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101.
102.
目的:利用核因子κBp65特异性小干涉核糖核酸抑制肿瘤坏死因子α诱导的关节滑膜细胞中一氧化氮合酶2和环氧合酶2的表达,探讨基因治疗类风湿性关节炎的新方法。方法:实验于2005-03/2006-03在北京大学医学部中心实验室(国家级)完成。①实验材料:清洁级健康近交系SD大鼠10只;一氧化氮合酶2,环氧合酶2,3-磷酸甘油醛脱氢酶引物(由北京奥科生物公司合成);肿瘤坏死因子α(Sigma公司);核因子κBp65特异性小干涉核糖核酸和转染条件由北京大学运动医学研究所陈连旭博士提供。②实验干预:切取大鼠髋关节和膝关节的滑膜体外培养滑膜细胞。利用脂质体siPORTTMLipid将核因子κBp65特异性小干涉核糖核酸转染滑膜细胞,再加入肿瘤坏死因子α刺激。阴性对照为任意编码的小干涉核糖核酸,阳性对照为针对3-磷酸甘油醛脱氢酶的小干涉核糖核酸。③实验评估:提取滑膜细胞中的核蛋白,利用电泳迁移率试验检测核因子κB的活性;提取滑膜细胞的核糖核酸和总蛋白,利用反转录聚合酶链反应和蛋白质免疫印记法从信使核糖核酸和蛋白质两水平检测一氧化氮合酶2和环氧合酶2的表达。结果:①肿瘤坏死因子α和核因子κBp65特异性小干涉核糖核酸对核因子κB转录活性的影响:与正常滑膜细胞相比,肿瘤坏死因子α可以显著提高核因子κB的结合能力,而事先转染小干涉核糖核酸48h,再用肿瘤坏死因子α刺激,核因子κB的结合能力又显著降低。②核因子κBp65特异性小干涉核糖核酸对核因子κB下游因子的影响:在培养的滑膜细胞中,肿瘤坏死因子α可以显著增加一氧化氮合酶2和环氧合酶2的表达;在转染小干涉核糖核酸抑制核因子κBp65的表达后再用肿瘤坏死因子α刺激,一氧化氮合酶2和环氧合酶2的表达被抑制。结论:①核因子κBp65特异性小干涉核糖核酸可降低肿瘤坏死因子α诱导的滑膜细胞中核因子κB的转录活性,抑制其下游因子一氧化氮合酶2和环氧合酶2的表达。②核因子κBp65特异性小干涉核糖核酸可用于基因治疗类风湿性关节炎的试验研究。 相似文献
103.
尼莫地平对烫伤大鼠脑内ZO-1 mRNA及血脑屏障通透性的影响 总被引:2,自引:0,他引:2
目的:观察尼莫地平对严重烫伤大鼠脑内紧密连接相关蛋白ZO-1mRNA及血脑屏障通透性的影响。方法:实验于2005-04/10在南昌大学基础医学院应用解剖实验室完成。①取健康SD大鼠132只分为正常对照组12只、烫伤组60只,尼莫地平组60只,后两组又设烫伤后1,3,6,12,24h5个时间点,每个时间点12只,其中6只用于脑组织伊文思蓝含量的测定,剩余6只用于ZO-1mRNA的检测。②烫伤组和尼莫地平组大鼠100℃开水烫伤15s,造成背部30%体表总面积Ⅲ度烧伤。尼莫地平组大鼠于烫伤后即刻腹腔注射尼莫地平(0.5mg/kg),其他2组不给药。③各组大鼠于相应的时间点麻醉并处死动物取材,应用化学定量方法检测大鼠脑组织内伊文思蓝含量,运用RT-PCR方法检测大鼠脑内ZO-1mRNA的表达变化。结果:经补充后132只大鼠进入结果分析。①大脑伊文思蓝含量:正常对照组为(10.18±1.79)μg/g,烫伤组伤后1,3,6,12h均高于正常对照组(P<0.05),其高峰在烫伤后6h,为(20.00±0.58)μg/g;尼莫地平组伤后1,6,12h均低于烫伤组(P<0.01),烫伤后6h时为(16.74±0.78)μg/g。②小脑伊文思蓝含量:正常对照组为(12.90±1.32)μg/g,烫伤组伤后1,3,6,12h均高于正常对照组(P<0.05),其高峰在烫伤后6h,为(31.3±1.47)μg/g;尼莫地平组伤后1,3,6,12h均低于烫伤组(P<0.01),烫伤后6h时为(21.05±2.36)μg/g。③脑组织ZO-1mRNA的表达:烫伤组烫伤后3,6,12,24h分别为正常对照组的(0.1235±0.0158),(0.1890±0.0531),(0.2014±0.0412),(0.1555±0.0163)倍(P<0.01);尼莫地平组较烫伤组高,以烫伤后3,6h最为明显,分别为烫伤组的3.96及1.81倍(P<0.01).结论:①严重烫伤后血脑屏障通透性增高,脑内ZO-1mRNA表达下降。②烫伤后早期应用尼莫地平能防止脑内ZO-1mRNA表达下降,并能起到保护血脑屏障功能的作用。 相似文献
104.
