丙肝病毒核心蛋白对肝门部胆管癌细胞增殖和细胞凋亡的调控作用

目的　探讨丙肝病毒核心蛋白 (HCVC蛋白 )在肝门部胆管癌发生和发展中的作用。方法　采用过氧化物酶 抗过氧化酶 (PAP)法检测 36例肝门部胆管癌组织中HCVC蛋白的表达 ,原位末端标记技术 (ISEL)和链霉亲合素 生物素技术 (SLAB)分别检测肝门部胆管癌中的细胞凋亡指数 (AI)和细胞增殖指数 (PI)。结果　 36例肝门部胆管癌患者中HCVC蛋白阳性表达率为61 .1 % (2 2 /36) ,AI和PI的平均值分别为 (3 .46± 0 .62 ) %和 (46 .43± 1 2 .59) % ,HCVC蛋白阳性表达组中AI明显低于HCVC蛋白阴性表达组 (P <0 .0 1 ) ,而PI在HCVC蛋白阳性组中明显高于HCVC蛋白阴性组 (P <0 .0 1 )。结论　HCVC蛋白可能有助于肝门部胆管癌细胞增殖 ,抑制细胞凋亡的发生率     

肾细胞癌中bcl-2、p53、增殖细胞核抗原表达与细胞增殖和凋亡

目的 探讨肾细胞癌(RCC)中bcl—2、p53、增殖细胞核抗原(PCNA)表达与细胞增殖、凋亡及病理参数之间的关系。方法 应用链霉亲和素辣根过氧化物酶(SABC)法分析34例RCC标本中bcl—2、p53和PCNA蛋白的表达，应用末端脱氧核苷酸转移酶介导的脱氧三磷酸尿苷苦(dUTP)缺口末端标记(TUNEL)法检测细胞凋亡。结果 34例RCC标本中，15(44．1％)例bcl-2阳性表达，表达阳性率与增殖指数(PI)、凋亡指数(AI）及RCC病理学参数无关；仅有3例p53表达阳性；PI为6．0％--24．0％(平均为12．3％)，AI为2．0％--8．0％(平均为5．4％)；PI与肿瘤分级、分期密切关系，AI与肿瘤分级有明显关系。结论 明显增高的PI和AI与肿瘤恶性表型有关，提示在RCC中肿瘤细胞过度增殖伴有频繁的凋亡发生。     

胰腺癌组织中细胞凋亡与增殖相关性的研究

目的　通过对胰腺癌组织中细胞凋亡与增殖相关性的研究 ,探讨其在胰腺癌发生发展中的作用。方法　采用原位末端标记、增殖细胞核抗原免疫组织化学染色和HE染色的方法对 32例胰腺癌和 14例慢性胰腺炎组织中细胞凋亡指数 (AI)、增殖指数 (PI)和分裂细胞指数 (MI)进行检测。结果　胰腺癌组织中的AI(3.37± 2 .38)、PI(46 .6 8± 2 .2 9)、MI(0 .31± 0 .12 )均明显高于慢性胰腺炎(0 .5 1± 0 .2 3、5 .0 8± 2 .82、0 .0 6± 0 .0 3,P <0 .0 0 1) ,癌组织的PI/AI(2 1.16± 17.44 )高于慢性胰腺炎(9 .6 0± 2 .15 ,P <0 .0 5 ) ,癌组织中AI与PI呈负相关 ,随肿瘤进展 ,PI/AI值增大。结论　细胞增殖增多、细胞凋亡相对减少 ,共同促进胰腺癌的发生发展。     

Survivin表达与脑胶质瘤增殖、凋亡及血管生成的关系

Survivin是凋亡蛋白抑制因子（IAP）家族的一个新成员，具有强大的抗细胞凋亡、促有丝分裂以及促血管生成作用，并与人类多种肿瘤的形成密切相关。本研究检测了Survivin蛋白在脑胶质瘤中的表达水平，进一步分析了其与脑胶质瘤恶性增殖、凋亡以及血管生成的关系。     

