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Non-symmetrical correspondence analysis (NSCA) is a very practical statistical technique for the identification of the structure
of association between asymmetrically related categorical variables forming a contingency table. This paper considers some
tools that can be used to numerically and graphically explore in detail the association between these variables and include
the use of confidence regions, the establishment of the link between NSCA and the analysis of variance of categorical variables,
and the effect of imposing linear constraints on a variable.
The authors would like to thank the anonymous referees for their comments and suggestions during the preparation of this paper. 相似文献
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为提高赛车在中低速下的加速能力,针对传统模糊控制依赖操作人员的经验、控制精度较低等缺点,提出一种基于自适应神经模糊推理系统的电动赛车加速驱动控制优化方法。该方法以当前加速踏板开度对应的最高车速为驾驶员期望车速,以驾驶员期望车速与实际车速的偏差及其变化率为输入变量,以加速踏板修正系数为输出变量,将加速踏板修正系数与当前加速踏板开度相乘得到修正后的加速踏板开度。Matlab/Simulink仿真与实车测试结果表明:在对加速踏板采用相同的操作控制下,优化后的驱动控制方法增加了赛车加速踏板的开度;在加速结束时刻,赛车车速的仿真值较优化前提高209%,实测值较优化前提高174%。 相似文献
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Albagha OM Wani SE Visconti MR Alonso N Goodman K Brandi ML Cundy T Chung PY Dargie R Devogelaer JP Falchetti A Fraser WD Gennari L Gianfrancesco F Hooper MJ Van Hul W Isaia G Nicholson GC Nuti R Papapoulos S Montes Jdel P Ratajczak T Rea SL Rendina D Gonzalez-Sarmiento R Di Stefano M Ward LC Walsh JP Ralston SH;Genetic Determinants of Paget's Disease 《Nature genetics》2011,43(7):685-689
Paget's disease of bone (PDB) is a common disorder characterized by focal abnormalities of bone remodeling. We previously identified variants at the CSF1, OPTN and TNFRSF11A loci as risk factors for PDB by genome-wide association study. Here we extended this study, identified three new loci and confirmed their association with PDB in 2,215 affected individuals (cases) and 4,370 controls from seven independent populations. The new associations were with rs5742915 within PML on 15q24 (odds ratio (OR) = 1.34, P = 1.6 × 10(-14)), rs10498635 within RIN3 on 14q32 (OR = 1.44, P = 2.55 × 10(-11)) and rs4294134 within NUP205 on 7q33 (OR = 1.45, P = 8.45 × 10(-10)). Our data also confirmed the association of TM7SF4 (rs2458413, OR = 1.40, P = 7.38 × 10(-17)) with PDB. These seven loci explained ~13% of the familial risk of PDB. These studies provide new insights into the genetic architecture and pathophysiology of PDB. 相似文献
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FL Muller S Colla E Aquilanti VE Manzo G Genovese J Lee D Eisenson R Narurkar P Deng L Nezi MA Lee B Hu J Hu E Sahin D Ong E Fletcher-Sananikone D Ho L Kwong C Brennan YA Wang L Chin RA DePinho 《Nature》2012,488(7411):337-342
Inactivation of tumour-suppressor genes by homozygous deletion is a prototypic event in the cancer genome, yet such deletions often encompass neighbouring genes. We propose that homozygous deletions in such passenger genes can expose cancer-specific therapeutic vulnerabilities when the collaterally deleted gene is a member of a functionally redundant family of genes carrying out an essential function. The glycolytic gene enolase 1 (ENO1) in the 1p36 locus is deleted in glioblastoma (GBM), which is tolerated by the expression of ENO2. Here we show that short-hairpin-RNA-mediated silencing of ENO2 selectively inhibits growth, survival and the tumorigenic potential of ENO1-deleted GBM cells, and that the enolase inhibitor phosphonoacetohydroxamate is selectively toxic to ENO1-deleted GBM cells relative to ENO1-intact GBM cells or normal astrocytes. The principle of collateral vulnerability should be applicable to other passenger-deleted genes encoding functionally redundant essential activities and provide an effective treatment strategy for cancers containing such genomic events. 相似文献
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Hashibe M McKay JD Curado MP Oliveira JC Koifman S Koifman R Zaridze D Shangina O Wünsch-Filho V Eluf-Neto J Levi JE Matos E Lagiou P Lagiou A Benhamou S Bouchardy C Szeszenia-Dabrowska N Menezes A Dall'Agnol MM Merletti F Richiardi L Fernandez L Lence J Talamini R Barzan L Mates D Mates IN Kjaerheim K Macfarlane GJ Macfarlane TV Simonato L Canova C Holcátová I Agudo A Castellsagué X Lowry R Janout V Kollarova H Conway DI McKinney PA Znaor A Fabianova E Bencko V Lissowska J Chabrier A Hung RJ 《Nature genetics》2008,40(6):707-709
