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Copy的相关文献在1995年到2022年内共计152篇,主要集中在自动化技术、计算机技术、肿瘤学、轻工业、手工业 等领域,其中期刊论文137篇、专利文献15篇;相关期刊94种,包括电脑迷、电脑知识与技术、软件等; Copy的相关文献由213位作者贡献,包括蒋兴浩、吴培森、岳峰等。

Copy—发文量

期刊论文>

论文:137 占比:90.13%

专利文献>

论文:15 占比:9.87%

总计:152篇

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Copy

-研究学者

  • 蒋兴浩
  • 吴培森
  • 岳峰
  • 张国富
  • 苏兆品
  • 丁峰
  • 任兴发
  • 何沛松
  • 刘焕
  • 吴俞醒
  • 期刊论文
  • 专利文献

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    • Ioannis A Voutsadakis
    • 摘要: BACKGROUND BRIP1 is a helicase that partners with BRCA1 in the homologous recombination(HR) step in the repair of DNA inter-strand cross-link lesions. It is a rare cause of hereditary ovarian cancer in patients with no mutations of BRCA1 or BRCA2. The role of the protein in other cancers such as gastrointestinal(GI) carcinomas is less well characterized but given its role in DNA repair it could be a candidate tumor suppressor similarly to the two BRCA proteins.AIM To analyze the role of helicase BRIP1(FANCJ) in GI cancers pathogenesis.METHODS Publicly available data from genomic studies of esophageal, gastric, pancreatic,cholangiocarcinomas and colorectal cancers were interrogated to unveil the role of BRIP1 in these carcinomas and to discover associations of lesions in BRIP1 with other more common molecular defects in these cancers.RESULTS Molecular lesions in BRIP1 were rare(3.6% of all samples) in GI cancers and consisted almost exclusively of mutations and amplifications. Among mutations,40% were possibly pathogenic according to the Onco KB database. A majority of BRIP1 mutated GI cancers were hyper-mutated due to concomitant mutations in mismatch repair or polymerase ε and δ1 genes. No associations were discovered between amplifications of BRIP1 and any mutated genes. In gastroesophageal cancers BRIP1 amplification commonly co-occurs with ERBB2 amplification.CONCLUSION Overall BRIP1 molecular defects do not seem to play a major role in GI cancers whereas mutations frequently occur in hypermutated carcinomas and co-occur with other HR genes mutations. Despite their rarity, BRIP1 defects may present an opportunity for therapeutic interventions similar to other HR defects.
    • 络小可1
    • 摘要: 在很多人眼中,自我评价是简历中的最形式化的一个板块,所以一般写得很随意,甚至去网上copy一份别人的评价贴到自己简历中就完事。
    • 老万1
    • 摘要: Q:在网页浏览器进行操作时,往往会一次性打开多个不同的网页链接,但是有时由于工作等原因,需要关掉电脑去忙别的工作。返回以后如何快速打开曾经访问过的网页链接?A:如果使用的是谷歌浏览器,或者是在其基础上开发的浏览器,可以通过应用商店安装一款名为“Copy All Uris”的功能扩展。以后当要离开电脑时,只需要点击该扩展图标,在弹出的对话框中点击“Copy”按钮,就能将所有打开的网页链接地址进行批量复制。
    • Soad Samir; Eid Emary; Khaled Elsayed; Hoda Onsi
    • 摘要: Copy-move offense is considerably used to conceal or hide several data in the digital image for specific aim, and onto this offense some portion of the genuine image is reduplicated and pasted in the same image. Therefore, Copy-Move forgery is a very significant problem and active research area to check the confirmation of the image. In this paper, a system for Copy Move Forgery detection is proposed. The proposed system is composed of two stages: one is called the detection stages and the second is called the refine detection stage. The detection stage is executed using Speeded-Up Robust Feature (SURF) and Binary Robust Invariant Scalable Keypoints (BRISK) for feature detection and in the refine detection stage, image registration using non-linear transformation is used to enhance detection efficiency. Initially, the genuine image is picked, and then both SURF and BRISK feature extractions are used in parallel to detect the interest keypoints. This gives an appropriate number of interest points and gives the assurance for finding the majority of the manipulated regions. RANSAC is employed to find the superior group of matches to differentiate the manipulated parts. Then, non-linear transformation between the best-matched sets from both extraction features is used as an optimization to get the best-matched set and detect the copied regions. A number of numerical experiments performed using many benchmark datasets such as, the CASIA v2.0, MICC-220, MICC-F600 and MICC-F2000 datasets. With the proposed algorithm, an overall average detection accuracy of 95.33% is obtained for evaluation carried out with the aforementioned databases. Forgery detection achieved True Positive Rate of 97.4% for tampered images with object translation, different degree of rotation and enlargement. Thus, results from different datasets have been set, proving that the proposed algorithm can individuate the altered areas, with high reliability and dealing with multiple cloning.
