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  • 1
    Electronic Resource
    Electronic Resource
    Soldier defensive secretions of two rare nearctic desert termite species
    Amsterdam : Elsevier
    Biochemical Systematics and Ecology 16 (1988), S. 213-216 
    Details
    ISSN: 0305-1978
    Keywords: 4,11-epoxy-cis-eudesmane ; Amitermes coachellae ; Amitermes emersoni ; Amitermitinae ; Isoptera ; Termitidae ; biogeography ; phylogeny ; soldier defensive secretions ; terpenes
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0305-1978(88)90099-3
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  • 2
    Electronic Resource
    Electronic Resource
    Chemical heterogeneity of soldier defensive secretions in the desert subterranean termite, Amitermes wheeleri
    Amsterdam : Elsevier
    Biochemical Systematics and Ecology 14 (1986), S. 661-664 
    Details
    ISSN: 0305-1978
    Keywords: Amitermes wheeleri ; Isoptera ; Termitidae ; chemosystematics ; defensive secretions ; intraspecific variation ; sesquiterpenoids ; termite soldiers
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0305-1978(86)90049-9
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  • 3
    Electronic Resource
    Electronic Resource
    Identification of the defensive secretion from soldiers of the North American termite,Amitermes wheeleri (Desneux) (Isoptera: Termitidae) (1983)
    Springer
    Journal of chemical ecology 9 (1983), S. 1293-1305 
    Details
    ISSN: 1573-1561
    Keywords: Amitermes wheeleri ; Isoptera ; Termitidae ; termite soldiers ; defensive secretion ; ant repellents ; α-bisabolene ; β-bisabolene ; α2-bisabolene ; Iridomyrmex humilis ; Pogonomyrmex rugosus ; sesquiterpenes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Head capsule extracts ofAmitermes wheeleri soldiers yielded an isomeric mixture (67 μg/ soldier) of three sesquiterpene hydrocarbons identified by EIMS, [13C]-, and [1H]NMR as (+)-(S,Z)-α-bisabolene (53%), (+)-(R)-β-bisabolene (16%), and (−)-(Z)-α2-bisabolene (31%). When alarmed, the termite soldiers secreted the fluid onto the head surface surrounding the efferent pore of the frontal gland reservoir. A defensive function for the soldier secretion was indicated by the avoidance behavior displayed toward alarmed soldiers by the antagonistic ants,Pogonomyrmex rugosus andIridomyrmex humilis. Laboratory studies demonstrated that the sesquiterpene mixture is repellent to foragingI. humilis workers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00994798
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  • 4
    Electronic Resource
    Electronic Resource
    Drywood termite feeding deterrents in sugar pine and antitermitic activity of related compounds (1983)
    Springer
    Journal of chemical ecology 9 (1983), S. 39-55 
    Details
    ISSN: 1573-1561
    Keywords: Feeding deterrents ; drywood termites ; Incisitermes minor ; Isoptera ; Kalotermitidae ; sugar pine ; Pinus lambertiana ; fatty acids α-halogenated acids ; esters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The feeding deterrent activity of sapwood extracts of sugar pine,Pinus lambertiana Dougl., and related compounds was determined against immatures of the western drywood termite,Incisitermes minor (Hagen). A bioassay was designed to quantify reductions in termite feeding caused by deterrent chemicals. Crude extracts and isolated fractions of sugar pine were deterrent and not preferred byI. minor at 0.5 mg/cm2. Fatty acids occurring in sugar pine extracts had a broad range of deterrent activity. Long-chain saturated fatty acids were deterrent at 0.25 and 0.05 mg/cm2. Unsaturated or intermediate length (C8-C14) acids, many not found in sugar pine wood, were less active than long-chain saturated acids. Related alpha-halogenated compounds were highly deterrent at 0.05 mg/cm2 regardless of chain length or presence of a carboxylic acid moiety. Deposits of 2-iodooctadecanoic acid reduced termite feeding at 5 μg/cm2, while 2-bromooctadecanoic acid had deterrent activity comparable to commercial wood preservatives. None of the halogenated compounds tested were termiticidal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00987769
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  • 5
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    Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-21
