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  • Male  (8)
  • Chemistry
  • 2005-2009  (8)
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  • 1
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    Somatic mutations affect key pathways in lung adenocarcinoma (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-25
    Description: Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694412/" 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/PMC2694412/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Li -- Getz, Gad -- Wheeler, David A -- Mardis, Elaine R -- McLellan, Michael D -- Cibulskis, Kristian -- Sougnez, Carrie -- Greulich, Heidi -- Muzny, Donna M -- Morgan, Margaret B -- Fulton, Lucinda -- Fulton, Robert S -- Zhang, Qunyuan -- Wendl, Michael C -- Lawrence, Michael S -- Larson, David E -- Chen, Ken -- Dooling, David J -- Sabo, Aniko -- Hawes, Alicia C -- Shen, Hua -- Jhangiani, Shalini N -- Lewis, Lora R -- Hall, Otis -- Zhu, Yiming -- Mathew, Tittu -- Ren, Yanru -- Yao, Jiqiang -- Scherer, Steven E -- Clerc, Kerstin -- Metcalf, Ginger A -- Ng, Brian -- Milosavljevic, Aleksandar -- Gonzalez-Garay, Manuel L -- Osborne, John R -- Meyer, Rick -- Shi, Xiaoqi -- Tang, Yuzhu -- Koboldt, Daniel C -- Lin, Ling -- Abbott, Rachel -- Miner, Tracie L -- Pohl, Craig -- Fewell, Ginger -- Haipek, Carrie -- Schmidt, Heather -- Dunford-Shore, Brian H -- Kraja, Aldi -- Crosby, Seth D -- Sawyer, Christopher S -- Vickery, Tammi -- Sander, Sacha -- Robinson, Jody -- Winckler, Wendy -- Baldwin, Jennifer -- Chirieac, Lucian R -- Dutt, Amit -- Fennell, Tim -- Hanna, Megan -- Johnson, Bruce E -- Onofrio, Robert C -- Thomas, Roman K -- Tonon, Giovanni -- Weir, Barbara A -- Zhao, Xiaojun -- Ziaugra, Liuda -- Zody, Michael C -- Giordano, Thomas -- Orringer, Mark B -- Roth, Jack A -- Spitz, Margaret R -- Wistuba, Ignacio I -- Ozenberger, Bradley -- Good, Peter J -- Chang, Andrew C -- Beer, David G -- Watson, Mark A -- Ladanyi, Marc -- Broderick, Stephen -- Yoshizawa, Akihiko -- Travis, William D -- Pao, William -- Province, Michael A -- Weinstock, George M -- Varmus, Harold E -- Gabriel, Stacey B -- Lander, Eric S -- Gibbs, Richard A -- Meyerson, Matthew -- Wilson, Richard K -- P50 CA070907/CA/NCI NIH HHS/ -- R01 CA154365/CA/NCI NIH HHS/ -- U19 CA084953/CA/NCI NIH HHS/ -- U19 CA084953-050003/CA/NCI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1069-75. doi: 10.1038/nature07423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center at Washington University, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948947" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma, Bronchiolo-Alveolar/*genetics ; Female ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Lung Neoplasms/*genetics ; Male ; Mutation/*genetics ; Proto-Oncogenes/genetics
    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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  • 2
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    Defective lipolysis and altered energy metabolism in mice lacking adipose triglyceride lipase (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-06
    Description: Fat tissue is the most important energy depot in vertebrates. The release of free fatty acids (FFAs) from stored fat requires the enzymatic activity of lipases. We showed that genetic inactivation of adipose triglyceride lipase (ATGL) in mice increases adipose mass and leads to triacylglycerol deposition in multiple tissues. ATGL-deficient mice accumulated large amounts of lipid in the heart, causing cardiac dysfunction and premature death. Defective cold adaptation indicated that the enzyme provides FFAs to fuel thermogenesis. The reduced availability of ATGL-derived FFAs leads to increased glucose use, increased glucose tolerance, and increased insulin sensitivity. These results indicate that ATGL is rate limiting in the catabolism of cellular fat depots and plays an important role in energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haemmerle, Guenter -- Lass, Achim -- Zimmermann, Robert -- Gorkiewicz, Gregor -- Meyer, Carola -- Rozman, Jan -- Heldmaier, Gerhard -- Maier, Robert -- Theussl, Christian -- Eder, Sandra -- Kratky, Dagmar -- Wagner, Erwin F -- Klingenspor, Martin -- Hoefler, Gerald -- Zechner, Rudolf -- F 3001/Austrian Science Fund FWF/Austria -- F 3002/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 May 5;312(5774):734-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biosciences, University of Graz, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675698" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/metabolism ; Adipose Tissue/anatomy & histology/*enzymology/metabolism ; Adipose Tissue, Brown/enzymology ; Animals ; Blood Glucose/metabolism ; Carboxylic Ester Hydrolases/deficiency/genetics/*metabolism ; Cell Size ; *Energy Metabolism ; Fatty Acids, Nonesterified/blood/metabolism ; Female ; Heart Failure/pathology ; Homeostasis ; Insulin/blood ; Isoproterenol/pharmacology ; Kidney/metabolism ; Lipase/deficiency/genetics/*metabolism ; Lipids/blood ; *Lipolysis/drug effects ; Male ; Mice ; Myocardium/metabolism/pathology ; Myocytes, Cardiac/cytology/metabolism ; Oxygen Consumption ; Testis/metabolism ; Thermogenesis ; Triglycerides/*metabolism ; Ventricular Dysfunction, Left/physiopathology
