Exosomes derived from umbilical cord mesenchymal stem cells alleviate viral myocarditis through activating AMPK/mTOR‐mediated autophagy flux pathway

Human umbilical cord mesenchymal stem cell‐derived exosomes (hucMSC‐exosomes) have been implicated as a novel therapeutic approach for tissue injury repair and regeneration, but the effects of hucMSC‐exosomes on coxsackievirus B3 (CVB3)‐induced myocarditis remain unknown. The object of the present study is to investigate whether hucMSC‐exosomes have therapeutic effects on CVB3‐induced myocarditis (VMC). HucMSC‐exosomes were identified using nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM) and Western blot. The purified hucMSC‐exosomes tagged with PKH26 were tail intravenously injected into VMC model mice in vivo and used to administrate CVB3‐infected human cardiomyocytes (HCMs) in vitro, respectively. The effects of hucMSC‐exosomes on myocardial pathology injury, proinflammatory cytokines and cardiac function were evaluated through haematoxylin and eosin (H&E) staining, quantitative polymerase chain reaction (qPCR) and Doppler echocardiography. The anti‐apoptosis role and potential mechanism of hucMSC‐exosomes were explored using TUNEL staining, flow cytometry, immunohistochemistry, Ad‐mRFP‐GFP‐LC3 transduction and Western blot. In vivo results showed that hucMSC‐exosomes (50 μg iv) significantly alleviated myocardium injury, shrank the production of proinflammatory cytokines and improved cardiac function. Moreover, in vitro data showed that hucMSC‐exosomes (50 μg/mL) inhibited the apoptosis of CVB3‐infected HCM through increasing pAMPK/AMPK ratio and up‐regulating autophagy proteins LC3II/I, BECLIN‐1 and anti‐apoptosis protein BCL‐2 as well as decreasing pmTOR/mTOR ratio, promoting the degradation of autophagy flux protein P62 and down‐regulating apoptosis protein BAX. In conclusion, hucMSC‐exosomes could alleviate CVB3‐induced myocarditis via activating AMPK/mTOR‐mediated autophagy flux pathway to attenuate cardiomyocyte apoptosis, which will be benefit for MSC‐exosome therapy of myocarditis in the future.     

Dihydromyricetin increases endothelial nitric oxide production and inhibits atherosclerosis through microRNA-21 in apolipoprotein E-deficient mice

Natural products were extracted from traditional Chinese herbal emerging as potential therapeutic drugs for treating cardiovascular diseases. This study examines the role and underlying mechanism of dihydromyricetin (DMY), a natural compound extracted from Ampelopsis grossedentata, in atherosclerosis. DMY treatment significantly inhibits atherosclerotic lesion formation, proinflammatory gene expression and the influx of lesional macrophages and CD4-positive T cells in the vessel wall and hepatic inflammation, whereas increases nitric oxide (NO) production and improves lipid metabolism in apolipoprotein E-deficient (Apoe^−/−) mice. Yet, those protective effects are abrogated by using NOS inhibitor L-NAME in Apoe^−/− mice received DMY. Mechanistically, DMY decreases microRNA-21 (miR-21) and increases its target gene dimethylarginine dimethylaminohydrolase-1 (DDAH1) expression, an effect that reduces asymmetric aimethlarginine (ADMA) levels, and increases endothelial NO synthase (eNOS) phosphorylation and NO production in cultured HUVECs, vascular endothelium of atherosclerotic lesions and liver. In contrast, systemic delivery of miR-21 in Apoe^−/− mice or miR-21 overexpression in cultured HUVECs abrogates those DMY-mediated protective effects. These data demonstrate that endothelial miR-21-inhibited DDAH1-ADMA-eNOS-NO pathway promotes the pathogenesis of atherosclerosis which can be rescued by DMY. Thus, DMY may represent a potential therapeutic adjuvant in atherosclerosis management.     

A Review on Additives for Halide Perovskite Solar Cells

Additives are widely adopted for efficient, stable, and hysteresis‐free perovskite solar cells and play an important role in various breakthroughs of perovskite solar cells (PSCs). Herein the various additives adopted for PSCs are reviewed and their functioning mechanism and influence on device performance is described. The main roles of additives, modulating morphology of perovskite films, stabilizing phase of formamidinium (FA) and cesium (Cs)‐based perovskites, adjusting energy level alignment in PSCs, suppressing nonradiative recombination in perovskites, eliminating hysteresis, enhancing operational stability of PSCs, are summarized.     