    Description: The genetics of renal cancer is dominated by inactivation of the VHL tumour suppressor gene in clear cell carcinoma (ccRCC), the commonest histological subtype. A recent large-scale screen of approximately 3,500 genes by PCR-based exon re-sequencing identified several new cancer genes in ccRCC including UTX (also known as KDM6A), JARID1C (also known as KDM5C) and SETD2 (ref. 2). These genes encode enzymes that demethylate (UTX, JARID1C) or methylate (SETD2) key lysine residues of histone H3. Modification of the methylation state of these lysine residues of histone H3 regulates chromatin structure and is implicated in transcriptional control. However, together these mutations are present in fewer than 15% of ccRCC, suggesting the existence of additional, currently unidentified cancer genes. Here, we have sequenced the protein coding exome in a series of primary ccRCC and report the identification of the SWI/SNF chromatin remodelling complex gene PBRM1 (ref. 4) as a second major ccRCC cancer gene, with truncating mutations in 41% (92/227) of cases. These data further elucidate the somatic genetic architecture of ccRCC and emphasize the marked contribution of aberrant chromatin biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030920/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varela, Ignacio -- Tarpey, Patrick -- Raine, Keiran -- Huang, Dachuan -- Ong, Choon Kiat -- Stephens, Philip -- Davies, Helen -- Jones, David -- Lin, Meng-Lay -- Teague, Jon -- Bignell, Graham -- Butler, Adam -- Cho, Juok -- Dalgliesh, Gillian L -- Galappaththige, Danushka -- Greenman, Chris -- Hardy, Claire -- Jia, Mingming -- Latimer, Calli -- Lau, King Wai -- Marshall, John -- McLaren, Stuart -- Menzies, Andrew -- Mudie, Laura -- Stebbings, Lucy -- Largaespada, David A -- Wessels, L F A -- Richard, Stephane -- Kahnoski, Richard J -- Anema, John -- Tuveson, David A -- Perez-Mancera, Pedro A -- Mustonen, Ville -- Fischer, Andrej -- Adams, David J -- Rust, Alistair -- Chan-on, Waraporn -- Subimerb, Chutima -- Dykema, Karl -- Furge, Kyle -- Campbell, Peter J -- Teh, Bin Tean -- Stratton, Michael R -- Futreal, P Andrew -- 077012/Wellcome Trust/United Kingdom -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- R01 CA113636/CA/NCI NIH HHS/ -- R01 CA134759/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Jan 27;469(7331):539-42. doi: 10.1038/nature09639. Epub 2011 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Renal Cell/*genetics ; Cell Line, Tumor ; Disease Models, Animal ; Gene Expression Regulation ; Gene Knockdown Techniques ; Humans ; Kidney Neoplasms/*genetics ; Mice ; Mutation/*genetics ; Nuclear Proteins/*genetics/*metabolism ; Pancreatic Neoplasms/genetics ; Transcription Factors/*genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-30
    Description: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530898/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biankin, Andrew V -- Waddell, Nicola -- Kassahn, Karin S -- Gingras, Marie-Claude -- Muthuswamy, Lakshmi B -- Johns, Amber L -- Miller, David K -- Wilson, Peter J -- Patch, Ann-Marie -- Wu, Jianmin -- Chang, David K -- Cowley, Mark J -- Gardiner, Brooke B -- Song, Sarah -- Harliwong, Ivon -- Idrisoglu, Senel -- Nourse, Craig -- Nourbakhsh, Ehsan -- Manning, Suzanne -- Wani, Shivangi -- Gongora, Milena -- Pajic, Marina -- Scarlett, Christopher J -- Gill, Anthony J -- Pinho, Andreia V -- Rooman, Ilse -- Anderson, Matthew -- Holmes, Oliver -- Leonard, Conrad -- Taylor, Darrin -- Wood, Scott -- Xu, Qinying -- Nones, Katia -- Fink, J Lynn -- Christ, Angelika -- Bruxner, Tim -- Cloonan, Nicole -- Kolle, Gabriel -- Newell, Felicity -- Pinese, Mark -- Mead, R Scott -- Humphris, Jeremy L -- Kaplan, Warren -- Jones, Marc D -- Colvin, Emily K -- Nagrial, Adnan M -- Humphrey, Emily S -- Chou, Angela -- Chin, Venessa T -- Chantrill, Lorraine A -- Mawson, Amanda -- Samra, Jaswinder S -- Kench, James G -- Lovell, Jessica A -- Daly, Roger J -- Merrett, Neil D -- Toon, Christopher -- Epari, Krishna -- Nguyen, Nam Q -- Barbour, Andrew -- Zeps, Nikolajs -- Australian Pancreatic Cancer Genome Initiative -- Kakkar, Nipun -- Zhao, Fengmei -- Wu, Yuan Qing -- Wang, Min -- Muzny, Donna M -- Fisher, William E -- Brunicardi, F Charles -- Hodges, Sally E -- Reid, Jeffrey G -- Drummond, Jennifer -- Chang, Kyle -- Han, Yi -- Lewis, Lora R -- Dinh, Huyen -- Buhay, Christian J -- Beck, Timothy -- Timms, Lee -- Sam, Michelle -- Begley, Kimberly -- Brown, Andrew -- Pai, Deepa -- Panchal, Ami -- Buchner, Nicholas -- De Borja, Richard -- Denroche, Robert E -- Yung, Christina K -- Serra, Stefano -- Onetto, Nicole -- Mukhopadhyay, Debabrata -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Gallinger, Steven -- Hruban, Ralph H -- Maitra, Anirban -- Iacobuzio-Donahue, Christine A -- Schulick, Richard D -- Wolfgang, Christopher L -- Morgan, Richard A -- Lawlor, Rita T -- Capelli, Paola -- Corbo, Vincenzo -- Scardoni, Maria -- Tortora, Giampaolo -- Tempero, Margaret A -- Mann, Karen M -- Jenkins, Nancy A -- Perez-Mancera, Pedro A -- Adams, David J -- Largaespada, David A -- Wessels, Lodewyk F A -- Rust, Alistair G -- Stein, Lincoln D -- Tuveson, David A -- Copeland, Neal G -- Musgrove, Elizabeth A -- Scarpa, Aldo -- Eshleman, James R -- Hudson, Thomas J -- Sutherland, Robert L -- Wheeler, David A -- Pearson, John V -- McPherson, John D -- Gibbs, Richard A -- Grimmond, Sean M -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- P01CA134292/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50CA062924/CA/NCI NIH HHS/ -- R01 CA097075/CA/NCI NIH HHS/ -- R01 CA97075/CA/NCI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Nov 15;491(7424):399-405. doi: 10.1038/nature11547. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kinghorn Cancer Centre, 370 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Carcinoma, Pancreatic Ductal/*genetics/*pathology ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genome/*genetics ; Humans ; Kaplan-Meier Estimate ; Mice ; Mutation ; Pancreatic Neoplasms/*genetics/*pathology ; Proteins/genetics ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    The mutational landscapes of genetic and chemical models of Kras-driven lung cancer (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-11-05
    Description: Next-generation sequencing of human tumours has refined our understanding of the mutational processes operative in cancer initiation and progression, yet major questions remain regarding the factors that induce driver mutations and the processes that shape mutation selection during tumorigenesis. Here we performed whole-exome sequencing on adenomas from three mouse models of non-small-cell lung cancer, which were induced either by exposure to carcinogens (methyl-nitrosourea (MNU) and urethane) or by genetic activation of Kras (Kras(LA2)). Although the MNU-induced tumours carried exactly the same initiating mutation in Kras as seen in the Kras(LA2) model (G12D), MNU tumours had an average of 192 non-synonymous, somatic single-nucleotide variants, compared with only six in tumours from the Kras(LA2) model. By contrast, the Kras(LA2) tumours exhibited a significantly higher level of aneuploidy and copy number alterations compared with the carcinogen-induced tumours, suggesting that carcinogen-induced and genetically engineered models lead to tumour development through different routes. The wild-type allele of Kras has been shown to act as a tumour suppressor in mouse models of non-small-cell lung cancer. We demonstrate that urethane-induced tumours from wild-type mice carry mostly (94%) Kras Q61R mutations, whereas those from Kras heterozygous animals carry mostly (92%) Kras Q61L mutations, indicating a major role for germline Kras status in mutation selection during initiation. The exome-wide mutation spectra in carcinogen-induced tumours overwhelmingly display signatures of the initiating carcinogen, while adenocarcinomas acquire additional C 〉 T mutations at CpG sites. These data provide a basis for understanding results from human tumour genome sequencing, which has identified two broad categories of tumours based on the relative frequency of single-nucleotide variations and copy number alterations, and underline the importance of carcinogen models for understanding the complex mutation spectra seen in human cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304785/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304785/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westcott, Peter M K -- Halliwill, Kyle D -- To, Minh D -- Rashid, Mamunur -- Rust, Alistair G -- Keane, Thomas M -- Delrosario, Reyno -- Jen, Kuang-Yu -- Gurley, Kay E -- Kemp, Christopher J -- Fredlund, Erik -- Quigley, David A -- Adams, David J -- Balmain, Allan -- 082356/Wellcome Trust/United Kingdom -- 