Out of the boxes,out of the silos: The need of interdisciplinary collaboration to reduce poor-quality medical products in the supply chain

In this paper, we argue that understanding and addressing the problem of poor-quality medical products requires a more interdisciplinary approach than has been evident to date. While prospective studies based on rigorous standardized methodologies are the gold standard for measuring the prevalence of poor-quality medical products and understanding their distribution nationally and internationally, they should be complemented by social science research to unpack the complex set of social, economic, and governance factors that underlie these patterns. In the following sections, we discuss specific examples of prospective quality surveys and of social science studies, highlighting the value of cross-sector partnerships in driving high-quality, policy-relevant research in this area.     

锁骨钩钢板内固定术后钢板钩与肩峰匹配性影像学研究

目的通过测量锁骨钩钢板内固定术后患者影像学资料，分析发生肩峰骨侵蚀的原因是否与钢板钩-肩峰匹配度相关。 方法回顾性分析2015年8月1日至2018年8月31日期间在上海市浦东医院骨科就诊的210例患者的影像学资料，210例患者均因肩锁关节脱位或锁骨远端骨折行锁骨钩钢板内固定治疗，其中男110例、女100例；年龄24~76岁，平均（44.60±8.75）岁；肩锁关节脱位70例，锁骨远端骨折140例。测量术后及终末随访患者肩锁关节正位X线片相关数据，按锁骨钩钢板术后是否发生肩峰骨侵蚀，将纳入患者分为3组：无骨侵蚀组（A组）、伴钢板钩移位骨侵蚀组（B组）、不伴移位的骨侵蚀组（C组），分别测量钢板钩-肩峰的匹配度（β），统计分析术后发生肩峰骨侵蚀与钢板钩-肩峰匹配度之间的关系。 结果纳入研究的210例患者术后随访24~64周，平均（32.0±6.5）周。A组患者115例，B组患者54例，C组患者41例。A组匹配度β（3.72±0.48）mm与B组β¹（6.91±0.84）mm比较差异有统计学意义（P<0.05）；A组匹配度β（3.72±0.48）mm与C组β²（5.88±0.65）mm比较差异有统计学意义（P<0.05）；B组匹配度β¹（6.91±0.84）mm与C组β²（5.88±0.65）mm比较差异有统计学意义（P<0.05）。 结论锁骨钩钢板内固定术后是否发生肩峰骨侵蚀与钢板钩-肩峰匹配度β存在明显相关性，钢板钩与肩峰之间的匹配度越好，β值越小，发生肩峰骨侵蚀的可能性更小。     

Non-canonical role of Hippo tumor suppressor serine/threonine kinase 3 STK3 in prostate cancer

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New approaches to moderate CRISPR-Cas9 activity: Addressing issues of cellular uptake and endosomal escape

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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.