环氧合酶2特异性抑制剂Celecoxib治疗强直性脊柱炎的疗效观察

Celecoxib是一种环氧合酶2(COX-2)特异性抑制剂,临床试验证实可用以改善骨关节炎和风湿性关节炎患者的症状、体征。作者研究评估Celecoxib治疗强直性脊柱炎(AS)的短期疗效。     

人肝癌细胞中COX-2与MDR/P-gp表达相关性研究

观察人肝癌细胞中特异性环氧合酶-2(Cyclooxygenase-2,COX-2)与MDR／P—gp表达变化,探讨二者在Celecoxib诱导细胞凋亡中的意义。采用免疫组化法、流式细胞技术以及RT-PCR观察Celecoxib诱导肝癌细胞凋亡过程中COX-2与MDR／P—gP表达的变化。Celecoxib诱导肝癌细胞呈时间、剂量依赖性;细胞周期分布改变,G0／G1期细胞比例增加;COX-2与MDR／P—gp表达减弱,但非线性相关。Celecoxib可能通过降低COX-2、MDR／P—gp表达,影响细胞周期分布,发挥抗肿瘤作用。     

塞来昔布对人淋巴瘤细胞株Raji增殖、凋亡及存活素表达的影响

目的观察选择性COX-2抑制剂塞米昔布(Celecoxib)对Raji细胞增殖、凋亡及细胞周期分布的影响,并检测存活素(Survivin)在细胞中的表达情况。方法应用流式细胞术(FCM)分析Celecoxib对人Burkitt淋巴瘤Raji细胞周期的影响并检测细胞凋亡及存活素在细胞中的表达情况,应用RT-PCR法检测细胞中SurvivinmRNA的表达水平。结果 Celecoxib各浓度组作用于Raji细胞24、48、72h后吸光度值与对照组相比均有显著性差异(P0.05),同时各浓度组之间以及时间组之间有显著性差异(P0.05)。Celecoxib各浓度组作用于Raji细胞48h后各浓度组间Cele-coxib对细胞凋亡率和细胞周期的影响、下调Survivin蛋白表达下调SurvivinmRNA相对表达量具有显著性差异(P0.05)。结论 Celecoxib能够通过诱导凋亡抑制Raji细胞的增殖,其机制可能与抑制Survivin表达有关。     

Celecoxib对胃癌细胞凋亡的影响

目的:研究选择性环氧合酶-2(COX-2)抑制剂Celecoxib对人胃癌细胞株SGC7901凋亡的影响.方法:采用MTT法测定人胃癌细胞株SGC7901分别在1×10-5,1×10-6,1×10-7,1×10-8,1×10-9mol/L的Celecoxib作用48h后生长抑制情况;流式细胞术(FCM)观察Celecoxib对SGC7901细胞凋亡的影响;采用免疫细胞化学染色观察Survivin的表达.结果:Celecoxib浓度为1×10-5-1×10-9mol/L时,对SGC7901细胞的生长均有抑制作用,以1×10-5mol/L浓度的抑制作用最为显著,其抑制率为30.03%;1×10-5mol/LCelecoxib作用12,24,48h后,细胞凋亡比例较对照组均明显增加,48h凋亡率达17.83%;1×10-5mol/LCelecoxib作用后,Survivin的表达自用药3h起下降,24h最明显.结论:Celecoxib可诱导SGC7901细胞的凋亡,其可能的作用机制为抑制细胞Survivin基因的表达.     