13031/Cancer Research UK/United Kingdom -- A12401/Cancer Research UK/United Kingdom -- A13031/Cancer Research UK/United Kingdom -- A14356/Cancer Research UK/United Kingdom -- F31 CA180669/CA/NCI NIH HHS/ -- F31 CA180715/CA/NCI NIH HHS/ -- R01 CA111834/CA/NCI NIH HHS/ -- R01 CA184510/CA/NCI NIH HHS/ -- T32 GM007175/GM/NIGMS NIH HHS/ -- T32GM007175/GM/NIGMS NIH HHS/ -- U01 CA084244/CA/NCI NIH HHS/ -- U01 CA141455/CA/NCI NIH HHS/ -- U01 CA176287/CA/NCI NIH HHS/ -- U01 CA84244/CA/NCI NIH HHS/ -- UO1 CA176287/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2015 Jan 22;517(7535):489-92. doi: 10.1038/nature13898. Epub 2014 Nov 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA [2] Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, California 94158, USA. ; Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA. ; Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK. ; Department of Pathology, University of California San Francisco, San Francisco, California 94143, USA. ; Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; Science for Life Laboratory, Department of Oncology-Pathology, Karolinska Institute, Stockholm 171 21, Sweden. ; 1] Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA [2] Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363767" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/chemically induced/genetics ; Animals ; Carcinogens/toxicity ; Carcinoma, Non-Small-Cell Lung/chemically induced/genetics ; Cell Transformation, Neoplastic/*chemically induced/*genetics ; DNA Copy Number Variations/genetics ; Disease Progression ; Female ; Genes, ras/*genetics ; Genomic Instability/genetics ; Germ-Line Mutation/genetics ; Humans ; Lung Neoplasms/*chemically induced/*genetics ; Male ; Methylnitrosourea/toxicity ; Mice ; Models, Genetic ; Mutation/*genetics ; Oncogene Protein p21(ras)/*genetics ; Point Mutation/genetics ; Proto-Oncogene Proteins p21(ras)/*genetics ; Urethane/toxicity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 8
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    The deubiquitinase USP9X suppresses pancreatic ductal adenocarcinoma (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-16
    Description: Pancreatic ductal adenocarcinoma (PDA) remains a lethal malignancy despite much progress concerning its molecular characterization. PDA tumours harbour four signature somatic mutations in addition to numerous lower frequency genetic events of uncertain significance. Here we use Sleeping Beauty (SB) transposon-mediated insertional mutagenesis in a mouse model of pancreatic ductal preneoplasia to identify genes that cooperate with oncogenic Kras(G12D) to accelerate tumorigenesis and promote progression. Our screen revealed new candidate genes for PDA and confirmed the importance of many genes and pathways previously implicated in human PDA. The most commonly mutated gene was the X-linked deubiquitinase Usp9x, which was inactivated in over 50% of the tumours. Although previous work had attributed a pro-survival role to USP9X in human neoplasia, we found instead that loss of Usp9x enhances transformation and protects pancreatic cancer cells from anoikis. Clinically, low USP9X protein and messenger RNA expression in PDA correlates with poor survival after surgery, and USP9X levels are inversely associated with metastatic burden in advanced disease. Furthermore, chromatin modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X expression in human PDA cell lines, indicating a clinical approach for certain patients. The conditional deletion of Usp9x cooperated with Kras(G12D) to accelerate pancreatic tumorigenesis in mice, validating their genetic interaction. We propose that USP9X is a major tumour suppressor gene with prognostic and therapeutic relevance in PDA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376394/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perez-Mancera, Pedro A -- Rust, Alistair G -- van der Weyden, Louise -- Kristiansen, Glen -- Li, Allen -- Sarver, Aaron L -- Silverstein, Kevin A T -- Grutzmann, Robert -- Aust, Daniela -- Rummele, Petra -- Knosel, Thomas -- Herd, Colin -- Stemple, Derek L -- Kettleborough, Ross -- Brosnan, Jacqueline A -- Li, Ang -- Morgan, Richard -- Knight, Spencer -- Yu, Jun -- Stegeman, Shane -- Collier, Lara S -- ten Hoeve, Jelle J -- de Ridder, Jeroen -- Klein, Alison P -- Goggins, Michael -- Hruban, Ralph H -- Chang, David K -- Biankin, Andrew V -- Grimmond, Sean M -- Australian Pancreatic Cancer Genome Initiative -- Wessels, Lodewyk F A -- Wood, Stephen A -- Iacobuzio-Donahue, Christine A -- Pilarsky, Christian -- Largaespada, David A -- Adams, David J -- Tuveson, David A -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- CA106610/CA/NCI NIH HHS/ -- CA122183/CA/NCI NIH HHS/ -- CA128920/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- K01 CA122183/CA/NCI NIH HHS/ -- K01 CA122183-05/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50CA62924/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Apr 29;486(7402):266-70. doi: 10.1038/nature11114.