Acetylsalicylic acid alleviates chilling injury of postharvest loquat (Eriobotrya japonica Lindl.) fruit

Loquat (Eriobotrya japonica Lindl. cv. Luoyangqing) is a chilling-sensitive fruit and therefore has a limited postharvest life. While fruit stored at 5 °C retained its acceptable quality after 39 days, fruit stored at 0 °C had chilling injury with the symptoms of tissue browning and lignification, decrease in percentage juice, increase in superoxide free radical production, electric conductivity and lignification enzyme activities, including phenylalanine ammonia lyase (PAL), cinnamyl alcohol dehydrogenase (CAD), and guaiacol-peroxidase (G-POD). Such chilling injury symptoms became more severe after fruit were moved to 20 °C shelf life. A postharvest application of 1 mmol/L aqueous acetylsalicylic acid (ASA, a derivative of salicylic acid) to loquat fruit significantly alleviated chilling injury symptoms, inhibited accumulation of superoxide free radical, and reduced PAL, CAD, and G-POD activities. ASA treatment impairing the accumulation of superoxide free radical may prevent chilling injury and lignification in loquat.     

Dietary Trans Fats Enhance Doxorubicin‐Induced Cardiotoxicity in Mice

This study investigated the combined effects of trans fat diet (TFD) and doxorubicin upon cardiac oxidative, inflammatory, and coagulatory stress. TFD increased trans fatty acid deposit in heart (P < 0.05), and decreased protein C and antithrombin‐III activities in circulation (P < 0.05). TFD plus doxorubicin treatment elevated activities of plasminogen activator inhibitor‐1, lactate dehydrogenase, and creatine phosphokinase (P < 0.05). This combination also raised xanthine oxidase activity, and enhanced cardiac levels of reactive oxygen species, interleukin (IL)‐6, IL‐10, tumor necrosis factor‐alpha, and monocyte chemoattractant protein‐1 than TFD or doxorubicin treatment alone (P < 0.05). TFD alone increased cardiac nuclear factor kappa B (NF‐κB) activity (P < 0.05), but failed to affect expression of NF‐κB and mitogen‐activated protein kinase (MAPK) (P > 0.05). Doxorubicin treatment alone augmented cardiac activity, mRNA expression, and protein production of NF‐κB and MAPK (P < 0.05). TFD plus doxorubicin treatment further upregulated cardiac expression of NF‐κB p65, p‐p38, and p‐ERK1/2 (P < 0.05). These findings suggest that TFD exacerbates doxorubicin‐induced cardiotoxicity.     

嗜热链球菌grx02对酒精性肝损伤大鼠保护作用的分子机制

研究了嗜热链球菌grx02对急性酒精性肝损伤大鼠模型的保护作用机制。建立了急性酒精性肝损伤大鼠模型,观察嗜热链球菌grx02对急性酒精性肝损伤大鼠血清转氨酶以及炎症细胞因子的改善作用。结果表明,酒精可诱导大鼠血清谷氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、丙二醛(MDA)水平显著升高,;血清、肝匀浆中肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、白介素-8(IL-8)细胞因子水平显著升高;乙醇脱氢酶(ADH)、还原性谷胱甘肽(GSH)、增加谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性显著下降,与对照组比较均有显著性差异。结论:grx02可能通过抑制炎性因子,增强抗氧化酶系活性、抑制氧化应激引发的肝损伤,对大鼠急性酒精性肝损伤发挥保护作用。     

丹参素对大鼠局灶性脑缺血再灌注损伤的保护作用

目的研究丹参素对大鼠局灶性脑缺血再灌注损伤的保护作用,并初步探讨其作用机制.方法用线栓法制备大鼠局灶性脑缺血再灌注损伤模型,通过神经功能学评分、苏木素和伊红(HE)染色及流式细胞术检测丹参素对大鼠脑缺血再灌注损伤后行为学、缺血侧脑组织病理形态学及神经细胞凋亡的影响.结果丹参素可明显改善脑缺血大鼠神经功能缺损体征,减轻脑组织病理形态学损伤,降低神经细胞凋亡百分率.结论丹参素对大鼠局灶性脑缺血再灌注损伤具有保护作用,其作用机制可能与抑制神经细胞凋亡有关.     

