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  • 1
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    Maximum entropy analysis of dispersed seismic signals (1986)
    In:  Geophysics, Roma, Acad. Roy. des Sciences, vol. 51, no. 51, pp. 2225-2234, pp. B04102, (ISBN: 0-12-018847-3)
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    Publication Date: 1986
    Keywords: Dispersion ; Group veloc. ; Maximum entropy
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    BIBLIOGRAPHY SEISMOLOGY
  • 2
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    Velocity analysis of SH-channel wave in the Schwalbach seam at Ensdorf colliery (1988)
    In:  Geophysics, Roma, Acad. Roy. des Sciences, vol. 53, no. 51, pp. 298-317, pp. B04102, (ISBN: 0-12-018847-3)
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    Publication Date: 1988
    Keywords: Channel waves ; Love-waves ; Mining geophysics ; SH waves
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    BIBLIOGRAPHY SEISMOLOGY
  • 3
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    High resolution analysis of dispersed seismic signals (1986)
    Earth Sciences
    In:  Dissertation Oxford University, Hanscom Air Force Base, Earth Sciences, vol. 10, no. PL-TR-91-2215, pp. 1-147
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    Publication Date: 1986
    Keywords: PIC ; gab ; Dispersion ; Seismology
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    BIBLIOGRAPHY SEISMOLOGY
  • 4
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    Characterization of the lipopolysaccharide produced by Pasteurella multocida serovars 6, 7 and 16: Identification of lipopolysaccharide genotypes L4 and L8 (2015)
    Oxford University Press
    Details
    Publication Date: 2015-01-30
    Description: Pasteurella multocida is an important veterinary pathogen that produces a wide range of lipopolysaccharide (LPS) structures, many of which mimic host glycoproteins. In this study, we complete our analysis of the LPS produced by the P. multocida Heddleston serovars by reporting the LPS structure and the LPS outer core biosynthesis loci of the type strains representing Heddleston serovars 6, 7 and 16. Genetic analysis revealed that the type strains representing serovars 6 and 7 share the same LPS outer core biosynthesis locus which we have designated LPS genotype L4. Comparative bioinformatic analysis revealed that although the serovar 16 type strain contained a different LPS locus, L8, there was a significant degree of nucleotide identity between the L4 and L8 loci. Structural analysis revealed that the LPS glycoforms produced by the L4 and L8 strains all contained the highly conserved inner core produced by all other P. multocida strains examined to date. The residues within the LPS outer core produced by the L4 and L8 strains were either Gal or derivatives of Gal; unlike all other P. multocida Heddleston type strains examined there are no heptosyltransferases encoded in the L4 and L8 outer core biosynthesis loci. The structure of the L4 LPS outer core produced by the serovar 6 type strain consisted of β-Gal-(1-3)-β- N -acetylgalactosamine (Gal N Ac)-(1-4)-β-Gal N Ac3 O Ac-(1-4)-α-Gal N Ac3 O Ac-(1-3)-β-Gal, whereas the serovar 7 type strain produced a highly truncated LPS outer core containing only a single β-Gal residue. The structure of the L8 LPS outer core produced by the serovar 16 type strain consisted of β-Gal-(1-3)-β-Gal N Ac-(1-4)-(α-Gal N Ac-(1-3)-)-α-Gal N Ac.
    Print ISSN: 0959-6658
    Electronic ISSN: 1460-2423
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 5
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    Insights into Krabbe disease from structures of galactocerebrosidase [Biochemistry] (2011)
    National Academy of Sciences
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    Publication Date: 2011-09-14
