脂多糖对核转录因子-κB的激活在人肺非小细胞肺癌获得性耐药细胞中的作用

目的 本研究旨在通过检测脂多糖(lipopolysaccharide ,LPS)作用后人非小细胞肺癌耐药株细胞内核转录因子(nuclear factor-κB,NF)-κB p65表达量的变化,探讨LPS作用下NF-κB表达量的增高与吉非替尼获得性耐药产生的相关性.方法 成功诱导非小细胞肺癌细胞株HCC827对吉非替尼产生稳定的获得性耐药后,按设置的分组用LPS及吉非替尼处理细胞,采用CCK-8法检测处理后吉非替尼对细胞的半数抑制浓度(IC50值),并与各自对照组相比较.细胞增殖曲线显示LPS作用对细胞增殖的影响.采用克隆形成实验显示LPS作用后对细胞增殖的影响.采用蛋白质印迹法检测LPS及吉非替尼处理后耐药株HCC827/GR-8-1细胞中凋亡相关蛋白caspase-3、Bcl-2等蛋白的表达量,并检测NF-κB蛋白的表达量,探讨LPS作用后激活的NF-κB对细胞吉非替尼敏感性的调节.结果 LPS处理后,可以显著降低耐药细胞对吉非替尼的敏感性,细胞克隆形成实验及增殖曲线显示LPS并无明显促进细胞的增殖作用,但可以降低细胞对吉非替尼的敏感性.蛋白质免疫印迹结果显示,与对照组相比较,LPS可抑制Caspase-3等相关促凋亡蛋白的表达,而相应凋亡抑制蛋白Bcl-2的表达上升.LPS处理48 h后NF-κB的表达量显著上调.LPS通过调节NF-κB表达量上升而参与细胞耐药机制的产生.结论 经LPS作用后的非小细胞肺癌细胞对吉非替尼敏感性降低,LPS处理后细胞的NF-κB表达量显著增高,增高的NF-κB表达量与细胞对吉非替尼的药物敏感性下降相关.     

全程个体化心理干预对脾切除术患者围术期焦虑抑郁影响的研究

目的分析全程个体化的心理干预对脾脏切除患者术前术后焦虑抑郁的影响。方法将95例拟行脾脏切除术患者随机分为对照组(45例)和实验组(50例),对照组接受常规护理,实验组接受全程个体化心理干预,用焦虑自评量表(SAS)和抑郁自评量表(SDS)评定比较患者在确定手术之日(术前4~5 d)、术前1 d、术后第4天的心理状态。结果实验组的SAS和SDS评分均较对照组低,2组术前1 d及术后第4天的评分比较有显著性差异(P<0.05)。结论全程个体化心理干预可显著改善脾脏切除患者围术期的焦虑抑郁情绪。     

亚甲基四氢叶酸还原酶基因多态和叶酸摄取与乳腺癌的发病风险

Objective To evaluate the relationship between dietary folate intake and genetic polymorphisms of 5, 10-methylenetetrahydrofolate reductase (MTHFR) with reference to breast cancer risk. Methods A case-control study was conducted with 669 cases and 682 population-based controls in Jiangsu province of China. MTHFR C677T and AI298C genotypes were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods. Dietary folate intake was assessed by using an 83-item food frequency questionnaire. Odds ratios (OR) were estimated with an unconditional logistic model. Results The frequencies of MTHFR C677T C/C, C/T and T/T genotypes were 32. 37% (202/624), 48. 88% (3051624) and 18. 75% (117/624) in cases and 37. 66% (235/624), 48.24% (301/624) and 14. 10% (88/624) in controls,respectively. The difference in distribution was significant (X2=6. 616, P=0. 037), the T/T genotype being associated with an elevated OR for breast cancer (1.62, 95% CI: 1.14 -2. 30). The frequencies of MTHFR A1298C A/A,A/C and C/C were 71.47% (446/624), 27.08% (169/624) and 1.44% (9/624) in cases and 68. 11% (425/624) ,30. 13% (188/624) and 1.76% (11/624) in controls, with no significant differences found (X2=1.716, P=0. 424). Folate intake of cases [(263.00±137. 38)μg/d]was significantly lower than that of controls [(285. 12±149. 61)μg/d](t=-2. 830,P=0. 005). Compared with the lowest tertile (≤199. 08μg/d) of folate intake,the adjusted OR for breast cancer in the top tertile (≥315.μg/d) was 0. 70 (95% CI:0. 53 -0. 92). Among individuals with the MTHFR A1298C A/A genotype,adjusted OR for breast cancer were 0. 89 (95% CI: 0. 62 -1.27)and 1.69 (95% CI: 1.20 -2. 36) for the second to the third tertite of folato intake compared with thehighest folate intake group (Xtrend2=11. 372, P=0. 001). Conclusion The findings of the present study suggest that MTHFR genetic polymorphisms, and dietary intake of folate may modify susceptibility to breast cancer.     

