核因子κB活性抑制剂对皮瓣缺血-再灌注后CD11b/CD18及细胞间黏附分子-1表达的影响

目的 观察皮瓣缺血-再灌注(I/R)期间,核因子(NF)-κB活性抑制剂对外周血中性粒细胞(PMN)表面CD11b/CD18及皮瓣血管内皮细胞细胞间黏附分子(ICAM)-1表达的影响,探讨其预防I/R损伤的确切机制.方法 雄性SD大鼠30只,随机分为:假手术组(A组);I/R组(B组);I/R+PDTC处理组(C组).制备右侧下腹岛状皮瓣I/R模型.C组于再灌注前5 min,静注PDTC(300 mg/kg体重).采用流式细胞术及免疫组织化学法,分别检测缺血前、再灌注不同时点外周血PMN CD11b/CD18及皮瓣血管内皮ICAM-1表达.行组织学观察,并测定皮瓣存活比例.结果 A组CD11b/CD18及ICAM-1均呈低表达;B组CD11b/CD18于再灌注3、6 h,ICAM-1于再灌注6 h表达均明显上调,较A组差异有统计学意义(P＜0.01).C组再灌注3、6 h CD11b/CD18及ICAM-1表达较B组显著降低(P＜0.01).C组再灌注6 h PMN浸润及组织破坏程度较B组明显减轻,皮瓣存活比例显著提高(P＜0.01).结论 NF-κB活性抑制剂对I/R皮瓣的保护机制之一是下调CD11b/CD18及ICAM-1表达,减轻PMN向皮瓣内的黏附及渗出.     

异氟醚预处理对兔局灶性脑缺血再灌注时降钙素基因相关肽和NF-κB的影响

目的 探讨异氟醚预处理对兔局灶性脑缺血再灌注时降钙素基因相关肽( CGPP)和NF-κB水平的影响.方法 新西兰纯系家兔54只,雌雄不拘,体重2.0～2.5 kg,采用随机数字表法,将其随机分为3组(n＝18):假手术组(S组)、脑缺血再灌注组(I/R组)和异氟醚预处理(I组).麻醉下气管内插管,机械通气,S组和I/R组静脉输注咪达唑仑维持麻醉;I组吸人1.4％异氟醚30 min后洗脱10 min进行异氟醚预处理,然后制备脑缺血再灌注损伤模型,在脑缺血再灌注损伤过程中静脉输注咪达唑仑,3组静脉输注芬太尼和维库溴铵.I/R组和I组采用线栓法制备局灶性脑缺血再灌注损伤模型,于缺血2h时进行再灌注.分别于麻醉前和再灌注即刻、1h、2h、3h、4h、5h时取耳中央动脉血样,测定血浆CGRP浓度,各时点取完血样后立即处死动物,测定脑组织神经元NF-κB活性及其表达.结果 与S组比较,I/R组血浆CGRP浓度、脑组织神经元NF-κB活性升高,脑组织NF-κB表达上调(P<0.05);与I/R组比较,I组血浆CGRP浓度升高,脑组织神经元NF-κB活性降低,脑组织NF-κB表达下调(P<0.05).结论 异氟醚预处理减轻兔脑缺血再灌注损伤的机制与促进CGRP释放及抑制神经元NF-κB功能有关.     