MT2A对脂多糖介导的人肺毛细血管内皮细胞损伤的保护作用

目的:探索不同浓度的金属硫蛋2A(Metallothionein 2A, MT2A)对脂多糖(Lipopolysaccharid, LPS)介导的人肺微血管内皮细胞损伤的保护作用。方法:培养人肺毛细血管内皮细胞株(Human lung microvascular endothelial cells, HPMVECs),经过一定浓度LPS溶液进行刺激后,利用不同浓度的MT2A与对照组共同培养,一段时间后观察炎性介质IL-6、TNF-α释放的量及荧光显微镜观察组HPMVECs骨架形态变化。结果:各组TNF-α浓度均在0 h最低,随之逐渐升高,到6 h达到高峰;从各时间点来看,除0 h各组TNF-α浓度无显著差异外(F=0.717, P=0.549),其余各时间点B1、B2、B3均显著高于A组(均P0.05)。各组中IL-6浓度均在0 h最低,A组在2 h达到高峰,随后逐渐下降;B1组在4 h达到高峰,随之下降;B2、B3组从0 h开始逐渐升高,到6 h达到峰值;从各时间点来看,除0 h各处理因素无显著差异外(F=2.341, P=0.092),其余各时间点B1、B2、B3均低于A组(均P0.05)。A组6 h小时后纤维状肌动蛋白(F-actin)明显解聚,分布明显减少,应力纤维排列紊乱或者消失;B1组、B2组、B3组6 h小时后,与A组相比,F-actin的分布明显较多,应力纤维排列较为整齐。结论:LPS刺激人肺毛细血管内皮细胞有明显损伤效应,加入MT2A后细胞相关炎性因子释放量、细胞骨架损伤情况明显减轻,表明一定浓度的MT2A对LPS介导的肺毛细血管损伤有明显保护作用。     

紫叶小檗刺的形态与发生——对小檗属植物刺的重新认识

针对目前人们对小檗属植物刺的来源存在不同见解,本研究通过实体解剖及石蜡切片技术,以紫叶小檗为代表研究小檗属植物刺的形态和发生,结果表明,紫叶小檗的刺均为叶刺,而非茎刺,明确了小檗属的刺为叶的变态。     

不同剂量熊果酸干预糖尿病小鼠视网膜病变的作用及机制研究

目的:探究不同剂量熊果酸(UA)干预糖尿病小鼠视网膜病变的作用及机制。方法:选取雄性健康C57BL/6小鼠60只,其中50只按50 mg/kg的剂量一次性往小鼠尾静脉注射新鲜配置的四氯嘧啶生理盐水溶液构建小鼠糖尿病视网膜病变模型,随机分为5组,每组10只,分别为模型组、阳性对照组(小鼠玻璃体注射3μL 40 mg/m L的曲安奈德),低剂量UA干扰组(小鼠玻璃体注射3μL剂量为0.5μg/μL的UA)、中剂量UA干扰组(小鼠玻璃体注射3μL剂量为1.0μg/μL的UA),高剂量UA干扰组(小鼠玻璃体注射3μL剂量为2.0μg/μL的UA),余下10只小鼠作为正常对照组。观察各组小鼠对胰岛素敏感性、视网膜内糖代谢情况、小鼠视网膜神经节细胞(RGCs)凋亡情况,比较各组小鼠视网膜组织中血管内皮生长因子(VEGF)、环氧化酶-2(COX-2)、基质金属蛋白酶2(MMP-2)蛋白及其mRNA的表达情况。结果:建模后,正常对照组胰岛素抵抗指数(HOMA-IR)、视网膜含糖量、葡萄糖转运体-1(GLUT-1)与葡萄糖转运体-3(GLUT-3)含量、RGCs凋亡率、视网膜组织中VEGF、COX-2、MMP-2蛋白及其mRNA的表达量低于模型组(P0.05);经干扰后,阳性对照组、不同剂量UA干扰组HOMA-IR、视网膜含糖量、GLUT-1、GLUT-3的含量、RGCs凋亡率、视网膜组织中VEGF、COX-2、MMP-2蛋白及其mRNA的表达量低于模型组(P0.05),且随UA干扰剂量的升高而降低(P0.05)。结论:UA能够降低HOMA-IR和视网膜糖代谢能力,抑制RGCs的凋亡,对VEGF、COX-2、MMP-2蛋白及其mRNA的表达具有一定的抑制作用,高剂量UA对糖尿病小鼠视网膜病预防治疗效果较好。     

