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  • 1
    Publication Date: 2015-02-13
    Description: Author(s): Min He, Rainer J. Fries, and Ralf Rapp We calculate open heavy-flavor (HF) production in Au+Au collisions at √ s NN =62.4 GeV utilizing a nonperturbative transport approach as previously applied in nuclear collisions at top Relativistic Heavy Ion Collider (RHIC) and Large Hadron Collider (LHC) energies. The effects of hot QCD matter are tre... [Phys. Rev. C 91, 024904] Published Thu Feb 12, 2015
    Keywords: Relativistic Nuclear Collisions
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
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  • 2
    Publication Date: 2015-02-12
    Description: Author(s): Matthew Heffernan, Paul Hohler, and Ralf Rapp Electromagnetic (EM) radiation off strongly interacting matter created in high-energy heavy-ion collisions (HICs) encodes information on the high-temperature phases of nuclear matter. Microscopic calculations of thermal EM emission rates are usually rather involved and not readily accessible to broa... [Phys. Rev. C 91, 027902] Published Wed Feb 11, 2015
    Keywords: Relativistic Nuclear Collisions
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
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  • 3
    Publication Date: 2011-11-10
    Description: Author(s): Hendrik van Hees, Charles Gale, and Ralf Rapp [Phys. Rev. C 84, 054906] Published Wed Nov 09, 2011
    Keywords: Relativistic Nuclear Collisions
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
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  • 4
    Publication Date: 2012-04-11
    Description: Author(s): Min He, Rainer J. Fries, and Ralf Rapp We reexamine the use of ideal hydrodynamics to describe bulk- and multistrange-hadron observables in nuclear collisions at the Relativistic Heavy Ion Collider. Toward this end we augment the 2+1-dimensional code azhydro by employing (a) an equation of state based on recent lattice-QCD computations m... [Phys. Rev. C 85, 044911] Published Tue Apr 10, 2012
    Keywords: Relativistic Nuclear Collisions
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
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  • 5
    Publication Date: 2012-07-11
    Description: Author(s): Min He, Rainer J. Fries, and Ralf Rapp We calculate diffusion and hadronization of heavy quarks in high-energy heavy-ion collisions, implementing the notion of a strongly coupled quark-gluon plasma in both micro- and macroscopic components. The diffusion process is simulated using relativistic Fokker-Planck dynamics for elastic scatterin... [Phys. Rev. C 86, 014903] Published Tue Jul 10, 2012
    Keywords: Relativistic Nuclear Collisions
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
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  • 6
    Publication Date: 2014-03-11
    Description: Author(s): Gojko Vujanovic, Clint Young, Björn Schenke, Ralf Rapp, Sangyong Jeon, and Charles Gale The invariant mass spectrum and the elliptic flow of lepton pairs produced in relativistic heavy-ion collisions at RHIC are studied with viscous hydrodynamics. The effects of viscous corrections on dilepton observables are explored. The lepton pairs originating from charm quarks evolving in the visc... [Phys. Rev. C 89, 034904] Published Mon Mar 10, 2014
    Keywords: Relativistic Nuclear Collisions
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-27
    Description: Blood pressure is influenced by multiple genetic loci whose identities are largely unknown. A restriction fragment length polymorphism (RFLP) in the renin gene was found between Dahl salt-hypertension-sensitive (S) and Dahl salt-hypertension-resistant (R) rats. In an F2 population derived from crossing S and R rats, the renin RFLP cosegregated with blood pressure. One dose of the S-rat renin allele was associated with an increment in blood pressure of approximately 10 mmHg, and two doses of this allele increased blood pressure approximately 20 mmHg. From this it can be definitively concluded that in the rat the renin gene is, or is closely linked to, one of the genes regulating blood pressure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rapp, J P -- Wang, S M -- Dene, H -- HL-07357/HL/NHLBI NIH HHS/ -- HL-20176/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 27;243(4890):542-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Medical College of Ohio, Toledo 43699.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2563177" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Blood Pressure/drug effects ; Blotting, Southern ; DNA Probes ; Female ; Genotype ; Hypertension/*genetics ; Male ; *Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Rats ; Rats, Inbred Strains ; Renin/*genetics ; Sodium Chloride/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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  • 8
    Publication Date: 2013-04-19
