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61.
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。 相似文献
62.
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。 相似文献
63.
Histopathological characterisation of effects of the mouse Pax6 missense mutation on eye development
Thaya Ramaesh Steven E. Williams Catriona Paul Kanna Ramaesh John D. West 《Experimental eye research》2009,89(2):263-273
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 Pax6Leca4 mutation and compare them to published observations on Pax6 alleles that are functionally equivalent to Pax6− null alleles (such as Pax6Sey and Pax6Sey-Neu) and human inherited eye diseases. Ocular features of homozygous Pax6Leca4/Leca4 and heterozygous Pax6Leca4/+ embryos at E12.5-E18.5, heterozygous Pax6Leca4/+ young mice at P18 and heterozygous Pax6Leca4/+ adults at 12 weeks were analysed histologically with their wild-type Pax6+/+ littermates. Homozygous Pax6Leca4/Leca4 fetuses died perinatally with no eyes although an optic cup rudiment with pigmented cells developed. Pax6Leca4/+ mice were microphthalmic and a range of other severe ocular phenotypes affected both the anterior and the posterior segments. In contrast to Pax6+/−, the Pax6Leca4/+ 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 Pax6Leca4/+ lacked some eye abnormalities commonly seen in Pax6Sey/+ and Pax6Sey-Neu/+ eyes, in most respects their eyes were more severely affected. These differences probably reflect both differences between the Pax6Leca4 and the Pax6Sey-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 Pax6Leca4/+ ocular abnormalities were similar to those present in human Peters' anomaly and persistent hyperplastic primary vitreous (PHPV) so Pax6Leca4/+ mice provide a useful model for some inherited eye diseases. 相似文献
64.
采用~(125)I 标记小鼠抗人IL—2受体(P55)的抗Tac(CD_(25))单克隆抗体,成功地建立了人IL—2受体的免疫放射分析法,动态观察了人外周血淋巴细胞经PHA 刺激24、48和72h 后IL—2受体表达的时间曲线,通过Scatchard 作图分析表明~(125)I—抗Tac 单克隆抗体与PHA 活化的上述三个时间点的T 淋巴细胞的最大结合容量(B_(max))分别为43000位点/细胞、54000位点/细胞和61000位点/细胞。本研究为临床IL—2受体检测提供一种简便的免疫放射测定法。 相似文献
65.
Carmine Zoccali Renke Maas Sebastiano Cutrupi Patrizia Pizzini Piero Finocchiaro Francesco Cambareri Vincenzo Panuccio Carmela Martorano Friedrich Schulze Giuseppe Enia Giovanni Tripepi Rainer Boger 《Nephrology, dialysis, transplantation》2007,22(3):801-806
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. 相似文献
66.
明玉华 《现代中西医结合杂志》2007,16(27):3940-3942
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。 相似文献
67.
应用鸡卵清蛋白致敏和刺激小鼠复制过敏性气道炎症反应模型研究血小板激活因子选择性拮抗剂YM-264对抗原引起气道嗜酸性粒细胞(EOS)浸润的影响。结果发现,正常小鼠支气管肺泡灌洗液(BALF)中未见到EOS;致敏小鼠给予抗原多次反复吸入刺激后,BALF中EOS急剧增多。在YM-264治疗各组中,YM-264的不同剂量分别导致EOS数下降27.0%、48.2%及67.9%。还发现YM-264抑制EOS对气道的浸润伴随着白细胞介素(IL)-5水平的明显下降。提示YM-264通过抑制IL-5的产生从而抑制了EOS在气道的聚集。 相似文献
68.
目的:研究重组人内皮细胞衍生的白细胞介素-8(IL8)对失血性休克的作用.方法:大鼠股动脉放血至MABP532kPa,维持90min,复制晚期失血性休克模型.输血后,静脉注射IL8250μg·kg-1.放免法测定血浆ET1和6KPGF1α含量.结果:给予IL8后,MABP显著提高,休克状态改善,2h存活率相应提高;休克晚期血浆ET1水平比正常明显升高(21±4vs82±18ng·L-1,P<001),血浆6KPGF1α含量明显降低(107±12vs157±11ng·L-1,P<001).IL8显著降低血浆ET1水平(10±4ng·L-1,P<001),提高血浆6KPGF1α含量(368±16ng·L-1,P<001).结论:IL8具有较好的抗休克作用. 相似文献
69.
