Background: Expression confusion of tripartite motif (TRIM) family proteins has been associated with various cellular processes such as immune disorders, neurological-related diseases, protein degradation, and tumorigenesis. Therefore, we aim to explore the function and clinical significance of TRIM family proteins in chemotherapy resistance in ovarian cancer. Methods: Western blot analysis and immunohistochemistry (IHC) assay were conducted to assess the protein expression levels of TRIM37 in both ovarian cancer cell lines and patient tissues. Furthermore, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were conducted to detect the effect of TRIM37 on 50% inhibitory concentration (IC50). The rate of apoptotic cells was conducted using fluorescence-activated cell sorting (FACS) assays. Moreover, Luciferase assays were performed to detect the luciferase reporter activity. Additionally, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were conducted to detect the pro-cancer effect of TRIM37. Results: We found that TRIM37 was increased in ovarian cancer tissues, showing partial response to cisplatin chemotherapy (p < 0.01). The high TRIM37 expression was linked to a worse overall survival prognosis and lower disease-free survival rate in our cancer tissue samples and public ovarian cancer databases (p < 0.001,p < 0.01). Functionally, overexpression of TRIM37 endows cisplatin resistance in ovarian cancer cells. However, inhibition of TRIM37 counteracted this resistance in ovarian cancer. Additionally, TRIM37 was found to activate the wnt//3-catenin signaling pathway. Conclusions: Our findings indicate that TRIM37 contributes to enhanced cisplatin resistance in ovarian cancer, suggesting its potential as a promising chemotherapy biomarker.

Chemotherapy is a common drug for lung cancer. Nevertheless, the development of drug resistance greatly limits their clinical efficacy. Therefore, to reduce drug resistance, we need to constantly explore new treatments. This study is aimed at determining the role of rhein in the proliferation and metastasis of lung cancer cell. Our study found that rhein significantly inhibits the proliferation and migration of lung cancer cells. Additionally, the mRNA expression and protein levels of Snail, MMP2, and MMP9 are decreasing in lung cancer cells treated by rhein. Our results showed that rhein plays a vital role in proliferation and metastasis of chemosensitive and chemoresistant lung cancer cells, and the mechanism may be related to the Stat3/Snail/MMP2/MMP9 pathway.

Waveguide-based spin-photon interfaces on the GaAs platform have emerged as a promising system for a variety of quantum information applications directly integrated into planar photonic circuits. The coherent control of spin states in a quantum dot can be achieved by applying circularly polarized laser pulses that may be coupled into the planar waveguide vertically through radiation modes. However, proper control of the laser polarization is challenging since the polarization is modified through the transformation from the far field to the exact position of the quantum dot in the nanostructure. Here, we demonstrate polarization-controlled excitation of a quantum-dot electron spin and use that to perform coherent control in a Ramsey interferometry experiment. The Ramsey interference reveals an inhomogeneous dephasing time of 2.2 +/- 0.1 ns, which is comparable to the values so far only obtained in bulk media. We analyze the experimental limitations in spin initialization fidelity and Ramsey contrast and identify the underlying mechanisms.

The spin of an electron is a promising memory state and qubit. Connecting spin states that are spatially far apart will enable quantum nodes and quantum networks based on the electron spin. Towards this goal, an integrated spin-photon interface would be a major leap forward as it combines the memory capability of a single spin with the efficient transfer of information by photons. Here, we demonstrate such an efficient and optically programmable interface between the spin of an electron in a quantum dot and photons in a nanophotonic waveguide. The spin can be deterministically prepared in the ground state with a fidelity of up to 96%. Subsequently, the system is used to implement a single-spin photonic switch, in which the spin state of the electron directs the flow of photons through the waveguide. The spin-photon interface may enable on-chip photon-photon gates, single-photon transistors and the efficient generation of a photonic cluster state.

