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  • 1
    Publication Date: 2002
    Keywords: Subduction zone ; Seismicity ; Refraction seismics ; Velocity depth profile ; Japan ; OBS ; GJI
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  • 2
    Publication Date: 2000
    Keywords: Geol. aspects ; Earthquake ; Plate tectonics ; Subduction zone ; GRL ; 0325 ; 3040 ; 8010
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  • 3
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    In:  Earth planet. Sci. Lett., Philadelphia, 4, vol. 217, no. 1-2, pp. 77-84, pp. B05318, (ISSN: 1340-4202)
    Publication Date: 2003
    Keywords: Subduction zone ; Seismicity ; Earthquake ; Japan ; EPSL
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  • 4
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    In:  Geophys. Res. Lett., Taipei, EGS, vol. 32, no. 20, pp. 105-121, pp. L20310, (ISSN: 1340-4202)
    Publication Date: 2005
    Keywords: Deep seismic sounding (espec. cont. crust) ; Reflection seismics ; 4D ; Aftershocks ; Earthquake asperities ; Fracture ; Earthquake ; Seismology ; Rock mechanics ; Physical properties of rocks ; GRL ; 3225 ; Mathematical ; Geophysics: ; Numerical ; approximations ; and ; analysis ; (4260) ; 3653 ; Mineralogy ; and ; Petrology: ; Fluid ; flow ; 7230 ; Seismology: ; Seismicity ; and ; tectonics ; (1207, ; 1217, ; 1240, ; 1242) ; 7240 ; Subduction ; zones ; (1207, ; 1219, ; 1240)
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  • 5
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    In:  Earth and Planetary Science Letters, Tokyo, Railway Tech. Res. Inst., vol. 203, no. 1, pp. 255-263, pp. L09308, (ISSN: 1340-4202)
    Publication Date: 2002
    Keywords: Subduction zone ; Plate tectonics ; rupture ; area ; Fracture ; Japan ; EPSL
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  • 6
    Publication Date: 2015-07-12
    Description: Global network modeling of distal regulatory interactions is essential in understanding the overall architecture of gene expression programs. Here, we developed a Bayesian probabilistic model and computational method for global causal network construction with breast cancer as a model. Whereas physical regulator binding was well supported by gene expression causality in general, distal elements in intragenic regions or loci distant from the target gene exhibited particularly strong functional effects. Modeling the action of long-range enhancers was critical in recovering true biological interactions with increased coverage and specificity overall and unraveling regulatory complexity underlying tumor subclasses and drug responses in particular. Transcriptional cancer drivers and risk genes were discovered based on the network analysis of somatic and genetic cancer-related DNA variants. Notably, we observed that the risk genes were functionally downstream of the cancer drivers and were selectively susceptible to network perturbation by tumorigenic changes in their upstream drivers. Furthermore, cancer risk alleles tended to increase the susceptibility of the transcription of their associated genes. These findings suggest that transcriptional cancer drivers selectively induce a combinatorial misregulation of downstream risk genes, and that genetic risk factors, mostly residing in distal regulatory regions, increase transcriptional susceptibility to upstream cancer-driving somatic changes.