MK886和Celecoxib抑制胰腺癌SW1990细胞生长及血管生成的实验研究

目的 观察5-脂氧合酶拮抗剂MK886、环氧化酶2拮抗剂Celeeoxib干预SW1990细胞后对细胞增殖及血管内皮生长因子(VEGF)mRNA表达的影响.方法 应用不同浓度的MK886、Celecoxib 以及两者联合处理SW1990细胞,采用胆囊收缩素(CCK-8)法检测细胞的增殖,RT-PCR法检测细胞白三烯B4受体1(BLT1) mRNA、前列腺素2(PGE2) mRNA、VEGF mRNA的表达.结果 10μmol/LMK886或20 mmol/L Celecoxib处理24h后,SW1990细胞的增殖受到明显抑制(1.80±0.06比1.65±0.10;2.04 ±0.03比1.86 ±0.02,P＜0.05),且随药物浓度的增加,细胞的增殖抑制更明显.两拮抗剂联合干预12h后,SW1990细胞的增殖即受到非常明显的抑制(1.72±0.05比1.52±0.05,P＜0.01).Celecoxib处理细胞48 h后,细胞BLT1、VEGF mRNA表达与对照组比较无明显变化,但PGE2 mRNA的表达明显减少(37.50比71.50,P＜0.05);MK886或MK886+ Celecoxib联合处理细胞后,细胞BLT1、VEGF mRNA表达明显减少(40.30、22.75比126.50,P＜0.05),而PGE2 mRNA的表达与对照组比较无明显变化.结论 花生四烯酸的两条代谢途径均与胰腺癌的发生及增殖有密切关系,同时抑制两条途径可显著抑制胰腺癌细胞的增殖.     

环氧合酶-2在非酒精性脂肪肝中的表达及其致病的可能机制

环氧合酶-2(COX-2)的过度表达与许多炎症性疾病有关,然而对它在非酒精性脂肪肝(NAFLD)中的表达和作用机制知之甚少.Celecoxib是特异性的COX-2抑制剂[1].我们通过建立大鼠NAFLD动物模型,同时在模型组中给予celecoxib进行干预治疗,研究COX-2在NAFLD中的作用,以便进一步探讨其在NAFLD中的致病机制.     

Celecoxib诱导SKOV3细胞株凋亡的机制探讨

目的探讨塞米昔布（Celecoxib）是否通过抑制Survivin表达来诱导人卵巢浆液性乳头状囊腺癌（SKOV3）细胞株的凋亡。方法选择SKOV3细胞株分成4组：对照组、Celecoxib组、转染空质粒组和Survivin转染组。各组细胞应用流式细胞仪检测细胞的凋亡率，应用Western印迹方法检测Survivin蛋白的表达。结果应用Celecoxib处理后，SKOV3细胞株的凋亡率上升，而Survivin蛋白表达明显下降，与对照组相比，差异具有显著性（P〈O．05）。转染了Survivin基因后，Survivin蛋白表达上调，而凋亡率明显下降，与Celecoxib组及转染空质粒组相比，差异具有显著性（P〈0．05）。结论Celecoxib可以诱导SKOV3细胞株的凋亡，这种凋亡是通过抑制Survivin蛋白的表达来实现的。     

Celecoxib对急性胰腺炎相关性肺损伤ICAM-1表达的影响

目的探讨Celecoxib对急性胰腺炎相关性肺损伤细胞间黏附分子1（ICAM-1）表达的影响。方法逆行胰胆管注射4%牛磺胆酸钠诱导SD大鼠急性出血坏死性胰腺炎模型（AHNP）。实验随机分为假手术组、AHNP组及Celecoxib预处理组,动态观察3、6和12 h肺组织中丙二醛（MDA）和髓过氧化物酶（MPO）含量,免疫组化检测ICAM-1蛋白表达。结果AHNP组肺组织MDA和MPO含量进行性增加,Celecoxib在各时间点均显著降低了AH-NP大鼠肺组织MPO活性及MDA水平（P〈0.05）;AHNP组ICAM-1表达上调,主要表达于血管内皮细胞,Celecoxib处理后表达显著下调（P〈0.05）。结论Celecoxib抑制ICAM-1的表达,可能是其减轻AHNP大鼠肺组织炎性损伤的重要环节之一。     

Celecoxib inhibits proliferation and induces apoptosis via prostaglandin E2 pathway in human cholangiocarcinoma cell lines