    Description: Zebrafish have become a popular organism for the study of vertebrate gene function. The virtually transparent embryos of this species, and the ability to accelerate genetic studies by gene knockdown or overexpression, have led to the widespread use of zebrafish in the detailed investigation of vertebrate gene function and increasingly, the study of human genetic disease. However, for effective modelling of human genetic disease it is important to understand the extent to which zebrafish genes and gene structures are related to orthologous human genes. To examine this, we generated a high-quality sequence assembly of the zebrafish genome, made up of an overlapping set of completely sequenced large-insert clones that were ordered and oriented using a high-resolution high-density meiotic map. Detailed automatic and manual annotation provides evidence of more than 26,000 protein-coding genes, the largest gene set of any vertebrate so far sequenced. Comparison to the human reference genome shows that approximately 70% of human genes have at least one obvious zebrafish orthologue. In addition, the high quality of this genome assembly provides a clearer understanding of key genomic features such as a unique repeat content, a scarcity of pseudogenes, an enrichment of zebrafish-specific genes on chromosome 4 and chromosomal regions that influence sex determination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3703927/" 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/PMC3703927/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howe, Kerstin -- Clark, Matthew D -- Torroja, Carlos F -- Torrance, James -- Berthelot, Camille -- Muffato, Matthieu -- Collins, John E -- Humphray, Sean -- McLaren, Karen -- Matthews, Lucy -- McLaren, Stuart -- Sealy, Ian -- Caccamo, Mario -- Churcher, Carol -- Scott, Carol -- Barrett, Jeffrey C -- Koch, Romke -- Rauch, Gerd-Jorg -- White, Simon -- Chow, William -- Kilian, Britt -- Quintais, Leonor T -- Guerra-Assuncao, Jose A -- Zhou, Yi -- Gu, Yong -- Yen, Jennifer -- Vogel, Jan-Hinnerk -- Eyre, Tina -- Redmond, Seth -- Banerjee, Ruby -- Chi, Jianxiang -- Fu, Beiyuan -- Langley, Elizabeth -- Maguire, Sean F -- Laird, Gavin K -- Lloyd, David -- Kenyon, Emma -- Donaldson, Sarah -- Sehra, Harminder -- Almeida-King, Jeff -- Loveland, Jane -- Trevanion, Stephen -- Jones, Matt -- Quail, Mike -- Willey, Dave -- Hunt, Adrienne -- Burton, John -- Sims, Sarah -- McLay, Kirsten -- Plumb, Bob -- Davis, Joy -- Clee, Chris -- Oliver, Karen -- Clark, Richard -- Riddle, Clare -- Elliot, David -- Threadgold, Glen -- Harden, Glenn -- Ware, Darren -- Begum, Sharmin -- Mortimore, Beverley -- Kerry, Giselle -- Heath, Paul -- Phillimore, Benjamin -- Tracey, Alan -- Corby, Nicole -- Dunn, Matthew -- Johnson, Christopher -- Wood, Jonathan -- Clark, Susan -- Pelan, Sarah -- Griffiths, Guy -- Smith, Michelle -- Glithero, Rebecca -- Howden, Philip -- Barker, Nicholas -- Lloyd, Christine -- Stevens, Christopher -- Harley, Joanna -- Holt, Karen -- Panagiotidis, Georgios -- Lovell, Jamieson -- Beasley, Helen -- Henderson, Carl -- Gordon, Daria -- Auger, Katherine -- Wright, Deborah -- Collins, Joanna -- Raisen, Claire -- Dyer, Lauren -- Leung, Kenric -- Robertson, Lauren -- Ambridge, Kirsty -- Leongamornlert, Daniel -- McGuire, Sarah -- Gilderthorp, Ruth -- Griffiths, Coline -- Manthravadi, Deepa -- Nichol, Sarah -- Barker, Gary -- Whitehead, Siobhan -- Kay, Michael -- Brown, Jacqueline -- Murnane, Clare -- Gray, Emma -- Humphries, Matthew -- Sycamore, Neil -- Barker, Darren -- Saunders, David -- Wallis, Justene -- Babbage, Anne -- Hammond, Sian -- Mashreghi-Mohammadi, Maryam -- Barr, Lucy -- Martin, Sancha -- Wray, Paul -- Ellington, Andrew -- Matthews, Nicholas -- Ellwood, Matthew -- Woodmansey, Rebecca -- Clark, Graham -- Cooper, James D -- Tromans, Anthony -- Grafham, Darren -- Skuce, Carl -- Pandian, Richard -- Andrews, Robert -- Harrison, Elliot -- Kimberley, Andrew -- Garnett, Jane -- Fosker, Nigel -- Hall, Rebekah -- Garner, Patrick -- Kelly, Daniel -- Bird, Christine -- Palmer, Sophie -- Gehring, Ines -- Berger, Andrea -- Dooley, Christopher M -- Ersan-Urun, Zubeyde -- Eser, Cigdem -- Geiger, Horst -- Geisler, Maria -- Karotki, Lena -- Kirn, Anette -- Konantz, Judith -- Konantz, Martina -- Oberlander, Martina -- Rudolph-Geiger, Silke -- Teucke, Mathias -- Lanz, Christa -- Raddatz, Gunter -- Osoegawa, Kazutoyo -- Zhu, Baoli -- Rapp, Amanda -- Widaa, Sara -- Langford, Cordelia -- Yang, Fengtang -- Schuster, Stephan C -- Carter, Nigel P -- Harrow, Jennifer -- Ning, Zemin -- Herrero, Javier -- Searle, Steve M J -- Enright, Anton -- Geisler, Robert -- Plasterk, Ronald H A -- Lee, Charles -- Westerfield, Monte -- de Jong, Pieter J -- Zon, Leonard I -- Postlethwait, John H -- Nusslein-Volhard, Christiane -- Hubbard, Tim J P -- Roest Crollius, Hugues -- Rogers, Jane -- Stemple, Derek L -- 095908/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- 1 R01 DK55377-01A1/DK/NIDDK NIH HHS/ -- P01 HD022486/HD/NICHD NIH HHS/ -- P01 HD22486/HD/NICHD NIH HHS/ -- R01 GM085318/GM/NIGMS NIH HHS/ -- R01 OD011116/OD/NIH HHS/ -- R01 RR010715/RR/NCRR NIH HHS/ -- R01 RR020833/RR/NCRR NIH HHS/ -- England -- Nature. 2013 Apr 25;496(7446):498-503. doi: 10.1038/nature12111. Epub 2013 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23594743" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes/genetics ; Conserved Sequence/*genetics ; Evolution, Molecular ; Female ; Genes/genetics ; Genome/*genetics ; Genome, Human/genetics ; Genomics ; Humans ; Male ; Meiosis/genetics ; Molecular Sequence Annotation ; Pseudogenes/genetics ; Reference Standards ; Sex Determination Processes/genetics ; Zebrafish/*genetics ; Zebrafish Proteins/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1984-06-01
