TSLC1和MPP3在胰腺癌中的表达及其意义

目的:探讨TSLC1和MPP3两种蛋白在胰腺癌中的表达和临床病理意义.方法:采用免疫组织化学S-P法检测37例胰腺癌组织、12例胰腺炎组织和10例正常胰腺组织中TSLC1和MPP3两种蛋白的表达.结果:TSLC1、MPP3蛋白在胰腺癌组织中的阳性表达率均明显低于在正常胰腺组织和胰腺炎组织中的表达(21.62%vs70.00%,75.00%;27.03%vs80.00%,66.67%,P<0.05或0.01).TSLC1和MPP3蛋白的异常表达均与胰腺癌的分化程度、淋巴结转移和TNM分期相关(均P<0.05),而与患者的性别、年龄、部位和病理分型无关.在37例胰腺癌中TSLC1与MPP3蛋白表达呈显著正相关(rs=0.715,P<0.01).结论:胰腺癌中存在TSLC1和MPP3基因的失活和蛋白表达下调,两者可能通过TSLC1-MPP3级联反应共同参与胰腺癌的发生、发展和转移.     

铜绿假单胞菌注射液对肺癌A549细胞自噬及PI3 K/Akt通路的影响

目的 探究铜绿假单胞菌注射液(PA-MSHA)对肺癌A549细胞自噬及磷脂酰肌醇-3激酶(PI3K)/蛋白激酶B(Akt)通路的影响.方法 体外培养人肺癌A549细胞,随机分为空白对照组、LY294002组(加入20μmol/L LY294002),PA-MSHA干预组(加入0.5×109/mL、1.0×109/mL、...     

脂肪因子补体C1q/肿瘤坏死因子相关蛋白3对胰岛素抵抗的3T3-L1脂肪细胞胰岛素信号通路影响的研究

目的 观察脂肪因子补体C1q/肿瘤坏死因子相关蛋白3(CTRP3)对IR的3T3-L1脂肪细胞胰岛素信号通路的影响. 方法 以软脂酸培养构建IR的3T3-L1脂肪细胞模型,分为对照组、CTRP3(10、50、250 ng/ml)干预组及CTRP3(250 ng/ml)+渥曼青霉素(Wortmannin)[磷脂酰肌醇3激酶(PI3K)抑制剂]干预组.以葡萄糖氧化酶法检测葡萄糖消耗量,以Western blot检测PI3K及蛋白激酶B[PKB(ser437)]蛋白相对表达量. 结果 与对照组相比,CTRP3干预组(10、50、250 ng/ml)葡萄糖消耗量分别增加了22.1％、42.9％及76.6％(P均＜0.01),PI3K蛋白相对表达量分别增加了62.5％、100.0％及137.5％(P均＜0.01),PKB(ser437)蛋白相对表达量分别增加了46.4％、160.7％及192.9％(P均＜0.01);与CTRP3(250 ng/ml)干预组相比,CTRP3 (250 ng/ml) +Wortmannin干预组葡萄糖消耗量下降53.2％ (P＜0.01),PI3K及PKB(ser437)蛋白相对表达量分别下降了43.4％及56.1％(P均＜0.01). 结论 脂肪因子CTRP3可能通过改善胰岛素信号转导增加IR的3T3-L1脂肪细胞IS.     

Influence of −308 A/G polymorphism in the tumor necrosis factor α gene on etanercept treatment in rheumatoid arthritis

Objective

To determine whether the ?308 A/G tumor necrosis factor α (TNFα) gene polymorphism can predict the outcome of etanercept therapy in 86 patients with rheumatoid arthritis (RA), as already observed in patients treated with infliximab.

Methods

Eighty‐six RA patients treated with etanercept were genotyped for ?308 A/G TNFα gene polymorphism by polymerase chain reaction and melting curve analysis, using specific gene primers and probes. Patients were subdivided into group A (G/A genotype) and group G (G/G genotype). We compared clinical responses to etanercept between groups A and G after 6 months, using the Disease Activity Score in 28 joints (DAS28). After 12‐month treatment, 48 of 86 patients were evaluated again.

Results

Of 86 patients, 18 (21%) belonged in group A and 68 (79%) belonged in group G. After 6‐month treatment, 55.6% of patients in group A and 82.4% of patients in group G had DAS28 improvement >1.2 (P = 0.027 by chi‐square). The mean ± SD DAS28 improvement was 1.69 ± 1.31 in group A and 2.23 ± 1.19 in group G (P = 0.098 by t‐test). After 1‐year treatment 48 patients were tested again: 10 (21%) belonged in group A and 38 (79%) belonged in group G. Forty percent of patients in group A and 87% in group G had DAS28 improvement >1.2 (P = 0.005 by chi‐square). The mean ± SD DAS28 improvement was 1.334 ± 1.37 in group A and 2.29 ± 1.47 in group G (Mann‐Whitney U test = 115, P = 0.0057).

Conclusion

RA patients with a ?308 G/G TNFα genotype respond to etanercept better than patients with a ?308 A/G genotype.