卡维地洛对不稳定型心绞痛患者血浆炎症因子的影响

目的观察卡维地洛对不稳定型心绞痛（UAP）患者高敏C反应蛋白（hs-CRP）、白介素-6（IL-6）及细胞间可溶性黏附分子1（sICAM-1）水平的影响。方法UAP患者62例采用完全随机化方法分成对照组（n=30）和治疗组（n=32）,在常规抗血小板、扩血管治疗基础上,对照组予美托洛尔（12.5mg,2次/d×3d）口服,治疗组服卡维地洛（6.25mg,2次/d×3d）,在治疗前后分别测定hs-CRP、IL-6、sICAM-1值。结果对照组和治疗组在治疗前hs-CRP、IL-6、sICAM-1均无显著性差异;用药后两组3指标均较用药前显著降低（P<0.05）;治疗组在用药后IL-6、sI-CAM-1显著低于对照组（P<0.05）。同时,用药后两组患者的心率、血压、心肌耗氧量均较用药前显著降低（P<0.05）,治疗组的心肌耗氧量显著低于对照组（P<0.05）。结论卡维地洛可显著降低UAP患者的炎症因子IL-6、sICMA-1水平。     

用逆转录—聚合酶链反应法对类胰岛素生长因子cDNA的扩增

逆转录-聚合酶链反应(RT-PCR)法是将PCR方法与逆转录法结合应用,可快速高效地扩增某一基因的全cDNA。类胰岛素生长因子-I(IGF-I)在人染色体中只有一个基因,全长超过45kb,并有内含子,其cDNA却只有几百个bp,为了表达得到IGF-I,本文利用RT-PCR方法,从胎肝提出的混合mRNA中,筛选并扩增了IGF-I的cDNA。经过分子克隆与测序,证明不需制备胎肝cDNA库,即可快速获得IGF-I的cDNA。     

18F-FDG符合线路显像与同机CT融合在肿瘤诊断的应用

【目的】评价~(18)F-FDG符合线路显像及同机CT图像融合在肿瘤诊断中的价值。【方法】经病理确诊或临床确诊为恶性肿瘤的病人79例,良性肿块病人19例进行~(18)F-FDG符合线路显像及同机CT图像融合检查,经COSEM重建,结果与解剖显像比较。【结果】①~(18)F-FDG符合显像诊断恶性肿瘤的敏感性、特异性、准确率、阳性预测值和阴性预测值分别为92.4％、89.5％、91.8％、97.3％和73.9％,解剖显像分别为79.8％、63.2％、76.5％、90.0％和42.9％。②同部位显像比较中,~(18)F-FDG显像病灶探测数为302个,而解剖显像为286个。③同机CT融合明显提高对肺部近纵隔、膈缘及腹部等部位的定位诊断。【结论】~(18)F-FDG符合线路显像较解剖显像更好地对恶性肿瘤作出鉴别诊断,并且能探测到更多的恶性病灶,同机CT融合较大地提高定位诊断的准确性,具有重要的临床价值,值得临床广泛应用。     

18氟-氟化脱氧葡萄糖在下咽部肿瘤诊断中的作用

目的：研究^18氟—氟化脱氧葡萄糖(^18F-FDG)在下咽部肿瘤诊断中的作用。方法：20例下咽部肿瘤患者均接受^18F-FDG检查及CT、全组内镜(食管、咽喉、气管镜)检查。结果：20例下咽部肿瘤患者^18F-FDG检查结果显示：2例阴性；18例肿瘤原发部位有同位素浓集，其中5例伴异位同位素浓集。对此5例患者进一步临床、病理检查证实：1例食管部占位，2例肺部病变，2例为良性改变。^18F-FDG检查结果显示的病变范围与CT、内镜检查相符。结论：^18F-FDG检查可以提高下咽部肿瘤、尤其是隐匿的并发肿瘤诊断的准确性，明确病变范围，为临床治疗提供依据；同时又是一个简单、易行的下咽部肿瘤的随访检查手段。     

丹参与雷公藤多甙联合治疗急性坏死性胰腺炎的实验研究

目的　探讨丹参与雷公藤多甙联合应用对急性坏死性胰腺炎 (acutenecrotizingpancreatitis,ANP)的治疗作用。 方法　采用单次过量 2 0 %L 精氨酸 (10 0 0mg/ 10 0g大鼠体重 )皮下注射建立ANP动物模型。测定血清淀粉酶、TNF α、IL 1β水平 ,并观察胰腺组织的病理变化。根据血清淀粉酶、TNF α、IL 1β水平及胰腺组织的变化来评价胰腺炎的严重程度。 结果　大鼠皮下注射过量L 精氨酸后 ,血清淀粉酶、TNF α、IL 1β水平升高 ,胰腺变性坏死。丹参与雷公藤多甙联合治疗ANP ,可显著降低血清淀粉酶、抑制炎症细胞因子的过度生成 ,组织受损程度明显减轻。结论　丹参与雷公藤多甙联合应用对ANP动物模型具有很好治疗效果 ,可能具有临床应用价值     

