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  • Humans  (45)
  • American Association for the Advancement of Science (AAAS)  (45)
  • American Institute of Physics (AIP)
  • American Physical Society (APS)
  • Nature Publishing Group
  • Oxford University Press
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  • American Association for the Advancement of Science (AAAS)  (45)
  • American Institute of Physics (AIP)
  • American Physical Society (APS)
  • Nature Publishing Group
  • Oxford University Press
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  • 1
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    Susceptibility locus for Alzheimer's disease on chromosome 10 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-12-23
    Beschreibung: The apolipoprotein E (APOE) gene is the only genetic risk factor that has so far been linked to risk for late-onset Alzheimer's disease (LOAD). However, 50 percent of Alzheimer's disease cases do not carry an APOE4 allele, suggesting that other risk factors must exist. We performed a two-stage genome-wide screen in sibling pairs with LOAD to detect other susceptibility loci. Here we report evidence for an Alzheimer's disease locus on chromosome 10. Our stage one multipoint lod score (logarithm of the odds ratio for linkage/no linkage) of 2.48 (266 sibling pairs) increased to 3.83 in stage 2 (429 sibling pairs) close to D10S1225 (79 centimorgans). This locus modifies risk for Alzheimer's disease independent of APOE genotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, A -- Holmans, P -- Marshall, H -- Kwon, J -- Meyer, D -- Ramic, D -- Shears, S -- Booth, J -- DeVrieze, F W -- Crook, R -- Hamshere, M -- Abraham, R -- Tunstall, N -- Rice, F -- Carty, S -- Lillystone, S -- Kehoe, P -- Rudrasingham, V -- Jones, L -- Lovestone, S -- Perez-Tur, J -- Williams, J -- Owen, M J -- Hardy, J -- Goate, A M -- AG16208/AG/NIA NIH HHS/ -- AG5681/AG/NIA NIH HHS/ -- U24 AG021886/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2304-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125144" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Age of Onset ; Aged ; Alleles ; Alzheimer Disease/*genetics ; Apolipoprotein E4 ; Apolipoproteins E/genetics ; Chromosomes, Human, Pair 10/*genetics ; Genetic Linkage ; Genetic Markers ; *Genetic Predisposition to Disease ; Genotype ; Humans ; Lod Score ; Nuclear Family ; Odds Ratio
    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)
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  • 2
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    Regional mu opioid receptor regulation of sensory and affective dimensions of pain (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2001-07-14
    Beschreibung: The endogenous opioid system is involved in stress responses, in the regulation of the experience of pain, and in the action of analgesic opiate drugs. We examined the function of the opioid system and mu-opioid receptors in the brains of healthy human subjects undergoing sustained pain. Sustained pain induced the regional release of endogenous opioids interacting with mu-opioid receptors in a number of cortical and subcortical brain regions. The activation of the mu-opioid receptor system was associated with reductions in the sensory and affective ratings of the pain experience, with distinct neuroanatomical involvements. These data demonstrate the central role of the mu-opioid receptors and their endogenous ligands in the regulation of sensory and affective components of the pain experience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zubieta, J K -- Smith, Y R -- Bueller, J A -- Xu, Y -- Kilbourn, M R -- Jewett, D M -- Meyer, C R -- Koeppe, R A -- Stohler, C S -- R01 DE 12059/DE/NIDCR NIH HHS/ -- R01 DE 12743/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2001 Jul 13;293(5528):311-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Mental Health Research Institute, Medical School, The University of Michigan, Ann Arbor, MI 48104-1687, USA. zubieta@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11452128" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Amygdala/physiology ; Analgesics, Opioid/administration & dosage ; Brain/*physiology ; Brain Mapping ; Female ; Fentanyl/administration & dosage/*analogs & derivatives ; Humans ; Magnetic Resonance Imaging ; Male ; Masseter Muscle ; Opioid Peptides/physiology ; *Pain ; Pain Measurement ; Receptors, Opioid, mu/*physiology ; Thalamus/physiology ; 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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  • 3
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    Rapid progression to AIDS in HIV+ individuals with a structural variant of the chemokine receptor CX3CR1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-03-24
    Beschreibung: Human immunodeficiency virus (HIV) enters cells in vitro via CD4 and a coreceptor. Which of 15 known coreceptors are important in vivo is poorly defined but may be inferred from disease-modifying mutations, as for CCR5. Here two single nucleotide polymorphisms are described in Caucasians in CX3CR1, an HIV coreceptor and leukocyte chemotactic/adhesion receptor for the chemokine fractalkine. HIV-infected patients homozygous for CX3CR1-I249 M280, a variant haplotype affecting two amino acids (isoleucine-249 and methionine-280), progressed to AIDS more rapidly than those with other haplotypes. Functional CX3CR1 analysis showed that fractalkine binding is reduced among patients homozygous for this particular haplotype. Thus, CX3CR1-I249 M280 is a recessive genetic risk factor in HIV/AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faure, S -- Meyer, L -- Costagliola, D -- Vaneensberghe, C -- Genin, E -- Autran, B -- Delfraissy, J F -- McDermott, D H -- Murphy, P M -- Debre, P -- Theodorou, I -- Combadiere, C -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2274-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Immunologie Cellulaire et Tissulaire, Centre National de la Recherche Scientifique UMR 7627, Hopital Pitie-Salpetriere, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731151" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acquired Immunodeficiency Syndrome/genetics/*physiopathology/virology ; Case-Control Studies ; Chemokine CX3CL1 ; *Chemokines, CX3C ; Chemokines, CXC/metabolism ; Chromosomes, Human, Pair 3 ; Cohort Studies ; Disease Progression ; European Continental Ancestry Group/genetics ; Genetic Variation ; Genotype ; HIV/physiology ; HIV Infections/genetics/*physiopathology/virology ; Haplotypes ; Homozygote ; Humans ; Leukocytes, Mononuclear/metabolism ; Linkage Disequilibrium ; Membrane Proteins/metabolism ; Mutation ; Polymorphism, Restriction Fragment Length ; *Polymorphism, Single Nucleotide ; Polymorphism, Single-Stranded Conformational ; Receptors, Cytokine/*genetics/*physiology ; Receptors, HIV/*genetics/*physiology ; Survival Analysis
