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1.
目的检测原发性高血压患者血清可溶性细胞间粘附因子(sICAM-1)水平并探讨其与一氧化氮(NO)及过氧化脂质水平的相关性.方法采用ELISA法测定血清sICAM-1浓度,分别用硝酸还原酶法、硫代巴比妥酸(TBA)法及黄嘌呤氧化酶法检测NO水平、丙二醛(MDA)含量及超氧化物岐化酶(SOD)活性.结果与正常对照组相比,65例原发性高血压病患者血清sICAM-1浓度和MDA含量升高(P<0.01),而NO水平和SOD活性降低(P<0.01).相关分析发现血清sICAM-1浓度和MDA含量呈正相关(r=0.94,P<0.01),而与NO水平和SOD活性水平呈负相关(r=-0.58、r=-0.93,P值均<0.01).结论原发性高血压患者血清sICAM-1明显升高,且与机体氧化应激增强及NO降低有关.  相似文献   

2.
探讨可溶性细胞间黏附分子1( sICAM-1)和透明质酸(HA)能否反映Graves眼病(GO)的疾病活动性.用ELISA方法检测48例GO患者(眼病组)的sICAM-1、HA水平,同时检测30例单纯Graves甲状腺功能亢进患者作为对照组.与对照组相比,眼病组的血清sICAM-1、HA水平明显增高(P<0.05);且眼病组活动期的血清sICAM-1、HA水平明显高于稳定期(P<0.05).Pearson相关性分析显示眼病组的血清sICAM-1、HA水平均与眼病活动分数(CAS)呈显著正相关(r=0.53,P<0.01;r=0.46,P<0.01),且sICAM-1与HA亦呈正相关(r=0.31,P<0.05).GO患者外周血sICAM-1、HA水平可作为评价GO活动性的指标.  相似文献   

3.
急性出血性脑血管病脑脊液中sICAM-1含量分析   总被引:1,自引:1,他引:0  
目的观察脑出血、蛛网膜下腔出血后脑脊液中可溶性细胞间黏附分子-1(sICAM-1)的变化.方法采用酶联免疫吸附试验检测脑出血、蛛网膜下腔出血后脑脊液中sICAM-1的含量.结果正常人脑脊液中sICAM-1含量低微,而脑出血、蛛网膜下腔出血病人脑脊液中sICAM-1含量显著升高(P<0.01),动态观察表明脑出血第1天已达高峰,第3天后开始下降,但仍维持在较高水平.结论脑脊液中sICAM-1含量显著升高可反映脑组织损伤后的炎性反应程度,脑出血后第1天脑组织局部的炎症应激反应明显加强.  相似文献   

4.
目的 观察不同类型男性冠心病患者血清睾酮、游离睾酮与可溶性细胞间黏附分子-1(soluble intercellular adhesion molecule-1,sICAM-1)水平改变及互相间相关关系,进一步探讨睾酮与sICAM-1在男性急性冠状动脉综合征(acute coronary syndrome,ACS)发病中的作用.方法 冠心病患者分为急性心肌梗死(acute myocardial infarction,AMI)组、不稳定型心绞痛(unstable angina pectoris,UA)组、稳定型心绞痛(stable angina pectoris,SA)组,每组30例患者,另设健康对照组30例,比较各组间血清睾酮、游离睾酮与sICAM-1水平差异并分析其相关性.结果 AMI组和UA组血清游离睾酮与sICAM-1水平与对照组差异有统计学意义(P<0.01),ACS患者血清游离睾酮与sICAM-1水平之间呈负相关(P<0.01).结论 血清游离睾酮与sICAM-1水平改变与ACS的发生有关,它们可作为评价冠状动脉粥样硬化斑块稳定性与病变严重程度的一个参考指标,并为临床预防和治疗ACS开辟了新的途径.  相似文献   