亚甲基四氢叶酸还原酶基因多态和叶酸摄取与乳腺癌的发病风险

Objective To evaluate the relationship between dietary folate intake and genetic polymorphisms of 5, 10-methylenetetrahydrofolate reductase (MTHFR) with reference to breast cancer risk. Methods A case-control study was conducted with 669 cases and 682 population-based controls in Jiangsu province of China. MTHFR C677T and AI298C genotypes were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods. Dietary folate intake was assessed by using an 83-item food frequency questionnaire. Odds ratios (OR) were estimated with an unconditional logistic model. Results The frequencies of MTHFR C677T C/C, C/T and T/T genotypes were 32. 37% (202/624), 48. 88% (3051624) and 18. 75% (117/624) in cases and 37. 66% (235/624), 48.24% (301/624) and 14. 10% (88/624) in controls,respectively. The difference in distribution was significant (X2=6. 616, P=0. 037), the T/T genotype being associated with an elevated OR for breast cancer (1.62, 95% CI: 1.14 -2. 30). The frequencies of MTHFR A1298C A/A,A/C and C/C were 71.47% (446/624), 27.08% (169/624) and 1.44% (9/624) in cases and 68. 11% (425/624) ,30. 13% (188/624) and 1.76% (11/624) in controls, with no significant differences found (X2=1.716, P=0. 424). Folate intake of cases [(263.00±137. 38)μg/d]was significantly lower than that of controls [(285. 12±149. 61)μg/d](t=-2. 830,P=0. 005). Compared with the lowest tertile (≤199. 08μg/d) of folate intake,the adjusted OR for breast cancer in the top tertile (≥315.μg/d) was 0. 70 (95% CI:0. 53 -0. 92). Among individuals with the MTHFR A1298C A/A genotype,adjusted OR for breast cancer were 0. 89 (95% CI: 0. 62 -1.27)and 1.69 (95% CI: 1.20 -2. 36) for the second to the third tertite of folato intake compared with thehighest folate intake group (Xtrend2=11. 372, P=0. 001). Conclusion The findings of the present study suggest that MTHFR genetic polymorphisms, and dietary intake of folate may modify susceptibility to breast cancer.     

亚甲基四氢叶酸还原酶基因多态和叶酸摄取与乳腺癌的发病风险

Objective To evaluate the relationship between dietary folate intake and genetic polymorphisms of 5, 10-methylenetetrahydrofolate reductase (MTHFR) with reference to breast cancer risk. Methods A case-control study was conducted with 669 cases and 682 population-based controls in Jiangsu province of China. MTHFR C677T and AI298C genotypes were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods. Dietary folate intake was assessed by using an 83-item food frequency questionnaire. Odds ratios (OR) were estimated with an unconditional logistic model. Results The frequencies of MTHFR C677T C/C, C/T and T/T genotypes were 32. 37% (202/624), 48. 88% (3051624) and 18. 75% (117/624) in cases and 37. 66% (235/624), 48.24% (301/624) and 14. 10% (88/624) in controls,respectively. The difference in distribution was significant (X2=6. 616, P=0. 037), the T/T genotype being associated with an elevated OR for breast cancer (1.62, 95% CI: 1.14 -2. 30). The frequencies of MTHFR A1298C A/A,A/C and C/C were 71.47% (446/624), 27.08% (169/624) and 1.44% (9/624) in cases and 68. 11% (425/624) ,30. 13% (188/624) and 1.76% (11/624) in controls, with no significant differences found (X2=1.716, P=0. 424). Folate intake of cases [(263.00±137. 38)μg/d]was significantly lower than that of controls [(285. 12±149. 61)μg/d](t=-2. 830,P=0. 005). Compared with the lowest tertile (≤199. 08μg/d) of folate intake,the adjusted OR for breast cancer in the top tertile (≥315.μg/d) was 0. 70 (95% CI:0. 53 -0. 92). Among individuals with the MTHFR A1298C A/A genotype,adjusted OR for breast cancer were 0. 89 (95% CI: 0. 62 -1.27)and 1.69 (95% CI: 1.20 -2. 36) for the second to the third tertite of folato intake compared with thehighest folate intake group (Xtrend2=11. 372, P=0. 001). Conclusion The findings of the present study suggest that MTHFR genetic polymorphisms, and dietary intake of folate may modify susceptibility to breast cancer.     

乳腺癌复发转移与基因表达的相关性研究

目的:研究BCL2L2、CCNA1、CD44、CTSD和MAP2K7基因表达与乳腺癌复发转移特性的关系.方法:81例乳腺癌患者术后5年随访期内出现复发者为研究组(41例)和未复发仍存活者为对照组(40例).提取所有病例石蜡包埋组织的RNA,质量鉴定后,应用实时定量RT-PCR芯片技术平行检测BCL2L2、CCNA1、CD44、CTSD和MAP2K7基因的表达,分析各基因表达差异与乳腺癌复发转移之间的关系.结果:CCNA1、CD44和MAP2K7基因在复发病例中均高表达(57.5%、66.7%和58.5%),而BCL2L2和CTSD基因在复发组中低表达(56.1%和53.7%),BCL2L2、CCNA1、CD44、CTSD和MAP2K7基因表达水平在复发与未复发组间差异均有统计学意义,P均<0.05.BCL2L2和CTSD基因是乳腺癌复发转移的危险因素.CCNA1、CD44和MAP2K7基因对乳腺癌复发转移是保护因素.结论:实时定量RT-PCR芯片技术能快速、准确地检测肿瘤相关特性基因AR、CCND1和ESR2的表达.乳腺癌术后BCL2L2、CCNA1、CD44、CTSD和MAP2K7基因的差异表达分析可做为预防和控制该病复发的新线索.     

