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  • Humans  (45)
  • Male  (23)
  • American Association for the Advancement of Science (AAAS)  (55)
  • 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)  (55)
  • American Institute of Physics (AIP)
  • American Physical Society (APS)
  • Nature Publishing Group
  • Oxford University Press
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  • 1
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    Dosage compensation proteins targeted to X chromosomes by a determinant of hermaphrodite fate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: In many organisms, master control genes coordinately regulate sex-specific aspects of development. SDC-2 was shown to induce hermaphrodite sexual differentiation and activate X chromosome dosage compensation in Caenorhabditis elegans. To control these distinct processes, SDC-2 acts as a strong gene-specific repressor and a weaker chromosome-wide repressor. To initiate hermaphrodite development, SDC-2 associates with the promoter of the male sex-determining gene her-1 to repress its transcription. To activate dosage compensation, SDC-2 triggers assembly of a specialized protein complex exclusively on hermaphrodite X chromosomes to reduce gene expression by half. SDC-2 can localize to X chromosomes without other components of the dosage compensation complex, suggesting that SDC-2 targets dosage compensation machinery to X chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawes, H E -- Berlin, D S -- Lapidus, D M -- Nusbaum, C -- Davis, T L -- Meyer, B J -- GM30702/GM/NIGMS NIH HHS/ -- T32 GM07127/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1800-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/*genetics/physiology ; *Caenorhabditis elegans Proteins ; *DNA-Binding Proteins ; Disorders of Sex Development ; *Dosage Compensation, Genetic ; Female ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Helminth Proteins/genetics/*physiology ; Male ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic ; Repressor Proteins/genetics/*physiology ; *Sex Determination Processes ; Transgenes ; X Chromosome/genetics/*metabolism
    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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  • 2
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    Susceptibility locus for Alzheimer's disease on chromosome 10 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-23
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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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
    Publication Date: 2001-07-14
    Description: 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〉
    Keywords: 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
    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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    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
    Publication Date: 2000-03-24
    Description: 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〉
    Keywords: 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
    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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    Calling it something other than cloning (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-10
    Description: 〈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〉
    Keywords: *Blastocyst ; *Cloning, Organism/legislation & jurisprudence ; Humans ; *Life ; Semantics ; *Stem Cells ; Terminology as Topic
    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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    Antiphase oscillation of the left and right suprachiasmatic nuclei (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-29
    Description: An unusual property of the circadian timekeeping systems of animals is rhythm "splitting," in which a single daily period of physical activity (usually measured as wheel running) dissociates into two stably coupled components about 12 hours apart; this behavior has been ascribed to a clock composed of two circadian oscillators cycling in antiphase. We analyzed gene expression in the hypothalamic circadian clock, the suprachiasmatic nucleus (SCN), of behaviorally "split" hamsters housed in constant light. The results show that the two oscillators underlying the split condition correspond to the left and right sides of the bilaterally paired SCN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de la Iglesia, H O -- Meyer, J -- Carpino, A Jr -- Schwartz, W J -- R01 NS24542/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):799-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. hacho@bio.umass.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052942" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Arginine Vasopressin/genetics/metabolism ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/*physiology ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cricetinae ; *Gene Expression ; Helix-Loop-Helix Motifs ; In Situ Hybridization ; Light ; Male ; Mesocricetus ; Motor Activity ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Suprachiasmatic Nucleus/metabolism/*physiology ; Transcription Factors/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Multiple representations of pain in human cerebral cortex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: 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〉
    Keywords: 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
    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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    Lateralization of phonetic and pitch discrimination in speech processing (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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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
    Publication Date: 1992-11-13
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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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
    Publication Date: 1989-06-16
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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