    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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  • 3
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    Diminishing reciprocal fairness by disrupting the right prefrontal cortex (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: Humans restrain self-interest with moral and social values. They are the only species known to exhibit reciprocal fairness, which implies the punishment of other individuals' unfair behaviors, even if it hurts the punisher's economic self-interest. Reciprocal fairness has been demonstrated in the Ultimatum Game, where players often reject their bargaining partner's unfair offers. Despite progress in recent years, however, little is known about how the human brain limits the impact of selfish motives and implements fair behavior. Here we show that disruption of the right, but not the left, dorsolateral prefrontal cortex (DLPFC) by low-frequency repetitive transcranial magnetic stimulation substantially reduces subjects' willingness to reject their partners' intentionally unfair offers, which suggests that subjects are less able to resist the economic temptation to accept these offers. Importantly, however, subjects still judge such offers as very unfair, which indicates that the right DLPFC plays a key role in the implementation of fairness-related behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knoch, Daria -- Pascual-Leone, Alvaro -- Meyer, Kaspar -- Treyer, Valerie -- Fehr, Ernst -- K24 RR018875/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):829-32. Epub 2006 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Empirical Research in Economics, University of Zurich, Blumlisalpstrasse 10, 8006 Zurich, Switzerland. dknoch@iew.unizh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023614" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Decision Making ; Functional Laterality ; *Games, Experimental ; Humans ; Interpersonal Relations ; Judgment ; Male ; Prefrontal Cortex/*physiology ; *Social Behavior ; Transcranial Magnetic Stimulation
    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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  • 4
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    Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: New strategies for prevention and treatment of type 2 diabetes (T2D) require improved insight into disease etiology. We analyzed 386,731 common single-nucleotide polymorphisms (SNPs) in 1464 patients with T2D and 1467 matched controls, each characterized for measures of glucose metabolism, lipids, obesity, and blood pressure. With collaborators (FUSION and WTCCC/UKT2D), we identified and confirmed three loci associated with T2D-in a noncoding region near CDKN2A and CDKN2B, in an intron of IGF2BP2, and an intron of CDKAL1-and replicated associations near HHEX and in SLC30A8 found by a recent whole-genome association study. We identified and confirmed association of a SNP in an intron of glucokinase regulatory protein (GCKR) with serum triglycerides. The discovery of associated variants in unsuspected genes and outside coding regions illustrates the ability of genome-wide association studies to provide potentially important clues to the pathogenesis of common diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diabetes Genetics Initiative of Broad Institute of Harvard and MIT, Lund University, and Novartis Institutes of BioMedical Research -- Saxena, Richa -- Voight, Benjamin F -- Lyssenko, Valeriya -- Burtt, Noel P -- de Bakker, Paul I W -- Chen, Hong -- Roix, Jeffrey J -- Kathiresan, Sekar -- Hirschhorn, Joel N -- Daly, Mark J -- Hughes, Thomas E -- Groop, Leif -- Altshuler, David -- Almgren, Peter -- Florez, Jose C -- Meyer, Joanne -- Ardlie, Kristin -- Bengtsson Bostrom, Kristina -- Isomaa, Bo -- Lettre, Guillaume -- Lindblad, Ulf -- Lyon, Helen N -- Melander, Olle -- Newton-Cheh, Christopher -- Nilsson, Peter -- Orho-Melander, Marju -- Rastam, Lennart -- Speliotes, Elizabeth K -- Taskinen, Marja-Riitta -- Tuomi, Tiinamaija -- Guiducci, Candace -- Berglund, Anna -- Carlson, Joyce -- Gianniny, Lauren -- Hackett, Rachel -- Hall, Liselotte -- Holmkvist, Johan -- Laurila, Esa -- Sjogren, Marketa -- Sterner, Maria -- Surti, Aarti -- Svensson, Margareta -- Svensson, Malin -- Tewhey, Ryan -- Blumenstiel, Brendan -- Parkin, Melissa -- Defelice, Matthew -- Barry, Rachel -- Brodeur, Wendy -- Camarata, Jody -- Chia, Nancy -- Fava, Mary -- Gibbons, John -- Handsaker, Bob -- Healy, Claire -- Nguyen, Kieu -- Gates, Casey -- Sougnez, Carrie -- Gage, Diane -- Nizzari, Marcia -- Gabriel, Stacey B -- Chirn, Gung-Wei -- Ma, Qicheng -- Parikh, Hemang -- Richardson, Delwood -- Ricke, Darrell -- Purcell, Shaun -- F32 DK079466/DK/NIDDK NIH HHS/ -- F32 DK079466-01/DK/NIDDK NIH HHS/ -- K23 DK067288/DK/NIDDK NIH HHS/ -- K23 DK080145/DK/NIDDK NIH HHS/ -- K23 DK080145-01/DK/NIDDK NIH HHS/ -- K23 DK65978-04/DK/NIDDK NIH HHS/ -- K23-HL083102/HL/NHLBI NIH HHS/ -- U01 HG004171/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1331-6. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and Massachusetts Institute of Technology (MIT), Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463246" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics ; Aged ; Alleles ; Blood Glucose/analysis ; Case-Control Studies ; Chromosome Mapping ; Chromosomes, Human, Pair 9/genetics ; Diabetes Mellitus, Type 2/*genetics ; Female ; Genetic Markers ; *Genetic Predisposition to Disease ; *Genome, Human ; Genotype ; Haplotypes ; Humans ; Insulin Resistance/genetics ; Insulin-Like Growth Factor Binding Proteins/genetics ; Introns ; Male ; Meta-Analysis as Topic ; Middle Aged ; *Polymorphism, Single Nucleotide ; Quantitative Trait, Heritable ; Triglycerides/*blood
    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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  • 5
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    Neural mechanisms of a genome-wide supported psychosis variant (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Schizophrenia is a devastating, highly heritable brain disorder of unknown etiology. Recently, the first common genetic variant associated on a genome-wide level with schizophrenia and possibly bipolar disorder was discovered in ZNF804A (rs1344706). We show, by using an imaging genetics approach, that healthy carriers of rs1344706 risk genotypes exhibit no changes in regional activity but pronounced gene dosage-dependent alterations in functional coupling (correlated activity) of dorsolateral prefrontal cortex (DLPFC) across hemispheres and with hippocampus, mirroring findings in patients, and abnormal coupling of amygdala. Our findings establish disturbed connectivity as a neurogenetic risk mechanism for psychosis supported by genome-wide association, show that rs1344706 or variation in linkage disequilibrium is functional in human brain, and validate the intermediate phenotype strategy in psychiatry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esslinger, Christine -- Walter, Henrik -- Kirsch, Peter -- Erk, Susanne -- Schnell, Knut -- Arnold, Claudia -- Haddad, Leila -- Mier, Daniela -- Opitz von Boberfeld, Carola -- Raab, Kyeon -- Witt, Stephanie H -- Rietschel, Marcella -- Cichon, Sven -- Meyer-Lindenberg, Andreas -- New York, N.Y. -- Science. 2009 May 1;324(5927):605. doi: 10.1126/science.1167768.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, University of Heidelberg, J5, 68159 Mannheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407193" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Affective Symptoms/genetics/physiopathology ; Bipolar Disorder/genetics/physiopathology ; Brain Mapping ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Hippocampus/*physiology ; Humans ; Kruppel-Like Transcription Factors/*genetics ; Magnetic Resonance Imaging ; Male ; Mental Processes ; Phenotype ; *Polymorphism, Single Nucleotide ; Prefrontal Cortex/*physiology ; Schizophrenia/*genetics/physiopathology
    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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  • 6
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    Transoceanic migration, spatial dynamics, and population linkages of white sharks (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: The large-scale spatial dynamics and population structure of marine top predators are poorly known. We present electronic tag and photographic identification data showing a complex suite of behavioral patterns in white sharks. These include coastal return migrations and the fastest known transoceanic return migration among swimming fauna, which provide direct evidence of a link between widely separated populations in South Africa and Australia. Transoceanic return migration involved a return to the original capture location, dives to depths of 980 meters, and the tolerance of water temperatures as low as 3.4 degrees C. These findings contradict previous ideas that female white sharks do not make transoceanic migrations, and they suggest natal homing behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonfil, Ramon -- Meyer, Michael -- Scholl, Michael C -- Johnson, Ryan -- O'Brien, Shannon -- Oosthuizen, Herman -- Swanson, Stephan -- Kotze, Deon -- Paterson, Michael -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):100-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wildlife Conservation Society, 2300 Southern Boulevard, Bronx, NY 10460, USA. rbonfil@wcs.