目的：探讨着色性干皮病基因A（XPA）单核苷酸多态性与广东地区女性乳腺癌易感性的关系。方法采用病例－对照研究方法纳入乳腺癌患者130例（病例组）和健康对照者188例（对照组），采用聚合酶链反应－限制性片段长度多态性分析两组人群XPA－4G／A多态性的基因型。结果病例组与对照组中杂合子基因型A／G在两组样本中的基因型频率差异无统计学意义（P＝0.857），纯合子基因型G／G在病例组的分布频率与对照组比较差异无统计学意义（ P＝0.103），但G／G基因型在乳腺癌患者中的基因型频率要低于在正常对照组中的分布频率。等位基因G和A在病例组和对照组中的分布频率差异接近有统计学意义的临界值（ OR＝0.782，95％CI＝0.568～1.077），对照组中G等位基因的基因型频率为病例组的1.28倍。结论 XPA－4G／A多态性与乳腺癌发病风险无相关性，但是等位基因G的携带者在健康人群中出现的频率更高，因此提示XPA－4G等位基因携带者发生乳腺癌的风险可能会降低。

A silicon nitride ring resonator with implanted ytterbium ions offers a means for greatly enhanced ion–light interactions in an integrated optics platform. Rare-earth ions in solids are of particular interest for quantum information storage and processing because of the long coherence times of the 4f states1. In the past few years, substantial progress has been made by using ensembles of ions2,3,4,5,6 and single ions7,8,9,10. However, the weak optical transitions within the 4f manifold pose a great challenge to the optical interaction with a single rare-earth ion on a single-photon level. Here, we demonstrate a ninefold enhanced ion–light interaction (Purcell effect11) in an integrated-optics-based, fibre-coupled silicon nitride (Si3N4) ring resonator with implanted ytterbium ions (Yb3+). We unveil the one-, two- and three-dimensional contributions to the Purcell factor as well as the temperature-dependent decoherence and depolarization of the ions. The results indicate that this cavity quantum electrodynamics (QED) system has the potential of interfacing single rare-earth ions with single photons on a chip.

Breast cancer already taken the first place of incidence in Chinese female cancer patients. TRPM8 is found to be over-expressed in breast cancer, but whether it promotes breast cancer aggressiveness remains unknown. In our study, TRPM8 was identified highly expressing in all the tested breast cancer cell lines including MCF-7, T47D, MDA-MB-231, BT549, SKBR3 and ZR-75-30, while it just could be detected in MCF-10A, the normal breast epithelial cell. Then four pairs of clinical samples were analyzed using Western blotting and the result showed that TRPM8 expression is higher in tumor tissues than in adjacent nontumor tissues. Subsequently, we established TRPM8 high-expressing MCF-7 cell line and TRPM8 knockout MDA-MB-231 cell line to explore expression status of cancer-related proteins. The Western blotting and immunofluorescence analysis outcomes demonstrated that TRPM8 might influence cancer cell metastasis by regulating the EMT phenotype via activating AKT/GSK-3β pathway, and the hypothesis had been supported by cell function tests. All the results demonstrated that TRPM8 significantly up-expressed in breast cancer cells and promoted their metastasis by regulating EMT via activating AKT/GSK-3β pathway, indicating TRPM8 gets the prospects of to be developed as medication or diagnostic indicator to be applied in clinical work.

DNA修复系统是人体抵御内外环境因素造成DNA损伤的重要系统，当DNA损伤不能及时修复，积累到一定程度导致基因组不稳定性升高，引起细胞增殖和分化失控，导致肿瘤发生［1-2］。因此，DNA 修复与肿瘤发生有着密不可分的联系。参与DNA修复的基因主要分为核苷酸切除修复（ nucleotide excision repair， NER ）基因、碱基切除修复（ base excision repair）基因、错配修复基因、双链断裂修复基因等。着色性干皮病基因A（ XPA）的主要作用是识别损伤DNA，在NER通路中， XPA 与 RPA、XPC、转录因子ⅡH （ TFⅡH ）、ERCC1-XPF复合体以及DNA聚合酶一起共同作用，完成损伤DNA的修复［3］。研究资料表明，DNA修复基因的多态性是决定肿瘤易感性的一个重要因素。目前XPA多态性与肿瘤发生之间的关系尚不明确，虽然目前国内外有关XPA基因多态性和肿瘤发病风险展开了关联研究，但是未能得到一致性的研究结果，在不同类型的肿瘤中其多态性与肿瘤的相关性也不同，考虑到XPA在DNA修复途径中的重要作用，本文对近年来XPA单核苷酸多态性与肿瘤易感性关系的相关研究进展综述如下。

Silicon nitride (Si3N4) optical ring resonators provide exceptional opportunities for low-loss integrated optics. Here we study the transmission through a multimode waveguide coupled to a Si3N4 ring resonator. By coupling single-mode fibers to both input and output ports of the waveguide we selectively excite and probe combinations of modes in the waveguide. Strong asymmetric Fano resonances are observed and the degree of asymmetry can be tuned through the positions of the input and output fibers. The Fano resonance results from the interference between modes of the waveguide and light that couples resonantly to the ring resonator. We develop a theoretical model based on the coupled mode theory to describe the experimental results. The large extension of the optical modes out of the Si3N4 core makes this system promising for sensing applications.