AIM: To evaluate the roles and mechanisms of celecoxib in inducing proliferation inhibition and apoptosis of human cholangiocarcinoma cell lines. METHODS: Cyclooxygenase-2-overexpressing human cholangiocarcinoma cell line QBC939 and cyclooxygenase2-deficient human cholangiocarcinoma cell line SK-CHA-1were used in the present study. The anti-proliferative effect was measured by methabenzthiazuron (MTT) assay;apoptosis was determined by transferase-mediated dUTP nick end labeling (TUNEL) detection and transmission electron microscopy (TEN). Cell cycle was analyzed by flow cytometry (FCM). The PGE2 levels in the supernatant of cultured cholangiocarcinoma cells were quantitated by enzyme-linked immunoabsordent assay (ELISA). RESULTS: Celecoxib suppressed the production of PGE2and inhibited the growth of QBC939 cells. Celecoxib at 10,20, and 40 μmol/L inhibited PGE2 production by 26 %,58 %, and 74 % in QBC939 cells. The PGE2 level was much lower constitutively in SK-CHA-1 cells (18.6±3.2)compared with that in QBC939 (121.9±5.6) cells (P＜0.01)and celecoxib had no significant influence on PGE2 level in the SK-CHA-1 cells. The PGE2 concentration in SK-CHA-1cells also reduced but not significantly after treatment with celecoxib. The PGE2 concentration in SK-CHA-1 cells was (16.5±2.9) ng/well, (14.8±3.4) ng/well, (13.2±2.0) ng/well and (12.6±3.1) ng/well respectively, when pre-treated with 1 Jmol/L, 10 Jmol/L, 20 Jmol/L and 40 Jmol/L of celecoxib for 48 h (P＞0.05, vs control). The anti-proliferation effect of celecoxib (20 Jmol/L) on QBC939 cells was time-dependent,it was noticeable on day 2 (OD490=0.23±0.04) and became obvious on day 3 (OD490=0.31±0.07) to day 4 (OD490=0.25±0.06), and the OD490 in the control group (day 1)was 0.12±0.03 (P＜0.01, vscontrol). The anti-proliferation effect of celecoxib could be abolished by the addition of 200 pg/mL PGE2. The proliferation of SK-CHA-1 cells was inhibited slightly by celecoxib, the cell density OD490 in the presence of celecoxib and in control group was 0.31±0.04 and 0.42±0.03 respectively on day 2 (P＞0.05), 0.58±0.07 and 0.67±0.09 respectively on day 3 (P＞0.05), and 0.71±0.08 and 0.78±0.06 respectively on day 4 (P＞0.05). Celecoxib induced proliferation inhibition and apoptosis by G1-S cell cycle arrest: the percentage of QBC939 cells in G0-G1 phase after treatment with 40 Jmol/L (74.66±6.21) and 20 Jmol/L (68.63±4.36) celecoxib increased significantly compared with control cells (54.41±5.12, P＜0.01). The percentage of SK-CHA-1 cells in G0-G1 phase after treatment with various concentrations of celecoxib didn't change significantly compared with control cells. The TUNEL index was much higher in QBC939 cells treated with 20 Jmol/L celecoxib for 2 d (0.063±0.018) and for 4 d (0.102±0.037) compared with control cells (0.017±0.004, P＜0.01). CONCLUSION: The currentin vitro study indicates that inhibition of proliferation and induction of apoptosis in human cholangiocarcinoma cells by cyclooxygenase-2 specific inhibitor celecoxib may involve in COX-dependent mechanisms and PGE2 pathway. Celecoxib as a chemopreventive and chemotherapeutic agent might be effective primarily on COX2-expressing cholangiocarcinoma.     

