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  • 2015-2019
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  • 1
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    The neural basis of altruistic punishment (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-08-31
    Beschreibung: Many people voluntarily incur costs to punish violations of social norms. Evolutionary models and empirical evidence indicate that such altruistic punishment has been a decisive force in the evolution of human cooperation. We used H2 15O positron emission tomography to examine the neural basis for altruistic punishment of defectors in an economic exchange. Subjects could punish defection either symbolically or effectively. Symbolic punishment did not reduce the defector's economic payoff, whereas effective punishment did reduce the payoff. We scanned the subjects' brains while they learned about the defector's abuse of trust and determined the punishment. Effective punishment, as compared with symbolic punishment, activated the dorsal striatum, which has been implicated in the processing of rewards that accrue as a result of goal-directed actions. Moreover, subjects with stronger activations in the dorsal striatum were willing to incur greater costs in order to punish. Our findings support the hypothesis that people derive satisfaction from punishing norm violations and that the activation in the dorsal striatum reflects the anticipated satisfaction from punishing defectors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Quervain, Dominique J-F -- Fischbacher, Urs -- Treyer, Valerie -- Schellhammer, Melanie -- Schnyder, Ulrich -- Buck, Alfred -- Fehr, Ernst -- New York, N.Y. -- Science. 2004 Aug 27;305(5688):1254-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Psychiatry Research, University of Zurich, Lenggstrasse 31, 8029 Zurich, Switzerland. quervain@bli.unizh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15333831" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Altruism ; Brain Mapping ; Caudate Nucleus/*physiology/radionuclide imaging ; Corpus Striatum/*physiology/radionuclide imaging ; *Emotions ; Frontal Lobe/physiology/radionuclide imaging ; Games, Experimental ; Humans ; Male ; *Personal Satisfaction ; Prefrontal Cortex/physiology/radionuclide imaging ; *Punishment ; Reward ; Surveys and Questionnaires ; Thalamus/physiology/radionuclide imaging ; Tomography, Emission-Computed
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Reactivation of the paternal X chromosome in early mouse embryos (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-01-31
    Beschreibung: It is generally accepted that paternally imprinted X inactivation occurs exclusively in extraembryonic lineages of mouse embryos, whereas cells of the embryo proper, derived from the inner cell mass (ICM), undergo only random X inactivation. Here we show that imprinted X inactivation, in fact, occurs in all cells of early embryos and that the paternal X is then selectively reactivated in cells allocated to the ICM. This contrasts with more differentiated cell types where X inactivation is highly stable and generally irreversible. Our observations illustrate that an important component of genome plasticity in early development is the capacity to reverse heritable gene silencing decisions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mak, Winifred -- Nesterova, Tatyana B -- de Napoles, Mariana -- Appanah, Ruth -- Yamanaka, Shinya -- Otte, Arie P -- Brockdorff, Neil -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):666-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉X inactivation group, MRC Clinical Sciences Centre, ICSM, Hammersmith Hospital, London, W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14752160" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylation ; Animals ; Blastocyst/physiology ; Cell Cycle Proteins/genetics/metabolism ; Chromosomal Proteins, Non-Histone/genetics/metabolism ; Chromosomes, Mammalian/physiology ; *Dosage Compensation, Genetic ; Embryo, Mammalian/*physiology ; Embryonic and Fetal Development ; Female ; *Gene Expression Regulation, Developmental ; Genomic Imprinting ; Histones/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Morula/physiology ; Polycomb Repressive Complex 2 ; Proteins/genetics/metabolism ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/genetics/metabolism ; X Chromosome/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-06-19
