The paper studies coseismic effect of the great earthquake and teleseismic recorded by the YongChun well water level.The ability of recording earthquake of the YongChun well water level is improved before and after Septermber 2007.This phenomenon is probably caused by earthquake intensity and frequency of Fujian province.During the process of earthquake preparation,the change of the regional stress field leads to the change of the stress state of the aquifer,which caused the changes of the ability of recording earthquakes of the YongChun well.The paper also elaborates the characteristics of coseismic effect of this well water level:the maximum amplitude coseismic effect of this well water is directly proportional to magnitude and is inversely proportional to the epicentral distance overall.The ability of recording earthquakes of the same well has certain direct.

目的:探讨乳腺癌组织中多药耐药基因 (MDR1) 和膜联蛋白 (Anxa2) 表达的相关性及其与乳腺癌转移的关系.方法:应用荧光定量PCR的方法检测20例配对的乳腺导管内癌、100例乳腺浸润性导管癌、70例癌旁正常组织中MDR1和Anxa2 mRNA的相对表达情况.结果:MDR1 mRNA在乳腺导管内癌中的表达水平明显高于癌旁正常组织 (P=0.005),乳腺浸润性导管癌组织中mRNA的表达明显高于癌旁正常组织 (P=0.017) 和导管内癌 (P=0.019 6).Anxa2 mRNA在乳腺导管内癌中表达与癌旁正常组织相比无显著性差异 (P=0.188 9),但是在乳腺浸润性导管癌组织中的表达明显高于导管内癌 (P=0.000 8) 和癌旁正常组织 (P<0.000 1); MDR1和Anxa2 mRNA的表达升高均与患者出现淋巴结转移有关 (P<0.01); 2种基因在乳腺浸润性导管癌中的表达呈正相关 (P<0.000 1).结论:在肿瘤进展过程中,MDR1和Anxa2 mRNA表达上调与乳腺癌的淋巴结转移有关,二者之间表达具有正相关提示肿瘤细胞的多药耐药的获得和肿瘤侵袭转移之间有着密切联系.

目的:研究Annexin a2的表达对人乳腺癌细胞MDA-MB-231增殖、迁移和侵袭能力的影响.方法:采用小干扰RNA技术下调人乳腺癌细胞中Annexin a2的表达,并筛选单克隆细胞株,得到实验组克隆,阴性对照组命名为control.采用Westernblot(WB)技术检测Annexin a2蛋白水平的变化,噻唑蓝(MTT)比色法研究其对MDA-MB-231细胞的存活、增殖能力的影响;采用划痕实验、侵袭实验观察其对细胞迁移和侵袭能力的影响;免疫沉淀法检测与Annexin a2相互作用的蛋白分子.结果:WB检测发现siRNA干扰后MDA-MB-231细胞中Annexin a2的蛋白表达水平明显下降,MTT增殖实验显示Annexin a2下降组细胞克隆在72、96h的增殖能力明显低于亲本和control组细胞(P 均＜0.05),同时细胞迁移和侵袭能力也显著下降,差异具有统计学意义(P＜0.05);免疫沉淀法证实Annexin a2与热休克蛋白27(HSP27)之间存在相互作用.结论:人乳腺癌细胞MDA-MB-231具有较强的迁移和侵袭能力,Annexin a2蛋白水平下降可以明显抑制其增殖、迁移和侵袭能力,研究提示Annexin a2与HSP27的相互作用有可能在乳腺癌的发生、浸润和转移中起调节作用.

Objective To study the effects of Annexin a2 on the proliferation,colony formation and cell cycle of human breast cancer cell line MDA-MB-231 and to explore the possible molecular mechanism.Methods Small interfering RNA(siRNA) technology was used to knock down the expression of Annexin a2 in MDA-MB-231 cells and monoclonal cell strains were screened.The expression level of Annexin a2 was detected by Western blot;the activities of proliferation and colony formation were examined by MTT,the changes of cell cycle were evaluated by flow cytometry;coimmunoprecipitation and immunofluresence were applied to detect proteins interacted with Annexin a2.Results Annexin a2 siRNA effectively knocked down the expression of Annexin a2.The cell proliferation and the colony formation were depressed,moreover,the proportion of G0/G1 stage of cell cycle increased,the percentage of G2/M and S stage decreased significantly.It was discovered that Annexin a2 binding with STAT3 by coimmunoprecipitation analysis.Conclusion The knockdown of Annexin a2 inhibited the proliferation and colony formation of tumor cells,and approved that Annexin a2 interacted with STAT3,which might participate in regulating the proliferation of breast cancer.