胃癌组织中Survivin、C-erbB-2及Ki-67的表达及其临床意义

目的观察凋亡抑制蛋白Survivin在胃癌组织中的表达,探讨其表达与C-erbB-2、Ki- 67增殖指数的相关性及其临床意义。方法应用免疫组织化学法检测92例胃癌组织中Survivin、C-erbB-2、Ki-67的表达,分析Survivin表达与临床病理因素、预后、C-erbB-2表达及Ki-67增殖指数的关系。结果Survivin在胃癌组织中的表达率为37%,正常胃组织中未见表达。Survivin表达与胃癌细胞分化、浸润深度、淋巴结转移、TNM分期明显相关(P＜0．05),Survivin阳性表达的5年生存率(26．5%)明显低于阴性表达者(51．7%,P＜0．05)。C-erhB-2表达率为47-8%,C-erbB-2在Sur- vivin阳性表达组的表达率(76．5%)明显高于在Survivin阴性表达组(31．0%,P＜0．05),Survivin阳性表达的胃癌组织Ki-67增殖指数(43．74±19．32)%明显高于Survivin阴性表达的胃癌组织增殖指数(21．87±19．40)%(P＜0．05)。结论Survivin表达可作为判断胃癌恶性程度和预后的重要指标,与C-erbB-2表达正相关,可促进胃癌细胞增殖。     

膀胱移行细胞癌组织survivin和bcl-2的表达及其相关性

目的研究凋亡抑制基因survivin和bcl-2在膀胱移行细胞癌(BTCC)组织中的表达、对肿瘤细胞凋亡的影响及其二者的相关性,探讨survivin在BTCC发生、发展和细胞凋亡调控中的作用。方法分别采用逆转录聚合酶链反应(RT-PCR)和免疫组织化学法检测45例BTCC组织中survivinmRNA和bcl-2蛋白的表达,并采用DNA原位末端标记(TUNEL)法检测细胞凋亡指数(AI)。结果SurvivinmRNA和bcl-2蛋白在BTCC组织中的阳性表达率分别为71.11%和51.11%。Survivin的高表达与BTCC的淋巴转移密切相关(P<0.05),与病理分级有一定关系;而与患者性别、年龄、临床分期、肿瘤直径和肿瘤发生情况等均无相关性。bcl-2的表达与临床病理特征等均无相关。Survivin和bcl-2表达阳性的AI分别为(4.23±0.68)%和(4.29±0.67)%,均显著低于阴性表达(8.79±1.10)%和(8.85±1.15)%,即与细胞的AI呈负相关。相关性检验表明survivin与bcl-2表达密切相关(χ2=9.338,P<0.05)。结论Survivin在BTCC组织中的高表达提示其可能参与BTCC的发生和发展,可作为判断其预后的重要参考指标。Survivin可能与bcl-2在BTCC细胞凋亡的调控方面起着协同作用。     

胃癌组织的细胞凋亡和增殖与其临床分期的关系研究

目的探讨胃癌组织中细胞凋亡和增殖细胞核抗原的表达与胃癌临床分期的关系。方法利用脱氧核糖核酸末端转移酶介导的dUTP缺口末端标记(TUNEL)技术及增殖细胞核抗原(PCNA)免疫组织化学染色法,检测40例手术切除的胃癌标本中组织细胞的凋亡指数(AI)及增殖指数(PI),分析两者及其比例与胃癌TNM分期的关系。结果胃癌组织中细胞凋亡指数和增殖指数分别为(4.3±1.2)％和(49.8±15.9)％,凋亡/增殖比率为0.11±0.07,与癌周正常黏膜组织比较,差异有显著性意义(P<0.01);随着TNM分期的进展,胃癌细胞的凋亡指数降低,增殖指数升高,凋亡/增殖比率则逐渐下降,其差异有显著性意义(P<0.05,P<0.01)。结论细胞凋亡的减少和细胞增殖的增多与胃癌的发生发展有明显的关系,两者及其比率可作为进展期胃癌的预后监测指标之一。     

Survivin的表达与直肠癌细胞凋亡、血管形成及预后的关系

目的:探讨直肠癌凋亡抑制基因Survivin的表达、细胞凋亡及血管形成的关系及临床意义.方法:用末端脱氧核糖核酸转移酶介导的TUNEL法和免疫组织化学技术检测50例直肠癌细胞凋亡指数(AI)、Survivin的表达及微血管密度(MVD).结果:50例直肠癌组织中Survivin阳性表达率56%(28/50),其表达与AI及MVD相关,Survivin阴性表达组的5年生存率(81.3%)显著优于阳性表达组(50%;P＜0.05);Cox模型多因素分析表明,Survivin及AI指数可作为临床预后判断的指标.结论:凋亡抑制基因Survivin的异常表达与直肠癌细胞凋亡抑制、血管形成及不良预后密切有关.     

