胶质淋巴系统——脑部疾病机制研究新方向

胶质淋巴系统是一个主要由星形胶质细胞水通道蛋白4介导的依靠动脉、静脉周围血管间隙的脑脊液-脑组织液交换流动的系统，是阿尔茨海默病、脑卒中、帕金森病、失眠、抑郁症等脑病的共同特征，是一条新的脑代谢途径，可以清除包括β-淀粉样蛋白、乳酸在内的代谢产物。本文综合分析了全球有关胶质淋巴系统在脑部疾病的研究，得出：胶质淋巴系统可能为神经退行性疾病等发病机制和诊治策略研究带来新视角；胶质淋巴系统有望为一些脑部疾病诊断提供新的有效证据；胶质淋巴系统可能是脑部疾病治疗给药方式的新途径。     

3-硝基-1,2,4-三唑-5-酮的毒理学特性

3-硝基-1,2,4-三唑-5-酮（NTO）是一种不敏感含能材料，因其爆轰速度和压力与六氢-1,3,5-三硝基-1,3,5-三嗪（RDX）相似，合成和运输安全，已逐渐成为传统含能材料的替代品。近年来，随着国内外对含能材料毒性研究的不断深入，已证实NTO对生物体及生态系统具有多种毒性效应，主要表现为对哺乳动物的睾丸毒性。本文从生物代谢、生物毒性及生态毒性三个方面对NTO毒性进行系统概述，展望今后NTO毒性的研究方向，以期为NTO的职业健康风险评估提供可靠的毒理学基础。     

SimMan3G高级模拟人在急危重症护理学综合实训中的应用

目的探讨SimMan3G高级模拟人在急危重症护理学综合实训中的应用效果。方法以某大学三年级的全体护理本科生为研究对象,进行SimMan3G高级模拟人教学,通过自身前后对照,比较教学前后护生的评判性思维能力及团队合作能力的差异,并分析护生在SimMan3G高级模拟人教学中的行为表现及对教学的满意度。结果SimMan3G高级模拟人教学后护生的评判性思维能力及团队合作能力提高,且差异有统计学意义(P<0.05);护生对SimMan3G高级模拟人教学的所有条目满意度均在90%以上。结论护生对SimMan3G高级模拟人教学满意度较高,SimMan3G高级模拟人教学有助于提高护生的评判性思维能力及团队合作能力。     

Knockdown of DEAD-box 51 inhibits tumor growth of esophageal squamous cell carcinoma via the PI3K/AKT pathway

BACKGROUND Esophageal squamous cell carcinoma(ESCC)is one of the most prevalent malignancies that seriously threaten people’s health worldwide.DEAD-box helicase 51(DDX51)is a member of the DEAD-box(DDX)RNA helicase family,and drives or inhibits tumor progression in multiple cancer types.AIM To determine whether DDX51 affects the biological behavior of ESCC.METHODS The expression of DDX51 in ESCC tumor tissues and adjacent normal tissues was detected by Immunohistochemistry(IHC)analyses and quantitative PCR(qPCR).We knocked down DDX51 in ESCC cell lines by using a small interfering RNA(siRNA)transfection.The proliferation,apoptosis,and mobility of DDX51 siRNAtransfected cells were detected.The effect of DDX51 on the phosphoinositide 3-kinase(PI3K)/AKT pathway was investigated by western blot analysis.A mouse xenograft model was established to investigate the effects of DDX51 knockdown on ESCC tumor growth.RESULTS DDX51 exhibited high expression in ESCC tissues compared with normal tissues and represented a poor prognosis in patients with ESCC.Knockdown of DDX51 induced inhibition of ESCC cell proliferation and promoted apoptosis.Moreover,DDX51 siRNA-expressing cells also exhibited lower migration and invasion rates.Investigations into the underlying mechanisms suggested that DDX51 knock down induced inactivation of the PI3K/AKT pathway,including decreased phosphorylation levels of phosphate and tensin homolog,PI3K,AKT,and mammalian target of rapamycin.Rescue experiments demonstrated that the AKT activator insulin-like growth factor 1 could reverse the inhibitory effects of DDX51 on ESCC malignant development.Finally,we injected DDX51 siRNA-transfected TE-1 cells into an animal model,which resulted in slower tumor growth.CONCLUSION Our study suggests for the first time that DDX51 promotes cancer cell proliferation by regulating the PI3K/AKT pathway;thus,DDX51 might be a therapeutic target for ESCC.     

本刊有关文稿中法定计量单位的书写要求

本刊发表的学术论文执行GB 3100~3102-1993《量和单位》中有关量、单位和符号的规定及其书写规则,具体使用参照中华医学会杂志社编写的《法定计量单位在医学上的应用》第3版(人民军医出版社2001年版)一书.