丙戊酸钠通过EGFR下调CD44表达抑制胶质瘤细胞生长

目的:探讨丙戊酸钠通过抑制A172胶质瘤细胞表皮生长因子受体（epidermal growth factor receptor，EGFR）的活化，下调CD44表达，进而调节细胞生长的机制。方法:实时荧光定量PCR和Western blot检测A172胶质瘤细胞中CD44以及siRNA下调CD44表达的情况，MTT检测CD44和丙戊酸钠对细胞生长的影响，Western blot检测丙戊酸钠对细胞中p-EGFR、EGFR和CD44表达影响。结果:丙戊酸钠抑制A172胶质瘤细胞生长，并具有浓度依赖性。A172胶质瘤细胞表达CD44，siRNA下调CD44表达后，细胞生长较正常组显著减缓。活化EGFR促进A172胶质瘤CD44蛋白表达，而EGFR的抑制剂Lapatinib可显著抑制上述效应。丙戊酸钠抑制EGFR磷酸化，下调CD44蛋白表达。结论:丙戊酸钠抑制A172胶质瘤细胞的生长。抑制A172胶质瘤细胞中EGFR的活化，下调CD44的表达，是丙戊酸钠抑制胶质瘤细胞生长的其中一个机制。     

Magnesium intake and primary liver cancer incidence and mortality in the Prostate,Lung, Colorectal and Ovarian Cancer Screening Trial

Epidemiological studies on magnesium intake and primary liver cancer (PLC) are scarce, and no prospective studies have examined the associations of magnesium intake with PLC incidence and mortality. We sought to clarify whether higher magnesium intake from diet and supplements was associated with lower risks of PLC incidence and mortality in the US population. Magnesium intake from diet and supplements was evaluated through a food frequency questionnaire in a cohort of 104,025 participants. Cox regression was employed to calculate hazard ratios for PLC incidence and competing risk regression was employed to calculate subdistribution hazard ratios for PLC mortality. Restricted cubic spline regression was employed to test nonlinearity. We documented 116 PLC cases during 1,193,513.5 person-years of follow-up and 100 PLC deaths during 1,198,021.3 person-years of follow-up. Total (diet + supplements) magnesium intake was found to be inversely associated with risks of PLC incidence (hazard ratio_{tertile 3 vs. 1}: 0.44; 95% confidence interval: 0.24, 0.80; p_trend = 0.0065) and mortality (subdistribution hazard ratio_{tertile 3 vs. 1}: 0.37; 95% confidence interval: 0.19, 0.71; p_trend = 0.0008). Similar results were obtained for dietary magnesium intake. Nonlinear inverse dose–response associations with PLC incidence and mortality were observed for both total and dietary magnesium intakes (all p_nonlinearity < 0.05). In summary, in the US population, a high magnesium intake is associated with decreased risks of PLC incidence and mortality in a nonlinear dose–response manner. These findings support that increasing the consumption of foods rich in magnesium may be beneficial in reducing PLC incidence and mortality.     

“5+3”背景下医学生感官系统技能培训体系建设

为探索以器官-系统为中心的整合课程的教学改革，本项目在“5＋3”医学生中进行了针对感官系统的临床技能培训新体系建设。根据当前医学教育改革发展的趋势和要求，结合目前临床技能教学的现状，项目整合了包括耳鼻咽喉科、眼科及皮肤科的基础与临床教学内容，设计了新的临床技能培训体系，其中包括编写新的教材，制定新的教学大纲，由专门的教学组负责实施，培训方式包括模拟训练和床旁实战训练，考核方法包括操作能力考核和临床病例考核，培训内容则涵盖各专业常规操作技能。经过实践运用，证实该培训体系能快速有效地提升学生的临床操作技能，取得了良好的教学效果。     

