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。     

白介素-6、血管内皮生长因子、D-二聚体对CSDH的影响

目的探讨血肿局部炎症、假膜新血管生成、局部纤溶状况及其在CSDH发生、发展中的作用。进而探讨CSDH的发病机制，并为CSDH的治疗及预防复发提供理论依据。方法以78例CSDH患者作为病例组，20例健康人作为正常对照组。采用ELISA法测定患者血清及血肿液中VEGF及IL-6的含量。比较患者末梢静脉血及血肿液中四种因子的含量变化并与正常对照组比较。结果病例组血肿液FDP、d-dimer检测均为阳性，血液为阴性；正常对照组血液FDP、d-dimer检测均为阴性；病例组血清VEGF含量与正常对照组比较差异无统计学意义。血肿液中VEGF浓度高于血清中。病例组血清IL-6浓度与正常对照组差异无统计学意义，血肿液中IL-6浓度高于血清中。CSDH患者血肿液VEGF、IL-6水平没有相关性。结论CSDH患者血肿液局部纤溶亢进，局部VEGF分泌旺盛，新血管生成活跃，局部炎症活跃，可导致CSDH不断扩大而参与CSDH发病机制。抗炎治疗、抑制VEGF的生理作用、有选择的对病人施行促凝治疗，可成为部分CSDH病人保守治疗及预防复发的有效手段。     

云南东川非铀矿山矿工血清IL-2、IL-6、TNF-α检测及其基因多态性的初步研究

目的 通过对云南非铀矿山矿工血清IL-2、IL-6和TNF-α浓度及基因多态性位点的检测,对氡致非铀矿山矿工机体生物效应进行初步探讨。方法 血清中IL-2、IL-6和TNF-α的浓度测定采用双抗夹心ABC-ELISA法。TNF-α(-308,G→A)检测基因型采用基因体外扩增限制性片段长度多态性分析方法,IL-2(-330, T→G)基因型检测采用PCR体外扩增后测序的方法。结果 矿工组与对照组比较,年龄(F＝1.07,P>0.05),工龄(F＝0.40,P>0.05),血清IL-2浓度(F＝0.71,P>0.05),血清IL-6浓度(F＝1.09,P>0.05),血清TNF-α浓度(F＝0.95,P>0.05),IL-2基因型频度(χ²=0.02,P>0.05)和TNF-α基因型频度(χ²=2.21,P>0.05),差异均无统计学意义。结论 云南东川非铀矿山矿工血清IL-2、IL-6和TNF-α平均浓度有下降的趋势, TNF-α(-308,A A)基因型频度有增高的趋势。     

Histopathological characterisation of effects of the mouse Pax6 missense mutation on eye development

Mutations in PAX6/Pax6 lead to a variety of ocular anomalies in humans and mice. The aim of the study was to characterise the ocular abnormalities caused by the missense Pax6^Leca4 mutation and compare them to published observations on Pax6 alleles that are functionally equivalent to Pax6⁻ null alleles (such as Pax6^Sey and Pax6^Sey-Neu) and human inherited eye diseases. Ocular features of homozygous Pax6^Leca4/Leca4 and heterozygous Pax6^Leca4/+ embryos at E12.5-E18.5, heterozygous Pax6^Leca4/+ young mice at P18 and heterozygous Pax6^Leca4/+ adults at 12 weeks were analysed histologically with their wild-type Pax6^+/+ littermates. Homozygous Pax6^Leca4/Leca4 fetuses died perinatally with no eyes although an optic cup rudiment with pigmented cells developed. Pax6^Leca4/+ mice were microphthalmic and a range of other severe ocular phenotypes affected both the anterior and the posterior segments. In contrast to Pax6^+/−, the Pax6^Leca4/+ eyes had no goblet cells in the corneal epithelium, the iris was not hypoplastic and there was no lens-corneal epithelial plug. However, microphthalmia was more severe, corneal vascularisation occurred earlier (during fetal stages), pigmented cells were present in the vitreous and corneal stroma and the ciliary body was malformed or abnormal. These results show that, although Pax6^Leca4/+ lacked some eye abnormalities commonly seen in Pax6^Sey/+ and Pax6^Sey-Neu/+ eyes, in most respects their eyes were more severely affected. These differences probably reflect both differences between the Pax6^Leca4 and the Pax6^Sey-Neu mutations and differences in modifier gene expression in different genetic backgrounds. The presence of pigmented cells in the cornea is a novel observation. Some Pax6^Leca4/+ ocular abnormalities were similar to those present in human Peters' anomaly and persistent hyperplastic primary vitreous (PHPV) so Pax6^Leca4/+ mice provide a useful model for some inherited eye diseases.     

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。     

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.     

BcL-2、Bax、CD44V6在乳腺癌表达及预后的研究

目的探讨影响乳腺癌患者预后的因素,协助临床制定手术方式及术后治疗方案。方法选择80例各型乳腺癌患者的标本,应用免疫组化SP方法,检测乳腺癌组织中癌基因BcL-2、Bax及黏附因子CD44V6的表达情况。结果乳腺癌中BcL-2、Bax及CD44V6的表达情况与肿瘤组织学分级、瘤体直径。有无转移及患者术后存活时间均有显著性相关(P<0.05或0.01)。结论BcL-2高表达、Bax低表达、CD44V6低表达的患者组织学分级好,肿瘤体积小,淋巴结转移少,术后存活时间长,这部分患者可做肿物扩大切除而保留乳房或即使已做乳房切除,术后也可减少放疗及化疗剂量。