    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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    Calling it something other than cloning (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-07-10
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Eli -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):51-2; author reply 51-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12102093" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Blastocyst ; *Cloning, Organism/legislation & jurisprudence ; Humans ; *Life ; Semantics ; *Stem Cells ; Terminology as Topic
    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)
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  • 5
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    Multiple representations of pain in human cerebral cortex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1991-03-15
    Beschreibung: The representation of pain in the cerebral cortex is less well understood than that of any other sensory system. However, with the use of magnetic resonance imaging and positron emission tomography in humans, it has now been demonstrated that painful heat causes significant activation of the contralateral anterior cingulate, secondary somatosensory, and primary somatosensory cortices. This contrasts with the predominant activation of primary somatosensory cortex caused by vibrotactile stimuli in similar experiments. Furthermore, the unilateral cingulate activation indicates that this forebrain area, thought to regulate emotions, contains an unexpectedly specific representation of pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talbot, J D -- Marrett, S -- Evans, A C -- Meyer, E -- Bushnell, M C -- Duncan, G H -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de neurophysiologie comportementale, Faculte de medecine dentaire, Universite de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2003220" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Animals ; Anxiety/physiopathology ; Brain Mapping ; Cerebral Cortex/*physiology ; Functional Laterality ; Hot Temperature ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology ; 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)
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  • 6
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    Lateralization of phonetic and pitch discrimination in speech processing (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1992-05-08
    Beschreibung: Cerebral activation was measured with positron emission tomography in ten human volunteers. The primary auditory cortex showed increased activity in response to noise bursts, whereas acoustically matched speech syllables activated secondary auditory cortices bilaterally. Instructions to make judgments about different attributes of the same speech signal resulted in activation of specific lateralized neural systems. Discrimination of phonetic structure led to increased activity in part of Broca's area of the left hemisphere, suggesting a role for articulatory recoding in phonetic perception. Processing changes in pitch produced activation of the right prefrontal cortex, consistent with the importance of right-hemisphere mechanisms in pitch perception.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zatorre, R J -- Evans, A C -- Meyer, E -- Gjedde, A -- New York, N.Y. -- Science. 1992 May 8;256(5058):846-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589767" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acoustic Stimulation ; Auditory Cortex/anatomy & histology/*physiology/radionuclide imaging ; Functional Laterality ; Humans ; Magnetic Resonance Imaging ; *Phonetics ; *Pitch Discrimination ; Reference Values ; Speech ; *Speech Perception ; Tomography, Emission-Computed/methods
    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)
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  • 7
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    Assignment of a locus for familial melanoma, MLM, to chromosome 9p13-p22 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1992-11-13
    Beschreibung: Linkage analysis of ten Utah kindreds and one Texas kindred with multiple cases of cutaneous malignant melanoma (CMM) provided evidence that a locus for familial melanoma susceptibility is in the chromosomal region 9p13-p22. The genetic markers analyzed reside in a candidate region on chromosome 9p21, previously implicated by the presence of homozygous deletions in melanoma tumors and by the presence of a germline deletion in an individual with eight independent melanomas. Multipoint linkage analysis was performed between the familial melanoma susceptibility locus (MLM) and two short tandem repeat markers, D9S126 and the interferon-alpha (IFNA) gene, which reside in the region of somatic loss in melanoma tumors. An analysis incorporating a partially penetrant dominant melanoma susceptibility locus places MLM near IFNA and D9S126 with a maximum location score of 12.71. Therefore, the region frequently deleted in melanoma tumors on 9p21 presumably contains a locus that plays a critical role in predisposition to familial melanoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannon-Albright, L A -- Goldgar, D E -- Meyer, L J -- Lewis, C M -- Anderson, D E -- Fountain, J W -- Hegi, M E -- Wiseman, R W -- Petty, E M -- Bale, A E -- CA 42014/CA/NCI NIH HHS/ -- CA 48711/CA/NCI NIH HHS/ -- RR 00064/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1148-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439824" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Aged ; Aged, 80 and over ; Base Sequence ; Child ; Chromosome Aberrations ; *Chromosomes, Human, Pair 9 ; Dysplastic Nevus Syndrome/genetics ; Female ; Genes, Tumor Suppressor ; Genetic Markers ; Humans ; Lod Score ; Male ; Melanoma/*genetics ; Middle Aged ; Molecular Sequence Data ; Pedigree ; Skin Neoplasms/*genetics ; Texas ; Utah
