肝脏肿瘤细胞诱导T淋巴细胞PD-1表达及功能研究

目的研究肝脏肿瘤细胞系细胞HepG2细胞与HepG2．2．15细胞对T淋巴细胞程序性死亡分子1（PD-1）表达的影响及PD-1的作用。方法HepG2细胞、HepG2．2．15细胞分别和Jurkat细胞共同培养后,标记流式抗体,流式细胞检测仪检测Jurkat细胞PD-1的表达,ELISA检测并比较阻断组与对照组培养上清中细胞因子含量,单核细胞直接细胞毒性测定法检测并比较阻断组与对照组T淋巴细胞杀伤能力即OD值的改变。结果肝脏肿瘤细胞能诱导T淋巴细胞PD-1的表达,共培养2d时表达率分别为16．17％±2．5％（HepG2细胞）和17．43％±2．2％（HepG2．2．15细胞）;阻断组培养上清中IL-2、IFN-γ、IL-10浓度分别为202．9±53．0pg/ml、88．6±4．6pg/ml和63．7±13．4pg／ml,均明显高于对照组（102．9±53．0pg/ml、39．3±4．2pg/ml和34．6±13．7pg/m1）,P〈0．05;阻断组Jurkat细胞对HepG2．2．15细胞杀伤的OD值为0．29±0．06,明显高于对照组（0．19±0．09）,P〈0．05。结论肝脏肿瘤细胞能诱导T淋巴细胞PD-1的表达;阻断PD-1／PD—L1能提高T淋巴细胞分泌细胞因子的量和杀伤能力。     

云南红河地区哈尼族髋部骨折流行病学调查

目的调查云南省红河地区哈尼族髋部骨折流行病学情况.方法运用国际疾病分类编码第10版（ICD-10）为统一的诊断标准,采取随机整群抽样和调查者入户调查及现场访谈检查的方式对云南省红河地区哈尼族人群进行调查.结果本次共调查25834人,其中发现髋部骨折患者2人,均为60岁以上男性.本次调查60岁及以上人群2543人（男性1144人,女性1399人）中髋部骨折发病率为39.32/10万,患病率为0.79‰.结论云南省红河地区哈尼族髋部骨折发病率、患病率较低.     

Non-toxic dose chidamide synergistically enhances platinum-induced DNA damage responses and apoptosis in Non-Small-Cell lung cancer cells

Combination of low doses of histone deacetylases inhibitors and chemotherapy drugs is considered as one of the most promising strategies to increase the anticancer efficacy. Chidamide is a novel benzamide chemical class of HDAC inhibitor that selectively inhibited HDAC1, 2, 3 and 10. We sought to determine whether chidamide may enhance platinum-induced cytotoxicity in NSCLC cells. In this study, the combination of chidamide with carboplatin showed a good synergism on growth inhibition with the mean combination index value as 0.712 and 0.639 in A549 and NCI-H157 cells, respectively. The used concentration of chidamide was non-toxic on cells by itself as low as 0.3 μM. All of our experiments were comparisons between combination regimen and single carboplatin regimen in A549 and NCI-H157 cell lines. Phosphorylated histone H2A.X (γH2A.X), a hall marker of DNA damage response, was dramatically increased by the combination treatment. Cell cycle analysis by flow cytometry and phosphorylation level analysis of histone H3 (Ser10) by western blotting showed that combination treatment significantly increased the percentage of G2/M phase of cells. Mitochondrial membrane potential and cleaved-PARP1 level analysis indicate that chidamide synergistically enhances carboplatin-induced apoptosis. Additionally, synergistic effects of chidamide were found when it was combined with two other platinum drugs (cisplatin and oxaliplatin). The results suggest that Chidamide in combination with platinum drugs may be a novel therapeutic option for NSCLC.