5.
目的探讨外源性胰岛素与2型糖尿病(T2DM)血管病变的关系。方法将62例长期使用胰岛素治疗的T2DM病人作为胰岛素组,检测血清胰岛素、C肽、视黄醇结合蛋白4(RBP4)、可溶性细胞间黏附分子-1(sICAM-1);将54例口服降糖药物的T2DM病人作为对照组。比较两组血清胰岛素、C肽、RBP4、sICAM-1差异。结果胰岛素组血清胰岛素浓度较对照组升高(P0.01);C肽浓度较对照组降低(P0.01);血清RBP4浓度较对照组升高(P0.01);血清sICAM-1浓度较对照组升高(P0.01)。结论使用胰岛素治疗的T2DM病人,血清胰岛素浓度升高,且血清RBP4及sICAM-1含量升高,因此外源性胰岛素可能参与T2DM血管病变的发生与发展。  相似文献   

6.
目的 观察扩张型心肌病(DCM)心力衰竭患者血清肌钙蛋白 I(cTnI)、可溶性细胞间黏附分子(sICAM)-1、肌酸激酶同工酶(CK-MB)水平变化,并探讨其临床意义.方法 67例DCM心力衰竭患者(观察组),采用酶联荧光免疫法测定血清cTnI水平,ELISA法测定血清sICAM-1水平,免疫抑制法测定血清CK-MB水平,分析三种指标与患者病程和预后的关系;选择20例健康查体者为对照组.结果 观察组血清cTnI、sICAM-1水平均高于对照组,且随病程延长而增高,死亡者升高最显著(P<0.01);病程<1 a者血清CK-MB水平显著高于对照组,但随病程延长明显降低,死亡者降低最显著(P<0.01).结论 DCM心力衰竭患者血清cTnI、sICAM-1水平持续升高,CK-MB水平随病程延长先升后降;血清cTnI、sICAM-1、 CK-MB随病程延长而下降或短期内CK-MB明显升高,均提示预后不良.  相似文献   

7.
目的通过比较类风湿关节炎病人致动脉粥样硬化指数(AIP)和黏附分子(AM)的水平,研究RA病人中血清AIP和黏附分子的关系。方法测定60例RA病人中血清AIP和可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞间黏附分子-1(sVCAM-1)、E-选择素(E-selectin)的水平,并分别比较血沉、C反应蛋白(CRP)、指标,分析各指标间的相关性。结果与正常对照组比较,RA病人AIP水平有明显升高(0.83±0.31比0.21±0.18,P0.01)。RA病人血清sVCAM-1、sICAM-1、E-选择素与正常对照组比较有明显升高(P0.01。RA病人血清中的sVCAM-1、s-ICAM与AIP呈正相关(r=0.727,P0.01;r=0.501,P0.01),而E选择素与AIP之间无相关性。结论 RA病人致动脉粥样硬化指数和血清黏附分子水平明显增高,且s-VCAM、s-ICAM与AIP呈正相关。提示sVCAM-1、sICAM-1可能与RA病人动脉粥样硬化的发生起着一定的作用。  相似文献   

8.
目的:研究血清白细胞介素-6(IL-6)和细胞间黏附分子-1(ICAM-1)对急性胰腺炎严重程度的早期判断价值.方法:收集临床确诊的28例急性胰腺炎(AP)患者,分为重症急性胰腺炎(SAP)13例和轻症急性胰腺炎(MAP)15例两组,另选择10例体检健康人群作对照组(CG),分别测定血清IL-6和ICAM-1的浓度、并进行比较.结果:(1)发病24 h 内入院的SAP患者血清IL-6和ICAM-1浓度与MAP患者及对照组之间有显著性差异(P<0.01);而MAP患者与CG之间无显著性差异(P>0.05)(2)入院时SAP患者血清IL-6浓度与MAP患者及对照组之间有明显差异(P<0.01);入院后SAP患者的血清IL-6浓度逐渐下降,5 d后与MAP比较无显著性差异(P>0.05).(3)入院2 d后 SAP患者血清ICAM-1的浓度升高最明显,以后逐渐下降,但与MAP比较均有显著性差异(P<0.05).讨论:血清IL-6和ICAM-1对急性胰腺炎病情严重程度有早期判断价值.  相似文献   