枇杷叶紫珠化学成分及其细胞毒活性和抗炎活性

目的研究枇杷叶紫珠Callicarpa kochiana的化学成分及其细胞毒活性和抗炎活性。方法枇杷叶紫珠90%丙酮提取物采用硅胶、Sephadex LH-20、MCI、ODS、重结晶、半制备HPLC进行分离纯化,根据理化性质及波谱数据鉴定所得化合物的结构。采用CCK8法、Griess法、ELISA法测定化合物4~5的细胞毒活性和抗炎活性。结果从中分离得到5个化合物,分别鉴定为3,7,3’,4’-tetramethyl-quercetin (1)、pachypodol (2)、14α-hydroxyisopimaric acid(3)、14α-hydroxy-7,15-isopimaradien-18-oic acid (4)、(16R)-16,17-dihydroxyphyllolladan-3-one (5)。化合物4在一定浓度范围内对7种肿瘤细胞具有不同程度的抑制作用,并可以减少RAW264. 7细胞NO、IL-10、MCP-1、TNF-α的释放量。结论化合物1~5均为首次从该植物中分离得到,化合物4具有细胞毒活性和抗炎活性。     

仪器设备全生命周期管理软件的研究与实践

目的:本文分析仪器设备全生命周期管理系统,分享仪器设备管理系统基于药监系统日常管理工作的特色选型。方法:围绕设备全生命周期管理的理念,设计实施电子化设备采购管理、设备台账管理、设备维护维修管理等一系列流程。结果与结论:仪器设备全生命周期管理系统实现全资产、全业务和全过程的信息化管理覆盖。具有良好示范作用,可在药检系统推广使用。     

彩色超声引导下针刀治疗肩胛上神经卡压综合征临床疗效观察

目的:观察彩色超声引导下针刀治疗肩胛上神经卡压综合征的临床疗效。方法:选择本院治疗的肩胛上神经卡压综合征患者60例,随机分为观察组和对照组,每组30例。对照组给予小针刀松解治疗,观察组在彩色超声引导下给予小针刀松解治疗。结果:观察组有效率96.7%,对照组有效率86.7%,观察组高于对照组,差异有统计学意义(P<0.05);治疗1周后、1个月后随访,两组VAS评分均低于治疗前,且观察组低于对照组,差异有统计学意义(P<0.05);治疗1周后、1个月后随访,两组Constant-Murley肩关节评分均高于治疗前,且观察组高于对照组,差异有统计学意义(P<0.05)。结论:彩超引导下针刀局部松解治疗肩胛上神经卡压综合征,可减轻患者的疼痛,缩短肩关节活动功能恢复的时间。     

CDC42 promotes vascular calcification in chronic kidney disease

Vascular calcification is prevalent in patients with chronic kidney disease (CKD) and a major risk factor of cardiovascular disease. Vascular calcification is now recognised as a biological process similar to bone formation involving osteogenic differentiation of vascular smooth muscle cells (VSMCs). Cell division cycle 42 (CDC42), a Rac1 family member GTPase, is essential for cartilage development during endochondral bone formation. However, whether CDC42 affects osteogenic differentiation of VSMCs and vascular calcification remains unknown. In the present study, we observed a significant increase in the expression of CDC42 both in rat VSMCs and in calcified arteries during vascular calcification. Alizarin red staining and calcium content assay revealed that adenovirus-mediated CDC42 overexpression led to an apparent VSMC calcification in the presence of calcifying medium, accompanied with up-regulation of bone-related molecules including RUNX2 and BMP2. By contrast, inhibition of CDC42 by ML141 significantly blocked calcification of VSMCs in vitro and aortic rings ex vivo. Moreover, ML141 markedly attenuated vascular calcification in rats with CKD. Furthermore, pharmacological inhibition of AKT signal was shown to block CDC42-induced VSMC calcification. These findings demonstrate for the first time that CDC42 contributes to vascular calcification through a mechanism involving AKT signalling; this uncovered a new function of CDC42 in regulating vascular calcification. This may provide a potential therapeutic target for the treatment of vascular calcification in the context of CKD. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.