人体胸部侧向碰撞损伤程度的试验研究

本文以利用假人和滑车碰撞试验台所进行的模拟汽车侧向碰撞下人体胸部损伤的试验为基础,分析了车门侧壁与乘员之间不同性质的吸能材料对胸部损伤程度的影响。     

末敏弹毁伤概率计算及其影响因素分析

根据末敏弹工作过程和探测器采用的捕获准则,在对自行火炮进行易损性分析基础上,建立了末敏弹毁伤目标模型,并在此基础上采用蒙特卡罗法进行了大量的数值模拟计算,对结果进行了分析,找出了影响末敏弹性的最敏感因素,为末敏弹结构参数,性能参数的优化提供了依据。     

综合康复措施治疗脊髓损伤中枢性疼痛的临床观察

目的:探讨综合康复治疗措施对脊髓损伤后中枢性疼痛的治疗效果.方法:对31例脊髓损伤后中枢性疼痛患者采用阿米替林、按摩、心理治疗及经皮神经电刺激(TENS)进行治疗.采用McGill疼痛问卷(McGill pain questionnaire,MPQ)、疼痛视觉模拟评分法(Visual Analogous Score,V...     

川芎嗪预处理对大鼠视网膜缺血再灌注损伤后视网膜电流图的影响

目的:观察川芎嗪预处理对大鼠视网膜缺血再灌注损伤后视网膜电流图的影响.方法:采用前房灌注法建立大鼠视网膜缺血再灌注损伤模型,设置正常组、缺血再灌注组、5min缺血预适应组、川芎嗪预处理组,分别于缺血前,缺血30min时,再灌注1h,12h,24h,72h,168h检测双眼各时期FERGb波及OPs(O2)波波幅,分别计...     

532nm激光照射后的兔视网膜损伤修复

目的:观察532nm激光照射后的兔视网膜损伤和修复。方法:采用(光斑直径约为2mm、照射时间100s、能量密度200J/cm2、532nm)激光照射家兔视网膜后极部,连续观察1d、3d、7d、14d和28d后眼底及组织学改变。结果:照后1d可见明显水肿及出血。3d后凝固斑边界清晰,出血范围扩大,可见脉络膜成纤维细胞开始增生。14d后渗出和出血大部分吸收。28d后大量纤维组织增生及新生血管形成。结论:该照射剂量可以引起家兔视网膜较为严重的损伤,其修复存在一定的规律性。     

VEGF165基因修饰的神经干细胞对脑外伤大鼠的神经保护作用及机制

目的：探讨移植转染pDsVEGF165Redl-N1质粒的神经干细胞对脑外伤大鼠的神经保护作用及机制。方法：由新生大鼠脑组织分离培养神经干细胞,应用Lipofectamine2000介导pDsVEGF16sRed1-N1质粒转染神经干细胞;分别将PBS（A组）、神经干细胞（B组）、转基因神经干细胞（C组）移植到脑外伤大鼠局部损伤灶边缘;利用ELISA法检测转基因细胞在体内的表达情况,以免疫组化检测移植后局部损伤组织中微血管密度变化,通过NSS评分评价移植后大鼠神经功能的变化。结果：转基因细胞移植后在一定时间内持续表达VEGFl65,C组大鼠NSS评分从移植后第3天开始明显低于A组（P〈0．05）,而B组大鼠NSS评分则从移植后第7天开始明显低于A组（P〈0．05）,C组大鼠微血管密度从移植后第7天开始明显高于其他两组（P〈0．01）。结论：转基因神经干细胞表达的VEGF165既可以通过促进微血管再生和改善微循环发挥保护作用又可以直接作用于神经细胞发挥保护作用。