105.
Prevalence of cytomegalovirus antibody in hemophiliacs and homosexuals infected with human immunodeficiency virus type 1 总被引:1,自引:0,他引:1
We determined the prevalence of antibody to cytomegalovirus (CMV) in the sera of non-homosexual hemophilia patients and homosexual men infected with the human immunodeficiency virus type 1 (HIV-1). CMV antibody testing by latex agglutination revealed 33 of 58 HIV-1 infected hemophiliacs (57%) were antibody-positive compared with 54 of 54 HIV-1 infected asymptomatic non-hemophiliac homosexuals (100%) (p less than .001). Nine of 15 hemophiliacs (60%) with symptomatic HIV-1 infection were CMV antibody-positive. We also tested 22 HIV-1 antibody-negative hemophiliacs who had received non-heat treated factor concentrates. 14 of these 22 (64%) were CMV antibody-positive compared with 57% of HIV-1 antibody-positive hemophiliacs. We conclude 1) there is little correlation between transmission of HIV-1 and CMV by factor concentrates, 2) the presence of CMV antibody does not appear to be associated with clinical stage of HIV-1 infection in hemophiliacs, and 3) there may be a significant number of CMV antibody-negative hemophiliacs with HIV-1 infection at risk for primary infection and subsequent disease if CMV seronegative blood products are not provided for future transfusions. 相似文献
106.
Arnault Tauzide-Espariat Philipp Sievers Frdrique Larousserie Joseph Benzakoun Delphine Guillemot Gaëlle Pierron Mathilde Duchesne Emmanuelle Uro-Coste Alexandre Roux Alexandre Vasiljevic Tanguy Fenouil David Meyronet Karima Mokhtari Marc Polivka Audrey Rousseau Frdrique Bost-Bezeaud Samir Akoury Johan Pallud Chiara Benevello Lauren Hasty Albane Gareton Emmanule Lechapt Fabrice Chrtien Thomas Blauwblomme Kvin Beccaria Stphanie Puget Felix Sahm Pascale Varlet 《Brain pathology (Zurich, Switzerland)》2022,32(1):e13010
107.
STUDY OBJECTIVE--The aim was to evaluate the protective effect of verapamil during myocardial ischaemia and reperfusion. DESIGN--In vivo phosphorus-31 (31P) magnetic resonance spectroscopy was performed on rats pretreated with verapamil (mg.kg-1 intraperitoneal) and controls during a 45 min left coronary artery occlusion and 60 min reperfusion. In separate groups of animals, haemodynamic measurements were taken at baseline, during ischaemia, and during reperfusion. Infarct size was determined by staining with triphenyltetrazolium chloride. EXPERIMENTAL MATERIAL--Female Sprague-Dawley rats were used (control group n = 25, experimental group n = 24). MEASUREMENTS AND MAIN RESULTS--Infarct size was significantly reduced in the verapamil group compared to controls: 9.9(SEM 2.3)%, n = 19 v 28.5(2.7)%, n = 19, p less than 0.001 (infarct % of left ventricular mass). Myocardial phosphocreatine and ATP levels were reduced to similar levels in both verapamil and control animals after 45 min ischaemia: 56.8(3.4)%, n = 10, v 61.4(1.8)%, n = 11 NS; 67.7(2.7)%, n = 10 v 69.7(2.9)%, n = 11, NS (% of baseline value). After 60 min reflow, there was significant recovery of phosphocreatine [91.1(4.2)% of baseline, p less than 0.05] and ATP [86.8(2.7)% of baseline, p less than 0.05] in the verapamil group, but no recovery of high energy phosphates in controls [66.3(2.8), NS; 69.6(2.7), NS]. The left ventricular systolic pressure, heart rate, rate-pressure product, and maximum rate of left ventricular pressure development were similar prior to ischaemia, and during ischaemia in both groups. There was an inverse correlation between infarct size and the degree of phosphocreatine recovery after 60 min of reperfusion (PCr recovery (%) = -0.99 x infarct size (%) + 101; r = 0.91; p less than 0.01; n = 14). Furthermore, in a separate group of animals (n = 9), there was a significant correlation between the size of the ischaemic area at risk and the degree of phosphocreatine decline after 15 min of coronary occlusion (PCr reduction (%) = 0.91 x risk area (%) + 5.6; r = 0.97; p less than 0.01). CONCLUSIONS--Pretreatment with verapamil extends the ischaemic time after which reperfusion results in myocardial salvage in this model of ischaemia and reperfusion. This protective effect is independent of the haemodynamic determinants of myocardial oxygen demand and the degree of ATP and phosphocreatine depletion during the ischaemic period. In this model of reversible ischaemia, 31P magnetic resonance spectroscopy is useful for quantitating both the size of the ischaemic region during coronary artery occlusion and infarct size after reperfusion. 相似文献
108.