    • Kirsten H. Walen
    • 摘要: The objective herein was to connect the ontogeny process of diplochromosomal, amitotic, 4n-skewed division-system, to cytogenetic deficiency lesions in satellite, repetitive DNAs, especially in the chromosomal fragile sites, some 100 distributed over the genome. These latter studies had shown that chemical induced replication-stress led to un-replicated lesions in these fragile sites, which from inaccurate repair processes caused genomic instability. In the chain of events of the ontogeny process to the special tetraploidy, it was proposed that primary damaged human cells could undergo replication stress from repair-process present during cell replication, a suggestion verified by X-ray damaged cells producing the unstable fragile sites (see text). The cancer-importance for therapy is recognition of cell cycle change for the 4n derivative fitness-gained, diploid progeny cells. An open question is whether RB controlling G1 to S-period is mutated at this suggested tumorigenesis initiating phase, and if so, with what consequences for therapy. The fragile site studies further showed that repair of repetitive DNAs could produce two types of genomic changes: single gene mutations and CNVs, which were here shown to be chromosomally located on “borders” to repairing satellite lesions. This genomic placement was found to correspond to mutations identified in tumor sequencing (p53, Rb, MYC), favoring a bad luck location for their cancer “mutational nature”. The CNVs in cancers, are here seen as molecular expressions of long-known cytogenetic HSRs and DMs also with demonstrated origin from amplifications of single genes. Over-expression of oncogenes was hinted of being from duplications, but Drosophila genetics demonstrated the opposite, gene inactivation. The reduced eye-size from dominant, BAR-Ultra-Bar-eye phenotypes, was caused by duplications, inactivating the genetic system for eye-size. The finding of CNVs showing “evasion” of the immune system suggests, inactivation of immune-determining genetics. Since mutated genes on borders to satellite DNAs are a fact in hematological cancers, the 4n-skewed division-system is suggested to replace debated leukemogenesis with fitness-gain from molecular mutations. For these cancers the question is how normal bone marrow cells attain genomic damage for special tetraploidy, which was referred to studies of cells moving in artificial marrow-like substrate, needing serious attention.
    • Hui-Hong Jiang; Zhi-Yong Zhang; Xiao-Yan Wang; Xuan Tang; Hai-Long Liu; Ai-Li Wang; Hua-Guang Li; Er-Jiang Tang; Mou-Bin Lin
    • 摘要: BACKGROUND Lymphovascular invasion (LVI) is suggested to be an early and important step in tumor progression toward metastasis, but its prognostic value and genetic mechanisms in colorectal cancer (CRC) have not been well investigated. AIM To investigate the prognostic value of LVI in CRC and identify the associated genomic alterations. METHODS We performed a retrospective analysis of 1219 CRC patients and evaluated the prognostic value of LVI for overall survival by the Kaplan-Meier method and multivariate Cox regression analysis. We also performed an array-based comparative genomic hybridization analysis of 47 fresh CRC samples to examine the genomic alterations associated with LVI. A decision tree model was applied to identify special DNA copy number alterations (DCNAs) for differentiating between CRCs with and without LVI. Functional enrichment and protein-protein interaction network analyses were conducted to explore the potential molecular mechanisms of LVI. RESULTS LVI was detected in 150 (12.3%) of 1219 CRCs, and the presence was positively associated with higher histological grade and advanced tumor stage (both P < 0.001). Compared with the non-LVI group, the LVI group showed a 1.77-fold (95% confidence interval: 1.40-2.25, P < 0.001) increased risk of death and a significantly lower 5-year overall survival rate (P < 0.001). Based on the comparative genomic hybridization data, 184 DCNAs (105 gains and 79 losses) were identified to be significantly related to LVI (P < 0.05), and the majority were located at 22q, 17q, 10q, and 6q. We further constructed a decision tree classifier including seven special DCNAs, which could distinguish CRCs with LVI from those without it at an accuracy of 95.7%. Functional enrichment and proteinprotein interaction network analyses revealed that the genomic alterations related to LVI were correlated with inflammation, epithelial-mesenchymal transition, angiogenesis, and matrix remodeling. CONCLUSION LVI is an independent predictor for survival in CRC, and its development may correlate with inflammation, epithelial-mesenchymal transition, angiogenesis, and matrix remodeling.
    • 余露
    • 摘要: 意大利生物刺激素公司瓦拉格罗(Valagro)近日表示,其巴西团队将通过各种田间开放日和瓦拉格罗与主要经销商Agricola Famosa和Copy Fruit组织的学术会议,推出他们最新的生物刺激素产品RETROSAL。
    • Anders Lorentzen; Cathy Mitchelmore
    • 摘要: AIM To investigate if the down-regulation of N-myc Downstream Regulated Gene 2(NDRG2) expression in colorectal carcinoma(CRC) is due to loss of the NDRG2 allele(s).METHODS The following were investigated in the human colorectal cancer cell lines DLD-1, Lo Vo and SW-480: NDRG2 mRNA expression levels using quantitative reverse transcriptionpolymerase chain reaction(qRT-PCR); interaction of the MYC gene-regulatory protein with the NDRG2 promoter using chromatin immunoprecipitation; and NDRG2 promoter methylation using bisulfite sequencing.Furthermore, we performed qPCR to analyse the copy numbers of NDRG2 and MYC genes in the above three cell lines, 8 normal colorectal tissue samples and 40 CRC tissue samples.RESULTS As expected, NDRG2 mRNA levels were low in the three colorectal cancer cell lines, compared to normal colon.Endogenous MYC protein interacted with the NDRG2 core promoter in all three cell lines.In addition, the NDRG2 promoter was heavily methylated in these cell lines, suggesting an epigenetic regulatory mechanism.Unaltered gene copy numbers of NDRG2 were observed in the three cell lines.In the colorectal tissues, one normal and three CRC samples showed partial or complete loss of one NDRG2 allele.In contrast, the MYC gene was amplified in one cell line and in more than 40% of the CRC cases.CONCLUSION Our study suggests that the reduction in NDRG2 expression observed in CRC is due to transcriptional repression by MYC and promoter methylation, and is not due to allelic loss.
    • 鲍亚萍; 刘明华
    • 摘要: 紫色的苞片像可以旋钮的外壳,红色的花朵像探出半截的口红,惟妙惟肖。生机勃勃。是人抄袭了自然,还是自然copy了人?第一次听到口红花的名字还有点莫名其妙,及至见了花,方知所言不虚,名符其实(图1~2)。
    • Zarmiga Karunanithi; Else Marie Vestergaard; Mette H Lauridsen
    • 摘要: Genetic analyses of patients with transposition of the great arteries have identified rare copy number variations,suggesting that they may be significant to the aetiology of the disease.This paper reports the identification of a 16 p11.2 microduplication,a variation that has yet to be reported in association with transposition of the great arteries.The 16 p11.2 microduplication is associated with autism spectrum disorder and developmental delay,but with highly variable phenotypic effects.Autism and attention deficit disorders are observed more frequently in children with congenital heart disease than in the general population.Neonatal surgery is proposed as a risk factor,but as yet unidentified genetic abnormalities should also be taken into account.Thus,congenital heart abnormalities may constitute a part of the phenotypic spectrum associated with duplications at 16 p11.2.We suggest chromosomal microarray be considered part of the diagnostic work-up in patients with transposition of the great arteries.
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