This meta-analysis was conducted to examine whether the genotype status of Val158Met polymorphism in catechol-O-methyltransferase (COMT) is associated with endometrial and ovarian cancer risk. Eligible studies were identified by searching several databases for relevant reports published before January 1, 2014. Pooled odds ratios (ORs) were appropriately derived from fixed-effects or random-effects models. In total, 15 studies (1,293 cases and 2,647 controls for ovarian cancer and 2,174 cases and 2,699 controls for endometrial cancer) were included in the present meta-analysis. When all studies were pooled into the meta-analysis, there was no evidence for significant association between COMT Val158Met polymorphism and ovarian cancer risk (Val/Met versus Val/Val: OR=0.91, 95% CI=0.76-1.08; Met/Met versus Val/Val: OR=0.90, 95% CI=0.73-1.10; dominant model: OR=0.90, 95% CI=0.77-1.06; recessive model: OR=0.95, 95% CI=0.80-1.13). Similarly, no associations were found in all comparisons for endometrial cancer (Val/Met versus Val/Val: OR 0.97, 95% CI=0.77-1.21; Met/Met versus Val/Val: OR=1.02, 95% CI=0.73-1.42; dominant model: OR=0.98, 95% CI=0.77-1.25; recessive model: OR=1.02, 95% CI=0.87-1.20). In the subgroup analyses by source of control and ethnicity, no significant associations were found in any subgroup of population. This meta-analysis strongly suggests that COMT Val158Met polymorphism is not associated with increased endometrial and ovarian cancer risk.

The T241M polymorphism in the X-ray cross-complementing group 3 (XRCC3) had been implicated in cancer susceptibility. The previous published data on the association between XRCC3 T241M polymorphism and cancer risk remained controversial. Hence, we performed a meta-analysis to investigate the association between cancer susceptibility and XRCC3 T241M (61,861 cases and 84,584 controls from 157 studies) polymorphism in different inheritance models. We used odds ratios with 95% confidence intervals to assess the strength of the association. Overall, significantly increased cancer risk was observed in any genetic model (dominant model: odds ration [OR]=1.07, 95% confidence interval [CI]=1.00-1.13; recessive model: OR=1.15, 95% CI=1.08-1.23; additive model: OR=1.17, 95% CI=1.08-1.28) when all eligible studies were pooled into the meta-analysis. In further stratified and sensitivity analyses, the elevated risk remained for subgroups of bladder cancer and breast cancer, especially in Caucasians. In addition, significantly decreased lung cancer risk was also observed. In summary, this meta-analysis suggests the participation of XRCC3 T241M in the susceptibility for bladder cancer and breast cancer, especially in Caucasians, and XRCC3 T241M polymorphism is associated with decreased lung cancer risk. Moreover, our work also points out the importance of new studies for T241M association in some cancer types, such as gastric cancer, colorectal cancer, and melanoma skin cancer, where at least some of the covariates responsible for heterogeneity could be controlled, to obtain a more conclusive understanding about the function of the XRCC3 polymorphism in cancer development.

The regulation of gene expression,one of the important sections of biochemistry and molecular biology,is one of the fastest growing region in biology in these years.Therefore,we carried out research-based learning in some classes of our university.In this paper,the authors reported the methods and some practical experience in the research-based learning of regulation of gene expression.

Objective CYP4A11 oxidizes endogenous arachidonic acid to 20-hydroxyeicosatetraenoic acid, a renal vasoconstrictor and natriuretic in humans. Previous studies demonstrated an association between a functional variant (T8590C) of CYP4A11 and essential hypertension, though with conflicting results. To elucidate this relationship, a case-control study and meta-analysis were performed to assess the possible association of essential hypertension with CYP4A11 genetic variations. Methods Associations between the T8590C polymorphism and essential hypertension were examined in 328 unrelated cases and 297 age-matched controls in Han Chinese individuals. High-resolution melting was used to identify the CYP4A11 variant. To further investigate the association, we conducted a meta-analysis including eight studies published previously in July 2012. Results The frequency of the CYP4A11 T8590C polymorphism showed no significant difference between cases and controls (all P>0.05). However, the meta-analysis showed that the CYP4A11 T8590C polymorphism may increase the risk of essential hypertension in an additive model (OR: 1.15, 95% CI: 1.02–1.29, P = 0.02), a dominant model (OR: 1.06, 95% CI: 1.01–1.32, P = 0.03), a recessive model (OR: 1.52, 95% CI: 1.15–2.02, P = 0.003) and a homozygote contrast (OR: 1.38, 95% CI: 1.07–1.78, P = 0.01). Also, a significant relationship was observed among Caucasians in the additive model, the homozygote contrast, the recessive model and the dominant model (all P<0.05). However, no association was observed in an Asian population (all P>0.05). Conclusions This meta-analysis suggests there is a significant association between the CYP4A11 T8590C variant and essential hypertension, especially in Caucasians. The case-control study did not find a significant association among the Han Chinese population, but the controls were poorly matched and meaningful conclusions cannot therefore be made. Further large-scale studies are needed to clarify whether the CYP4A11 T8590C polymorphism is associated with hypertension risk in Asians or has a gender-specific effect.