9.
扩张型心肌病患者血清sICAM-1水平及其临床意义研究   总被引:1,自引:0,他引:1  
目的 探讨扩张型心肌病患者血清可溶性胞间黏附因子-1(sICAM-1)水平与扩张型心肌病的发生发展的关系及临床意义.方法 应用酶联免疫双抗体夹心法(ELISA)测定25例扩张型心肌病患者和15例健康对照组的血清sICAM-1水平.所有扩张型心肌病患者均经过超声心动图、X线胸片、心电图等多项检查证实,确属不明原因的心脏扩大伴有不同程度的心肌收缩功能减退,左室射血分数(LVEF)<35%者.结果 扩张型心肌病组血清sICAM-1明显高于对照组[(162.46±78.56)ng/ml,69.48 ng/ml,P<0.01];心功能Ⅱ级组血清sICAM-1高于对照组[(99.80±13.49)ng/ml,(69.48±16.86)ng/ml,P<0.05];心功能Ⅲ级组血清sICAM-1水平明显均高于心功能Ⅱ级组[(188.40±27.15)ng/ml,(99.80±13.49)ng/ml,P<0.01],心功能Ⅳ级组血清sICAM-1水平明显高于心功能Ⅲ级组[(370.85±49.97)ng/ml,(188.40±27.15)ng/ml,P<0.01].结论 扩张型心肌病患者血清中sICAM-1高表达,并且随着心衰加重,外周血清中sICAM-1的水平逐渐升高.在DCM中,sICAM-1可以作为一种无创性炎症活动的标记物  相似文献   

10.
目的 探讨急性心肌梗死(AMI)患者急诊经皮冠状动脉介入治疗(PCI)后白细胞介素8(IL-8)、可溶性细胞间黏附分子1(sICAM-1)变化与心肌灌注的关系. 方法急性ST段抬高型心肌梗死患者98例,接受急诊PCI治疗,于术前5 min,术后6 h、12 h、24 h分别抽取动脉血标本,采用酶联免疫双抗体夹心法(ELISA)检测ICAM-1及IL-8.PCI术后1个月做双核素心肌灌注显像(DISA SPECT)检查,根据心肌灌注程度分为心肌灌注不良组、心肌灌注良好组. 结果 IL-8在PCI术前5 min两组均已呈现升高趋势(P>0.05),术后6 h心肌灌注不良组进一步升高达峰值(P<0.01),术后12 h、24 h心肌灌注不良组[分别为(94.3±169.9)和(44.1±27.8)ng/L]仍高于心肌灌注良好组[分别为(27.4±26.8)和(21.5±12.2)ng/L,P<0.01和P<0.05].两组sICAM-1在PCI术前5 min比较,差异无统计学意义(P>0.05);术后6 h、12 h、24 h均持续高于心肌灌注良好组(P<0.05). 结论 急性心肌梗死PCI术后心肌灌注不良患者血浆IL-8、sICAM-1水平明显高于心肌灌注良好者,提示细胞因子IL-8、sICAM-1参与血运重建后心肌灌注障碍的发生、发展.  相似文献   

11.
目的 观察色素上皮衍生因子(PEDF)、血小板反应蛋白-1(TSP-1)在糖尿病大鼠肾脏的表达变化,探讨促血管生成素-1(Ang-1)对上述因子的影响. 方法 将雄性SD大鼠分正常对照(NC)组、DN组、空载处理(BV)组、Ang-1处理(AV)组.采用STZ腹腔注射诱导大鼠DN模型.成模8周后尾静脉注射Ang-1腺病毒载体.多时点检测24 hUAlb和肾组织PEDF、TSP-1蛋白及mRNA表达水平.结果 DN、BV、AV组24 hUAlb均升高,其中AV组于20周后降低(P<0.05).DN、BV、AV组肾组织PEDF蛋白及mRNA表达下调,TSP-1表达上调(P<0.05),其中AV组12周后肾组织PEDF和TSP-1mRNA及蛋白表达变化较DN、BV组改善明显(P<0.05). 结论 糖尿病大鼠肾脏PEDF、TSP-1异常表达参与DN发生发展,给予Ang-1可改善糖尿病大鼠肾脏PEDF、TSP-1异常表达.  相似文献   