    Keywords: Computational Methods, Genomics, Transcriptome Mapping - Monitoring Gene Expression
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
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  • 7
    Publication Date: 2002-08-17
    Description: Seismic reflection profiles reveal steeply landward-dipping splay faults in the rupture area of the magnitude (M) 8.1 Tonankai earthquake in the Nankai subduction zone. These splay faults branch upward from the plate-boundary interface (that is, the subduction zone) at a depth of approximately 10 kilometers, approximately 50 to 55 kilometers landward of the trough axis, breaking through the upper crustal plate. Slip on the active splay fault may be an important mechanism that accommodates the elastic strain caused by relative plate motion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Jin-Oh -- Tsuru, Tetsuro -- Kodaira, Shuichi -- Cummins, Phil R -- Kaneda, Yoshiyuki -- New York, N.Y. -- Science. 2002 Aug 16;297(5584):1157-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Frontier Research on Earth Evolution, Japan Marine Science and Technology Center, Yokosuka 237-0061, Japan. jopark@jamstec.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12183623" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2009-07-25
    Description: The iridescent metallic green beetle, Chrysina gloriosa, which selectively reflects left circularly polarized light, possesses an exoskeleton decorated by hexagonal cells (approximately 10 microm) that coexist with pentagons and heptagons. The fraction of hexagons decreases with an increase in curvature. In bright field microscopy, each cell contains a bright yellow core, placed in a greenish cell with yellowish border, but the core disappears in dark field. With use of confocal microscopy, we observe that these cells consist of nearly concentric nested arcs that lie on the surface of a shallow cone. We infer that the patterns are structurally and optically analogous to the focal conic domains formed spontaneously on the free surface of a cholesteric liquid crystal. These textures provide the basis for the morphogenesis as well as key insights for emulating the intricate optical response of the exoskeleton of scarab beetles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Vivek -- Crne, Matija -- Park, Jung Ok -- Srinivasarao, Mohan -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):449-51. doi: 10.1126/science.1172051.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Polymer, Textile, and Fiber Engineering, Georgia Institute of Technology, Atlanta, GA 30332, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628862" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beetles/*anatomy & histology/physiology/ultrastructure ; Color ; Microscopy, Confocal ; Optics and Photonics ; Radiation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2004-05-29
    Description: Silent-slip events have been detected at several subduction zones, but the cause of these events is unknown. Using seismic imaging, we detected a cause of the Tokai silent slip, which occurred at a presumed fault zone of a great earthquake. The seismic image that we obtained shows a zone of high pore fluid pressure in the subducted oceanic crust located down-dip of a subducted ridge. We propose that these structures effectively extend a region of conditionally stable slips and consequently generate the silent slip.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kodaira, Shuichi -- Iidaka, Takashi -- Kato, Aitaro -- Park, Jin-Oh -- Iwasaki, Takaya -- Kaneda, Yoshiyuki -- New York, N.Y. -- Science. 2004 May 28;304(5675):1295-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Frontier Research on Earth Evolution, Japan Agency for Marine-Earth Science and Technology, Showa-machi 3175-25 Kanazawa-ku, Yokohama 236-0001, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15166372" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2007-04-28
    Description: The epidermal growth factor receptor (EGFR) kinase inhibitors gefitinib and erlotinib are effective treatments for lung cancers with EGFR activating mutations, but these tumors invariably develop drug resistance. Here, we describe a gefitinib-sensitive lung cancer cell line that developed resistance to gefitinib as a result of focal amplification of the MET proto-oncogene. inhibition of MET signaling in these cells restored their sensitivity to gefitinib. MET amplification was detected in 4 of 18 (22%) lung cancer specimens that had developed resistance to gefitinib or erlotinib. We find that amplification of MET causes gefitinib resistance by driving ERBB3 (HER3)-dependent activation of PI3K, a pathway thought to be specific to EGFR/ERBB family receptors. Thus, we propose that MET amplification may promote drug resistance in other ERBB-driven cancers as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Engelman, Jeffrey A -- Zejnullahu, Kreshnik -- Mitsudomi, Tetsuya -- Song, Youngchul -- Hyland, Courtney -- Park, Joon Oh -- Lindeman, Neal -- Gale, Christopher-Michael -- Zhao, Xiaojun -- Christensen, James -- Kosaka, Takayuki -- Holmes, Alison J -- Rogers, Andrew M -- Cappuzzo, Federico -- Mok, Tony -- Lee, Charles -- Johnson, Bruce E -- Cantley, Lewis C -- Janne, Pasi A -- 1K12CA87723-01/CA/NCI NIH HHS/ -- GM41890/GM/NIGMS NIH HHS/ -- K08CA120060-01/CA/NCI NIH HHS/ -- P01 CA089021/CA/NCI NIH HHS/ -- P20CA90578-02/CA/NCI NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- R01-CA111560/CA/NCI NIH HHS/ -- R01CA114465-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 18;316(5827):1039-43. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology/therapeutic use ; CHO Cells ; Carcinoma, Non-Small-Cell Lung/drug therapy/genetics/*metabolism/*pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cricetinae ; Cricetulus ; Drug Resistance, Neoplasm ; Enzyme Inhibitors ; *Gene Amplification ; Humans ; Indoles/pharmacology ; Lung Neoplasms/drug therapy/genetics/metabolism/pathology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Proto-Oncogene Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-met ; Quinazolines/*pharmacology/therapeutic use ; Receptor, ErbB-3/*metabolism ; Receptors, Growth Factor/*genetics/metabolism ; *Signal Transduction ; Sulfones/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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