异氟醚和七氟醚对人肺癌细胞株A549细胞凋亡及CD44和CD54表达的影响

目的 评价异氟醚和七氟醚对人肺癌细胞株A549细胞凋亡及CD44和CD54表达的影响.方法 人肺癌细胞株A549接种于24孔培养板中,培养24 h后,随机分为对照组(C组)、异氟醚组(Iso组)和七氟醚组(Sev组),每组8孔.将培养板置于无菌密闭容器内,再置于37℃恒温水浴箱中.C组通入95%O2-5%CO2混合气体2 L/min,维持4 h;Iso组通入95%O2-5%CO2混合气体2 L/min 和异氟醚,维持异氟醚浓度1.7%4 h;Sev组通入95%O2-5%CO2混合气体2 L/min和七氟醚,维持七氟醚浓度2.5%4 h.处理完成后,放回37℃、5%CO2,培养箱中,继续培养24 h.分别于处理前、处理2、4 h和处理后24 h时,取A549细胞,检测细胞凋亡情况,计算细胞凋亡率;测定CD44和CD54的表达水平.结果 与处理前比较,Iso组处理4 h和处理后24 h时细胞凋亡率升高,Sev组处理2、4 h和处理后24 h时细胞凋亡率升高,Iso组和Sevo组处理2、4 h和处理后24 h时CD44和CD54表达下调(P<0.05);与C组比较,Iso组处理4 h和处理后24 h时细胞凋亡率升高,Sev组处理2、4 h和处理后24 h时细胞凋亡率升高,Iso组和Sevo组处理2、4 h和处理后24 h时CD44和CD54表达下调(P<0.05);与Iso组,Sevo组处理2、4 h和处理后24 h时细胞凋亡率升高(P<0.05),CD44和CD54表达差异无统计学意义(P>0.05).结论 异氟醚和七氟醚均可诱导人肺癌A549细胞凋亡,其中七氟醚作用较强.异氟醚和七氟醚均可抑制人肺癌A549细胞CD44和CD54的表达.     

卡巴胆碱对肠缺血/再灌注大鼠中性粒细胞CD11b/CD18表达和血清可溶性细胞间黏附分子-1浓度的影响

目的:观察胆碱能激动剂卡巴胆碱对肠缺血/再灌注大鼠中性粒细胞(PMN)上CD11b/CD18表达和血清可溶性细胞间黏附分子-1(sICAM-1)浓度的调节作用。方法:54只雄性Wistar大鼠随机分为假手术组(N组)、肠缺血/再灌注组(GI/R组)及卡巴胆碱干预组(Car组)。采用夹闭肠系膜上动脉45min后恢复灌流的方法制成GI/R模型;卡巴胆碱组在肠缺血15min后经幽门注入卡巴胆碱(100μg/kg)。于肠缺血45min(I45)及再灌注1h(R1)、2h(R2)、6h(R6)取肠系膜上静脉血,双抗体夹心酶联免疫吸附(ELISA)法测定血清sICAM-1浓度,流式细胞仪检测PMN上CD11b/CD18表达率。结果:肠系膜上静脉血中PMN表面黏附分子CD11b/CD18的表达在肠缺血和再灌注后各时相点均增加(P<0.01),R2和R6时增加幅度较大;卡巴胆碱干预组R6时CD11b/CD18阳性PMN比例减少(P<0.05)。血清sICAM-1浓度在R1～R6时均升高(P<0.05),而给予卡巴胆碱的动物R6时降低(P<0.05),其值接近N组。结论:卡巴胆碱能降低肠缺血/再灌注大鼠PMN上CD11b/ C...     

异氟醚预处理对局灶性脑缺血再灌注损伤大鼠缺血半暗带TLR4-MyD88信号通路的影响

目的 探讨异氟醚预处理对局灶性脑缺血再灌注损伤大鼠缺血半暗带TLR4-MyD88信号通路的影响.方法 成年雄性SD大鼠54只,体重250 ～ 280 g,采用随机数字表法,将其随机分为3组(n=18):假手术组(S组)、脑缺血再灌注组(I/R组)和异氟醚预处理组(IP组).S组仅分离血管不留置线栓;I/R组采用线栓法制备右侧局灶性脑缺血再灌注损伤模型,缺血2h,再灌注24 h;IP组吸入2.0％异氟醚2h,预处理结束后24h时制备右侧局灶性脑缺血再灌注损伤模型.于再灌注24 h时行神经功能缺陷评分,随后处死大鼠,每组随机抽取5只大鼠,取脑组织,测定脑梗死体积,采用Westernblot法和RT-PCR法检测大鼠右侧脑缺血半暗带区HSP60、TLR4、MyD88蛋白及mRNA的表达情况;每组剩余的3只大鼠,采用TUNEL法检测大鼠右侧脑缺血半暗带区细胞凋亡情况.结果 与S组比较,I/R组和IP组神经功能缺陷评分升高,脑梗死体积增大,右侧脑缺血半暗带区凋亡指数升高,HSP60、TLR4、MyD88蛋白及mRNA表达均上调(P＜0.05);与I/R组比较,IP组神经功能缺陷评分降低,脑梗死体积减小,右侧脑缺血半暗带区凋亡指数降低,HSP60、TLR4、MyD88蛋白及mRNA表达均下调(P＜0.05).结论 异氟醚预处理可保护脑缺血再灌注大鼠缺血半暗带,其机制可能与抑制大鼠脑缺血半暗带TLR4-MyD88信号通路有关.     

