Cold‐inducible RNA‐binding protein (CIRP) in inflammatory diseases: Molecular insights of its associated signalling pathways

Cold‐inducible RNA‐binding protein (CIRP) was previously identified as an intracellular stress‐response protein, which can respond to a variety of stress conditions by changing its expression and regulating mRNA stability through its binding site on the 3′‐UTR of its targeted mRNAs. Recently, extracellular CIRP (eCIRP) was discovered to be present in various inflammatory conditions and could act as a pro‐inflammatory factor. Genetic studies have demonstrated a key role for eCIRP in inflammatory conditions that led to the importance of targeting eCIRP in these diseases. Currently, the underlying mechanism of eCIRP‐induced inflammation is under intensive investigation and several signalling pathways are being explored. Here, we epitomized various signalling pathways that mediate the pro‐inflammatory effects of CIRP and also recapitulated all the CIRP‐derived peptides that can block the interaction between CIRP and its receptors in inflammatory setting.     

前瞻性护理干预在急性心力衰竭患者中的应用

目的探讨前瞻性护理干预在急性心力衰竭患者中的应用效果。方法选取2018年4月—2020年5月河南省某医院收治的122例急性心力衰竭患者为研究对象,采用随机数字表法分为观察组与对照组,每组61例。对照组患者采用常规护理,观察组患者采用前瞻性护理,比较2组患者的干预效果、并发症发生情况,干预前后焦虑自评量表(SAS)、抑郁自评量表(SDS)评分及护理满意度。结果观察组患者干预总有效率为95.08%,高于对照组的75.41%,差异有统计学意义(χ²=9.385,P=0.002)。观察组患者并发症发生率为3.28%,低于对照组的18.03%,差异有统计学意义(χ²=6.974,P=0.008)。2组患者干预后SAS及SDS评分均低于干预前,且观察组低于对照组,差异均有统计学意义(P<0.05)。观察组患者护理满意度为98.36%,高于对照组的86.89%,差异有统计学意义(χ²=4.319,P=0.038)。结论前瞻性护理干预用于急性心力衰竭患者,有助于改善患者负性情绪及减少并发症的发生。     

两种保留自主神经D3根治术治疗中低位直肠癌的安全性及生存质量比较

目的比较腹腔镜保留自主神经D3根治术与开腹术治疗中低位直肠癌的安全性及生存质量差异。 方法回顾性分析2015年6月至2017年8月间84例低位直肠癌患者资料，根据手术方式不同分为腹腔镜组(n＝46)和开腹组(n＝38)，应用SPSS21.0软件完成数据分析。手术相关指标采用( ±s)表示，独立样本t检验；并发症发生率、复发率及生存率等指标采用χ²检验；P<0.05为差异有统计学意义。 结果腹腔镜组患者的手术时间长于开腹组(P<0.05)，而术中出血量、住院时间、尿管保留时间、肛门排气时间均短于开腹组(均P<0.05)。腹腔镜组术后并发症总发生率为6.5%低于开腹组的26.3%(χ²＝4.6517，P<0.05)。两组患者1年局部复发率及生存率差异均无统计学意义(均P>0.05)。腹腔镜组患者术后10 d排尿功能、术后2个月勃起功能、术后2个月射精功能均优于开腹组(均P<0.05)。 结论腹腔镜保留自主神经D3根治术治疗中低位直肠癌安全性较高，复发率及生存率与开腹术相当，并能显著提高患者的生存质量，值得推广应用。     

智慧课堂融合任务驱动教学法在《医学影像学》教学中的应用

目的 探讨智慧课堂融合任务驱动教学法在《医学影像学》教学中的应用效果。方法 选取2018 年9 －12 月大连医科大学2015 级本科临床专业4 个班的学生，分为研究组64 名学生（接受智慧课堂融合任务驱动教学法教学），对照组64 名学生（接受传统授予式教学法教学）。教学结束后，通过随堂测试评价教学效果，内容包括学生客观考核与主观考评。应用SPSS 19.0 软件对数据进行统计分析。结果 研究组学生客观考核成绩（82.39±9.59）高于对照组（70±11.55），差异具有统计学意义（P ＜ 0.05）；研究组学生在激发学习兴趣（82.9% 比10.6%）、培养影像诊断思维能力及阅片技能（91.3% 比5.6%）、培养独立思考与解决问题能力（88.5% 比7.8%）、培养自主学习与科研创新思维（86.7% 比9.2%）均高于对照组学生，具有统计学意义（P ＜ 0.01）；两组学生对智慧课堂融合任务驱动教学法改革的认同感或对教学改革的期待（93.3% 比85.4%）无统计学意义。结论 智慧课堂融合任务驱动教学法，提高《医学影像学》教学质量显著，有助于激发学生的学习兴趣，培养学生的影像学诊断思维模式、良好的阅片习惯及技能。     

蟾蜍灵诱导人宫颈癌C33A细胞自噬作用的机理研究

目的:探讨蟾蜍灵诱导人宫颈癌C33A细胞自噬的作用。方法:不同浓度梯度的蟾蜍灵处理人宫颈癌C33A细胞，选用CCK－8法检测蟾蜍灵对人宫颈癌C33A细胞的杀伤作用。透射电镜观察给药后C33A细胞的自噬现象。流式细胞仪检测细胞内活性氧（ROS）水平，蛋白免疫印迹法检测自噬LC3蛋白表达及相关信号通路JNK、p-JNK蛋白表达。结果:蟾蜍灵对人宫颈癌C33A细胞的生长抑制作用呈时间-剂量依赖性。蟾蜍灵给药后可诱导C33A细胞发生自噬，蛋白印迹实验结果表明LC3蛋白表达随药物浓度升高而增加。蟾蜍灵诱导C33A细胞自噬发生与其促ROS水平升高激活了JNK信号通路有关。结论:蟾蜍灵诱导C33A细胞自噬的机制可能与通过ROS/JNK通路促进细胞自噬有关，以此发挥其抗肿瘤的作用。     

Knockdown of Urothelial Carcinoma-Associated 1 Suppressed Cell Growth and Migration Through Regulating miR-301a and CXCR4 in Osteosarcoma MHCC97 Cells

Liver cancer is one of the most common malignancies in the world and a leading cause of cancer-related mortality. Accumulating evidence has highlighted the critical role of long noncoding RNAs (lncRNAs) in various cancers. The present study aimed to explore the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in cell growth and migration in MHCC97 cells and its underlying mechanism. First, we assessed the expression of UCA1 in MHCC97 and three other cell lines by RT-qPCR. Then the expression of UCA1, miR-301a, and CXCR4 in MHCC97 cells was altered by transient transfection. The effects of UCA1 and miR-301 on cell viability, migration, invasion, and apoptosis were assessed. The results revealed that UCA1 expression was relatively higher in MHCC97 cells than in MG63, hFOB1.19, and OS-732 cells. Knockdown of UCA1 reduced cell viability, inhibited migration and invasion, and promoted cell apoptosis. However, the effect of UCA1 knockdown on cell growth and migration was blocked by miR-301a overexpression, whose expression was regulated by UCA1. We also found that miR-301a positively regulated CXCR4 expression. CXCR4 inhibition reversed the effect of miR-301a overexpression on cell growth and migration. Moreover, miR-301a activated the Wnt/ -catenin and NF- B pathways via regulating CXCR4. The present study demonstrated that UCA1 inhibition exerted an antigrowth and antimigration role in MHCC97 cells through regulating miR-301a and CXCR4 expression.