目的:研究PKCζ在肺腺癌组织中的表达与肿瘤侵袭、转移和预后的关系,初步分析PKCζ促进肿瘤转移的分子机制.方法:采用特异的PKC抑制剂抑制PKCζ的活性,观察PKCζ活性下降对肺腺癌A549细胞趋化运动和粘附能力的影响.选择临床及随访资料完整的48例肺腺癌患者,采用免疫组织化学法检测肺腺癌组织中PKCζ的表达情况,结合临床病理参数分析PKCζ表达与临床预后的关系.结果:PKC家族中的非典型PKC参与了肺癌细胞的趋化和黏附过程,通过抑制PKCζ的活性明显减弱了EGF诱导的A549细胞的趋化运动和对细胞外基质的黏附能力.25例(52%)患者肺腺癌组织中癌细胞PKCζ呈阳性表达且表达定位在胞浆;PKCζ蛋白表达与患者出现淋巴结转移有关(P<0.05),与性别、年龄、肿瘤大小、吸烟与否、远处转移和临床分期等其它临床病理参数无关;PKCζ表达与肺腺癌患者生存预后相关(P<0.05).结论:肺腺癌组织中PKCζ的高表达与肺癌患者出现淋巴结转移相关,有可能作为患者预后不良的指标及潜在的治疗靶点.

Folic acid and TAT peptide were conjugated on the octadecyl-quaternized, lysine-modified chitosan-cholesterol polymeric liposomes (FA-TATp-PLs) to investigate their potential feasibility for tumor-targeted drug delivery.

Targeting therapy is a promising strategy for enhancing the therapeutic potential of chemotherapeutic agents. In this study, we report the construction of a multifunctional drug delivery system, termed folic acid modified and TAT peptide conjugated PEGylated polymeric liposomes (FA-TATp-PLs), which is originally derived from octadecyl-quaternized lysine modified chitosan and cholesterol. Our data revealed that FA-TATp-PLs have a particle size of about 60 nm with a zeta potential of about 30 mV, a low burst release effect within the first day, a sustained release for the next 14 days in vitro as well as an instant cellular uptake by folate receptor-overexpressing KB human nasopharyngeal carcinoma cells. In vitro cytotoxicity of paclitaxel-loaded FA-TATp-PLs in KB cells was superior to that of Taxol(®). Furthermore, a comparable antitumor efficacy of paclitaxel-loaded FA-TATp-PLs and Taxol(®) was observed at the same doses in murine models bearing nasopharyngeal carcinoma. These results demonstrate that the paclitaxel formulation not only exhibits a higher antitumor activity but also significantly reduces the toxicity and improves the bioavailability as compared to that of free paclitaxel for the treatment of nasopharyngeal carcinoma. Taken together, our findings indicate that paclitaxel-loaded FA-TATp-PLs are a promising nano-sized drug formulation for future cancer therapy.

A GFC-HPLC method was established to determine the loading and encapsulation efficiency of paclitaxel in paclitaxel loaded polymeric liposomes.The analysis was performed on combining Sephadex G25 with Comatex C_(18)column(150mm×4.6mm,5μm),mobile phase for HPLC:methanol:acetonitrile:water(35:40:25,v/ v/v),flow rate:1.0mL/min,wavelength:227nm,injection volume:10μL.The linear range for paclitaxel was 2～64μg/mL(r=0.9997,n=5).The average recovery was 101.60%,and RSD was 0.74%.The method is simple and accurate for the measurement of loading and encapsulation efficiency of paclitaxel in polymeric liposomes.