以医院登记为基础的20万例恶性肿瘤患者生存报告

背景与目的：恶性肿瘤是全球重大的公共健康问题，患者生存率是评价恶性肿瘤诊治水平的重要指标。通过描述以医院登记为基础的20万例恶性肿瘤患者的生存情况，以真实世界数据从一个侧面反映我国恶性肿瘤的治疗效果。方法：纳入2008年1月1日—2017年12月31日之间在复旦大学附属肿瘤医院确诊为恶性肿瘤并接受住院治疗的患者共计202 542例。通过患者复诊病史资料、电话随访及死因数据链接等方式收集生存随访信息，随访统计时间截至2019年11月30日。应用寿命表法估计各个病种1年、3年和5年总生存率（overall survival，OS），以性别、年龄组、首次治疗时间分层。采用Kaplan-Meier生存曲线绘制各病种的总体生存曲线。结果：患者总体的1年、3年、5年OS分别为89.8%、77.4%和71.0%；男性患者5年OS为58.8%，女性患者为78.7%。在常见的恶性肿瘤中，甲状腺癌患者的5年OS最高，为98.6%；胰腺癌患者最低，为11.4%。2013—2017年首次治疗的乳腺癌、肺癌和肾癌患者5年OS分别为90.0%、55.9%和80.7%，显著高于2008—2012年首次治疗患者，其他肿瘤未见显著上升。结论：大部分恶性肿瘤患者经规范诊治可以获得较为理想的预后，女性生存情况显著优于男性，乳腺癌和肺癌患者的生存改善可能归功于新的临床治疗和早诊手段。     

miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2

In the present study, we investigated the role of miR-122 in hepatocarcinoma progression and explored the mechanism. In hepatocarcinoma tissues and cells, we used qRT-PCR to validate the miR-122 expression level. Next, we used colony formation by crystal violet staining assay to compare cell proliferation ability, and we used scratch test or Transwell assay to compare cell migration or invasion ability. We then conducted bioinformatics or luciferase reporter gene assay to prove the regulation effect of miR-122 on lamin B2 (LMNB2), and the biological function of LMNB2 was analyzed. We used nude mouse tumorigenicity assay to test the inhibition effect of miR-122 ASO therapy against hepatocarcinoma. miR-122 was reduced in hepatocarcinoma tissues compared to the paracarcinoma tissues, which was relatively low or high in hepatocarcinoma cell line SMMC7721 or Hep3B, and overexpressed miR-122 inhibited proliferation, migration, and invasion in hepatocarcinoma cells. Additionally, some reports showed that LMNB2 was regulated by miR-122, which inhibited the expression of LMNB2. Moreover, LMNB2 functioned to promote cell proliferation, migration, and invasion. We could achieve the inhibition of hepatocarcinoma using miR-122 therapy through decreasing LMNB2 expression in vivo. Our data indicated that miR-122 could inhibit hepatocellular carcinoma cell progression by targeting LMNB2 and as a therapeutic target for hepatocarcinoma treatment.     

从武汉抗疫看中医药文化认同与新的医学模式

从武汉抗疫中医药的投入使用情况,反思现代临床和国人所呈现出的中医药文化认同和就医习惯,探索其历史文化根源及社会因素与医学发展的内在关联。回顾历史,中医屡次临危受命,不负重托,如今大疫当前,中医药再次发挥了重要作用。故新时代探讨如何遵循中医药发展规律,传承精华、守正创新,坚持中医药原创优势,形成中医药学科优势整体化呈现的新模式医学,对提升全社会的中医药认知度具有重要意义。     

Functional Brain Network Classification for Alzheimer’s Disease Detection with Deep Features and Extreme Learning Machine

The human brain can be inherently modeled as a brain network, where nodes denote billions of neurons and edges denote massive connections between neurons.     

改进软腭牵拉暴露鼻咽手术治疗腺样体肥大

2013年5月至2014年2月对解放军107医院收治的80例腺样体肥大患者采用吸痰管牵拉软腭暴露鼻咽部,并在70°鼻内镜辅助下行肥大腺样体切除术,效果良好,现报告如下。1资料与方法1.1临床资料本组80例中,男43例,女37例,5~13岁,平均7岁,病程9个月~4年。临床症状均有不同程度夜寐打鼾、张口呼吸,伴有鼻塞。其中     

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。