    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)
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  • 8
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    The Fc and not CD4 receptor mediates antibody enhancement of HIV infection in human cells (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-06-16
    Beschreibung: Antibodies that enhance human immunodeficiency virus (HIV) infectivity have been found in the blood of infected individuals and in infected or immunized animals. These findings raise serious concern for the development of a safe vaccine against acquired immunodeficiency syndrome. To address the in vivo relevance and mechanism of this phenomenon, antibody-dependent enhancement of HIV infectivity in peripheral blood macrophages, lymphocytes, and human fibroblastoid cells was studied. Neither Leu3a, a monoclonal antibody directed against the CD4 receptor, nor soluble recombinant CD4 even at high concentrations prevented this enhancement. The addition of monoclonal antibody to the Fc receptor III (anti-FcRIII), but not of antibodies that react with FcRI or FcRII, inhibited HIV type 1 and HIV type 2 enhancement in peripheral blood macrophages. Although enhancement of HIV infection in CD4+ lymphocytes could not be blocked by anti-FcRIII, it was inhibited by the addition of human immunoglobulin G aggregates. The results indicate that the FcRIII receptor on human macrophages and possibly another Fc receptor on human CD4+ lymphocytes mediate antibody-dependent enhancement of HIV infectivity and that this phenomenon proceeds through a mechanism independent of the CD4 protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Homsy, J -- Meyer, M -- Tateno, M -- Clarkson, S -- Levy, J A -- AI-26471/AI/NIAID NIH HHS/ -- R01-AI-24499/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1357-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, School of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2786647" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acquired Immunodeficiency Syndrome/*immunology ; Animals ; Antibodies, Monoclonal ; Antibody-Dependent Cell Cytotoxicity ; Guinea Pigs ; HIV Antibodies/biosynthesis/*immunology ; HIV-1/*immunology ; HIV-2/*immunology ; Humans ; In Vitro Techniques ; Pan troglodytes ; Receptors, Fc/*physiology ; Receptors, HIV ; Receptors, Virus/*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)
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  • 9
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    Genome sequence diversity and clues to the evolution of variola (smallpox) virus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-07-29
    Beschreibung: Comparative genomics of 45 epidemiologically varied variola virus isolates from the past 30 years of the smallpox era indicate low sequence diversity, suggesting that there is probably little difference in the isolates' functional gene content. Phylogenetic clustering inferred three clades coincident with their geographical origin and case-fatality rate; the latter implicated putative proteins that mediate viral virulence differences. Analysis of the viral linear DNA genome suggests that its evolution involved direct descent and DNA end-region recombination events. Knowing the sequences will help understand the viral proteome and improve diagnostic test precision, therapeutics, and systems for their assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esposito, Joseph J -- Sammons, Scott A -- Frace, A Michael -- Osborne, John D -- Olsen-Rasmussen, Melissa -- Zhang, Ming -- Govil, Dhwani -- Damon, Inger K -- Kline, Richard -- Laker, Miriam -- Li, Yu -- Smith, Geoffrey L -- Meyer, Hermann -- Leduc, James W -- Wohlhueter, Robert M -- G0501257/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):807-12. Epub 2006 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Core Facility Branch, Division of Scientific Resources, National Center for Preparedness, Detection, and Control of Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30329, USA. jesposito@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873609" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): DNA, Viral/*genetics ; Disease Outbreaks ; *Evolution, Molecular ; Gene Deletion ; *Genetic Variation ; *Genome, Viral ; Genomics ; Humans ; Molecular Sequence Data ; Open Reading Frames ; Phylogeny ; Proteome/analysis/genetics ; Recombination, Genetic ; Sequence Analysis, DNA ; Smallpox/epidemiology/mortality/*virology ; Variola virus/classification/*genetics/isolation & purification/pathogenicity ; Viral Proteins/chemistry/genetics ; Virulence/genetics
    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)
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  • 10
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    Diminishing reciprocal fairness by disrupting the right prefrontal cortex (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-10-07
    Beschreibung: 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〉
    Schlagwort(e): Adult ; Decision Making ; Functional Laterality ; *Games, Experimental ; Humans ; Interpersonal Relations ; Judgment ; Male ; Prefrontal Cortex/*physiology ; *Social Behavior ; Transcranial Magnetic Stimulation
    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)
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