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210537" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Identification Systems ; *Animal Migration ; Animals ; Australia ; Behavior, Animal ; Cues ; Female ; Homing Behavior ; Indian Ocean ; Male ; Population Dynamics ; Satellite Communications ; Sex Characteristics ; Sharks/*physiology ; South Africa ; Swimming ; Temperature
    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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  • 7
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    Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-23
    Description: Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the host. The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer-Luehmann, Melanie -- Coomaraswamy, Janaky -- Bolmont, Tristan -- Kaeser, Stephan -- Schaefer, Claudia -- Kilger, Ellen -- Neuenschwander, Anton -- Abramowski, Dorothee -- Frey, Peter -- Jaton, Anneliese L -- Vigouret, Jean-Marie -- Paganetti, Paolo -- Walsh, Dominic M -- Mathews, Paul M -- Ghiso, Jorge -- Staufenbiel, Matthias -- Walker, Lary C -- Jucker, Mathias -- NS45357/NS/NINDS NIH HHS/ -- RR-00165/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1781-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tubingen, D-72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990547" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/*administration & dosage/*analysis/chemistry/pharmacology ; Amyloid beta-Protein Precursor/*administration & dosage/pharmacology ; Amyloidosis/*metabolism/pathology ; Animals ; Brain/pathology ; Brain Chemistry ; Brain Diseases/*metabolism/pathology ; Female ; Hippocampus/*chemistry/pathology ; Humans ; Male ; Mice ; Mice, Transgenic ; Protein Denaturation ; Time Factors ; Tissue Extracts
    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
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    A key role for similarity in vicarious reward (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-16
    Description: Humans appear to have an inherent prosocial tendency toward one another in that we often take pleasure in seeing others succeed. This fact is almost certainly exploited by game shows, yet why watching others win elicits a pleasurable vicarious rewarding feeling in the absence of personal economic gain is unclear. One explanation is that game shows use contestants who have similarities to the viewing population, thereby kindling kin-motivated responses (for example, prosocial behavior). Using a game show-inspired paradigm, we show that the interactions between the ventral striatum and anterior cingulate cortex subserve the modulation of vicarious reward by similarity, respectively. Our results support studies showing that similarity acts as a proximate neurobiological mechanism where prosocial behavior extends to unrelated strangers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2839480/" 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/PMC2839480/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mobbs, Dean -- Yu, Rongjun -- Meyer, Marcel -- Passamonti, Luca -- Seymour, Ben -- Calder, Andrew J -- Schweizer, Susanne -- Frith, Chris D -- Dalgleish, Tim -- MC_U105579214/Medical Research Council/United Kingdom -- MC_U105579215/Medical Research Council/United Kingdom -- U.1055.02.002.00001.01(79215)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 May 15;324(5929):900. doi: 10.1126/science.1170539.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cognition and Brain Sciences Unit, Medical Research Council (MRC), Cambridge CB2 7EF, UK. dean.mobbs@mrc-cbu.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443777" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Basal Ganglia/*physiology ; Brain Mapping ; Empathy ; Female ; Games, Experimental ; Gyrus Cinguli/*physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Prefrontal Cortex/*physiology ; *Reward ; Self Concept ; *Social Behavior ; *Social Desirability ; Young Adult
    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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