    Beschreibung: A major cause of aging is thought to result from the cumulative effects of cell loss over time. In yeast, caloric restriction (CR) delays aging by activating the Sir2 deacetylase. Here we show that expression of mammalian Sir2 (SIRT1) is induced in CR rats as well as in human cells that are treated with serum from these animals. Insulin and insulin-like growth factor 1 (IGF-1) attenuated this response. SIRT1 deacetylates the DNA repair factor Ku70, causing it to sequester the proapoptotic factor Bax away from mitochondria, thereby inhibiting stress-induced apoptotic cell death. Thus, CR could extend life-span by inducing SIRT1 expression and promoting the long-term survival of irreplaceable cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Haim Y -- Miller, Christine -- Bitterman, Kevin J -- Wall, Nathan R -- Hekking, Brian -- Kessler, Benedikt -- Howitz, Konrad T -- Gorospe, Myriam -- de Cabo, Rafael -- Sinclair, David A -- AG19719-03/AG/NIA NIH HHS/ -- AG19972-02/AG/NIA NIH HHS/ -- F32 CA097802/CA/NCI NIH HHS/ -- P01 AG027916/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG019972/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R01 GM068072/GM/NIGMS NIH HHS/ -- R37 AG028730/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 16;305(5682):390-2. Epub 2004 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15205477" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylation ; Adipose Tissue/metabolism ; Alleles ; Animals ; Antigens, Nuclear/metabolism ; *Apoptosis ; *Caloric Restriction ; Cell Line ; *Cell Survival ; DNA-Binding Proteins/metabolism ; Histone Deacetylases/genetics/*metabolism ; Humans ; Insulin/metabolism/pharmacology ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Kidney/metabolism ; Liver/metabolism ; Male ; Mitochondria/metabolism ; Mutation ; Proto-Oncogene Proteins/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; RNA, Small Interfering ; Rats ; Rats, Inbred F344 ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; bcl-2-Associated X Protein
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    A diarylquinoline drug active on the ATP synthase of Mycobacterium tuberculosis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-12-14
    Beschreibung: The incidence of tuberculosis has been increasing substantially on a worldwide basis over the past decade, but no tuberculosis-specific drugs have been discovered in 40 years. We identified a diarylquinoline, R207910, that potently inhibits both drug-sensitive and drug-resistant Mycobacterium tuberculosis in vitro (minimum inhibitory concentration 0.06 mug/ml). In mice, R207910 exceeded the bactericidal activities of isoniazid and rifampin by at least 1 log unit. Substitution of drugs included in the World Health Organization's first-line tuberculosis treatment regimen (rifampin, isoniazid, and pyrazinamide) with R207910 accelerated bactericidal activity, leading to complete culture conversion after 2 months of treatment in some combinations. A single dose of R207910 inhibited mycobacterial growth for 1 week. Plasma levels associated with efficacy in mice were well tolerated in healthy human volunteers. Mutants selected in vitro suggest that the drug targets the proton pump of adenosine triphosphate (ATP) synthase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andries, Koen -- Verhasselt, Peter -- Guillemont, Jerome -- Gohlmann, Hinrich W H -- Neefs, Jean-Marc -- Winkler, Hans -- Van Gestel, Jef -- Timmerman, Philip -- Zhu, Min -- Lee, Ennis -- Williams, Peter -- de Chaffoy, Didier -- Huitric, Emma -- Hoffner, Sven -- Cambau, Emmanuelle -- Truffot-Pernot, Chantal -- Lounis, Nacer -- Jarlier, Vincent -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):223-7. Epub 2004 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johnson & Johnson Pharmaceutical Research and Development, Turnhoutseweg 30, 2340 Beerse, Belgium. kandries@prdbe.jnj.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15591164" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Antitubercular Agents/chemistry/pharmacokinetics/*pharmacology/therapeutic use ; Bacterial Proton-Translocating ATPases/*antagonists & ; inhibitors/chemistry/metabolism ; Diarylquinolines ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Drug Resistance, Bacterial ; Drug Therapy, Combination ; Enzyme Inhibitors/chemistry/pharmacology/therapeutic use ; Humans ; Male ; Mice ; Microbial Sensitivity Tests ; Molecular Sequence Data ; Mycobacterium smegmatis/drug effects/enzymology/growth & development ; Mycobacterium tuberculosis/*drug effects/enzymology/growth & development ; Point Mutation ; Protein Subunits/antagonists & inhibitors/chemistry ; Quinolines/chemistry/pharmacokinetics/*pharmacology/*therapeutic use ; Tuberculosis/*drug therapy/microbiology ; Tuberculosis, Multidrug-Resistant/drug therapy/microbiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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