有氧运动对女大学生心脏功能及血清免疫球蛋白的影响

目的研究不同持续时间有氧运动对女大学生心脏功能及血清免疫球蛋白含量的影响。方法选取自愿参加的非体育专业女大学生45人,随机均分为对照组、60 m in运动组和120 m in运动组。运动组每周进行3次,共8周的有氧运动。分别测定运动前后安静心率、心功指数、血清免疫球蛋白（IgG、IgA、IgM）含量。结果45名女大学生均按计划完成运动试验。两种不同持续时间的有氧运动均未影响安静心率,但均显著改善心功指数,且120 m in组的改善效果显著优于60 m in组（P<0.05）。60 m in有氧运动仅可显著增加血清IgG含量（P<0.05）,而120 m in有氧运动对3种血清Ig均无明显影响。结论两种不同持续时间的有氧运动均可改善心脏功能,且120 m in运动的改善效果优于60 m in运动。     

陕西秦岭以北地区成人血脂水平的横断面调查

目的 评估陕西秦岭以北地区人群的血脂状况,描述血脂异常人群的流行病学特征.方法 采用多极分层抽样方法,根据2007年中国成人血脂异常防治指南,对陕西省秦岭以北地区3298名居民进行血脂状况的调查.结果 血脂异常的检出率为33.54%,标化率为32.11%.其中高胆固醇血症的检出率为8.13%,标化率为7.48%.高甘油三酯血症的检出率是16.89%,标化率是15.40%.低高密度脂蛋白血症的检出率为19.77%,标化率为19.72%.血脂异常、高甘油三酯血症、高胆固醇血症随着年龄的增加异常率逐渐升高.血脂异常的发生率在城市和农村之间没有差异,但男性远高于女性.吸烟和饮酒者的血脂异常率明显升高,糖尿病和高血压人群也显示出了较高的血脂异常率.Logistic多因素分析显示,血脂异常的危险因素包括性别、体质指数、高血压、糖尿病、教育程度.结论 陕西省秦岭以北地区具有较高的血脂异常发生率,需根据性别、肥胖程度、是否有糖尿病、高血压及受教育程度进行针对性的血脂防治.     

MicroRNAs与心肌缺血/再灌注损伤关系的研究进展

MicroRNA(miRNA)是一类体内生成,长度介于17~25 nt的非编码小RNA。此类RNA在翻译后的水平对基因表达发挥负调控作用,广泛参与生物体的生长发育及各种病理生理过程。近年研究表明,miRNA在心肌缺血/再灌注损伤(MIRI)中发挥重要作用,其参与了与MIRI有关的心肌细胞凋亡、热休克蛋白、离子通道以及细胞生存信号通路的调控,并可作为某些药物的作用靶点,为MIRI的治疗提供了新的思路。     

姜黄素后处理通过JAK2/STAT3信号通路拮抗心肌缺血/再灌注损伤

目的:观察姜黄素（curcumin,Cur）后处理对离体心肌缺血/再灌注损伤(ischemia and reperfusion injury,I/RI)的拮抗作用及其可能的机制。方法: 40只SD大鼠随机分为5组(n=8),即空白对照(Ctl组)、缺血/再灌注组(I/R组)、I/R+姜黄素后处理组(I/R+Cur组)、I/R+姜黄素后处理+AG490组(I/R+Cur+AG组)及AG490组（AG组）,AG490为JAK2/STAT3信号通路特异性阻断剂。采用离体大鼠心脏Langendoff逆行灌注模型,缺血60 min,再灌注60 min。分别于缺血前及再灌注后15 min、30 min、45 min和60 min,测定血流动力学各项指标,包括:心率（HR）、左心室发展压（LVDP）、左心室内压力上升的最大速率(+dp/dtmax)、冠脉流量（CF）、计算出心率压力指数（DP,LVDP×HR/1000）。用氯化三苯基四氮唑(TTC)染色法测定各组心肌梗死(MI)的面积,用Western blot检测各组JAK2、磷酸化JAK2(p-JAK2)、STAT3以及磷酸化STAT3(p-STAT3)的表达。结果: 与Ctl组比较,I/R组各时间点的收缩及舒张功能均显著降低(P<0.01),MI面积显著增加(P<0.01),磷酸化JAK2和STAT3的表达明显升高(P<0.01)。与I/R组比较,I/R+Cur组各时间点的心肌收缩及舒张功能下降程度明显减轻(P<0.01),MI的面积明显减少(P<0.01),p-JAK2和STAT3的表达更高(P<0.01)。与I/R+Cur组相比,I/R+Cur+AG组各时间点的收缩及舒张功能显著降低(P<0.01),MI的面积显著增加(P<0.01),p-JAK2和STAT3的表达显著下降(P<0.01);和Ctl组相比,AG组血流动力学和MI的面积无统计学差异。结论: Cur后处理对I/R大鼠心肌具有保护作用,其作用机制与JAK2/STAT3信号通路的活化有关。     

