞中的表达。向MDA-MB-231细胞中转染miR-32-5p mimic、miR-32-5p inhibitor及各自的对照（NC）序列，分别用CCK-8法、流式细胞术和Transwell实验检测过表达或抑制miR-32-5p对细胞增殖、凋亡和侵袭的影响。结果：从GEO数据库中获取的两个数据集共识别出两个差异miRNA，ENCORI数据库验证差异miRNA的表达发现miR-32-5p的表达水平与GEO数据库的结果一致，故选择其进行研究；预测得到198个miR-32-5p潜在的靶基因并鉴定出10个核心基因（DKK3、WNT2B、SFRP5、SFRP2、SFRP1、LRP6、WNT6、KREMEN1、NEDD4L、TRIP12），其中DKK3的度值最大可能在乳腺癌中较为重要，于是选择miR-32-5p/DKK3轴进行后续研究。miR-32-5p在3种乳腺癌细胞中的表达水平显著高于正常乳腺细胞（均P<0.01），其中以MDA-MB-231细胞中表达最高。双荧光素酶基因报告实验验证了miR-32-5p与DKK3基因的靶向结合及其对后者表达的负向调控。转染miR-32-5p mimic、miR-32-5p inhibitor后成功提高或抑制了MDA-MB-231细胞中miR-32-5p的表达。与对照组相比，过表达miR-32-5p可抑制MDA-MB-231细胞的凋亡而促进细胞增殖和侵袭（P<0.05或P<0.01），敲低miR-32-5p则起相反的作用（均P<0.01）。结论：miR-32-5p/DKK3轴可能是影响乳腺癌发生发展的关键通路，过表达miR-32-5p能够抑制乳腺癌MDA-MB-231细胞的凋亡而促进细胞增殖和侵袭。

Humans ; Carcinoma, Verrucous/pathology* ; Carcinoma, Squamous Cell/pathology* ; Bone Neoplasms ; Toes/pathology* ; Skin Neoplasms/pathology*