七氟醚预处理对局灶性脑缺血再灌注损伤大鼠海马TREK-1表达的影响

目的 探讨七氟醚预处理对局灶性脑缺血再灌注损伤大鼠海马机械敏感性钾通道TREK-1表达的影响.方法 健康雄性SD大鼠36只,体重240～280 g,随机分为3组(n=12):假手术组(S组)、局灶性脑缺血再灌注组(l/R组)和七氟醚预处理组(Sevo组).结扎右侧颈总动脉、颈外动脉,采用线栓法阻断颈内动脉2 h,再灌注24 h制备大鼠局灶性脑缺血再灌注损伤模型;Sevo组于缺血前1 h经半密闭的吸入箱持续吸入含2.5%七氟醚的02;S组仅分离并结扎右侧颈总动脉、颈外动脉,不置入线栓.各组于再灌注24 h时行神经功能缺陷评分后断头取脑,TIC染色后测定脑梗死体积,采用RT-PCR法测定海马TREK-1 mRNA的表达.结果 与S组相比,I/R组和Sevo组神经功能缺陷评分和脑梗死体积比升高(P<0.01);与I/R组相比,Sevo组神经功能缺陷评分和脑梗死体积比降低,海马TREK-1 mRNA表达上调(P<0.05).结论 七氟醚预处理可通过激活海马TREK-1减轻大鼠局灶性脑缺血再灌注损伤.     

异丙酚对大鼠脑缺血再灌注损伤时海马解偶联蛋白-2表达的影响

目的 探讨异丙酚对大鼠脑缺血再灌注损伤时海马解偶联蛋白-2(ucP-2)表达的影响.方法 健康雄性Wistar大鼠72只,体重250～300 g,随机分为3组,每组24只:对照组(C组)、缺血再灌注组(I/R组)和异丙酚组(P组).采用二血管阻断法建立前脑缺血再灌注模型.C组于暴露双侧颈总动脉后,左侧脑室注射生理盐水1 mg/kg;I/R组脑缺血10 min,再灌注即刻左侧脑室注射生理盐水1 mg/kg;P组脑缺血10 min,再灌注即刻左侧脑室注射异丙酚1 mg/kg.I/R组和P组分别于再灌注即刻、再灌注6、12和24 h(T1-4)时断头取脑分离海马组织.光镜下观察海马组织病理学;RT-PCR法检测海马UCP-2 mRNA表达;免疫组化法检测海马组织UCP-2蛋白表达.结果 与C组比较,I/R组各时点UCP-2 mRNA表达上调(P<0.05);与I/R组比较,P组T2-3时UCP-2 mRNA表达上调,T3时UCP-2蛋白表达上调(P<0.05).P组较I/R组脑组织病理损伤减轻.结论 异丙酚可减轻大鼠脑缺血再灌注损伤,其机制可能与其上调海马组织UCP-2表达有关.     