广西原发性肝癌抗血管生成治疗机制及围手术期肝功能评估研究

目的探讨广西原发性肝癌抗血管生成治疗机制和评估围手术期肝功能。方法通过体外分子生物学实验、体内动物实验、耐药实验结合肝癌患者生存资料进行分析;通过观察104例肝癌患者声脉冲辐射力成像(acoustic radiation force impulse,ARFI)评分与术后标准残肝体积(SRLV)进行直线回归分析;检测术前尿8-羟基脱氧鸟苷(8-OHd G)及外周血T淋巴细胞亚群CD4+、CD8+表达。结果 COX-2/PGE2信号通路可调控肝癌中血管内皮生长因子(VEGF)的上游靶点蛋白缺氧诱导因子2α(HIF-2α)的活性;PEG-SS-PLL有效地转染si VEGF,其细胞毒性可忽略不计,且在体外和体内均显著降低了VEGF在mRNA和蛋白水平的表达,抑制了肿瘤生长;重度代偿不全的SRLV的临界值为503 ml/m2。术前ARFI评分及术后SRLV进行直线回归方程为SRLV(ml/m2)=149.6×ARFI评分(m/s)+194.1。术前尿8-OHd G水平显著高于对照组[(16.15±4.96)ng/mg Cr vs(12.13±4.66)ng/mg Cr]。结论 COX-2/PGE2通路的特异性抑制剂Meloxicam或Celecoxib可明显增强肝癌分子靶向药物索拉菲尼的药物敏感性,PEG-SS-PLL/si VEGF可能被应用于肝细胞癌的抗血管生成基因治疗;联合SRLV及肝纤维化程度测定对原发性肝癌术前安全切肝量评估有重要指导价值,对伴中、重度肝纤维化病例安全SRLV临界值为503 ml/m2;尿8-OHd G在肝癌诊治及疗效评价中有较高应用价值。     

Overexpression of cyclooxygenase-2 in human HepG2, Bel-7402 and SMMC-7721 hepatoma cell lines and mechanism of cyclooxygenase-2 selective inhibitor celecoxib-induced cell growth inhibition and apoptosis

AIM: To investigate the cyclooxygenase-2 (COX-2) expression level in human HepG2, Bel-7402 and SMMC-7721 hepatoma cell lines and the molecular mechanism of COX-2 selective inhibitor celecoxib-induced cell growth inhibition and cell apoptosis. METHODS: Hepatoma cells were cultured and treated with celecoxib. Cell In situ hybridization (ISH) and immunocytochemistry were used to detect COX-2 mRNA and protein expression. Proliferating cell nuclear antigen and phosphorylated Akt were also detected by immunocytochemistry assay. Cell growth rates were assessed by 3-(4, 5-dimethylthiazol-2-yl-2, 5-diphenylte-trazolium (MTT) bromide colorimetric assay. Celecoxib-induced cell apoptosis was measured by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and flow cytometry (FCM). The phosphorylated Akt and activated fragments of caspase-9, caspase-3 were examined by Western blotting analysis. RESULTS: Increased COX-2 mRNA and protein expression were detected in all three hepatoma cell lines. Celecoxib could significantly inhibit cell growth and the inhibitory effect was in a dose- and time-dependent manner evidenced by MTT assays and morphological changes. The apoptotic index measured by TUNEL increased correspondingly with the increased concentration of celecoxib and the reaction time. With 50 μmol/L celecoxib treatment for 24 h, the apoptotic index of HepG2, BEL-7402 and SMMC-7721 cells was 25.01±3.08%, 26.40±3.05%, and 30.60±2.89%, respectively. Western blotting analysis showed remarkable activation of caspase-9, caspase-3 and dephosphorylation of Akt (Thr308). Immunocytochemistry also showed the reduction of PCNA expression and phosphorylation Akt (Thr308) after treatment with celecoxib. CONCLUSION: COX-2 mRNA and protein overexpression in HepG2, Bel-7402 and SMMC-7721 cell lines correlate with the increased cell growth rate. Celecoxib can inhibit proliferation and induce apoptosis of hepatoma cell strains in a dose- and time-dependent manner.     

