排序方式: 共有127条查询结果,搜索用时 15 毫秒
121.
Phase radiography with neutrons 总被引:1,自引:0,他引:1
Allman BE McMahon PJ Nugent KA Paganin D Jacobson DL Arif M Werner SA 《Nature》2000,408(6809):158-159
122.
Genome-wide atlas of gene expression in the adult mouse brain 总被引:1,自引:0,他引:1
Lein ES Hawrylycz MJ Ao N Ayres M Bensinger A Bernard A Boe AF Boguski MS Brockway KS Byrnes EJ Chen L Chen L Chen TM Chin MC Chong J Crook BE Czaplinska A Dang CN Datta S Dee NR Desaki AL Desta T Diep E Dolbeare TA Donelan MJ Dong HW Dougherty JG Duncan BJ Ebbert AJ Eichele G Estin LK Faber C Facer BA Fields R Fischer SR Fliss TP Frensley C Gates SN Glattfelder KJ Halverson KR Hart MR Hohmann JG Howell MP Jeung DP Johnson RA Karr PT Kawal R Kidney JM Knapik RH Kuan CL Lake JH Laramee AR 《Nature》2007,445(7124):168-176
Molecular approaches to understanding the functional circuitry of the nervous system promise new insights into the relationship between genes, brain and behaviour. The cellular diversity of the brain necessitates a cellular resolution approach towards understanding the functional genomics of the nervous system. We describe here an anatomically comprehensive digital atlas containing the expression patterns of approximately 20,000 genes in the adult mouse brain. Data were generated using automated high-throughput procedures for in situ hybridization and data acquisition, and are publicly accessible online. Newly developed image-based informatics tools allow global genome-scale structural analysis and cross-correlation, as well as identification of regionally enriched genes. Unbiased fine-resolution analysis has identified highly specific cellular markers as well as extensive evidence of cellular heterogeneity not evident in classical neuroanatomical atlases. This highly standardized atlas provides an open, primary data resource for a wide variety of further studies concerning brain organization and function. 相似文献
123.
Tomlins SA Laxman B Dhanasekaran SM Helgeson BE Cao X Morris DS Menon A Jing X Cao Q Han B Yu J Wang L Montie JE Rubin MA Pienta KJ Roulston D Shah RB Varambally S Mehra R Chinnaiyan AM 《Nature》2007,448(7153):595-599
Recently, we identified recurrent gene fusions involving the 5' untranslated region of the androgen-regulated gene TMPRSS2 and the ETS (E26 transformation-specific) family genes ERG, ETV1 or ETV4 in most prostate cancers. Whereas TMPRSS2-ERG fusions are predominant, fewer TMPRSS2-ETV1 cases have been identified than expected on the basis of the frequency of high (outlier) expression of ETV1 (refs 3-13). Here we explore the mechanism of ETV1 outlier expression in human prostate tumours and prostate cancer cell lines. We identified previously unknown 5' fusion partners in prostate tumours with ETV1 outlier expression, including untranslated regions from a prostate-specific androgen-induced gene (SLC45A3) and an endogenous retroviral element (HERV-K_22q11.23), a prostate-specific androgen-repressed gene (C15orf21), and a strongly expressed housekeeping gene (HNRPA2B1). To study aberrant activation of ETV1, we identified two prostate cancer cell lines, LNCaP and MDA-PCa 2B, that had ETV1 outlier expression. Through distinct mechanisms, the entire ETV1 locus (7p21) is rearranged to a 1.5-megabase prostate-specific region at 14q13.3-14q21.1 in both LNCaP cells (cryptic insertion) and MDA-PCa 2B cells (balanced translocation). Because the common factor of these rearrangements is aberrant ETV1 overexpression, we recapitulated this event in vitro and in vivo, demonstrating that ETV1 overexpression in benign prostate cells and in the mouse prostate confers neoplastic phenotypes. Identification of distinct classes of ETS gene rearrangements demonstrates that dormant oncogenes can be activated in prostate cancer by juxtaposition to tissue-specific or ubiquitously active genomic loci. Subversion of active genomic regulatory elements may serve as a more generalized mechanism for carcinoma development. Furthermore, the identification of androgen-repressed and insensitive 5' fusion partners may have implications for the anti-androgen treatment of advanced prostate cancer. 相似文献
124.
Weir BA Woo MS Getz G Perner S Ding L Beroukhim R Lin WM Province MA Kraja A Johnson LA Shah K Sato M Thomas RK Barletta JA Borecki IB Broderick S Chang AC Chiang DY Chirieac LR Cho J Fujii Y Gazdar AF Giordano T Greulich H Hanna M Johnson BE Kris MG Lash A Lin L Lindeman N Mardis ER McPherson JD Minna JD Morgan MB Nadel M Orringer MB Osborne JR Ozenberger B Ramos AH Robinson J Roth JA Rusch V Sasaki H Shepherd F Sougnez C Spitz MR Tsao MS Twomey D Verhaak RG Weinstock GM Wheeler DA Winckler W 《Nature》2007,450(7171):893-898
125.
Magnani F Mencuccini M Borghetti M Berbigier P Berninger F Delzon S Grelle A Hari P Jarvis PG Kolari P Kowalski AS Lankreijer H Law BE Lindroth A Loustau D Manca G Moncrieff JB Rayment M Tedeschi V Valentini R Grace J 《Nature》2007,447(7146):848-850
Temperate and boreal forests in the Northern Hemisphere cover an area of about 2 x 10(7) square kilometres and act as a substantial carbon sink (0.6-0.7 petagrams of carbon per year). Although forest expansion following agricultural abandonment is certainly responsible for an important fraction of this carbon sink activity, the additional effects on the carbon balance of established forests of increased atmospheric carbon dioxide, increasing temperatures, changes in management practices and nitrogen deposition are difficult to disentangle, despite an extensive network of measurement stations. The relevance of this measurement effort has also been questioned, because spot measurements fail to take into account the role of disturbances, either natural (fire, pests, windstorms) or anthropogenic (forest harvesting). Here we show that the temporal dynamics following stand-replacing disturbances do indeed account for a very large fraction of the overall variability in forest carbon sequestration. After the confounding effects of disturbance have been factored out, however, forest net carbon sequestration is found to be overwhelmingly driven by nitrogen deposition, largely the result of anthropogenic activities. The effect is always positive over the range of nitrogen deposition covered by currently available data sets, casting doubts on the risk of widespread ecosystem nitrogen saturation under natural conditions. The results demonstrate that mankind is ultimately controlling the carbon balance of temperate and boreal forests, either directly (through forest management) or indirectly (through nitrogen deposition). 相似文献
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Easton DF Pooley KA Dunning AM Pharoah PD Thompson D Ballinger DG Struewing JP Morrison J Field H Luben R Wareham N Ahmed S Healey CS Bowman R;SEARCH collaborators Meyer KB Haiman CA Kolonel LK Henderson BE Le Marchand L Brennan P Sangrajrang S Gaborieau V Odefrey F Shen CY Wu PE Wang HC Eccles D Evans DG Peto J Fletcher O Johnson N Seal S Stratton MR Rahman N Chenevix-Trench G Bojesen SE Nordestgaard BG Axelsson CK Garcia-Closas M Brinton L Chanock S Lissowska J Peplonska B Nevanlinna H 《Nature》2007,447(7148):1087-1093
Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r2 > 0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P < 10(-7)). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1). At the second stage, 1,792 SNPs were significant at the P < 0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach. 相似文献