PD Dr. J. Hörer MD PhD U. Stierle T. Hanke J.J. Takkenberg A.J.J.C. Bogers W. Hemmer J.G. Rein M. Hübler R. Hetzer H.H. Sievers R. Lange 《Zeitschrift für Herz-, Thorax- und Gef??chirurgie》2010,24(2):115-121
Objectives
To determine the durability of autografts and homografts after Ross operations in children.Patients and methods
The data of 152 children <16 years were analyzed using the Cox proportional hazards model and hierarchical multilevel modeling.Results
Autograft regurgitation increased with sinotubular junction diameter (p=0.028). The homograft gradient increased within the first 2 years (4.2 mmHg/year, p<0.001). Freedom from autograft and homograft reintervention at 10 years was 95.5±2.7% and 79.6±6.1%, respectively. Longer follow-up time was a risk factor for autograft reintervention (p=0.036). Use of an aortic homograft was a risk factor for conduit reintervention (p=0.013).Conclusions
Reinterventions are necessary for autograft regurgitation and homograft stenosis. Increasing sinotubular junction diameters explain autograft regurgitation. Using pulmonary homografts delays the development of a homograft gradient. 相似文献109.
Wang L Lawrence MS Wan Y Stojanov P Sougnez C Stevenson K Werner L Sivachenko A DeLuca DS Zhang L Zhang W Vartanov AR Fernandes SM Goldstein NR Folco EG Cibulskis K Tesar B Sievers QL Shefler E Gabriel S Hacohen N Reed R Meyerson M Golub TR Lander ES Neuberg D Brown JR Getz G Wu CJ 《The New England journal of medicine》2011,365(26):2497-2506
110.
Mueller SC Majcher-Peszynska J Mundkowski RG Uehleke B Klammt S Sievers H Lehnfeld R Frank B Thurow K Kundt G Drewelow B 《European journal of clinical pharmacology》2009,65(1):81-87
Objective Induction of CYP3A by St. John’s wort (SJW) products with high hyperforin content is well described. Since CYP3A induction
is mediated by hyperforin in a concentration-dependent manner, and SJW preparations differ significantly in hyperforin content,
the aim of the study was to evaluate the effect of an SJW powder with low hyperforin content on CYP3A function.
Methods Twenty healthy male volunteers received an SJW powder with low hyperforin content for 2 weeks. Midazolam plasma concentration
time profiles were characterized after a single oral dose of 7.5 mg midazolam on the day before and on the 14th day of SJW
medication.
Results Midazolam AUC0–∞ slightly decreased from 124.0 ± 62.5 ng/ml·h at baseline to 105.6 ± 53.2 ng/ml·h after SJW (P < 0.05), representing a mean 11.3% decrease (95% CI: −22.8 to 0.21). No significant change in midazolam Cmax, t1/2 and tmax was observed. For all pharmacokinetic parameters, the 90% CI for the geometric mean ratio of treatment over baseline were
within the no-effect boundaries of 0.70–1.43.
Conclusion Administration of an SJW product with low hyperforin content resulted in a mild induction of CYP3A not considered clinically
relevant. 相似文献