Preparation and activity of conjugate of monoclonal antibody HAb18 against hepatoma F(ab')(2) fragment and staphylococcal enterotoxin A

AIM: To prepare the conjugate of staphylococcal enterotoxin A (SEA) protein which is a bacterial SAg and the F(ab')(2) fragment of mAb HAb18 against human hepatocellular carcinoma (HCC), and identify its activity in order to use SAg in the targeting therapy of HCC. METHODS: MAb HAb18 was extracted from the abdominal dropsy of Balb/c mice, and was purified through chromatography column SP 40HR with Fast protein liquid chromatography (FPLC) system. The F(ab')(2) fragment of mAb HAb18 was prepared by papainic digestion method. The conjugate of mAb HAb18 F(ab')(2) fragment and SEA was prepared with chemical conjugating reagent N succinimidyl 3 (2-pyridyldithio) propionate (SPDP) and purified through chromatography column Superose 12 with FPLC system. The molecular mass and purity of each collected peak were identified with SDS-PAGE assay. The protein content was assayed by Lowry's method. The antibody activity of HAb18 F(ab')(2) against HCC in the conjugate was identified by indirect immunocytochemical ABC method, and the activity of SEA in the conjugate to activate peripheral blood mononuclear cells (PBMC) was identified with MTT assay. RESULTS: The IgG mAb HAb18 was extracted, and purified successfully. Immunocytochemical staining demonstrated that it reacted with most of HHCC cells of human HCC cell line. There were two peaks in the process of purification of the prepared HAb18 F(ab')(2) SEA conjugate. SDS-PAGE assay demonstrated that the molecular mass of the first peak was about 130 ku, and the second peak was the mixture of about 45 ku and a little 100 ku proteins. The immunocytochemical staining was similar in HAb18 F(ab') (2) SEA conjugate and HAb18 F(ab') (2), i.e.the cytoplasm and/or cell membranes of most HHCC cells were positively stained. The MTT assay showed that the optical absorbance (A) value at 490 nm of HAb18 F(ab') (2) SEA conjugate was 0.182 +/- 0.012, that of negative control was 0.033 +/- 0.009, and there was significant difference between them (P < 0.05). CONCLUSION: SPDP is a good protein conjugating reagent and can be used in preparing protein conjugate. The conjugate of mAb HAb18 F(ab') (2) fragment and SEA protein was prepared successfully in present study and can be used in the experimental study of HCC targeting therapy with the conjugate of SAg and anti HCC mAbs or their fragments.     

DIDS对I/RI心肌组织中信号分子PI3K/Akt及ROS的调控

目的:探讨氯离子通道阻断剂4,4-二异硫氰基芪-2,2′-二磺酸（4,4′-Diisothiocyanostilbene-2,2′-disulfonic acid,DIDS）对缺血/再灌注损伤(Ischemia/reperfusion injury,I/RI)心肌组织中信号分子磷脂酰肌醇-3激酶（Phosphoinositide-3 kinase,PI3K）/蛋白激酶B（Protein kinase B,Akt）及活性氧（ROS）的调控。方法: 常规建立SD大鼠I/RI心脏模型,32只,随机分成4组（n=8）,分为假手术组、I/R组、过氧化氢酶(CAT)组及DIDS组。伊文思蓝和红四氮唑（TTC）双染色法检测大鼠心肌梗死面积、荧光分光光度计法检测心肌组织中ROS的含量、用western blot 蛋白印迹法检测Akt和p-Akt的水平,TUNNEL法检测心肌细胞凋亡,以及检测血清肌酸激酶（CK）、乳酸脱氢酶（LDH）、超氧化物歧化酶(SOD)的活性及丙二醛（MDA）的含量。结果: ①与I/R组对比,DIDS组和CAT两组的心肌梗死面积、细胞凋亡数、血清CK、LDH的活性均明显减少（P<0.05）;但DIDS和CAT二组间无差异。②与I/R组对比,DIDS组和CAT组血清中MDA的含量明显减小;而SOD的活性明显升高（P<0.05）;与DIDS组比较,CAT组SOD的活性明显升高（P<0.05）、MDA的含量明显减少（P<0.05）。③与I/R组对比,CAT组和DIDS组心肌组织中ROS的含量显著降低（P<0.05）;CAT组较DIDS组降低的更明显（P<0.05）。④各组心肌组织中总Akt的表达无显著差异。与假手术组相比,I/R、DIDS 和CAT 3组p-Akt的水平均有明显升高（P<0.05）;DIDS组p-Akt的水平显著高于I/R和CAT组（P<0.05）;但I/R和CAT两组间无差异。结论: DIDS同时具有激活PI3K/Akt信号通路及降低ROS水平,减轻I/RI,达到保护心肌组织的作用。     