IL-4与IL-10联合诱导异种骨移植免疫耐受的体外研究

目的　探讨 IL - 4和 IL - 10在诱导异种骨移植免疫耐受中的作用。方法　反应细胞为 BAL B/c小鼠脾淋巴细胞 ,刺激细胞为新西兰白兔血淋巴细胞 ,刺激抗原为兔骨上清液。采用经典的混合淋巴细胞培养法及骨上清液与淋巴细胞混合培养法作为异种骨移植的体外实验模型。在各培养液中分别加入 IL - 4、IL - 10及两者联合应用 ,通过测定其 3H- Td R掺入率 ,观察不同细胞因子对刺激淋巴细胞增殖的影响。结果　无论在细胞刺激组还是骨上清液刺激组 ,IL- 4对淋巴细胞增殖均有显著抑制作用 (P<0 .0 0 1和 P<0 .0 5 ) ,IL- 10未表现出抑制作用 (P>0 .0 5 )。在两组 IL- 4和 IL - 10联合应用均产生比 IL - 4单独应用更为明显的细胞增殖抑制作用 (P<0 .0 0 1和 P<0 .0 5 )。结论　 IL - 4对由细胞或骨上清液刺激产生的淋巴细胞增殖均有很好的抑制作用 ,IL- 10没有表现出抑制作用 ;IL- 4与 IL- 10联合应用有协同抑制作用。     

17β-雌二醇对子宫内膜异位症患者在位子宫内膜间质细胞β-catenin mRNA和蛋白表达的影响

目的研究17β-雌二醇(17β-E2)对子宫内膜异位症(内异症)患者在位子宫内膜间质细胞β-catenin mRNA和蛋白表达的影响,探讨Wnt/β-catenin信号通路在介导雌激素促进内异症发生发展的作用。方法体外分离培养内异症患者在位子宫内膜间质细胞。用不同浓度17β-E2处理子宫内膜间质细胞48 h;此后选用10-10mol/L 17β-E2处理子宫内膜间质细胞12、24和48 h,逆转录聚合酶链反应(RT-PCR)和免疫印迹法(Western blotting)检测17β-E2处理前后子宫内膜间质细胞β-catenin mRNA和蛋白的表达水平。同法分析雌激素受体拮抗剂ICI182,780(10-6mol/L)对17β-E2促进β-catenin mRNA和蛋白表达的影响。免疫组织化学染色观察17β-E2作用后β-catenin在子宫内膜间质细胞中的定位。结果17β-E2能明显促进内异症患者在位子宫内膜间质细胞β-catenin mRNA和蛋白的表达,并呈剂量和时间依赖性,于10-10mol/L作用48 h最明显。雌激素受体拮抗剂ICI182,780能明显抑制17β-E2对子宫内膜间质细胞β-catenin mRNA和蛋白的表达。免疫组织化学染色发现17β-E2能促进β-catenin在子宫内膜间质细胞核内的表达。结论雌激素可能通过激活Wnt/β-catenin信号通路促进内异症在位子宫内膜的异位种植。     

Association between cord blood IgE and genetic polymorphisms of interleukin-4, the β-subunit of the high-affinity receptor for IgE, lymphotoxin-α, and tumor Necrosis factor-α

High cord blood immunoglobulin E (cbIgE) is known to be associated with increased risks of atopic diseases in childhood. The relationship between genetic polymorphisms and high cbIgE has not been well documented. A cross-sectional study was conducted to assess the association between cbIgE and genetic polymorphisms of interleukin (IL)-4 -590C/T, the beta-subunit of the high-affinity receptor for IgE (FcepsilonRI-beta) E237G, lymphotoxin (LT)-alphaNcoI alleles, and tumor necrosis factor (TNF)-alpha -308G/A. A total of 320 mother-neonate pairs were recruited from four maternity hospitals from different locations of Taiwan. Cord blood was obtained and assayed for cbIgE. Polymerase chain reaction followed by restriction fragment length polymorphism was used to assess the genotypes. Three hundred pairs of mothers and neonates were included in the final analysis. Infants with IL-4 -590 C allele were found to have higher risk of elevated cbIgE (> or =0.35 IU/ml, 24.3%) (p = 0.004). After adjusting for gender, birth order, maternal age, and history of allergic disease in maternal and paternal families, odds ratios for CC and CT genotypes were 4.41 and 3.16 (95% confidence interval 0.78-22.67, and 1.66-6.13), respectively, using TT genotype as reference. The genotypes of FcepsilonRI-beta, LT-alpha, and TNF-alpha were not associated with cbIgE before or after the adjustment. Our finding suggested a significant association of cbIgE with genetic polymorphism of IL-4 -590C/T, but not with the genotypes of FcepsilonRI-beta, LT-alpha, and TNF-alpha.     

Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.

BACKGROUND AND METHODS: The endogenous inhibitor of nitric oxide synthase (NOs) asymmetrical dimethyl-arginine (ADMA) has been implicated as a possible modulator of inducible NOs during acute inflammation. We examined the evolution in the plasma concentration of ADMA measured at the clinical outset of acute inflammation and after its resolution in a series of 17 patients with acute bacterial infections. RESULTS: During the acute phase of inflammation/infection, patients displayed very high levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin and nitrotyrosine. Simultaneous plasma ADMA concentration was similar to that in healthy subjects while symmetric dimethyl-arginine (SDMA) levels were substantially increased and directly related with creatinine. When infection resolved, ADMA rose from 0.62 +/- 0.23 to 0.80 +/- 0.18 micromol/l (+29%, P = 0.01) while SDMA remained unmodified. ADMA changes were independent on concomitant risk factor changes and inversely related with baseline systolic and diastolic pressure. Changes in the ADMA/SDMA ratio were compatible with the hypothesis that inflammatory cytokines activate ADMA degradation. CONCLUSIONS: Resolution of acute inflammation is characterized by an increase in the plasma concentration of ADMA. The results imply that ADMA suppression may actually serve to stimulate NO synthesis or that in this situation plasma ADMA levels may not reflect the inhibitory potential of this methylarginine at the cellular level.