胰腺腺泡细胞凋亡和Fas/Fas配体表达在大鼠胰腺移植急性排斥反应中的作用

目的探讨大鼠胰腺移植后细胞凋亡的变化、Fas/Fas配体(FasL)的表达及其与急性排斥反应的关系。方法实验分为同基因移植组和异基因移植组。分别于术后第3、5、7天处死受体,取移植胰腺,应用原位末端标记法(TUNEL)检测细胞凋亡,计算凋亡指数(AI),应用免疫组织化学及Westernblot检测Fas/FasL的表达。结果细胞凋亡主要发生在胰腺腺泡细胞,同基因移植组有散在的腺泡细胞凋亡,AI在术后无明显变化,Fas/FasL表达阴性;异基因移植组在术后第3、5、7天胰腺腺泡细胞凋亡发生率逐渐增加(28.40±3.75,39.40±5.59,57.30±8.53,P<0.01),Fas/FasL表达逐渐增强,AI与急性排斥反应程度呈显著正相关(rs=0.932,P<0.01)。结论胰腺腺泡细胞凋亡和Fas/FasL表达在胰腺移植急性排斥反应中发挥重要作用,凋亡指数对胰腺移植急性排斥反应的诊断有一定的参考价值。     

血管紧张素Ⅱ通过抑制AKT/蛋白激酶B磷酸化诱导肾小管上皮细胞凋亡

目的观察血管紧张素Ⅱ(AngⅡ)在诱导肾小管上皮细胞凋亡的信号传导是否有磷脂酰肌醇3激酶(PI3K)-AKT信号系统的参与,及该系统在诱导细胞凋亡中的作用。方法大鼠肾小管上皮细胞株NRK-52E分别与终浓度为0(对照组)、10-9mol/L、10-8mol/L、10-7mol/L、10-5mol/LAngⅡ共培养24h。用流式细胞仪检测细胞凋亡指数,用免疫组化方法检测增殖细胞核抗原(PCNA)的表达。Western印迹检测PI3K及磷酸化AKT和总AKT蛋白表达,AKT的磷酸化水平用473位丝氨酸磷酸化AKT(AKT-ser473)水平与总AKT水平的比值表示。结果随着AngⅡ浓度的增加,10-6mol/LAngⅡ组与对照组相比,凋亡指数显著增加[(22.7±1.41)%比(3.0±0.75)%,P<0.01]。而10-9mol/LAngⅡ组与对照组相比,PCNA指数显著增强[(47.54±2.6)%比(22.63±2.5)%,P<0.01]。与对照组相比,PI3K-p85蛋白的表达随AngⅡ浓度增加表现为先激活后抑制。AKT的磷酸化具有明显的AngⅡ浓度依赖性,随AngⅡ浓度的增加而逐渐受到抑制,并与细胞凋亡指数呈显著负相关(r=-0.90,P<0.01)。结论AngⅡ可以诱导肾小管上皮细胞凋亡并抑制细胞的增殖,可能部分是通过抑制PI3K-AKT信号传导途径实现的。     

The expression and significance of dishevelled in human glioma

Background

The proto-oncogene dishevelled (Dvl) is a critical component of the Wnt/β-catenin signaling pathway, and its elevated expression in various tumor types is associated with malignancy. However, a role for Dvl in glioma has not been explored.

Materials and methods

To determine whether Dvl expression is elevated in human glioma, we examined the protein levels in 67 human glioma samples and 3 normal brain specimens by Western blotting and immunohistochemistry. To investigate a possible association of Dvl with the malignant phenotype in glioma, the correlation of the Dvl immunoreactivity score (IRS) with β-catenin IRS, the tumor proliferation index (PI), and tumor invasion index (II) were determined for each sample.

Results

The Dvl IRS, β-catenin IRS, PI, and II increased significantly with the pathologic grade of glioma (P <0.001) with average scores of 3.46 ± 3.45, 3.92 ± 3.28, 30.93 ± 17.92, and 20.43 ± 11.79, respectively. Furthermore, the PI and II were significantly higher for the Dvl-positive group than the Dvl-negative group (P <0.001). Correlation analysis demonstrated that β-catenin IRS, PI, and II were positively correlated with Dvl IRS.

Conclusions

Dvl overexpression may contribute to the malignant proliferation and invasion of human glioma.     