    Description: Krabbe disease is a devastating neurodegenerative disease characterized by widespread demyelination that is caused by defects in the enzyme galactocerebrosidase (GALC). Disease-causing mutations have been identified throughout the GALC gene. However, a molecular understanding of the effect of these mutations has been hampered by the lack of structural data for this enzyme. Here we present the crystal structures of GALC and the GALC-product complex, revealing a novel domain architecture with a previously uncharacterized lectin domain not observed in other hydrolases. All three domains of GALC contribute residues to the substrate-binding pocket, and disease-causing mutations are widely distributed throughout the protein. Our structures provide an essential insight into the diverse effects of pathogenic mutations on GALC function in human Krabbe variants and a compelling explanation for the severity of many mutations associated with fatal infantile disease. The localization of disease-associated mutations in the structure of GALC will facilitate identification of those patients that would be responsive to pharmacological chaperone therapies. Furthermore, our structure provides the atomic framework for the design of such drugs.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    Biallelic inactivation of BRCA2 in Fanconi anemia (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-18
    Description: Fanconi anemia (FA) is a rare autosomal recessive cancer susceptibility disorder characterized by cellular hypersensitivity to mitomycin C (MMC). Six FA genes have been cloned, but the gene or genes corresponding to FA subtypes B and D1 remain unidentified. Here we show that cell lines derived from FA-B and FA-D1 patients have biallelic mutations in BRCA2 and express truncated BRCA2 proteins. Functional complementation of FA-D1 fibroblasts with wild-type BRCA2 complementary DNA restores MMC resistance. Our results link the six cloned FA genes with BRCA1 and BRCA2 in a common pathway. Germ-line mutation of genes in this pathway may result in cancer risks similar to those observed in families with BRCA1 or BRCA2 mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howlett, Niall G -- Taniguchi, Toshiyasu -- Olson, Susan -- Cox, Barbara -- Waisfisz, Quinten -- De Die-Smulders, Christine -- Persky, Nicole -- Grompe, Markus -- Joenje, Hans -- Pals, Gerard -- Ikeda, Hideyuki -- Fox, Edward A -- D'Andrea, Alan D -- P01HL54785/HL/NHLBI NIH HHS/ -- R01DK43889/DK/NIDDK NIH HHS/ -- R01HL52725/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 26;297(5581):606-9. Epub 2002 Jun 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology, Children's Hospital, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12065746" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; BRCA2 Protein/chemistry/genetics/*metabolism ; Cell Line ; DNA Damage ; Fanconi Anemia/*genetics ; Female ; Fibroblasts ; Frameshift Mutation ; Gene Silencing ; Genes, BRCA1 ; *Genes, BRCA2 ; Genetic Complementation Test ; Germ-Line Mutation ; Homozygote ; Humans ; Male ; Mitomycin/pharmacology ; Molecular Sequence Data ; *Mutation ; Pedigree ; Phenotype ; Protein Isoforms ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Synthesis and Pharmacology of (Pyridin-2-yl)methanol Derivatives as Novel and Selective Transient Receptor Potential Vanilloid 3 Antagonists (2016)
    American Chemical Society (ACS)
    Details
    Publication Date: 2016-05-03
    Description: Journal of Medicinal Chemistry DOI: 10.1021/acs.jmedchem.6b00287
    Topics: Chemistry and Pharmacology
    Published by American Chemical Society (ACS)
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  • 8
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    Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-08-13
    Description: Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182531/" 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/PMC3182531/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉International Multiple Sclerosis Genetics Consortium -- Wellcome Trust Case Control Consortium 2 -- Sawcer, Stephen -- Hellenthal, Garrett -- Pirinen, Matti -- Spencer, Chris C A -- Patsopoulos, Nikolaos A -- Moutsianas, Loukas -- Dilthey, Alexander -- Su, Zhan -- Freeman, Colin -- Hunt, Sarah E -- Edkins, Sarah -- Gray, Emma -- Booth, David R -- Potter, Simon C -- Goris, An -- Band, Gavin -- Oturai, Annette Bang -- Strange, Amy -- Saarela, Janna -- Bellenguez, Celine -- Fontaine, Bertrand -- Gillman, Matthew -- Hemmer, Bernhard -- Gwilliam, Rhian -- Zipp, Frauke -- Jayakumar, Alagurevathi -- Martin, Roland -- Leslie, Stephen -- Hawkins, Stanley -- Giannoulatou, Eleni -- D'alfonso, Sandra -- Blackburn, Hannah -- Martinelli Boneschi, Filippo -- Liddle, Jennifer -- Harbo, Hanne F -- Perez, Marc L -- Spurkland, Anne -- Waller, Matthew J -- Mycko, Marcin P -- Ricketts, Michelle -- Comabella, Manuel -- Hammond, Naomi -- Kockum, Ingrid -- McCann, Owen T -- Ban, Maria -- Whittaker, Pamela -- Kemppinen, Anu -- Weston, Paul -- Hawkins, Clive -- Widaa, Sara -- Zajicek, John -- Dronov, Serge -- Robertson, Neil -- Bumpstead, Suzannah J -- Barcellos, Lisa F -- Ravindrarajah, Rathi -- Abraham, Roby -- Alfredsson, Lars -- Ardlie, Kristin -- Aubin, Cristin -- Baker, Amie -- Baker, Katharine -- Baranzini, Sergio E -- Bergamaschi, Laura -- Bergamaschi, Roberto -- Bernstein, Allan -- Berthele, Achim -- Boggild, Mike -- Bradfield, Jonathan P -- Brassat, David -- Broadley, Simon A -- Buck, Dorothea -- Butzkueven, Helmut -- Capra, Ruggero -- Carroll, William M -- Cavalla, Paola -- Celius, Elisabeth G -- Cepok, Sabine -- Chiavacci, Rosetta -- Clerget-Darpoux, Francoise -- Clysters, Katleen -- Comi, Giancarlo -- Cossburn, Mark -- Cournu-Rebeix, Isabelle -- Cox, Mathew B -- Cozen, Wendy -- Cree, Bruce A C -- Cross, Anne H -- Cusi, Daniele -- Daly, Mark J -- Davis, Emma -- de Bakker, Paul I W -- Debouverie, Marc -- D'hooghe, Marie Beatrice -- Dixon, Katherine -- Dobosi, Rita -- Dubois, Benedicte -- Ellinghaus, David -- Elovaara, Irina -- Esposito, Federica -- Fontenille, Claire -- Foote, Simon -- Franke, Andre -- Galimberti, Daniela -- Ghezzi, Angelo -- Glessner, Joseph -- Gomez, Refujia -- Gout, Olivier -- Graham, Colin -- Grant, Struan F A -- Guerini, Franca Rosa -- Hakonarson, Hakon -- Hall, Per -- Hamsten, Anders -- Hartung, Hans-Peter -- Heard, Rob N -- Heath, Simon -- Hobart, Jeremy -- Hoshi, Muna -- Infante-Duarte, Carmen -- Ingram, Gillian -- Ingram, Wendy -- Islam, Talat -- Jagodic, Maja -- Kabesch, Michael -- Kermode, Allan G -- Kilpatrick, Trevor J -- Kim, Cecilia -- Klopp, Norman -- Koivisto, Keijo -- Larsson, Malin -- Lathrop, Mark -- Lechner-Scott, Jeannette S -- Leone, Maurizio A -- Leppa, Virpi -- Liljedahl, Ulrika -- Bomfim, Izaura Lima -- Lincoln, Robin R -- Link, Jenny -- Liu, Jianjun -- Lorentzen, Aslaug R -- Lupoli, Sara -- Macciardi, Fabio -- Mack, Thomas -- Marriott, Mark -- Martinelli, Vittorio -- Mason, Deborah -- McCauley, Jacob L -- Mentch, Frank -- Mero, Inger-Lise -- Mihalova, Tania -- Montalban, Xavier -- Mottershead, John -- Myhr, Kjell-Morten -- Naldi, Paola -- Ollier, William -- Page, Alison -- Palotie, Aarno -- Pelletier, Jean -- Piccio, Laura -- Pickersgill, Trevor -- Piehl, Fredrik -- Pobywajlo, Susan -- Quach, Hong L -- Ramsay, Patricia P -- Reunanen, Mauri -- Reynolds, Richard -- Rioux, John D -- Rodegher, Mariaemma -- Roesner, Sabine -- Rubio, Justin P -- Ruckert, Ina-Maria -- Salvetti, Marco -- Salvi, Erika -- Santaniello, Adam -- Schaefer, Catherine A -- Schreiber, Stefan -- Schulze, Christian -- Scott, Rodney J -- Sellebjerg, Finn -- Selmaj, Krzysztof W -- Sexton, David -- Shen, Ling -- Simms-Acuna, Brigid -- Skidmore, Sheila -- Sleiman, Patrick M A -- Smestad, Cathrine -- Sorensen, Per Soelberg -- Sondergaard, Helle Bach -- Stankovich, Jim -- Strange, Richard C -- Sulonen, Anna-Maija -- Sundqvist, Emilie -- Syvanen, Ann-Christine -- Taddeo, Francesca -- Taylor, Bruce -- Blackwell, Jenefer M -- Tienari, Pentti -- Bramon, Elvira -- Tourbah, Ayman -- Brown, Matthew A -- Tronczynska, Ewa -- Casas, Juan P -- Tubridy, Niall -- Corvin, Aiden -- Vickery, Jane -- Jankowski, Janusz -- Villoslada, Pablo -- Markus, Hugh S -- Wang, Kai -- Mathew, Christopher G -- Wason, James -- Palmer, Colin N A -- Wichmann, H-Erich -- Plomin, Robert -- Willoughby, Ernest -- Rautanen, Anna -- Winkelmann, Juliane -- Wittig, Michael -- Trembath, Richard C -- Yaouanq, Jacqueline -- Viswanathan, Ananth C -- Zhang, Haitao -- Wood, Nicholas W -- Zuvich, Rebecca -- Deloukas, Panos -- Langford, Cordelia -- Duncanson, Audrey -- Oksenberg, Jorge R -- Pericak-Vance, Margaret A -- Haines, Jonathan L -- Olsson, Tomas -- Hillert, Jan -- Ivinson, Adrian J -- De Jager, Philip L -- Peltonen, Leena -- Stewart, Graeme J -- Hafler, David A -- Hauser, Stephen L -- McVean, Gil -- Donnelly, Peter -- Compston, Alastair -- 068545/Z/02/Wellcome Trust/United Kingdom -- 075491/Z/04/Z/Wellcome Trust/United Kingdom -- 084702/Wellcome Trust/United Kingdom -- 085475/Wellcome Trust/United Kingdom -- 085475/B/08/Z/Wellcome Trust/United Kingdom -- 085475/Z/08/Z/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 898/Multiple Sclerosis Society/United Kingdom -- AI076544/AI/NIAID NIH HHS/ -- CA104021/CA/NCI NIH HHS/ -- G0100594/Medical Research Council/United Kingdom -- G0400017/Medical Research Council/United Kingdom -- G0700061/Medical Research Council/United Kingdom -- G0901310/Medical Research Council/United Kingdom -- G0901461/Medical Research Council/United Kingdom -- G19/2/Medical Research Council/United Kingdom -- K23N/S048869/PHS HHS/ -- NS032830/NS/NINDS NIH HHS/ -- NS049477/NS/NINDS NIH HHS/ -- NS049510/NS/NINDS NIH HHS/ -- NS067305/NS/NINDS NIH HHS/ -- NS19142/NS/NINDS NIH HHS/ -- NS26799/NS/NINDS NIH HHS/ -- NS43559/NS/NINDS NIH HHS/ -- PDA/02/06/016/Department of Health/United Kingdom -- R01 NS026799/NS/NINDS NIH HHS/ -- R01 NS049477/NS/NINDS NIH HHS/ -- R01 NS049477-06A1/NS/NINDS NIH HHS/ -- RR020092/RR/NCRR NIH HHS/ -- RR024992/RR/NCRR NIH HHS/ -- UL1 TR000448/TR/NCATS NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2011 Aug 10;476(7359):214-9. doi: 10.1038/nature10251.