烧伤早期伴发脓毒症患者血清PCT、hs-CRP、COR及WBC的动态变化及临床意义

目的:探讨烧伤早期伴发脓毒症患者血清降钙素原(PCT)、超敏C反应蛋白(hs-CRP)、皮质醇(COR)和白细胞计数(WBC)水平并分析其临床价值。方法:回顾性分析2014年12月至2018年1月本院收治的63例烧伤早期患者的临床资料,其中19例患者伴发脓毒症(脓毒症组),44例患者未伴发脓毒症(无脓毒症组),另选取30例于本院进行体检的志愿者作为健康对照组,依据病情严重程度将脓毒症患者分为脓毒症休克组(n=4)、严重脓毒症组(n=7)、一般脓毒症组(n=8),依据预后情况分为预后良好组(n=13)和预后不良组(n=6)。动态检测并对比所有研究对象血清PCT、hs-CRP、COR和WBC水平。结果:无脓毒症组、脓毒症组血清PCT、hs-CRP、COR和WBC水平高于健康对照组,且脓毒症组高于无脓毒症组(P<0.05)。烧伤后7 d、11 d、15 d,脓毒症组血清PCT、hs-CRP、COR和WBC水平均高于无脓毒症组(P<0.05)。脓毒症休克组血清PCT、hs-CRP、COR和WBC水平高于严重脓毒症组、一般脓毒症组,且严重脓毒症组患者高于一般脓毒症组患者(P<0.05)。预后不良组血清PCT、hs-CRP、COR和WBC水平高于预后良好组(P<0.05)。结论:血清PCT、hs-CRP、COR和WBC水平在烧伤早期伴发脓毒症患者中水平异常升高,与病情严重程度有关,上述指标对预后判断有一定的临床参考价值。     

思维导图引导康复锻炼对胸腰椎肿瘤术后功能恢复的干预效果

目的:研究思维导图引导康复锻炼对胸腰椎肿瘤术后功能恢复的干预效果,为患者术后的康复提供指导。方法:选择我院2017年1月-2019年12月期间我院200例胸腰段肿瘤术后患者。按照随机数表法将其分为研究组与对照组。研究组采用思维导图引导康复锻炼措施,对照组采用常规术后康复锻炼措施。比较两组患者干预前后腰背部功能、日常生活活动能力、社会生活生存质量及康复质量的评分结果。结果:干预后研究组生活自理能力、疼痛情况、站立、坐位、步行、睡眠情况、社会生活的Oswestry功能障碍(ODI)指数明显低于对照组,差异有统计学意义(P0.05)。干预后研究组Barthel指数以及Fugl-Meyer评分明显高于对照组,差异有统计学意义(P0.05)。干预后研究组社会功能缺陷筛选量表(SDSS)评分与生存质量测定量表(QOLI)评分明显优于对照组,差异有统计学意义(P0.05)。干预后研究组患者的躯体症状、心理状态及康复状况评分明显高于对照组,差异有统计学意义(P0.05)。结论:思维导图引导康复锻炼对胸腰椎肿瘤术后功能恢复有着较为理想的效果,值得临床推广运用。     

基于磁驱动技术的空肠营养管的设计

目的:为解决目前床旁鼻肠管快速置入成功率低这一临床难题,该文提出一种基于磁驱动技术的空肠营养管的设计。方法:分析了现有空肠营养管置管过程中的动力因素,结合磁驱动技术原理,提出了通过体外旋转磁场带动体内感应磁体螺旋式前进的设计方案,以期缩短空肠营养管的飘管时间。结果:该设计包括磁性空肠营养管和体外磁力驱动装置两部分。其中磁性空肠营养管由管体和感应磁头两部分构成,感应磁头包括磁体内核和硅胶外壳。磁力驱动装置由多极磁体和手持式微型电机组成。操作时通过体外磁力驱动装置发出大旋转磁场带动空肠营养管的感应磁头做轴向旋转运动,可加速空肠营养管在肠道内的移动,达到缩短飘管时间的目的。结论:该设计基于磁驱动技术原理,设计巧妙,符合磁力学原理,操作简单,具有临床应用潜力。     

关节镜下同期行冻结肩松解术对肩袖损伤患者的治疗效果评估

目的:评估关节镜下同期行冻结肩松解术对肩袖损伤患者的治疗效果。方法:选择2015年3月到2018年3月在我院诊治的肩袖损伤患者70例进行研究,按随机数表法将其分为观察组(n=36)和对照组(n=34)。对照组采用传统小切口肩袖修复术治疗,观察组采用关节镜下同期行冻结肩松解术进行治疗。比较两组治疗后疗效、手术时间、术中出血量、住院时间、疼痛减轻时间、治疗前后VAS、美国肩肘外科协会评分(ASES)、Contant-Muley评分的变化情况。结果:治疗后,观察组总有效率为94.44%,显著高于对照组(73.53%,P0.05);观察组手术时间、术中出血量、住院时间及疼痛减轻时间均显著低于对照组(P0.05);两组VAS、ASES、Contant-Muley评分较治疗前均显著改善(P0.05),且观察组VAS评分明显低于对照组,ASES及Contant-Muley评分显著高于对照组(P0.05)。结论:关节镜下同期行冻结肩松解术治疗肩袖损伤的临床疗效显著优于传统小切口肩袖修复术治疗,其可显著促进关节功能恢复,并减轻患者痛苦。