乳化异氟醚预处理对大鼠局灶性脑缺血再灌注时海马腺苷A1受体表达的影响

目的 探讨乳化异氟醚预处理对大鼠局灶性脑缺血再灌注时海马腺苷A1(AA1)受体表达的影响.方法 健康雄性SD大鼠88只,体重280～320 g,采用随机数字表法,将其随机分为7组:假手术组(S组,n=16)、缺血再灌注组(I/R组,n=16)、乳化异氟醚预处理组(EI组,n=16)、乳化异氟醚溶剂组(LE组,n=16)、乳化异氟醚+AA1受体拮抗剂8-环戊基-1,3-二丙基黄嘌呤(DPCPX)组(ED组,n=8)、DPCPX组(DP组,n=8)和DPCPX溶剂二甲基亚砜组(DM组,n=8).采用大脑中动脉阻塞法制备局灶性脑缺血再灌注损伤模型.于缺血前24h,I/R组、EI组和LE组分别腹腔注射生理盐水、8％乳化异氟醚和脂肪乳剂10.5 ml/kg,DP组和DM组分别腹腔注射DPCPX 1 mg/kg和二甲基亚砜2.5mg/kg,S组于相应时点腹腔注射生理盐水10.5 ml/kg; ED组于腹腔注射8％乳化异氟醚前30 min腹腔注射DPCPX 1 mg/kg.各组于再灌注24h时取8只大鼠,进行神经功能缺陷评分,然后处死,取脑组织,测定脑梗死体积;S组、I/R组、EI组和LE组于再灌注24 h时处死8只大鼠,取脑组织,采用Western blot法检测海马AA1受体的表达水平.结果 与S组比较,其余各组神经功能缺陷评分和脑梗死体积百分比升高,I/R组和LE组海马AA1受体表达下调,EI组海马AA1受体表达上调(P＜0.01);与I/R组比较,EI组神经功能缺陷评分和脑梗死体积百分比降低,海马AA1受体表达上调(P＜0.05或0.01);与EI组比较,LE组、ED组、DP组和DM组神经功能缺陷评分和脑梗死体积百分比升高(P＜0.05或0.01).结论 乳化异氟醚预处理减轻大鼠局灶性脑缺血再灌注损伤的机制可能与上调海马AA1受体表达有关.     

异氟醚、七氟醚和地氟醚预处理对脑缺血再灌注损伤大鼠海马CBS/H2S、iNOS/NO和HO-1/CO的影响

目的 研究异氟醚、七氟醚和地氟醚预处理对脑缺血再灌注损伤大鼠海马CBS／H，S、iNOS／NO和HO-1／CO的影响，探讨吸入麻醉药脑保护作用的机制。方法30只Wistar大鼠随机分为5组（n=6）：对照组（C组）、脑缺血再灌注组（I／R组）、异氟醚组（I组）、七氟醚组（S组）和地氟醚组（D组）。采用四动脉阻断法建立大鼠全脑缺血再灌注模型。Ⅰ组、S组和D组夹闭两侧颈总动脉前分别吸入氧气＋0．65MAC的异氟醚、七氟醚和地氟醚30min，C组和I／R组吸入氧气。缺血20min，再灌注12h后处死大鼠，取海马，测定大鼠海马组织中HS、NO、CO、cAMP和cGMP含量和CBS，iNOS和HO活性以及CBS—mRNA、iNOS，mRNA和HO—1-mRNA的表达水平；电镜下观察海马线粒体的变化。结果与C组相比，I／R组海马组织CO、H2S、NO、cAMP、cGMP含量和HO、CBS、iNOS活性升高，CBS—mRNA、iNOS-mRNA和HO-1-mRNA表达升高，海马神经细胞线粒体变性率升高（P〈0．01）；与I／R组相比，Ⅰ组、D组和S组CO含量和HO活性升高，H2S、NO、cAMP含量和CBS、iNOS活性降低，CBS—mRNA和iNOS-mRNA表达降低而HO-1-mRNA表达升高，线粒体变性率降低（P〈0．05或0．01）。结论 异氟醚、七氟醚和地氟醚预处理可通过抑制CBS／142S、iNOS／NO，激活HO-1／CO，减轻了大鼠脑缺血再灌注损伤。     

