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991.
李静 《国际中华应用心理学杂志》2005,2(3):235-237
本文根据心理学的基本观点,讨论了孔子的心理学思想,着重讨论了孔子学习心理学思想,普通心理学的思想,社会心理学的思想,建议我们应继承和发扬我国优秀的文化遗产和传统,挖掘其积极价值,促进我国心理学的发展。 相似文献
992.
Lei C Dongqing Z Yeqing S Oaks MK Lishan C Jianzhong J Jie Q Fang D Ningli L Xinghai H Daming R 《European journal of human genetics : EJHG》2005,13(7):823-828
Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is important for downregulation of T-cell activation, and CTLA-4 gene polymorphisms have been implicated as risk factors for rheumatoid arthritis (RA). Previous studies of the association between the +49 polymorphism of the CTLA-4 gene in RA have provided conflicting results. In order to determine association of the CTLA-4 gene with RA in Chinese Han population, we used denaturing gradient gel electrophoresis (DGGE) to genotype polymorphisms of four SNPs (MH30, +49, CT60 and JO31) of the CTLA-4 gene in 326 RA patients and 250 healthy controls. Furthermore, meta-analysis of all available studies relating +49 polymorphism to the risk of RA was performed to confirm the disease association. Among the SNPs examined, the genotype frequencies of CTLA-4 +49 and CT60 in RA patients differed significantly from controls (P=0.028 and 0.007). In addition, the distribution of four haplotypes constructed by these two SNPs was significantly different between patients and controls (chi(2)=10.58, d.f. =3, P=0.014). The meta-analysis also revealed that in both European and Asian populations, the CLTA-4 +49 G allele was associated with the risk of RA. These results suggested that the CTLA-4 gene might be involved in the susceptibility to RA in the Chinese Han population and both +49 and CT60 of CTLA-4 gene might be the causal variants in RA disease. 相似文献
993.
目的观察青蒿琥酯(artesunate,Art)对人食管癌Eca-109细胞系的抑瘤作用,并进一步探讨ATt诱导肿瘤细胞周期阻滞与CDC25A、TGF-β表达的关系。方法体外培养人食管癌Eca-109细胞系及正常人外周血单个核细胞(hPBMC),利用MTT法测定细胞增殖;采用流式细胞术(FCM)测定细胞周期;应用RT.PCR方法检测CDC25AmRNA表达,应用Western blot方法检测蛋白表达。结果Art能显著抑制Eca-109细胞的增殖,ICS0为(68.80±0.76)μmol/L,而对hPBMC的增殖则没有明显抑制作用。低浓度Art可将细胞阻滞于G0/G1期,S期细胞显著减少,当浓度达到100μmol/L时,细胞阻滞于G2/M期。Art可显著抑制Eca-109细胞CDC25AmRNA及蛋白表达,同时显著上调TGF-β的蛋白表达水平。结论Art可抑制肿瘤细胞生长,上调TGF-β表达,抑制CDC25A表达。 相似文献
994.
995.
本文主要介绍了奔腾计算机和步进电机的接口电路,提出了步进电机匀加速的控制算法,探讨了在 Windows 环境下以 Visual C++实现步进电机匀加速的实现途径和多任务环境下匀加速程序的设计方法。 相似文献
996.
目的:研究阿尔茨海默病(AD)血清中抗Aβ抗体与淀粉样蛋白结合的特性。方法:以AD患者和健康老人的血清作一抗,①用组织淀粉样斑块免疫反应(TAPIR)观察与Tg2576鼠脑内老年斑结合能力;②Western blot检测与Aβ42-GST融合蛋白的结合能力;③将Aβ42与PC12细胞培养,加入健康老人和AD患者的血清后,MTT法观察PC12细胞存活率。结果:AD患者的血清中抗Aβ抗体与成熟老年斑和Aβ42-GST融合蛋白的结合能力较弱;加入AD血清后,PC12细胞的A值较健康老人血清相比下降明显(P<0.01)。结论:AD血清中抗Aβ抗体对淀粉样蛋白可能存在着免疫耐受。 相似文献
997.