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Li Ka Shing Centre, Cambridge Research Institute, Cancer Research UK, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anoikis/genetics ; Carcinoma, Pancreatic Ductal/*enzymology/genetics/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Endopeptidases ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms/*enzymology/genetics/pathology ; U937 Cells ; Ubiquitin Thiolesterase/*genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    A fractal analysis of quaternary, Cenozoic-Mesozoic, and Late Pennsylvanian sea level changes (1993)
    In:  Other Sources
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    Publication Date: 2019-07-13
    Description: Sea level changes are related to both climatic variations and tectonic movements. The fractal dimensions of several sea level curves were compared to a modern climatic fractal dimension of 1.26 established for annual precipitation records. A similar fractal dimension (1.22) based on delta(O-18/O-16) in deep-sea sediments has been suggested to characterize climatic change during the past 2 m.y. Our analysis indicates that sea level changes over the past 150,000 to 250,000 years also exhibit comparable fractal dimensions. Sea level changes for periods longer than about 30 m.y. are found to produce fractal dimensions closer to unity and Missourian (Late Pennsylvanian) sea level changes yield a fractal dimension of 1.41. The fact that these sea level curves all possess fractal dimensions less than 1.5 indicates that sea level changes exhibit nonperiodic, long-run persistence. The different fractal dimensions calculated for the various time periods could be the result of a characteristic overprinting of the sediment recored by prevailing processes during deposition. For example, during the Quaternary, glacio-eustatic sea level changes correlate well with the present climatic signature. During the Missourian, however, mechanisms such as plate reorganization may have dominated, resulting in a significantly different fractal dimension.
    Keywords: GEOPHYSICS
    Type: Journal of Geophysical Research (ISSN 0148-0227); 98; B12; p. 21963-21967
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  • 10
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    Application of X-ray imaging techniques to auroral monitoring (1981)
    In:  Other Sources
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    Publication Date: 2019-07-13
    Description: The precipitation of energetic particles into the ionosphere produces bremsstrahlung X-rays and K-alpha line emission from excited oxygen and nitrogen. If viewed from a spacecraft in a highly elliptical polar orbit, this soft (0.3 - 3.0 keV) X-radiation will provide an almost uninterrupted record of dayside and nightside auroras. A grazing incidence X-ray telescope especially designed for such auroral monitoring is described. High photon collection efficiency will permit exposure times of approximately 100 seconds during substorms. Spectrophotometry will allow users to derive the energy spectrum of the precipitating particles. If placed in a 15 earth-radius orbit, the telescope can produce auroral X-ray images with 30 km resolution. Absolute position of X-ray auroras can be established with a small optical telescope co-aligned with the X-ray telescope. Comparison of X-ray and optical images will establish the height and global distribution of X-ray aurorae, relative to well-known optical auroras, thus melding the new X-ray results with knowledge of optical auroras.
    Keywords: GEOPHYSICS
    Type: Symposium on the Effect of the Ionosphere on Radiowave Systems; Apr 14, 1981 - Apr 16, 1981; Washington, DC
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