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Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

炎症性肠病（IBD）是一种多因素导致的慢性非特异性自身免疫性疾病，发病机制复杂。Toll 样受体 （TLR）是模式识别受体，可诱导炎症反应。TLR在IBD中异常表达，在IBD的发生发展中占重要地位。TLR通过髓 样分化因子（MyD88）依赖性通路和MyD88非依赖性通路影响肠黏膜屏障与免疫细胞分化，参与IBD的发生发展； TLR与IBD并发症密切相关，TLR下游炎症因子可促进肠纤维化，诱导炎症相关性结直肠癌，还可促进IBD患者血 栓形成；临床可基于TLR基因多态性治疗IBD并判断预后，益生菌或内外源性调控物质可通过TLR通路改善IBD 病情。 [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

第 10号染色体同源丢失性磷酸酶—张力蛋白基因（PTEN）是一种可以调节多种生理和病理过程的抑癌 基因，通过调节丝裂原活化蛋白激酶（MAPK）/细胞外信号调节激酶（ERK）、磷脂酰肌醇 3-激酶（PI3K）/丝氨酸/苏 氨酸蛋白激酶（AKT）/哺乳动物雷帕霉素靶蛋白（mTOR）、IκB激酶（IKK）/核因子-κB（NF-κB）途径参与了多种疾病 的发生与发展；MAPK/ERK途径不仅调控了细胞增殖，侵袭和转移过程，而且参与了细胞外基质降解和血管生成的 过程；PI3K/AKT/mTOR途径促进细胞增殖和抗凋亡能力，并调节由血管内皮生长因子介导的血管生成；IKK/NF-κB 途径可通过影响炎症因子的表达从而使盆腔微环境失衡。子宫内膜异位症是一种具有恶性行为的良性疾病，目前 仍无有效的治疗手段，仅可通过药物或手术治疗缓解症状；异位内膜细胞中PTEN表达显著降低，促进了异位内膜 的增殖和抗凋亡能力，并因其盆腔微环境失衡而使异位内膜细胞易于种植与存活；PTEN对血管生成的调节作用在 异位内膜细胞的存活中亦发挥了重要的作用。 [ABSTRACT FROM AUTHOR]

多聚嘧啶区结合蛋白1（PTBP1）是一种已知的转录后基因表达调节因子，可以调控mRNA的可变剪接、翻 译、稳定性和定位，具有多种与RNA代谢相关的分子功能.PTBP1在多种恶性肿瘤中高表达，并可以通过影响肿瘤 细胞的能量代谢、增殖、凋亡和转移等方式促进胶质瘤、结直肠癌、乳腺癌等肿瘤的恶性进展，具有作为临床诊断标 志物和治疗靶标的潜力. [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To establish the human breast MDA-MB-231 cells stably expressing HMGA2 protein. Methods Total RNA of MDA-MB-231 cells in the logarithmic phase were extracted, and cDNA of HMGA2 gene was reversely tran­scribed. The recombinant pLVX-HMGA2 expression vector was acquired by inserting the target fragments which were ac­quired by PCR technology into the lentiviral expression plasmid pLVX-IRES-Puro. The forward and reverse primers, contai­ning EcoR1 and BamH1 restriction enzyme sites, were designed according to their CDS sequences. The recombinant lenti- virus carrying HMGA2 gene was obtained by co-transfecting HEK293T cells with the packaging plasmid，and the culture supernatant containing the lentiviral particles was collected. The recombinant plasmid was identified by bacterial colonies PCR，double restriction enzyme digestion，plasmid PCR，and sequencing comparison. MDA-MB-231 cells were divided in­to two groups. The cells in the experimental group were infected by the lentivirus carrying HMGA2 gene，simultaneously， the control group was infected by the lentivirus carrying only expression vector. Puromycin (1 pg/mL) was used to screen out the infected cells after 48 hours so as to obtain a cell line for stable expression. The mRNA and protein expression of HMGA2 was detected by Western blotting and real-time fluorescent quantitative PCR. Results The relative expression levels of HMGA2 mRNA in the observation group and the control group were 10 273.93 ±4 290. 77 and 1.18 ±0.81，re­spectively， and significant difference was found between these two groups (P < 0. 05 ). The relative expression levels of HMGA2 protein in the observation group and the control group were 1.570 ±0.080 and 0. 110 ±0.002，and the difference between the two groups was statistically significant ( P <0. 05 ) . Conclusion The breast cancer cell line MDA-MB-231 stably expressing HMGA2 is successfully established. [ABSTRACT FROM AUTHOR]