Nicoletta Desideri Isabella Sestili Maria Luisa Stein Stefano Manarini Giuseppe Dell'Elba Chiara Cerletti 《Archiv der Pharmazie》1997,330(4):100-106
6-[(4-Quinolinyl)oxy]hexanoic acids and the corresponding esters were designed and synthesized as inhibitors of the production of arachidonic acid metabolites. The inhibitory activities were assayed in vitro by evaluation of serum leukotriene B4 and thromboxane B2 production. While all 6-[(4-quinolinyl)oxy]hexanoic acids and their esters proved to be inactive, the N-alkyl-4-quinolones, obtained as by-products in their synthesis, were found to be a new class of leukotriene biosynthesis inhibitors. 相似文献
70.
Characterization of the human cytochrome P450 enzymes involved in the metabolism of dihydrocodeine 总被引:1,自引:0,他引:1
L. C. Kirkwood R. L. Nation & A. A. Somogyi 《British journal of clinical pharmacology》1997,44(6):549-555
Aims Using human liver microsomes from donors of the CYP2D6 poor and extensive metabolizer genotypes, the role of individual cytochromes P-450 in the oxidative metabolism of dihydrocodeine was investigated.
Methods The kinetics of formation of N- and O -demethylated metabolites, nordihydrocodeine and dihydromorphine, were determined using microsomes from six extensive and one poor metabolizer and the effects of chemical inhibitors selective for individual P-450 enzymes of the 1A, 2A, 2C, 2D, 2E and 3A families and of LKM1 (anti-CYP2D6) antibodies were studied.
Results Nordihydrocodeine was the major metabolite in both poor and extensive metabolizers. Kinetic constants for N -demethylation derived from the single enzyme Michaelis-Menten model did not differ between the two groups. Troleandomycin and erythromycin selectively inhibited N -demethylation in both extensive and poor metabolizers. The CYP3A inducer, α-naphthoflavone, increased N -demethylation rates. The kinetics of formation of dihydromorphine in both groups were best described by a single enzyme Michaelis-Menten model although inhibition studies in extensive metabolizers suggested involvement of two enzymes with similar K m values. The kinetic constants for O -demethylation were significantly different in extensive and poor metabolizers. The extensive metabolizers had a mean intrinsic clearance to dihydromorphine more than ten times greater than the poor metabolizer. The CYP2D6 chemical inhibitors, quinidine and quinine, and LKM1 antibodies inhibited O -demethylation in extensive metabolizers; no effect was observed in microsomes from a poor metabolizer.
Conclusions CYP2D6 is the major enzyme mediating O -demethylation of dihydrocodeine to dihydromorphine. In contrast, nordihydrocodeine formation is predominantly catalysed by CYP3A. 相似文献
Methods The kinetics of formation of N- and O -demethylated metabolites, nordihydrocodeine and dihydromorphine, were determined using microsomes from six extensive and one poor metabolizer and the effects of chemical inhibitors selective for individual P-450 enzymes of the 1A, 2A, 2C, 2D, 2E and 3A families and of LKM1 (anti-CYP2D6) antibodies were studied.
Results Nordihydrocodeine was the major metabolite in both poor and extensive metabolizers. Kinetic constants for N -demethylation derived from the single enzyme Michaelis-Menten model did not differ between the two groups. Troleandomycin and erythromycin selectively inhibited N -demethylation in both extensive and poor metabolizers. The CYP3A inducer, α-naphthoflavone, increased N -demethylation rates. The kinetics of formation of dihydromorphine in both groups were best described by a single enzyme Michaelis-Menten model although inhibition studies in extensive metabolizers suggested involvement of two enzymes with similar K
Conclusions CYP2D6 is the major enzyme mediating O -demethylation of dihydrocodeine to dihydromorphine. In contrast, nordihydrocodeine formation is predominantly catalysed by CYP3A. 相似文献