37℃凝血温度下正常人和哮喘患者血清ECP水平的测定 总被引:5,自引:0,他引:5
室温(20℃)是广泛接受的血清ECP测定凝血温度,但存在一些问题。设想体温37℃可能是血清ECP测定的有效凝血温度。为此,对68例急性发作的哮喘患者在37℃凝血温度下血清ECP水平进行分析,比较凝血温度分别为20℃和37℃时同一患者血样本的ECP水平变化,结果发现37℃下哮喘患者血清ECP水平(50.9±3.18μg/L)显著高于正常对照(17.27±1.36μg/L,P<0.01)。在68例病人中,37℃凝血下有28人血清ECP水平高于正常值,而20℃凝血下只有17人血清ECP水平高于正常值,两者间存在显著差异(P<0.05)。37℃凝血温度下血清ECP水平与哮喘症状计分显著相关(r=0.77,P<0.01)。此外,尚测定了37℃凝血温度下101位10~50岁的健康人血清ECP水平,结果显示37℃下正常人血清ECP水平的几何均数是17.81μg/L,血清ECP水平的正常值为70μg/L以下(95%的可信限)。本研究表明,在血清ECP的测定中设凝血温度为37℃不仅是有效、简化的方法,而且还可减少哮喘患者血清ECP水平的假阴性。 相似文献
998.
目的 探讨超声彩色脉搏波(UFPWV)技术在定量评价2型糖尿病患者颈动脉血管管壁弹性变化中的应用价值。方法 回顾性研究。纳入2018年7月-2019年3月蚌埠医学院第一附属医院收治的97例2型糖尿病患者为观察组,其中男47例、女50例,年龄20~74(46.6±9.3)岁;根据颈动脉内中膜厚度(IMT)将观察组分为颈动脉粥样斑块组(A组)、颈动脉内中膜增厚组(B组)和颈动脉内中膜正常组(C组),依据下肢动脉有无斑块将C组分为下肢动脉斑块组(C1组)、下肢动脉无斑块组(C2组)。选取2017年12月-2018年12月在蚌埠医学院第一附属医院体检中心血糖及颈动脉IMT正常的健康体检者64人为对照组,其中男25人、女39人,年龄20~74(44.3±12.0)岁。运用UFPWV采集脉搏波速度 (PWV),计算颈动脉收缩早期PWV(PWV-BS)及收缩晚期PWV(PWV-ES),分析各项参数组间的差异。结果 观察组中,A组颈动脉PWV-BS、PWV-ES分别为(9.51±1.25)m/s、(10.79±1.64)m/s,B组分别为(8.47±0.91)m/s、(9.81±1.05)m/s,C组分别为(7.97±0.77)m/s、(9.07±0.74)m/s,对照组颈动脉PWV-BS、PWV-ES分别为(6.10±1.00)m/s、(7.40±1.20)m/s,A组、B组、C组及对照组间颈动脉PWV-BS、PWV-ES测量值依次降低,差异均有统计学意义(P值均<0.05)。C组中,C1组颈动脉PWV-BS、PWV-ES分别为(7.83±0.85)m/s、(8.82±0.59)m/s,C2组分别为(8.14±0.64)m/s、(9.34±0.79)m/s, C1组PWV-ES显著高于C2组,差异有统计学意义(t=3.402,P<0.01),而两组间PWV-BS的差异无统计学意义(P>0.05)。结论 UFPWV技术可定量评价2型糖尿病患者颈动脉弹性变化,并可通过PWV-ES的改变评估颈动脉形态学正常的患者动脉粥样硬化的进展程度,对临床诊疗具有一定意义。 相似文献
999.