nNOS阳性神经元支配雄性大鼠球海绵体肌和坐骨海绵体肌

为了证实一氧化氮是否参与调节球海绵体肌和坐骨海绵体肌的功能 ,本研究用 CB-HRP逆行追踪结合 n NOS免疫细胞化学的技术 ,对支配雄性大鼠球海绵体肌和坐骨海绵体肌的神经元进行了研究 ,并结合 NADPH-d组化技术对雄性大鼠腰、骶髓的 NADPH-d阳性细胞和突起的分布进行了观察。结果发现 :( 1)支配球海绵体肌和坐骨海绵体肌的 Onuf核内存在着 CB-HRP与 n NOS双重反应细胞、CB-HRP阳性细胞、n NOS阳性细胞 ;n NOS阳性细胞还可见于后连合核、骶副交感核、背角等部位。( 2 ) NADPH-d阳性神经元在腰、骶髓主要位于中央管周围、后连合核、骶副交感核、背角等部位。本研究为 NO作为神经活性物质参与球海绵体肌和坐骨海绵体肌功能的调节提供了形态学证据     

社会因素与食管癌关系的病例对照研究

泰兴市 1996年食管癌死亡率为 77 5 2 / 10万 ,占癌症死亡率的 2 9 1% ,本研究探索影响泰兴市食管癌死亡水平居高不下的有关社会因素。1 材料与方法 :病例选自有泰兴市常住户口 ,于 1998年9月 1日～ 1999年 12月 1日发病并确诊为食管癌的新发病例。对照选取与病例同性别 ,年龄相差不超过 2岁 ,与病例居住在同村或同一街道的非肿瘤居民。采用 1∶1配对的病例对照研究方法。调查项目包括 :研究对象的一般状况 ,社会和经济因素 ,不良生活习惯与饮食习惯 (吸烟为每天吸烟 ,连续半年以上 ;饮酒为每周至少 1次 ,连续半年以上 )等。单因素和多因素…     

上消化道肿瘤高发区胃癌、食管癌病例对照研究

目的：探索泰兴市胃癌,食管癌的高危因素,方法,选择1998年9月1日－1999年12月31日期间430例胃癌和591例食管癌新发病例,按年龄,性别和居住地进行以人群为基础1：1配对的病例对照研究,分别采用Epi-info(6.04版）和SAS（6．12版）统计软件进行单因素和多因素分析。结果：单因素分析发现,经济状况差,吸烟,进食速度快,三餐不按时和既往患胃炎和胃溃疡,以及平时经常忧郁,长期处于精神压抑状态是泰兴地区胃和食管癌的共同危险因素,而有良好的人际关系,黄绿蔬菜的大量摄入,则可降低两种癌症的危险性,而饮高度白酒9OR＝2．71）,口味嗜咸（OR＝1．42）,喜爱吃烫食）OR＝2．21）,食管病变（OR＝6．62）和一级亲属中有人患食管癌（OR＝1．98）是食管癌的危险因素,多吃水果（OR＝0．68）则可降低患癌的危险性,多因素条件Logistic回归分析结果显示,既往有胃,食管病变,平时经常忧郁是胃,食管癌共同危险因素,进食速度快,三餐不按时,喜食烫食,过量饮高度白酒,一级亲属中有人患食管癌均作为食管癌的危险因素,而经常摄入黄绿蔬菜则作为胃癌保护因素进入回归方程,结论：精神因素,饮食相关因素及相关的上消化道病变对上消化道癌的发生影响十分明显。     

MICRONUCLEUS FORMATION IN VIVO IN LYMPHOCYTES OF HUMAN PERIPHERAL BLOOD AND INDIVIDUAL SUSCEPTIBILTY TO LUNG CANCER

目的 :探讨体内淋巴细胞微核形成与肺癌个体遗传易感性的关系。方法 :本组病例 -对照研究包括 95例确诊肺癌患者和90例对照。按末梢血微核法制备微核片。结果 :肺癌患者的自发和吸烟诱发的微核率 (MNF ,0 87‰和 1 6 4‰ )比对照人群的(0 47‰和 0 76‰ )有显著增加 (分别P <0 .0 5和P <0 .0 1)。结论 :肺癌患者是诱变效应易感人群 ;同时本研究首次证实 ,体内淋巴细胞微核形成是评价肺癌个体易感性的良好生物标志 ,MNF为 1‰和≥ 3‰的个体分别增加 5 5倍和 2 1 9倍的发生肺癌的相对危险性。