α-亚麻酸对糖尿病大鼠血管功能和氧化应激的影响

目的:观察α-亚麻酸（ALA）对糖尿病(DM)大鼠血管功能和氧化应激的影响,探讨ALA在DM血管并发症防治中的作用。方法: 将30只SD大鼠随机分为正常对照组、DM模型组和ALA治疗组［500 μg/(kg·d)］,每组10只。10只雄性SD大鼠以高脂饮食喂养4周后,腹腔注射链脲佐菌素（STZ）30 mg/kg建立Ⅱ型DM（T2DM）模型。4周后分离降主动脉,进行离体血管灌流观察血管的舒张功能,利用试剂盒测定灌流液中NO的含量以及血管组织中丙二醛（MDA）的含量、超氧化物岐化酶（SOD）和过氧化氢酶（CAT）的活性。结果: 与正常对照组相比,DM大鼠主动脉内皮依赖性舒张功能和NO的含量显著下降(P<0.01),ALA治疗可有效地减轻DM大鼠血管内皮功能障碍,增加NO的含量（均P<0.01）。另外,与正常对照组相比,DM大鼠血管组织中MDA的含量增加(P<0.01),抗氧化酶SOD和CAT的活性下降(P<0.01);ALA治疗可显著降低DM大鼠血管组织中MDA的含量(P<0.05),增加抗氧化酶SOD和CAT的活性(P<0.01)。结论: ALA可显著改善T2DM模型大鼠的血管内皮舒张功能障碍,其机制可能与减轻血管组织的氧化应激有关。     

口腔颌面部间隙感染诊疗专家共识

口腔颌面部间隙感染（oral and maxillofacial space infections,OMSI）是颌面部潜在筋膜间隙的感染,是口腔颌面部的常见疾病。OMSI病例具有耐药菌感染增多、重症感染增多、致死风险增加等特点。为提高OMSI的治愈率,其治疗原则与方法需与时俱进。因此,依据国内部分专家当前诊治OMSI的...     

视神经损伤后发生非折叠蛋白反应的超微证据

目的:探索视神经损伤后视网膜节细胞(retinal ganglion cell,RGC)及其纤维渐进性死亡机制。方法:利用包埋前与包埋后免疫金细胞化学标记技术结合电镜观察研究大鼠(n=15)视神经钳夹损伤后RGC与视神经干少突胶质细胞内的非折叠蛋白反应(unfolding protein response,UPR)。结果:视神经钳夹后,需肌醇酶1(inositol requiring enzyme 1,IRE1)在RGC与少突胶质细胞内胶体金标记数目增多,在钳夹0.5d后RGC内即有显著地增加(18.4±5.1～30.4±7.2个,P<0.05),随损伤时间延长,增多更为明显,在钳夹3d后达高峰(48.5±9.7个),IRE1在视神经干上的少突胶质细胞内增多时程变化与在RGC内相似。IRE1在RGC与少突胶质细胞内胶体金标记颗粒分布部位距离ER管腔距离增加为特征,在钳夹0.5d内神经干少突胶质细胞以及视网膜RGC内均表现非常明显的距离增加。结论:视神经钳夹导致损伤细胞触发UPR,UPR可能参与视神经损伤后RGC及其纤维渐进性死亡机制。     

VEGF gene therapy for the survival of transplanted fat tissue in nude mice.

The objective of this study was to determine the effects of adenovirus-mediated vascular endothelial growth factor (Ad-VEGF) on the angiogenesis and survival of free-fat tissue transplantation in nude mice. Thirty 6-week-old CD-1 nude male mice were injected with 1ml fat tissue (harvested by suction-assisted lipectomy from the breast of humans) in the subcutaneous of scalp and were randomised into three groups of 10 animals each. Group 1 was the study group, in which Ad-VEGF was mixed with transplanted fat tissue and injected into mice. In group 2, adenovirus-mediated green fluorescent protein (Ad-GFP) gene was mixed with transplanted fat tissue and injected into the mice. In group 3, normal saline alone was used. Both group 2 and group 3 are control groups. The animals were euthanised 15 weeks after the procedure. The fat survival weight and volume of the study group were significantly greater than those of two control groups (p<0.05). Light microscopical examination of haematoxylin and eosin-stained slides of the dissected fat 15 weeks after injection was performed in group 1 and group 2. Less cyst formation and fibrosis, indicating improved quality of the injected fat, can be obtained by the addition of Ad-VEGF. Vascular density was evaluated at the microvascular level through the use of light microscopic sections of the central part of the fat tissue at 15 weeks after injection by von Willebrand factor staining. Histological evaluation showed that capillary density increased markedly in the study group mice. Mice of the study group disclosed significantly higher VEGF protein levels detected by ELISA assay of plasma samples obtained from the mice after the fat injection (day 1, 4, 7 and 28; p<0.01) at each time point than the mice of the two control groups. The findings reported in this study indicate that the VEGF gene therapy can enhance the survival and the quality of grafted fat tissue, which may be due to induction of angiogenesis.