课堂教学是教学活动的中心环节,课堂教学的高效与否直接影响着学生获得知识的多少.着重分析了影响高校课堂教学高效的四大因素:无序的课堂学习纪律、不良的课堂学习习惯、单调的课堂教学手段以及乏味的课堂教学技巧等,对课堂教学效果所带来的负面影响,并有针对性地提出相应的解决方法:双重管理,创造轻松有序的课堂氛围,培养良好的学习习惯,增加课堂师生互动,运用多种教学技巧和手段,从而达到有效提升课堂教学效果的目的.

Background: There have been an increasing number of studies with evidence suggesting that the N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2) genotypes may be implicated in the development of colorectal cancer (CRC) and colorectal adenoma (CRA). So far the published data on this association has remained controversial, however. We performed a meta-analysis of case-cohort and case-control studies using a subset of the published data, with an aim to derive a better understanding of the underlying relationship.Methods/Principal Findings: A literature search was performed using Medline database for relevant studies published through October 31, 2011. A total of 39 publications were selected for this meta-analysis, including 11,724 cases and 16,215 controls for CRC, and 3,701 cases and 5,149 controls for CRA. In our pooled analysis of all these studies, the results of our meta-analysis suggested that the NAT1 genotype was not significantly associated with an elevated CRC risk (OR 0.99, 95% CI 0.91-1.07). We also found that individuals with the rapid NAT2 genotype did have an elevated risk of CRC (OR 1.07, 95% CI 1.01-1.13). There was no evidence for an association between the NAT1 and 2 rapid genotype and an elevated CRA risk (NAT1: OR 1.14, 95% CI 0.99-1.29; NAT2: OR 0.94, 95% CI 0.86-1.03).Conclusion: This meta-analysis suggests that individuals with NAT2 genotype had an elevated risk of CRC. There was no evidence for the association between NAT1 and 2 rapid genotype and CRA risk.

Lung cancer is the leading cause of cancer-related death in the world. To explore tumor biomarkers for clinical application, two-dimensional fluorescence difference gel electrophoresis and subsequent MALDI-TOF/TOF mass spectrometry were performed to identify proteins differentially expressed in 12 pairs of lung squamous cell tumors and their corresponding normal tissues. A total of 28 nonredundant proteins were identified with significant alteration in lung tumors. The up-regulation of isocitrate dehydrogenase 1 (IDH1), superoxide dismutase 2, 14-3-3ε, and receptor of activated protein kinase C1 and the down-regulation of peroxiredoxin 2 in tumors were validated by RT-PCR and Western blot analysis in independent 15 pairs of samples. Increased IDH1 expression was further verified by the immunohistochemical study in extended 73 squamous cell carcinoma and 64 adenocarcinoma clinical samples. A correlation between IDH1 expression and poor overall survival of non-small cell lung cancer (NSCLC) patients was observed. Furthermore, ELISA analysis showed that the plasma level of IDH1 was significantly elevated in NSCLC patients compared with benign lung disease patients and healthy individuals. In addition, knockdown of IDH1 by RNA interference suppressed the proliferation of NSCLC cell line and decreased the growth of xenograft tumors in vivo. These observations suggested that IDH1, as a protein promoting tumor growth, could be used as a plasma biomarker for diagnosis and a histochemical biomarker for prognosis prediction of NSCLC.