Alcohol is an important risk factor for upper aerodigestive cancers and is principally metabolized by alcohol dehydrogenase (ADH) enzymes. We have investigated six ADH genetic variants in over 3,800 aerodigestive cancer cases and 5,200 controls from three individual studies. Gene variants rs1229984 (ADH1B) and rs1573496 (ADH7) were significantly protective against aerodigestive cancer in each individual study and overall (P = 10(-10) and 10(-9), respectively). These effects became more apparent with increasing alcohol consumption (P for trend = 0.0002 and 0.065, respectively). Both gene effects were independent of each other, implying that multiple ADH genes may be involved in upper aerodigestive cancer etiology. 相似文献
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Tumour vascularization via endothelial differentiation of glioblastoma stem-like cells 总被引:2,自引:0,他引:2
Ricci-Vitiani L Pallini R Biffoni M Todaro M Invernici G Cenci T Maira G Parati EA Stassi G Larocca LM De Maria R 《Nature》2010,468(7325):824-828
Glioblastoma is a highly angiogenetic malignancy, the neoformed vessels of which are thought to arise by sprouting of pre-existing brain capillaries. The recent demonstration that a population of glioblastoma stem-like cells (GSCs) maintains glioblastomas indicates that the progeny of these cells may not be confined to the neural lineage. Normal neural stem cells are able to differentiate into functional endothelial cells. The connection between neural stem cells and the endothelial compartment seems to be critical in glioblastoma, where cancer stem cells closely interact with the vascular niche and promote angiogenesis through the release of vascular endothelial growth factor (VEGF) and stromal-derived factor 1 (refs 5-9). Here we show that a variable number (range 20-90%, mean 60.7%) of endothelial cells in glioblastoma carry the same genomic alteration as tumour cells, indicating that a significant portion of the vascular endothelium has a neoplastic origin. The vascular endothelium contained a subset of tumorigenic cells that produced highly vascularized anaplastic tumours with areas of vasculogenic mimicry in immunocompromised mice. In vitro culture of GSCs in endothelial conditions generated progeny with phenotypic and functional features of endothelial cells. Likewise, orthotopic or subcutaneous injection of GSCs in immunocompromised mice produced tumour xenografts, the vessels of which were primarily composed of human endothelial cells. Selective targeting of endothelial cells generated by GSCs in mouse xenografts resulted in tumour reduction and degeneration, indicating the functional relevance of the GSC-derived endothelial vessels. These findings describe a new mechanism for tumour vasculogenesis and may explain the presence of cancer-derived endothelial-like cells in several malignancies. 相似文献
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Effectiveness of the global protected area network in representing species diversity 总被引:7,自引:0,他引:7
Rodrigues AS Andelman SJ Bakarr MI Boitani L Brooks TM Cowling RM Fishpool LD Da Fonseca GA Gaston KJ Hoffmann M Long JS Marquet PA Pilgrim JD Pressey RL Schipper J Sechrest W Stuart SN Underhill LG Waller RW Watts ME Yan X 《Nature》2004,428(6983):640-643
The Fifth World Parks Congress in Durban, South Africa, announced in September 2003 that the global network of protected areas now covers 11.5% of the planet's land surface. This surpasses the 10% target proposed a decade earlier, at the Caracas Congress, for 9 out of 14 major terrestrial biomes. Such uniform targets based on percentage of area have become deeply embedded into national and international conservation planning. Although politically expedient, the scientific basis and conservation value of these targets have been questioned. In practice, however, little is known of how to set appropriate targets, or of the extent to which the current global protected area network fulfils its goal of protecting biodiversity. Here, we combine five global data sets on the distribution of species and protected areas to provide the first global gap analysis assessing the effectiveness of protected areas in representing species diversity. We show that the global network is far from complete, and demonstrate the inadequacy of uniform--that is, 'one size fits all'--conservation targets. 相似文献
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