靶向存活素基因短发卡RNA对人脑胶质母细胞瘤U251细胞在裸鼠体内生长的影响

目的观察靶向存活素基因的特异性短发卡RNA（shRNA）对人脑胶质母细胞瘤U251细胞裸鼠体内肿瘤生长和血管形成的影响。方法将U251细胞、稳定转染存活素基因shRNA真核表达载体pWH1-SR的U251细胞（U251-SR细胞）、稳定转染空载体pWH1的U251细胞（U251-P细胞）,分别接种于15只裸鼠背部皮下,每组5只,观测肿瘤生长情况。采用免疫组化SABC方法检测存活素、增殖细胞核抗原（PCNA）以及第八因子相关抗原（FⅧRAg）在各组肿瘤标本中的表达;采用TUNEL方法检测凋亡细胞,分别计算各组肿瘤标本的增殖指数（PI）、凋亡指数（AI）以及微血管密度（MVD）。结果与U251、U251-P组相比,U251-SR组裸鼠肿瘤形成时间延迟,肿瘤生长缓慢,肿瘤体积及重量均明显减小（P均〈0.01）;肿瘤标本存活素蛋白表达明显下调;PI和MVD明显减少,AI明显升高（P均〈0．01）。结论靶向存活素基因的shRNA能够在裸鼠体内明显抑制U251细胞的肿瘤生长和血管形成。     

术前选择性动脉灌注化疗对直肠癌细胞凋亡和增殖的影响

目的　探讨术前选择性动脉灌注化疗对直肠癌细胞凋亡和增殖的影响。　方法　　对114例直肠癌患者化疗前后的肿瘤组织及 12例正常直肠粘膜 ,分别采用TUNEL法和S P法测定细胞凋亡指数 (AI)和增殖指数 (PI)。　结果　本组患者化疗前及化疗后 7～ 12d ,AI分别为 5 81‰、10 99‰ ;PI分别为 49 2 7‰、5 7 38‰ ,差异均有显著性意义 (P <0 0 1) ;高PI组患者化疗后AI的增加值显著高于低PI组 ,差异均有显著性意义 (P <0 0 1)。　结论　术前选择性动脉灌注化疗能诱导直肠癌细胞凋亡 ,对高PI的癌细胞作用更加显著 ,并且能暂时抑制癌细胞增殖 ;化疗后 7～ 12d ,癌细胞增殖速度高于化疗前 ,提示化疗后应及时进行手术。     

L-arginine impacts pulmonary vascular structure in rats with an aortocaval shunt

BACKGROUND: The present study was designed to explore the therapeutic effect of L-arginine on the proliferation and apoptosis of pulmonary artery smooth muscle cells (SMCs) in high pulmonary blood flow-induced pulmonary hypertension and therefore to provide a basis for the mechanism by which L-arginine regulated pulmonary hypertension. MATERIALS AND METHODS: Twenty-one male SD rats were randomly divided into shunting group, shunting with L-arginine group, and control group. Abdominal aorta and inferior vena cava shunting was produced in rats of the shunting group and the shunting with L-arginine group. Pulmonary artery mean pressure (mPAP) and pulmonary vascular microstructure were analyzed. Immunohistochemistry for proliferative cell nuclear antigen (PCNA) and Fas expressions and TdT-mediated dUTP-biotin nick-end labeling (TUNEL) were used to detect cell proliferation and apoptosis, respectively. RESULTS: mPAP, RV/BW, and RV/LV + S were significantly increased in shunted rats compared to normal controls (P < 0.01, respectively). Pulmonary vascular structural remodeling developed in shunted rats. Proliferative index (PI), apoptotic index (AI), and the ratio of PI/AI of pulmonary artery SMCs in the rats of shunting group were elevated obviously (P < 0.01). Meanwhile, the expressing integral score of Fas was elevated in the shunting group (P < 0.01). However, L-arginine significantly attenuated pulmonary artery pressure and ameliorated pulmonary vascular structural remodeling. Also, it reduced PI and again augmented AI of pulmonary artery SMCs. The ratio of PI/AI was significantly reduced (P < 0.01). The expressing integral score of Fas was again augmented by L-arginine (P < 0.01). CONCLUSIONS: L-Arginine could inhibit proliferation and promote apoptosis of pulmonary artery SMCs in shunted rats.     

