三腔起搏器囊袋感染电极拔除1例

三腔心脏起搏器(CRT)和植入型心律转复除颤器(ICD)显著的治疗效果已为人们所公认,随着起搏工程技术的飞速发展,起搏治疗的适应症也不断拓宽,尤其对于扩张型心肌病所致的心衰患者,特别是心电图ORS≥0.12s者,单纯药物治疗常常不能取得满意的效果,植入CRT能够取得较为满意的结果.此类患者一旦发生起搏系统感染,有效的治疗方法是将已被污染的电极导线取出体外[1],但由于左室电极置于冠状静脉窦内,血管壁薄,且易与血管发生粘连,给电极的拔出带来困难.     

DHS加张力带固定治疗股骨粗隆严重粉碎骨折

目的:观察DHS加张力带在肌骨粗隆间严重粉碎骨折中的治疗效果。方法:采用DHS加张力带固定肌骨粗隆间严重粉碎骨折治疗30例,观察手术时间、骨折愈合时间和术后恢复优良率。结果:本组病例手术时间、骨折愈合时间和术后恢复优良率较理想。结论:DHS加张力带内固定在股骨粉隆间严重粉碎骨折的治疗中具有手术时间短、操作简单、骨折愈合疗效满意、早期功能锻炼等优点。     

中药消炎烧烫酊对烫伤家兔治疗作用的实验研究

目的:观察消炎烧烫酊对皮肤烫伤的作用。方法:采用家兔深Ⅱ度烫伤模型,18只家兔随机平均分成对照组、治疗1组、治疗2组共三组,每组6只。对照组创面涂抹75%酒精,4次/d;治疗1组创面涂抹消炎烧烫酊,2次/d;治疗2组涂抹消炎烧烫酊,4次/d。观察各组创面愈合过程;分别于治疗后48h、第6d取材,进行组织学检查。结果:治疗2组创面无感染,血液循环恢复快,上皮再生早。结论:消炎烧烫酊有抗感染,减少渗出和促进组织修复的作用,对Ⅱ度烫伤有明显疗效。     

《食品机械与设备》混合式教学模式探索与实践

利用优质在线课程及教学资源的优势进行混合式教学改革，构建“以学生为中心”的《食品机械与设备》混合式教学模式，突出新时期教学创新性。线上线下混合式教学使学生的学习更加灵活，提高了学生的参与度，其对课程内容、教学模式和评价考核体系等多方面进行组织和设计，为学生互学和深入探究提供条件，充分考虑学生的自主学习和扩展学习，培养学生形成良好的学习习惯，进而实现对学生各项能力的提升。《食品机械与设备》课程经过混合式教学改革和多个学期的实践积累，逐渐形成了大班授课、小组研讨和实验课的多元化混合教学模式，教学效果良好，将《食品机械与设备》的基础理论知识与前沿进展结合起来，学生学习效率显著提升，更容易理解所学知识。食品机械实验环节可以激发学生的学习兴趣，形成更加具有专业特色的教学培养模式，培养学生自主探索和独立思考的能力。     

灵孢多糖通过抑制TLR4/NF-κB通路改善EAE小鼠的髓鞘脱失北大核心CSCD

目的探究灵孢多糖(ganoderma lucidum polysaccharides,GLPS)对多发性硬化(multiple sclerosis,MS)动物模型实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)小鼠的保护作用及机制。方法将C57BL/6小鼠30只随机平均分为3组:正常对照组、EAE模型组、GLPS组(5 mg·kg^(-1))。采用结核分枝杆菌和MOG35-55建立小鼠EAE模型,观察GLPS对EAE小鼠体质量及神经功能障碍评分的影响;采用固蓝染色和HE染色观察小鼠脊髓冰冻切片髓鞘组织病理情况、免疫荧光观察MBP表达变化;利用流式细胞术检测小鼠脾脏、淋巴结中IL-17、Foxp3含量;通过Western blot检测小鼠脊髓组织中TLR4/NF-κB通路蛋白表达水平。结果与正常对照组比较,EAE模型组小鼠神经行为学评分升高,并且伴随体质量降低,脊髓组织大范围髓鞘脱失,呈现大量炎性细胞浸润,髓鞘标志蛋白MBP表达下调,TLR4/NF-κB通路蛋白表达水平升高。经GLPS干预后,EAE小鼠神经功能评分降低、体质量上升,髓鞘脱失改善,炎性细胞浸润减少,Foxp3的表达增加,IL-17的含量降低,TLR4/NF-κB通路蛋白表达降低。结论GLPS能够抑制MS动物模型EAE的发病进程,其作用机制可能是通过抑制TLR4/NF-κB炎症通路改善髓鞘脱失,从而发挥对中枢神经系统的保护作用。     

Procyanidin B2 protects H2O2-induced oxidative damage in PC12 cells by regulating PI3K/Akt and Nrf2/HO-l signaling pathways北大核心CSCD

Aim To explore the protective effect of proanthocyanidin B2 (PC-B2) on oxidative damage of PC 12 cells induced by hydrogen peroxide (H2 O2 ) and the related mechanism. Methods PC12 cells were treated with H2 O2 (200 μmol • L -1) for 24 h to establish oxidative damage model in vitro, and were randomly divided into normal group, normal + PC-B2 group, H2O2-induced model group and H2 O2 +PC-B2 group. Cell proliferation and cytotoxicity in each group were detected by CCK-8 and LDH assays, respectively. The expressions of MDA, SOD, CAT and GSH-Px were detected by ELISA kit. Cell apoptosis was observed by TUNEL staining. The expressions of apoptosis-related factors Bax, Bcl-2, caspase-3, p-PI3 K, p-Akt, PI3 K/Akt and Nrf2/HO-l pathway were detected by RT-PCR and Western blot. Results Compared with the normal group, the cell proliferation ability of the H2 O2 model group decreased, the contents of LDH and MDA increased, the contents of SOD, CAT and GSH-Px decreased, and the apoptosis was aggravated. After PCB2 intervention, the proliferation ability of PC 12 cells increased, the contents of LDH and MDA decreased, and the contents of SOD, CAT and GSH-Px increased. PC-B2 effectively inhibited the apoptosis of PC12 cells and up-regulated the expression of PI3K/Akt and Nrf2/HO-l proteins. Conclusions PC-B2 can protect PC12 cells from oxidative damage induced by H2 O2 and improve the apoptosis of PC 12 cells. The mechanism may be related to the activation of PI3K/Akt and Nrf2/HO-l signaling pathways. © 2023 Publication Centre of Anhui Medical University. All rights reserved.