12.
目的 探讨钙(Ca~(2+))/钙调素依赖蛋白激酶Ⅱ(CaMKⅡ)对Slingshot-1L(SSH-1L)活性的调控作用.方法 用脂质体法将含Myc-SSH-1L的重组质粒转染至MG63细胞,经不同浓度的钙离子载体A23187诱导10 min,蛋白印迹实验,观察P-cofilin、P-SSH1L、P-CaMK Ⅱ水平的变化;体内及体外实验检测CaMKⅡ对SSH-1L的磷酸化及活性调控作用.结果 当 A23187浓度为1 μmol/L时CaMK Ⅱ活性达到了最大,同时此浓度下P-cofilin水平以及SSH-1L的978位点丝氨酸的磷酸化水平升高.体外实验证实CaMK Ⅱ可使SSH-1L(WT)磷酸化,但是对其突变体SSH-1L(2 SA)无作用;同时CaMK Ⅱ明显抑制了SSH1L(WT)的活性,但对SSH-1L(2 SA)的活性无作用.结论 CaMKⅡ对SSH-1L的活性具有明显调控作用,且与SSH-1L的丝氨酸位点密切相关.  相似文献   

13.
Patients with β-thalassemia (thal) major are subject to peroxidative tissue injury by iron overload. Glutathione S-transferases work as antioxidants, and their activity is determined genetically. In this study, we used multiplex polymerase chain reaction (m-PCR) to analyze polymorphisms of two endogenous antioxidant agents, glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1), and to determine their roles in 41 patients with β-thal major. Our results showed that the GSTM1 and GSTT1 null genotypes were not associated with any incidence of endocrine dysfunction (including diabetes mellitus, hypogonadism, hypothyroidism, and growth hormone deficiency), liver function, or impaired left ventricular ejection fraction (LVEF). The GSTM1 null genotype, but not the GSTT1 null genotype, was associated with a decreased signal intensity ratio on cardiac magnetic resonance imaging (MRI). Our results suggest that genetic variations of the GSTM1 enzyme are associated with cardiac iron deposition in patients with β-thal major.  相似文献   

14.

Background

Currently, blockade of the programmed cell death 1 (PD-1)/PD-1 ligand 1 (PD-L1) signaling pathway has been proved one of the most promising immunotherapeutic strategies against cancer. Several antibodies have been developed to either block the PD-1 or its ligand PD-L1 are under development. So far, a series of phase I trials on PD-1/PD-L1 antibodies for non-small cell lung cancer (NSCLC) have been completed, without reports of results from phase II studies. Thus, we sought to perform a meta-analysis incorporating all available evidences to evaluate the efficacy and safety of PD-1 or PD-L1 inhibition therapy.

Methods

Electronic databases were searched for eligible literatures. Data of objective respond rate (ORR) and rate of adverse effects (AEs) with 95% confidence interval (CI) evaluated by immunohistochemistry (IHC) was extracted. The outcomes were synthesized based on random-effect model. Subgroup analyses were proposed.

Results

In overall, ORR in the whole population with PD-1 blockage treatment is 22.5% (95% CI: 17.6% to 28.2%). Additionally, the rate of Grade 3-4 AEs is 16.7% (95% CI: 6.5% to 36.8%) and drug-related death rate is 2.5% (95% CI: 1.3% to 4.6%). As for patients with PD-L1 inhibition therapy, an overall ORR is 19.5% (95% CI: 13.2% to 27.7%). A higher rate of Grade 3-4 AEs (31.7%, 95% CI: 14.2% to 56.5%) is observed with a lower drug-related death rate (1.8%, 95% CI: 0.4% to 8.3%). In exploratory analyses of anti-PD-1 agents, we observed that greater ORR was presented in the median-dose cohort (3 mg/kg) than that of both low-dose (1 mg/kg) and high-dose (10 mg/kg) cohort (low-dose vs. median-dose: OR =0.12, P=0.0002; median-dose vs. high-dose: OR =1.47, P=0.18).