Skeletal muscle insulin resistance in normoglycemic subjects with a strong family history of type 2 diabetes is associated with decreased insulin-stimulated insulin receptor substrate-1 tyrosine phosphorylation

Normoglycemic subjects with a strong family history of type 2 diabetes are insulin resistant, but the mechanism of insulin resistance in skeletal muscle of such individuals is unknown. The present study was undertaken to determine whether abnormalities in insulin-signaling events are present in normoglycemic, nonobese subjects with a strong family history of type 2 diabetes. Hyperinsulinemic-euglycemic clamps with percutaneous muscle biopsies were performed in eight normoglycemic relatives of type 2 diabetic patients (FH(+)) and eight control subjects who had no family history of diabetes (FH(-)), with each group matched for age, sex, body composition, and ethnicity. The FH(+) group had decreased insulin-stimulated glucose disposal (6.64 +/- 0.52 vs. 8.45 +/- 0.54 mg. kg(-1) fat-free mass. min(-1); P < 0.05 vs. FH(-)). In skeletal muscle, the FH(+) and FH(-) groups had equivalent insulin stimulation of insulin receptor tyrosine phosphorylation. In contrast, the FH(+) group had decreased insulin stimulation of insulin receptor substrate (IRS)-1 tyrosine phosphorylation (0.522 +/- 0.077 vs. 1.328 +/- 0.115 density units; P < 0.01) and association of PI 3-kinase activity with IRS-1 (0.299 +/- 0.053 vs. 0.466 +/- 0.098 activity units; P < 0.05). PI 3-kinase activity was correlated with the glucose disposal rate (r = 0.567, P = 0.02). In five subjects with sufficient biopsy material for further study, phosphorylation of Akt was 0.266 +/- 0.061 vs. 0.404 +/- 0.078 density units (P < 0.10) and glycogen synthase activity was 0.31 +/- 0.06 vs. 0.50 +/- 0.12 ng. min(-1). mg(-1) (P < 0.10) for FH(+) and FH(-) subjects, respectively. Therefore, despite normal insulin receptor phosphorylation, postreceptor signaling was reduced and was correlated with glucose disposal in muscle of individuals with a strong genetic background for type 2 diabetes.     

Survivin基因在原发性胆囊癌中的表达及其与P53,PCNA蛋白表达的关系

目的: 探讨Survivin基因在原发性胆囊癌(PGC)中的表达情况,以及与P53,PCNA蛋白表达的相互关系.方法: 逆转录聚合酶链反应(RT-PCR)法检测9例PGC新鲜癌组织Survivin mRNA表达,对38例PGC石蜡包埋组织应用免疫组织化学法检测Survivin,P53和PCNA蛋白的表达,并将结果进行相关分析.结果: 9例PGC新鲜癌组织中3例有Survivin mRNA表达.21例(55.2%)PGC Survivin蛋白表达阳性,而12例胆囊腺瘤中有2例表达,20例癌旁正常组织中则无表达.PGC Survivin蛋白表达阳性率显著高于胆囊良性病变和正常胆囊组织(P<0.01).Survivin蛋白在PGC中的表达与PCNA指数相关,与P53蛋白表达、PGC病理分级和Neiv分期无显著相关.结论: Survivin基因在PGC中存在高表达,Survivin基因表达上调通过不同的机制影响PGC细胞的凋亡和增殖,在PGC发生、发展过程中起作用.     

Can clinical factors estimate insulin resistance in type 1 diabetes?

An insulin resistance syndrome (IRS) score was developed based on clinical risk factors in adults with childhood-onset type 1 diabetes in the Epidemiology of Diabetes Complications (EDC) Study and was validated using euglycemic-hyperinsulinemic clamp studies. Hypertension, waist-to-hip ratio (WHR), triglyceride and HDL cholesterol levels, family history of type 2 diabetes, and glycemic control were risk factors used to define the score. A score of 1 (lowest likelihood IRS) to 3 (highest likelihood IRS) was assigned for each risk factor. Eligible subjects (n = 24) were recruited from the EDC cohort based on tertile of IRS score. Subjects received an overnight insulin infusion to normalize glucose levels, then underwent a 3-h euglycemic-hyperinsulinemic (60 mU x m(-2) x min(-1)) clamp. Glucose disposal rate (GDR) was determined during the last 30 min of the clamp. The GDR differed significantly by IRS group (9.65 +/- 2.99, 8.02 +/- 1.39, and 5.68 +/- 2.16 mg x kg(-1) x min(-1), P < 0.01). The GDR was inversely correlated with the IRS score (r = -0.64, P < 0.01). Using linear regression, the combination of risk factors that yielded the highest adjusted r2 value (0.57, P < 0.001) were WHR, hypertension, and HbA1. This study found that clinical risk factors can be used to identify subjects with type 1 diabetes who are insulin resistant, and it provides validation of a score based on clinical factors to determine the extent of insulin resistance in type 1 diabetes. This score will be applied to the entire EDC population in future studies to determine the effect of insulin resistance on complications.     