During gestation, placental blood flow, endothelial nitric oxide (NO) production, and endothelial cell nitric oxide synthase (eNOS) expression are elevated dramatically. Shear stress can induce flow-mediated vasodilation, endothelial NO production, and eNOS expression. Both the activity and expression of eNOS are closely regulated because it is the rate-limiting enzyme essential for NO synthesis. The authors adapted CELLMAX artificial capillary modules to study the effects of pulsatile flow/shear stress on ovine fetoplacental artery endothelial (OFPAE) cell NO production, eNOS expression, and eNOS phosphorylation. This model allows for the adaptation of endothelial cells to low physiological flow environments and thus prolonged shear stresses. The cells were grown to confluence at 3 dynes/cm2, then were exposed to 10, 15, or 25 dynes/cm2 for up to 24 h and NO production, eNOS mRNA, and eNOS protein expression were elevated by shear stress in a graded fashion (p < .05). Production of NO by OFPAE cells exposed to pulsatile shear stress was de novo; i.e., inhibited by L-NMMA (N(G)-monomethyl-L-arginine) and reversed by excess NOS substrate L-arginine. Rises in NO production at 25 dynes/cm2 (8-fold) exceeded (p < .05) that seen for eNOS protein (3.6-fold) or eNOS mRNA (1.5-fold). Acute rises in NO production with shear stress occurred by eNOS activation, whereas prolonged NO rises were via elevations in both eNOS expression and enzyme activation. The authors therefore used Western analysis to investigate the signaling mechanisms underlying pulsatile shear stress-induced increases in eNOS phosphorylation and protein expression by "flow-adapted" OFPAE cells. Increasing shear stress from 3 to 15 dynes/cm2 very rapidly increased eNOS Ser1177, ERK1/2 (extracellular signal-regulated kinase 1 and 2) and Akt, but not p38 MAPK (p38 mitogen-activated protein kinase) phosphorylation by Western analysis. Phosphorylation of eNOS Ser1177 under shear stress was elevated by 20 min, a response that was blocked by PI-3K (phosphatidylinositol 3-kinase) inhibitors wortmannin and LY294002, but not the MEK (MAPK kinase) inhibitor UO126. Basic fibroblast growth factor (bFGF) enhanced eNOS protein levels in static culture via a MEK-mediated mechanism, but it could not further augment the elevated eNOS protein levels induced by 15 dynes/cm2 shear stress. Blocking of either signaling pathways or p38 MAPK did not change the shear stress-induced increase in eNOS protein levels. Therefore, shear stress induced rapid eNOS phosphorylation on Ser1177 in OFPAE cells through a PI-3K-dependent pathway. The bFGF-induced rise in eNOS protein levels in static culture was much less than those observed under flow and was blocked by inhibiting MEK. Prolonged shear stress-stimulated increases in eNOS protein levels were not affected by inhibition of MEK- or PI-3K-mediated pathways. In conclusion, pulsatile shear stress greatly induces NO production by OFPAE cells through the mechanisms of both PI-3K-mediated eNOS activation and elevations in eNOS protein levels; bFGF does not further stimulate eNOS expression under flow condition. 相似文献
1000.
Wang FS Hong WG Cao Y Liu MX Jin L Hu LP Wang Z Feng TJ Hou J Zhang B Shi M Xu DP Lei ZY Wang B Liu ZD Ye JJ Peng L Qiu Y Winkler C 《Journal of acquired immune deficiency syndromes (1999)》2003,32(2):124-130
The aim of this study is to determine in indigenous Chinese ethnic groups the frequencies of the chemokine (SDF1 3'A) and chemokine receptors (CCR5 delta32, CCR5 m303, and CCR2b 64I) HIV-1/AIDS restriction alleles. The study includes two cohorts; the first comprised 3165 indigenous healthy subjects representing eight ethnic groups: Han (n = 1406), Uygur (n = 316), Mongolia (n = 134), Hui (n = 386), Tibetan (n = 330), Zhuang (n = 378), Dai (n = 101), and Jingbo (n =114). The second cohort consisted of 330 HIV-1-infected (86 subjects infected by sexual transmission and 198 subjects infected by HIV-1-contaminated blood or by sharing injection equipment; the remaining 46 subjects said nothing about HIV-1 transmission) and 474 HIV-1-uninfected Han Chinese belonging to one of two HIV-1 high-risk groups: intravenous drug users (n = 215) and individuals with sexually transmitted diseases (n = 259). Genotypes for the four genes were obtained using PCR (CCR5 delta32) or PCR-restriction fragment length polymorphism. Randomly selected amplified PCR products were further confirmed by direct DNA sequencing. The variant allele frequencies were determined to be 0% to 3.48% for CCR5 delta32, 0% for CCR5 m303, 16.23% to 28.79% for CCR2b 64I, and 17.70% to 27.76% for SDF1 3'A in Chinese healthy individuals from eight ethnic groups. These findings show that allele frequencies differ among the eight Chinese ethnic groups for CCR5 delta32, CCR2b 64I, and SDF1 3'A and that the CCR5 m303 and CCR5 delta32 mutant alleles were absent or infrequent in Chinese, which may be helpful for studies of specific anti-HIV-1 vaccine trials and coreceptor inhibitor drug targets in Chinese populations. Furthermore, we observed no significant differences in allele or genotypic frequencies between HIV-1-infected and HIV-1-uninfected groups from the Han ethnic group. Our finding is the first reporting that there is likely no effect of the examined polymorphisms in our study on HIV-1 transmission in the Chinese Han population, However, the genetic effects of these and other AIDS-modifying polymorphisms on the pathogenesis and clinical outcome of HIV-1/AIDS diseases is under investigation in Chinese populations. 相似文献