异氟醚对大鼠肺缺血再灌注损伤的保护作用

目的 探讨异氟醚对大鼠肺缺血再灌注损伤的保护作用。方法 120只SD雄性大鼠，随机分成4组（n=30）：假手术组（S组）、缺血再灌注组（IR组）、异氟醚-缺血再灌注组（ISO-IR组）和异氟醚组（ISO-S组）。IR组、ISO-IR组建立肺缺血再灌注模型，ISO-IR组吸入1MAC异氟醚30min时行肺缺血再灌注，ISO-S组吸入1MAC异氟醚，不进行肺缺血再灌注。分别在缺血45min、再灌注30、60、120min处死6只大鼠，测定肺组织湿干比（W／D）、髓过氧化物酶（MPO）活性、中性粒细胞（PMN）膜表面CD18和肺组织ICAM-1mRNA表达、支气管肺泡灌洗液（BALF）中自细胞计数、沉渣白细胞分类和总蛋白（TP）浓度，并进行肺组织病理学检查。结果 再灌注期间IR组肺组织W／D、MPO活性、CDl8和ICAM-1mRNA表达、BALF中PMN百分比、TP浓度及PMN膜表面CD18表达均升高。而异氟醚预先给药减弱了缺血再灌注诱导的上述指标的升高。肺组织病理学检查显示异氟醚预先给药减轻了肺缺血再灌注损伤。结论 通过抑制PMN浸润和肺组织ICAM-1mRNA及CD18表达上调，缺血前吸入异氟醚对肺缺血再灌注损伤有一定的保护作用。     

Influence of CD14 polymorphism on CD14 expression in patients with extensive burns

We sought to investigate the association of CD14 genotype with the risk of mortality after burn, and we also attempted to evaluate whether CD14-159 C/T polymorphism affects the kinetics and extent of CD14 expression as well as its release, and TNF-alpha expression in burned patients. The study involved 64 patients in Chinese Han population incurring burns covering more than 30% of the total body surface area. CD14 polymorphism was determined by polymerase chain reaction (PCR) and subsequent restriction fragment length polymorphism (RFLP) analysis. Meanwhile, leukocyte CD14 mRNA expression and soluble CD14 (sCD14) levels were measured during a 28-day observation period. TNF-alpha mRNA and protein levels were also determined in patients with different genotypes of CD14. On day 21 after burn, CD14 mRNA expression and sCD14 levels were significantly higher in TT homozygotes than in CC genotypes (1.33+/-0.36 microg/ml vs. 0.75+/-0.28 microg/ml and 16.1+/-4.6 microg/ml vs. 9.7+/-3.4 microg/ml, P<0.05), and these values were also higher in non-survivors than in survivors (1.32+/-0.40 microg/ml vs. 0.87+/-0.32 microg/ml and 14.8+/-4.5 microg/ml vs. 11.1+/-4.8 microg/ml, P<0.05). In addition, TNF-alpha mRNA and protein levels were significantly lower in both CC homozygotes and survivors than in TT genotypes or non-survivors during the 28-day observation period (P<0.05). However, TT genotype did not impart an increased risk for burn mortality in this small study. In conclusion, CD14-159 C/T polymorphism might be associated with the kinetics and extent of CD14 expression as well as its release, and it was also related to TNF-alpha expression. However, this study did not confirm CD14-159 C/T polymorphism was associated with the outcome of extensive burns.     

CD70 expression in thymic carcinoma

CD70, a type II transmembrane glycoprotein, is a member of the tumor necrosis factor (TNF) family that mediates the interaction between B- and T-lymphocytes. CD70 has been shown to be expressed by malignant lymphoma, especially Hodgkin's disease, and by nasopharyngeal carcinoma, both of which are frequently associated with Epstein-Barr virus (EBV). In this study, we investigated the expression of CD70 in epithelial cells of various types of thymic epithelial tumors and its association with EBV. Immunohistochemical expression of CD70 was studied on frozen tissue. In a series of 27 thymic epithelial tumors, including thymic carcinomas (n = 8), atypical thymomas (n = 5), thymomas (n = 13), and thymic carcinoid (n = 1), 7 (88%) thymic carcinomas and 1 (20%) atypical thymoma showed positive immunoreactivity for CD70, whereas CD70 was not detected in other tumors. Twenty-four intrathoracic malignant epithelial tumors of nonthymic origin, including lung (n = 17), esophagus (n = 5), and mesothelium (n = 2), showed no immunoreactivity for CD70. Northern blot analysis also revealed that CD70 messenger RNA was expressed in 2 of 2 thymic carcinomas, 0 of 2 atypical thymomas. and 0 of 2 thymomas. All of the 27 thymic epithelial tumors were EBV-negative as assessed by EBV-encoded small RNA in situ hybridization. The expression of CD70 is closely related to the pathogenesis of thymic carcinoma but unrelated to EBV infection in the thymus.     