Conclusions

Anti-PD-1 and anti PD-L1 antibodies showed objective responses in approximately one fourth NSCLC patients with a tolerable adverse-effect profile. In addition, median-dose (3 mg/kg) might be a preferential dosage of anti-PD-1 agents.  相似文献   

15.
Significant mortalities of racing pigeons occurred in Australia in late 2011 associated with a pigeon paramyxovirus serotype 1 (PPMV-1) infection. The causative agent, designated APMV-1/pigeon/Australia/3/2011 (P/Aus/3/11), was isolated from diagnostic specimens in specific pathogen free (SPF) embryonated eggs and was identified by a Newcastle Disease virus (NDV)-specific RT-PCR and haemagglutination inhibition (HI) test using reference polyclonal antiserum specific for NDV. The P/Aus/3/11 strain was further classified as PPMV-1 using the HI test and monoclonal antibody 617/161 by HI and phylogenetic analysis of the fusion gene sequence. The isolate P/Aus/3/11 had a slow haemagglutin-elution rate and was inactivated within 45 min at 56 °C. Cross HI tests generated an R value of 0.25, indicating a significant antigenic difference between P/Aus/3/11 and NDV V4 isolates. The mean death time (MDT) of SPF eggs infected with the P/Aus/3/11 isolate was 89.2 hr, characteristic of a mesogenic pathotype, consistent with other PPMV-1 strains. The plaque size of the P/Aus/3/11 isolate on chicken embryo fibroblast (CEF) cells was smaller than those of mesogenic and velogenic NDV reference strains, indicating a lower virulence phenotype in vitro and challenge of six-week-old SPF chickens did not induce clinical signs. However, sequence analysis of the fusion protein cleavage site demonstrated an 112RRQKRF117 motif, which is typical of a velogenic NDV pathotype. Phylogenetic analysis indicated that the P/Aus/3/11 isolate belongs to a distinct subgenotype within class II genotype VI of avian paramyxovirus type 1. This is the first time this genotype has been detected in Australia causing disease in domestic pigeons and is the first time since 2002 that an NDV with potential for virulence has been detected in Australia.  相似文献   

16.
The interaction of adhesion receptors on lymphocytes with their ligands over endothelial cells provides the mechanism by which lymphocytes infiltrate target tissues in autoimmune diseases. Primary Sjogren's syndrome (SS) is associated with lymphocytic infiltration in exocrine glands. The aim of this study was to examine levels of expression of adhesion molecules by peripheral blood lymphocytes from patients with SS (before and after stimulation). Peripheral blood lymphocytes from 16 patients with primary SS and from 15 controls were stained directly or cultured for 72 h with and without phytohaemagglutinin (PHA). Indirect immunofluorescence with monoclonal antibodies and flow cytometry were used. The following molecules were detected in patients before culture: CD18 (mean percentage 94%), CD11a (94%), CD11b (39%), CD54 (23%), CD58 (62%), CD44 (Hermes-1; 82%), CD49-d (VLA-4; 80%), CD25 (11%) and LECAM-1 (62%). After stimulation with PHA, there was an increase in the levels of CD18 (2.5-fold), CD11a (2.3-fold), CD54 (10.2-fold), CD58 (2.5-fold), CD44 (2.4-fold), CD49d (3.4-fold) and CD25 (62-fold) on lymphocytes from both patients and controls. The number of positive cells and level of expression did not differ from the controls, except in the case of unstimulated, cultured lymphocytes in which the levels of CD44 and LECAM-1 were increased more in patients than in normal controls. The increase in the level of in vitro expression of CD44 (P< 0.05) and LECAM-1 (P< 0.002) on lymphocytes from patients with primary SS reached statistical significance when compared to similarly cultured lymphocytes from controls. The regulation of LECAM-1 and CD44 expression in patients with SS may contribute to the immunopathogenesis of this desease by increased tethering or rolling (early adhesive events) of lymphocytes over endothelial cells. Such molecules may be involved in lymphocytic homing to tissues in SS.  相似文献   