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21833088" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Differentiation/immunology ; Europe/ethnology ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genome-Wide Association Study ; HLA-A Antigens/genetics ; HLA-DR Antigens/genetics ; HLA-DRB1 Chains ; Humans ; Immunity, Cellular/genetics/*immunology ; Major Histocompatibility Complex/genetics ; Multiple Sclerosis/*genetics/*immunology ; Polymorphism, Single Nucleotide/genetics ; Sample Size ; T-Lymphocytes, Helper-Inducer/cytology/immunology
    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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  • 9
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    In quest of virtual tests for structural composites (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-18
    Description: The difficult challenge of simulating diffuse and complex fracture patterns in tough structural composites is at last beginning to yield to conceptual and computational advances in fracture modeling. Contributing successes include the refinement of cohesive models of fracture and the formulation of hybrid stress-strain and traction-displacement models that combine continuum (spatially averaged) and discrete damage representations in a single calculation. Emerging hierarchical formulations add the potential of tracing the damage mechanisms down through all scales to the atomic. As the models near the fidelity required for their use as virtual experiments, opportunities arise for reducing the number of costly tests needed to certify safety and extending the design space to include material configurations that are too complex to certify by purely empirical methods.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cox, Brian -- Yang, Qingda -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1102-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Teledyne Scientific Co., 1049 Camino Dos Rios, Thousand Oaks, CA 91360, USA. bcox@teledyne.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110566" 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    The spatial extent and distribution of star formation in 3D-HST mergers at z ~ 1.5 (2013)
    Oxford University Press
    Details
    Publication Date: 2013-05-21
    Description: We present an analysis of the spatial distribution of star formation in a sample of 60 visually identified galaxy merger candidates at z  〉 1. Our sample, drawn from the 3D- HST survey, is flux limited and was selected to have high star formation rates based on fits of their broad-band, low spatial resolution spectral energy distributions. It includes plausible pre-merger (close pairs) and post-merger (single objects with tidal features) systems, with total stellar masses and star formation rates derived from multiwavelength photometry. Here we use near-infrared slitless spectra from 3D- HST which produce Hα or [O iii ] emission line maps as proxies for star formation maps. This provides a first comprehensive high-resolution, empirical picture of where star formation occurred in galaxy mergers at the epoch of peak cosmic star formation rate. We find that detectable star formation can occur in one or both galaxy centres, or in tidal tails. The most common case (58 per cent) is that star formation is largely concentrated in a single, compact region, coincident with the centre of (one of) the merger components. No correlations between star formation morphology and redshift, total stellar mass or star formation rate are found. A restricted set of hydrodynamical merger simulations between similarly massive and gas-rich objects implies that star formation should be detectable in both merger components, when the gas fractions of the individual components are the same. This suggests that z  ~ 1.5 mergers typically occur between galaxies whose gas fractions, masses and/or star formation rates are distinctly different from one another.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press
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