发育性髋关节脱位闭合复位后髋臼发育的研究

目的 通过回顾性研究,观察闭合复位治疗发育性髋关节脱位的临床疗效,动态分析闭合复位后髋臼发育的特点.方法 2002年1月-2005年12月,采用闭合复位治疗100例单侧发育性髋关节脱位患儿.男18例,女82例;年龄7～36个月,平均19.4个月.左侧68例,右侧32例.髋关节脱位按Zionts等方法分度,Ⅰ度15例,Ⅱ度50例,Ⅲ度26例,Ⅳ度9例.治疗时行内收肌切断与牵引74例,直接闭合复位26例.按四级功能评价标准判定临床疗效;于复位前、复位后第3、6、9和12个月动态测量患、健侧髋关节的髋臼指数(acetabular index,AI)和髋臼深度与宽度比值[acetabular index of depth to width,AI(D/W)],并进行相关比较.结果 治疗12个月功能恢复总优良率达88.00%.复位后12个月,患侧AI由治疗前(37.17±2.17).下降至(27.02 ±3.54).,AI(D/W)由22.06%±1.65%增长至29.80%±3.56%,各时间点比较差异均有统计学意义(P<0.01);患侧AI下降幅度、AI(D/W)增长幅度明显快于健侧(P<0.01).复位后1～3个月、10～12个月AI分别为(3.22±1.42).和(3.41±2.03). 9 AI(D/W)分别为2.69%±1.83%和2.33%±1.13%,明显快于其他时间段(P<0.01);各时间段患侧AI下降幅度、AI(D/W)增长幅度均明显快于同期健侧(P<0.01).复位后12个月,7～12月龄、13～18月龄A1分别为(13.71±396).和(11.48±4.15).,AI(D/W)分别为9.95%±3.81%和8.28%±3.58%,明显快于其他年龄段患儿(P<0.05);各年龄段患侧AJ、AI(D/W)变化速度均明显快于健侧(P<0.01).结论 闭合复位治疗发育性髋关节脱位操作简便,治疗效果良好,在治疗后12个月内,患侧髋臼发育速度明显快于健侧;患侧髋臼的发育高峰期在复位后1～3个月和10～12个月;患儿年龄<18个月为闭合复位治疗发育性髋关节脱位的最佳时期.     

细胞膜磷脂变化与大肠癌发生及肝转移关系的研究

目的　探讨大肠癌原发灶、癌旁肠粘膜及肝转移灶组织中细胞膜磷脂的变化 ,研究细胞膜磷脂代谢及其信号转导途径与大肠癌发生及肝转移的关系。　方法　采用高效液相色谱法 ,检测 48例大肠癌原发灶、癌旁肠粘膜、肝转移灶中细胞膜磷脂酰肌醇 (PI)、磷脂酰丝氨酸 (PS)、磷脂酰乙醇胺 (PE)和磷脂酰胆碱 (PC) ,对比分析不同膜磷脂组分含量变化。　结果　 48例大肠癌患者癌旁肠粘膜、原发灶、肝转移组织中细胞不同膜磷脂含量 (mg/g) ,PI为 :0 92± 0 12、1 5 7± 0 14、1 5 4±0 15 ;PC含量为 :5 6 47± 5 33、10 8 5 7± 6 37、116 35± 6 85。原发灶和肝转移组织中PI、PC含量高于癌旁粘膜组织 (F =36 3 10 ,870 10 ,P <0 0 1)。 3种组织中PE(mg/g)含量分别为 :18 2 3± 3 5 6、42 0 2± 4 33、79 5 1± 5 5 2 ,肝转移组织中PE含量显著高于原发灶和癌旁组织 (F =1149 6 3,P <0 0 1)。肝转移组与无肝转移组癌原发灶中PI、PS、PC含量差异无显著性意义 (t=3 5 5 ,P >0 0 5 )。但肝转移组中转移灶PE含量显著增高 (t=115 87,P <0 0 1)。　结论　大肠癌发生及肝转移过程中细胞膜磷脂有明显变化 ,PI、PC增高与大肠癌发生有关 ,PE增高与癌细胞浸润、肝转移发生有关