17.
[目的]探讨肝肺综合征(HPS)的发病机制.[方法]采用胆总管结扎(CBDL)术制备大鼠HPS模型,观察肺组织肾上腺髓质素(ADM)、内皮素-1(ET-1)及其受体(ETRA和ETRB)的表达和分布.[结果]在大鼠HPS形成过程中,血浆和肺组织中ADM、ET-1水平动态升高,且与肺泡-动脉氧分压差(A-aDO2)正相关;HPS大鼠肺组织中ADM、内皮素前体原(ppET-1 mRNA)的表达较假手术组明显增强,差异均有统计学意义(P<0.05).HPS大鼠肺血管ETRA的分布及染色强度与假手术组比较无明显变化,而ETRB在远端肺小动脉和小静脉内膜上表达明显增强.图像分析结果显示CBDL 5周(w)组大鼠ETRA染色面积、平均积分光密度值与假手术组比较差异无统计学意义(P>0.05),而CBDL 5 w组大鼠ETRB染色面积和平均积分光密度值明显高于假手术组,差异均有统计学意义(P<0.05).[结论]扩血管物质ADM和缩血管物质ET-1的共同作用可能参与HPS的发生,肺组织中升高的ET-1可能更多地通过与在肺血管表达增强的ETRB结合从而扩张肺血管.  相似文献   

18.
目的探讨锌α2糖蛋白(AZhGP1)与肝细胞癌(HCC)发生、发展和转移的关系。方法二乙基亚硝胺(DEN)构建肝硬化和HCC大鼠模型,以过表达AZGP1基因干扰的HepG2细胞液构建裸鼠皮下成瘤和肝原位移植模型。免疫组织化学、蛋白免疫和PCR检测AZGP1和TGFβ1的表达。结果AZGP1 mRNA在正常肝组织、肝硬化和肝癌中的表达分别为(0.98±0.02)、(0.52±0.03)、(0.20±0.02);而TGFβ1的基因和蛋白表达在肝硬化和肝癌组织中呈现显著上调。AZGP1过表达的HepG2细胞接种裸鼠构建皮下肿瘤(HepG2-AZGP1组)。与对照组(HepG2-GFP组)比较,肿瘤大小无差异。裸鼠肝内移植术6周后,HepG2-GFP组57%和HepG2-AZGP1组14%发生肺转移(P=0.0157)。与HepG2-GFP组比较,HepG2-AZGP1组肝脏原发灶和肺转移灶结节数目明显减少,癌细胞异型性明显较轻。结论肝硬化进展至肝癌过程中抑癌基因.AZGP1发生缺失,伴随着失去阻抑TGFβ1作用。恢复AZGP1功能可能是一种新的有前途的治疗肝癌方法。  相似文献   

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目的 测定中华血吸虫线粒体细胞色素 C氧化酶亚基 1(CO1)和 NADH脱氢酶亚基 1(ND1)基因序列 ,并根据这些序列构建分子系统发生树 ,探讨中华血吸虫在裂体属内的系统发生位置。 方法 以 GNT- K法抽提虫体基因组 DNA,用特异引物 PCR扩增目的基因。PCR扩增产物经纯化后克隆于质粒载体 ,以纯化后的阳性质粒 DNA作为模板 ,M13(F/ R)为引物于 L icor测序仪测序。检索 Gen Bank,查找曼氏血吸虫等相关血吸虫两线粒体基因序列 ,作基因排序及比较分析后 ,用 PHYL IP和 MEGA以邻接法和最大简约法绘制系统发生树。 结果 克隆了中华血吸虫的 CO1和 ND1基因片段 ,并测定了两基因片段的核苷酸序列 ,根据这些序列构建了系统发生树。 结论 中华血吸虫 CO1和ND1基因的系统发生树结果一致。提示中华血吸虫归属于亚洲血吸虫组  相似文献   

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