特异性环氧合酶-2抑制剂预防胃癌的实验研究

目的 探讨特异性环氧合酶(COX)-2抑制剂塞来昔布(Celecoxib)对化学致癌剂(N-甲基-N′-硝基-亚硝基胍，MNNG)诱导的胃癌发生的影响。方法 86只二级雄性Wistar大鼠分为A、B、C、D、E、F共6组。A组(5只)：自由饮用蒸馏水不作特殊处理；B组(16只)：仅饮用含MNNG 100μg/ml的蒸馏水；C组(16只)：每天给予吲哚美辛3mg／kg；D组(17只)：每天给予塞来昔布5mg／kg；E组(16只)：每天给予塞来昔布10mg／kg；F组(16只)：每天给予塞来昔布20mg／kg。B～F组动物给予10％氯化钠(实验初6周)和饮水中加用MNNG(10μg／ml)，以诱导胃癌，持续40周，第48周时处死动物。观察、比较各组动物大体及组织学变化。结果 86只大鼠实验期间自然死亡26只(30％)，余60只完成实验研究。A、B、C、D、E、F组动物胃癌发生率分别为0％(0／5)、75．0％(12／16)、68．8％(11／16)、70．6％(12／17)、18．8％(3／16)和31．3％(5／16)。各组动物胃癌发生率(P=0．002)、多发数目(P=0．001)、肿瘤体积(P=0．009)差异有显著性。与B组相比，E组胃癌发生率(P=0．004)、多发数目(P=0．006)和肿瘤体积(P=0．02)显著降低。C组与B组相比差异无显著性。结论本研究提示塞来昔布对MNNG诱导的大鼠胃癌有预防作用，而吲哚美辛未见此效果。     

Celecoxib-induced gastrointestinal,liver and brain lesions in rats,counteraction by BPC 157 or L-arginine,aggravation by L-NAME

AIM To counteract/reveal celecoxib-induced toxicity and NO system involvement. METHODS Celecoxib(1 g/kg b.w. ip) was combined with therapy with stable gastric pentadecapeptide BPC 157(known to inhibit these lesions, 10 μg/kg, 10 ng/kg, or 1 ng/kg ip) and L-arginine(100 mg/kg ip), as well as NOS blockade [N(G)-nitro-L-arginine methyl ester(L-NAME)](5 mg/kg ip) given alone and/or combined immediately after celecoxib. Gastrointestinal, liver, and brain lesions and liver enzyme serum values in rats were assessed at 24 h and 48 h thereafter. RESULTS This high-dose celecoxib administration, as a result of NO system dysfunction, led to gastric, liver, and brain lesions and increased liver enzyme serum values. The L-NAME-induced aggravation of the lesions was notable for gastric lesions, while in liver and brain lesions the beneficial effect of L-arginine was blunted. L-arginine counteracted gastric, liver and brain lesions. These findings support the NO system mechanism(s), both NO system agonization(L-arginine) and NO system antagonization(L-NAME), that on the whole are behind all of these COX phenomena. An even more complete antagonization was identified with BPC 157(at both 24 h and 48 h). A beneficial effect was evident on all the increasingly negative effects of celecoxib and L-NAME application and in all the BPC 157 groups(L-arginine + BPC 157; L-NAME + BPC 157; L-NAME + L-arginine + BPC 157). Thus, these findings demonstrated that BPC 157 may equally counteract both COX-2 inhibition(counteracting the noxious effects of celecoxib on all lesions) and additional NOS blockade(equally counteracting the noxious effects of celecoxib + L-NAME). CONCLUSION BPC 157 and L-arginine alleviate gastrointestinal, liver and brain lesions, redressing NSAIDs' post-surgery application and NO system involvement.     