Objective To observe the anti-enterovirus type 71 (EV71 ) effects of Houttuvnia cordata Thunb water extract and its main ingredients, including chlorogenic acid, rutin, spasinin, and quercetin in vitro. Methods The RD cells (derived from human rhabdomyosarcoma cells) were divided into the Houttuvnia cordata group, hyperoside group, quercetin group, rutin group, chlorogenic acid group, and control group. Cells in the Houttuyniae cordata group were given water extracts of Houttuvnia coidata at the concentrations of 5 000. 2 500. 1 250. 625. and 313 mg/L; cells in the quercetin and rutin groups were added with quercetin and rutin at the concentrations of 10. 00, 5. 00, 2. 50. 1.25 . and 0.63 mg/mL; cells in the hyperoside and chlorogenic acid groups were given hyperoside and chlorogenic acid, respectively, with the concentrations of 4. 00, 2.00. 1.00, 0.50, and0.25 mg/mL; cells in the control group were added with the cell culture fluid. We observed the cytopathic effect (CPE) and calculated the inhibition rate of virus replication, half maximal inhibitory concentration (IC50) , inhibition rate of virus growth, inhibition rate of virus adsorption, vims inactivation rate, and virus penetration rate. Results The inhibition rate of virus replication in the Houttuvnia cordata group and quercetin group was higher than that in the other four groups, and the inhibition rate increased with the increasing concentrations ( all P < 0. 05 ). The inhibition rate of virus growth in the hyperin and rutin groups was higher than that in the other four groups ( all Pc 0.05). The inhibition rate of virus adsorption in the hyperin and Houttuynia cordata group was higher than that in the other four groups ( all P < 0. 05). The water extract and its main components of Houttuynia cordata had no effect in inactivating the virus. No inhibitory effect on virus penetration was observed in each group at 15 and 30 min. At 60 min. the inhibition rate of virus penetration was higher in houttuyniae, quercetin, rutin and chlorogenic acid groups than in the hypero-side group and control group ( all P <0. 05 ). The inhibition rate of virus penetration of the quercetin group and rutin group decreased with the decreasing drug concentrations, but increased in the chlorogenic acid group. Conclusions The water extract of Houttuynia cordata Thunb and its main components all have the effect of anti-EV71 in vitro, but had no effect in inactivating the virus. Quercetin has the effect of inhibiting virus replication. Hyperin and rutin block the growth of the virus, hyperoside can inhibit virus adsorption, and quercetin, rutin, chlorogenic acid can inhibit the virus penetration. [ABSTRACT FROM AUTHOR]

Objective To construct the lentiviral vector of human DNA methyltransferase 3A (DNMT3A) and to establish the stable breast caner MDA-MB-231 cell line. Methods The total RNA was extracted from MDA-MB-231 cells and cDNA containing DNMT3A was inverse transcribed. DNMT3A fragment containing EcoR I and BamH I sites was amplified by PCR and was inserted into pLVX-IRES-Hyg lentiviral vector. Then the recombinant expression vector pLVX-FLAG-DNMT3A was co-transfected into 293T cell line with packaging plasmids, and the culture supermatant containing the lentiviral particles was collected to infect MDA-MB-231 cells. After 48 h, 1 μg/μ puromycin was used to screen the infected cells, so as to obtain a cell line with stable expression. The protein and mRNA expression levels of DNMT3 A were detected by Western blotting and PCR. Results Bacteria colonies PCR, double restriction enzyme digestion, plasmid PCR identification, and DNA sequencing demonstrated the lentiviral vector pLVX-FLAG-DNMT3A was constructed. MDA-MB-231 cells were infected by the lentivirus, and the protein and mRNA expression of DNMT3A was significantly up-regulated following screening with puromycin. Conclusions The DNMT3A gene lentiviral vector pLVX-FLAG-DNMT3A is constructed successfully. The cell line stably expressing DNMT3A is screened in MDA-MB-231 cells, which provides an in vitro model for further study of molecular function and mechanism of DNMT3A in human breast cancer. [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

目的探讨急性ST段抬高型心肌梗死（STEMI)患者发生非梗死血管闭塞性病变的危险因素。 方法120例老年（⩾65岁）STEMI患者人院后均行选择性冠状动脉造影确定是否合并非梗死血管闭塞性病变，其 中合并非梗死血管闭塞性病变21例（观察组）、不合并非梗死血管闭塞性病变者99例（对照组）$收集两组性别、年 龄、左室射血分数（LVEF)、LDL-C、梗死冠状动脉支数等临床病理资料。采用单因素及多因素Log-K分析法分析 STEMI患者合并非梗死血管闭塞性病变的危险因素。结果两组性别分布、合并糖尿病比例、LVEF比较，P均< %.。5;两组年龄、吸烟史、合并高血压比例、[0^、梗死动脉支数比较，P均>%35。^5--多因素分析结果显示， 男性（01 = 1.027、P <0.05)、合并糖尿病（01 = 1.531、P <0.05 )、LVEF 降低（0R = 1.338、P <0.05)是 STEMI 患者 发生非梗死血管闭塞性病变的危险因素。结论男性、合并糖尿病、LVEF降低是老年STEMI患者发生非梗死血管 性病 的危 因 。 [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)