    Description: Crude extracts of rat atria reduced the basal amount of aldosterone released from rat zona glomerulosa cells and partially inhibited aldosterone stimulation by adrenocorticotropic hormone and angiotensin II. The destruction of this activity by trypsin suggests that the active factor is a peptide, possibly atrial natriuretic factor. These data suggest that atrial natriuretic factor affects sodium excretion by the kidneys both directly and through the inhibition of aldosterone production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, K -- Mulrow, P J -- Franco-Saenz, R -- Snajdar, R -- Rapp, J -- New York, N.Y. -- Science. 1984 Jun 1;224(4652):992-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6326267" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/pharmacology ; Aldosterone/*biosynthesis ; Angiotensin II/pharmacology ; Animals ; *Atrial Function ; Dogs ; Female ; Kidney/drug effects/metabolism ; Mineralocorticoid Receptor Antagonists/pharmacology ; Natriuresis/drug effects ; Rats ; Rats, Inbred Strains ; Trypsin/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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  • 10
    Publication Date: 2015-12-18
    Description: Variant rs351855-G/A is a commonly occurring single-nucleotide polymorphism of coding regions in exon 9 of the fibroblast growth factor receptor FGFR4 (CD334) gene (c.1162G〉A). It results in an amino-acid change at codon 388 from glycine to arginine (p.Gly388Arg) in the transmembrane domain of the receptor. Despite compelling genetic evidence for the association of this common variant with cancers of the bone, breast, colon, prostate, skin, lung, head and neck, as well as soft-tissue sarcomas and non-Hodgkin lymphoma, the underlying biological mechanism has remained elusive. Here we show that substitution of the conserved glycine 388 residue to a charged arginine residue alters the transmembrane spanning segment and exposes a membrane-proximal cytoplasmic signal transducer and activator of transcription 3 (STAT3) binding site Y(390)-(P)XXQ(393). We demonstrate that such membrane-proximal STAT3 binding motifs in the germline of type I membrane receptors enhance STAT3 tyrosine phosphorylation by recruiting STAT3 proteins to the inner cell membrane. Remarkably, such germline variants frequently co-localize with somatic mutations in the Catalogue of Somatic Mutations in Cancer (COSMIC) database. Using Fgfr4 single nucleotide polymorphism knock-in mice and transgenic mouse models for breast and lung cancers, we validate the enhanced STAT3 signalling induced by the FGFR4 Arg388-variant in vivo. Thus, our findings elucidate the molecular mechanism behind the genetic association of rs351855 with accelerated cancer progression and suggest that germline variants of cell-surface molecules that recruit STAT3 to the inner cell membrane are a significant risk for cancer prognosis and disease progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ulaganathan, Vijay K -- Sperl, Bianca -- Rapp, Ulf R -- Ullrich, Axel -- HL-102923/HL/NHLBI NIH HHS/ -- HL-102924/HL/NHLBI NIH HHS/ -- HL-102925/HL/NHLBI NIH HHS/ -- HL-102926/HL/NHLBI NIH HHS/ -- HL-103010/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):570-4. doi: 10.1038/nature16449. Epub 2015 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Biochemistry, Department of Molecular Biology, Am Klopferspitz 18, 82152, Martinsried. Germany. ; Max Planck Institute for Heart and Lung Research, Molecular Mechanisms of Lung Cancer, Parkstrasse 1, 61231 Bad Nauheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26675719" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs/genetics ; Amino Acid Sequence ; Animals ; Binding Sites/genetics ; Breast Neoplasms/genetics/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Disease Models, Animal ; Disease Progression ; Exons/genetics ; Female ; Gene Knock-In Techniques ; *Germ-Line Mutation ; Humans ; Lung Neoplasms/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Phosphorylation ; Phosphotyrosine/metabolism ; Polymorphism, Single Nucleotide/genetics ; Receptor, Fibroblast Growth Factor, Type 4/chemistry/*genetics/*metabolism ; STAT3 Transcription Factor/*metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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