COX-2抑制剂联合survivin反义寡核苷酸抗胰腺癌BxPC-3细胞的效应

目的:探讨COX-2抑制剂和survivin反义寡核苷酸联合应用对胰腺癌BxPC-3细胞的抗肿瘤效应及其可能机制.方法:应用胰腺癌BxPC-3细胞进行研究,将BxPC-3细胞分为4组:A组(对照组),B组(Celecoxib 80μmol/L)组,C组(300 nmol/L survivin ASODN),D组(80μmol/L celecoxib 300 nmol/L survivin ASODN).采用MTT检测细胞增殖.流式细胞仪检测细胞凋亡率,caspase-3试剂盒检测caspase-3活性,并用RT-PCR检测Bcl-2、survivin和Mcl-1的mRNA国的变化.结果:将80μmol/L celecoxib和300 nmol/L survivin反义寡核苷酸单独或联合作用于胰腺癌BxPC-3细胞24h和48h,D组细胞的存活率明显低于B,C组(24h:41.0%±0.4% vs 71.0%±2.2%,63.3%±4.5%;48h:34.2%±1.1% vs 61.6%±1.7%,55.0%±3%;P<0.01).作用24h后,流式细胞仪检测细胞凋亡率显示,D组细胞的凋亡率明显高于B,C组(30.33%±3.49% vs 11.93%±1.17%,22.07%±0.93%;P<0.01).caspase-3活性在B,C,D组明显高于对照组(0.04867±0.0021,0.02967±0.0021,0.08767±0.0042 vs 0.007±0.0001;P<0.01),D组细胞的caspase-3活性明显高于B,C组(0.08767±0.0042 vs 0.04867±0.0021,0.02967±0.0021;P<0.01).用100μmol/L塞来昔布作用于胰腺癌BxPC-3细胞24h后,survivin/β-actin和Mcl-1/β-actin的mRNA的比值明显低于对照组(0.68±0.05 vs 1.05±0.06,P<0.01),而Bcl-2/β-actin的mRNA的比值无明显变化(0.99±0.02 vs 1.07±0.06,P>0.05).结论:联合应用COX-2抑制剂塞来昔布和survivin反义寡核苷酸可明显诱导胰腺癌细胞的凋亡,抑制细胞增殖,并能够明显提高caspase-3活性.COX-2抑制剂塞来昔布诱导细胞凋亡可能通过survivin和Mcl-1途径,而非Bcl-2途径.     

载体介导的猪瘟病毒囊膜蛋白疫苗的研制现状

猪瘟病毒(CSFV)是一种常见的猪场感染病毒,常引起猪瘟,其防治疫苗研制备受关注。囊膜蛋白是一种有效的疫苗候选分子,本文综述伪狂犬病毒(rPRV-E2)、鸡痘病毒(rFPV-E0/E2)、Semliki森林病毒(rSFV-E2)、水疱性口炎病毒(rVSV-E2)、猪痘病毒(rSPV-E2)、腺病毒(rAdV-E2)、牛痘病毒(rVV-E2)、猪繁殖和呼吸综合征病毒(rPRRSV-E2)、杆状病毒(rBuV-E2)、猪霍乱沙门氏菌(rSc-E2)、鼠伤寒沙门氏菌(rSt-E2)、干酪乳杆菌(rLc-VP2-E290/E2-Tα1)、根癌农杆菌(rAt-E2)和酵母(rPP-E2)等载体介导的CSFV囊膜蛋白疫苗的构建及其免疫机制等方面研制现状。     

醛糖还原酶基因5’端(AC)n多态性对2型糖尿病患者红细胞醛糖还原酶活性的影响

目的　探讨醛糖还原酶 (AR)基因 5’端 (AC) n 的多态性对 2型糖尿病 (DM )红细胞AR活性的影响。方法　 16 3例 2型DM分为无微血管病变 (NDC)组 (6 6例 )和微血管病变 (DMAP)组(97例 ) ,正常对照 (CON)组 42例 ;另按AR基因 5’端 (AC) n 的等位基因类型分为DM携带Z 2等位基因 (DZ 2 )组 (5 4例 )、DM携带Z - 2等位基因 (DZ - 2 )组 (35例 )、DM同时携带Z 2和Z - 2等位基因 (Z 2 /Z - 2 )组 (18例 )、DM不携带Z 2和Z - 2等位基因 (X/X)组 (5 6例 )、对照者携带Z 2等位基因 (NZ 2 )组 (2 1例 )和对照者携带Z - 2等位基因 (NZ - 2 )组 (7例 )。用改良Sriratava法测定AR活性并比较其在各组间的差异。结果　DMAP组、NDC组和CON组间的AR活性 (ARA)差异有显著性 ,DMAP组最高 ,NDC组次之 ,CON组最低 (P <0 .0 0 1)。DM组携带Z - 2和Z 2等位基因各亚组中 ,DZ - 2组ARA最高 ,Z - 2 /Z 2和X/X组居中 ,DZ 2组最低 ,差异有显著性统计学意义(P <0 .0 0 1)。DZ - 2和NZ - 2组的ARA分别高于DZ 2和NZ 2组 ,DZ - 2和DZ 2组的ARA分别高于NZ - 2和NZ 2组 (P均 <0 .0 0 1)。结论　AR的激活对DMAP的发生和发展起重要作用。Z - 2等位基因可能是AR的激活因子 ,Z 2等位基因则为其抑制因子。     