CD147 expression in peritoneal injury

Background

Peritoneal injury is an important cause of technical failure of long-term peritoneal dialysis (PD). Encapsulating peritoneal sclerosis (EPS) is a severe complication of long-term PD with potentially life threatening consequences. CD147 is a glycoprotein with diverse functions including modulation of extracellular matrix via induction of matrix metalloproteinases, cell adhesion, and regulation of immune reactions. We hypothesized that CD 147 plays a role in the peritoneal cavity.

Methods

In this retrospective study, we localized CD147 by immunohistochemistry in peritoneal biopsies from uremic patients not on PD (n?=?8), on PD without signs of EPS (n?=?7), and in biopsies in patients with the diagnosis of EPS (n?=?7). Double immunofluorescence was used to co-localize α-smooth-muscle actin (α-SMA) and CD147 in selected biopsies from each group. Expression was scored semi-quantitatively.

Results

In biopsies from uremic controls, CD147 was prominently expressed in mesothelial cells, focally between fat cells and by some perivascular cells. In patients on PD, a similar distribution was present (although mesothelium was rarely conserved), with some focal accentuation. In EPS, layers of fibroblastic cells were positive for CD147. EPS biopsies demonstrated a significantly higher score in a blinded evaluation, compared to uremic patients. Cells expressing CD147 were α-SMA positive myofibroblasts as demonstrated by double immunofluorescence. Mean CD147 scores did not differ between patients with different transporter status.

Conclusions

This is the first study demonstrating CD147 on a major part of fibroblastic cells in EPS. Future studies need to address the role of these cells in this severe complication of long-term PD.

     

急性高容量血液稀释对全髋关节置换术患者血小板膜糖蛋白表达的影响

目的 评价急性高容量血液稀释(AHH)对全髋关节置换术患者血小板激活程度和血小板凝血功能的影响。方法 ASAⅠ～Ⅱ级骨科择期全髋关节置换术患者20例,随机分为羟乙基淀粉(HES)组和乳酸钠林格溶液(LR)组,每组10例。于静脉麻醉诱导后以25ml/kg的剂量和30ml·kg~(-1)·h~(-1)的速率分别输入HES和LR。采用流式细胞术定量测定诱导前(T_1)、AHH前(T_2)、输注开始后15min(T_3)、30min(T_4)和45min(T_5)血小板膜糖蛋白(CD62P和CD63)的表达量。结果 HES组T_3、T_4和T_5的CD62P表达水平较T_1有显著性增高(P<0.05或0.01),较T_2有非常显著性增高(P<0.01);两组T_2的CD62P表达水平较T_1显著性降低(P<0.05)。两组各时点的CD63表达水平均无明显变化。结论 HES术前、术中行AHH能明显增强血小板表面CD62P的表达,促进血小板活化。     

Changes in CD14 expression on monocytes and changes in serum soluble CD14 level during hemodialysis

Background. CD14 is a receptor of lipopolysaccharide (LPS) and LPS binding protein (LBP) complex expressed on monocytes, and changes in the cell surface CD14 expression are thought to be a marker of activation of these cells. CD14 is shed from the cell surface when monocytes are activated. In this study, we assessed the influence of dialyzer membrane material and dialysate purity on monocyte CD14 expression and serum soluble CD14 (sCD14) levels in chronic hemodialysis (HD) patients in vivo during HD. Methods. We measured LPS concentrations in dialysate at two institutions by limulus assay. From one institution where LPS was undetectable in dialysate over a 2-year period, we selected seven patients. In the first period of the study, they were treated with a regenerated cellulose (RC) dialyzer, and then they were treated with a polysulfone (PS) dialyzer. We named them the "RC group" and the "PS group", respectively. From the other institution, where dialysate was contaminated with LPS, we selected eight patients. They were treated with a PS dialyzer, and were named the "PS + LPS group". CD14 expression on monocytes and serum sCD14 concentrations were measured by flow cytometry analysis and enzyme-liked immunosorbent assay, respectively. Results. During HD, in the RC group, upregulation of CD14 expression across the dialyzer was greater than in the PS group. There was no significant variation in serum sCD14 levels during HD in the RC and PS groups, while in the PS + LPS group, serum sCD14 level on the venous side of the dialyzer was significantly increased at 30 and 180 min after the initiation of HD compared with the predialysis value, and at 30 and 180 min compared with the level on the arterial side of the dialyzer. These results suggest that the changes in CD14 expression reflected the effect of dialyzer membrane material, while the changes in serum sCD14 levels reflected the effect of LPS influx from the dialysate. Conclusion. Dialysate purity may be an important factor in preventing monocyte activation during HD. Received: April 13, 1999 / Accepted: July 16, 1999     