乳腺癌是女性最常见的恶性肿瘤,转移与复发是乳腺癌患者死亡的主要原因.研究与乳腺癌细胞转移相关的分子靶点对预防乳腺癌术后复发、提高疗效有重要意义.本研究以3组乳腺癌转移相关的基因表达谱数据(GSE2034,GSE2603,GSE12276)为分析材料,采用GeneSpring软件筛选乳腺癌原发瘤与转移瘤芯片数据的差异表达基因,结合生物信息学工具PATHER、STRING、pSTIING和文献挖掘工具iHOP对差异基因及其相互作用关系进行分析.结果显示,共筛选出乳腺癌转移共同差异基因147个,其中表达上调93个,表达下调54个.这些差异基因主要涉及细胞周期与增殖、细胞粘附、细胞迁移、血管形成及信号转导等生物通路和生物过程.差异基因编码蛋白间的相互作用主要集中在14个蛋白,且在更为复杂的网络图谱中仍可见其中9个基因(CXCR4、MMP1、MMP2、MMP3、CTGF、COL1A1、MEF2C、PTGS2及SPARC)在重要的节点位置.文献挖掘发现,COL1A1基因可能为新发现的乳腺癌转移候选基因,为乳腺癌转移的发病机制提供新的思路,也为转移性乳腺癌的分子诊断和个体化治疗奠定基础.

MicroRNAs (miRNAs) as a species of small non coding single stranded RNA of about 21–25 nucleotides have important roles in the development of different cancers. In present study, we found that the expression of miR-25 was up-regulated in 60 esophageal squamous cell carcinoma (ESCC) tissues compared with matched adjacent non-cancer tissues. Moreover, we demonstrated that the up-regulation of miR-25 was significantly correlated with the status of lymph node metastasis and TNM (Tumor, Node and Metastasis) stage. Furthermore, over-expression of miR-25 markedly promoted migration and invasion of ESCC cells. On the contrary, down-regulation of miR-25 inhibited the migration and invasion of cells. E-cadherin(CDH1) is a very important tumor metastasis suppressor. We further identified that miR-25 directly targeted CDH1 3′-untranslated region (3′UTR) and repressed the expression of CDH1. These results, for the first time, demonstrate that miR-25 promotes ESCC cell migration and invasion by suppressing CDH1 expression.

The oncogene, microRNA‐155, is significantly elevated in GBM (glioblastoma multiforme), regulating multiple genes associated with cancer cell proliferation, apoptosis and invasiveness. Thus, miR‐155 can theoretically become a target for enhancement of the chemotherapy in cancer. Down‐regulating miR‐155 to enhance the effect of taxol has not been studied in human GBM. Human GBM U251 cells were treated with taxol and the miR‐155 inhibitor alone or in combination. IC50 values were dramatically decreased in cells treated with miR‐155 inhibitor combined with taxol, to a greater extent than those treated with taxol alone. Furthermore, the miR‐155 inhibitor significantly enhanced apoptosis in U251 cells. The data suggest that miR‐155 blockage increased the chemosensitivity to taxol in GBM cells, making combined treatment an effective therapeutic strategy for controlling the growth by inhibiting EAG1 expression.

We read with great interest the recent Breast Cancer Research paper by Desrichard and colleagues [1] reporting the association between CHEK2 mutations and non-BRCA hereditary breast cancer risk.Th is report summarized the results of diff erent case-control studies to provide an overview of CHEK2 1100delC mutation and susceptibility to early-onset breast cancer (EOBC) and bilateral breast cancer (BBC).We believe there are signifi cant issues to note regarding the authors' study.To investigate the role of CHEK2 1100delC mutation in BBC susceptibility, Desrichard and colleagues performed a systematic review and pooled analysis based on fi ve studies.Notably, another study that showed contradictory results indicating that the 1100delC mutation might not be a modifi er in BBC [2] was not included in these analyses.Rashid and colleagues [3] have also shared their data, which failed to identify CHEK2 1100delC mutations among cases of BBC.Interestingly, the study by de Jong and colleagues [4] categorized individuals with BBC as unselected breast cancer cases.However, the BBC cases were included in the group of 192 patients identifi ed with early-onset/familial breast cancer from an Irish study [5].Hence, ongoing uncertainty exists and, in our opinion, the conclusion reached by Desrichard and colleagues may not be fully supported by the available data.An additional issue is the association between CHEK2 mutations and EOBC risk.Using the same search strategy as that of Desrichard and colleagues, we located three relevant case-control studies in PubMed comprising a total of 3,742 EOBC cases and 8,405 controls [6-8], which were not included in the pooled analy ses.Furthermore, we have combined all of the studies on European