老年人原发性肝癌的诊治

目的　进一步总结老年人原发性肝癌的特点和治疗经验。方法　对 1 2 5例 60岁以上老年原发性肝癌患者与 2 95例非老年原发性肝癌患者的临床资料进行回顾性分析。结果　老年组和非老年组中各项指标分别为 :HBsAg阳性率 51 .2 % (64 1 2 5)和 67.8% (2 0 0 2 95) ;小肝癌 (肿瘤直径 <5cm) 31 .2 % (39 1 2 5)和 2 6 .8% (79 2 95) ;大肝癌 (直径在 5～ 1 0cm) 4 9.6 % (62 1 2 5)和 40 .3 % (1 1 9 2 95) ;巨大肝癌 (肿瘤直径 >1 0cm) 1 9.2 % (2 4 1 2 5)和 32 .9% (97 2 95) ;伴有门静脉癌栓 1 2 .0 % (1 5 1 2 5)和 32 .5 % (96 2 95) ;术前血清甲胎蛋白 (AFP)阳性率 68.8%(86 1 2 5)和 67.8% (2 0 0 2 95) ;术前肝功能Child分级A级 52 % (65 1 2 5)和 63 .7% (1 88 2 95) ,B级 2 2 .4% (2 8 1 2 5)和 2 4 .7% (73 2 95) ,C级 2 5 .6 % (32 1 2 5)和 1 1 .6 % (34 2 95) ;手术切除率 2 7.2 % (34 1 2 5)和 42 .7% (1 2 6 2 95) ;中位生存时间为 44个月和 2 5个月。结论　老年组与非老年组术后生存率无明显差异 ;年龄并非手术禁忌证 ;以手术为主综合治疗同样是老年患者的重要治疗手段 ;老年组手术并发症并无升高 ;AFP结合腹部B超是早期诊断的主要方法。     

慢性阻塞性肺疾病患者动脉二氧化碳分压的相关因素分析

目的　评价慢性阻塞性肺疾病 (COPD)患者动脉二氧化碳分压 [Pa(CO2 ) ]与肺功能指标的多重相关关系及吸入支气管扩张剂后的影响。方法　 91例COPD患者随机分为 3组 ,测定Pa(CO2 )、第 1秒时间肺活量(FEV1)、呼出气平均CO2 分压 [Pe(CO2 ) ]、功能残气量 (FRC)、潮气量 (VT) ;分别吸入不同的支气管扩张剂后 ,重复上述测定。结果　用药前Pa(CO2 )与Pe(CO2 )、潮气量 (VT)呈显著负相关。Pa(CO2 )与Pe(CO2 )、FEV1、功能残气量 (FRC)呈显著负相关。用药后 ,这种关系依然存在 ,且Pa(CO2 )在各组均出现下降 (P均 <0 0 5 ) ,在溴化异丙托品组 ,Pa(CO2 )的改变值与FRC的改变值显著呈正相关 ,在联合吸入组 ,Pa(CO2 )的改变值与VD/VT的改变值呈显著正相关。结论　COPD患者Pa(CO2 )与Pe(CO2 )、VT呈显著负相关 ,Pa(CO2 )与Pe(CO2 )、FEV1、FRC呈显著负相关。在吸入支气管扩张剂后 ,依然存在这种关系且使Pa(CO2 )下降 ,但不同的药物影响机制不同