CD44和 CD54在结直肠癌肝转移中的表达意义

目的探讨结直肠癌肝转移患者血清中CD44和CD54含量与结直肠癌肝转移发生发展的关系,寻找一个稳定的早期诊断结直肠癌肝转移的生物学指标。方法应用酶联免疫吸附测定方法(ELISA)检测38例结直肠癌和21例结直肠癌肝转移患者以及40例健康成人(正常对照组)的血清CD44和CD54含量,并比较血清中CD44和CD54含量在治疗前后的变化。结果结直肠癌肝转移组和结直肠癌组血清中CD44和CD54含量明显高于正常对照组,且结直肠癌肝转移组较结直肠癌组含量也明显增高。结直肠癌肝转移组和结直肠癌组治疗后的血清CD44和CD54含量比治疗前下降。结论CD44和CD54可以作为临床早期诊断结直肠癌肝转移的生物学指标,同时也可以作为监测结直肠癌和结直肠癌肝转移预后的客观指标。     

CD14-159C/T基因多态性对全血培养CD14表达的影响

目的探讨CD14基因启动子-159C/T基因多态性对全血培养CD14mRNA表达及可溶性CD14(sCD14)浓度的影响。方法采集118例健康献血员血标本,用全血细胞培养模型检测内毒素刺激前后CD14mRNA表达及sCD14浓度的变化。采用聚合酶链反应(PCR)及限制性内切酶HaeⅢ对PCR产物的消化作用检测CD14基因多态性。同时,对内毒素刺激后肿瘤坏死因子α(TNF-α)诱生水平进行了分析。结果118例健康献血员中,等位基因T和C的频率分别为60.2%和39.8%;40例是T等位基因纯合子(TT),62例为杂合子(TC),还有16例基因型为CC。基因型TT与TC白细胞中CD14mRNA的表达及上清液sCD14浓度均明显高于CC纯合子(P<0.05或0.01)。并且TT纯合子TNF-α诱生水平为(352±215)pg/ml,显著高于基因型TC及CC[(261±163)pg/ml及(198±122)pg/ml,P<0.05]。结论内毒素受体CD14-159C/T基因多态性对全血培养CD14的表达及释放产生显著影响,并与内毒素诱导TNF-α的反应性相关。     

巨噬细胞CD40L表达在腹膜炎中的临床意义

目的：探讨巨噬细胞CD40配体（CD40L）表达与持续性不卧床腹膜透析（CAPD）腹膜炎发生发展的关系。方法：运用流式细胞仪观察CAPD患者急性腹膜炎时腹透透出液中巨噬细胞CD40L,表达,并与CAPD非腹膜炎患者比较,结果：急性腹膜炎发生时,透出液中表达CD40L阳性巨噬细胞数显著增多。巨噬细胞表达CD40L水平显著增加,与非腹膜炎患者比较有显著差异（P＜0．05,P＜0．01）,急性腹膜炎缓解后,患者透出液中表达CD40L阳性巨噬细胞数及巨噬细胞表达CD40L水平均较发作期显著降低（P＜0．05）,结论：CAPD腹膜炎时巨噬细胞高表达的CD40L对于限制腹膜炎的发生发展具有积极意义。