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  • Cells, Cultured  (135)
  • Adult  (87)
  • American Association for the Advancement of Science (AAAS)  (220)
  • American Chemical Society
  • Molecular Diversity Preservation International
  • Springer
  • 2020-2022
  • 1995-1999  (125)
  • 1980-1984  (95)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (220)
  • American Chemical Society
  • Molecular Diversity Preservation International
  • Springer
Years
Year
  • 1
    Publication Date: 1996-11-22
    Description: Despite its high prevalence, very little is known regarding genetic predisposition to prostate cancer. A genome-wide scan performed in 66 high-risk prostate cancer families has provided evidence of linkage to the long arm of chromosome 1 (1q24-25). Analysis of an additional set of 25 North American and Swedish families with markers in this region resulted in significant evidence of linkage in the combined set of 91 families. The data provide strong evidence of a major prostate cancer susceptibility locus on chromosome 1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, J R -- Freije, D -- Carpten, J D -- Gronberg, H -- Xu, J -- Isaacs, S D -- Brownstein, M J -- Bova, G S -- Guo, H -- Bujnovszky, P -- Nusskern, D R -- Damber, J E -- Bergh, A -- Emanuelsson, M -- Kallioniemi, O P -- Walker-Daniels, J -- Bailey-Wilson, J E -- Beaty, T H -- Meyers, D A -- Walsh, P C -- Collins, F S -- Trent, J M -- Isaacs, W B -- CA58236/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1371-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Human Genome Research, National Institutes of Health, Bethesda, MD, USA. jtrent@nchgr.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910276" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; *Chromosome Mapping ; *Chromosomes, Human, Pair 1 ; Dinucleotide Repeats ; *Genes ; Genetic Linkage ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Likelihood Functions ; Male ; Middle Aged ; North America ; Oncogenes ; Pedigree ; Prostatic Neoplasms/*genetics ; Risk Factors ; Statistics, Nonparametric ; Sweden
    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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  • 2
    Publication Date: 1999-07-10
    Description: The tumor necrosis factor (TNF) superfamily of cytokines includes both soluble and membrane-bound proteins that regulate immune responses. A member of the human TNF family, BLyS (B lymphocyte stimulator), was identified that induced B cell proliferation and immunoglobulin secretion. BLyS expression on human monocytes could be up-regulated by interferon-gamma. Soluble BLyS functioned as a potent B cell growth factor in costimulation assays. Administration of soluble recombinant BLyS to mice disrupted splenic B and T cell zones and resulted in elevated serum immunoglobulin concentrations. The B cell tropism of BLyS is consistent with its receptor expression on B-lineage cells. The biological profile of BLyS suggests it is involved in monocyte-driven B cell activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, P A -- Belvedere, O -- Orr, A -- Pieri, K -- LaFleur, D W -- Feng, P -- Soppet, D -- Charters, M -- Gentz, R -- Parmelee, D -- Li, Y -- Galperina, O -- Giri, J -- Roschke, V -- Nardelli, B -- Carrell, J -- Sosnovtseva, S -- Greenfield, W -- Ruben, S M -- Olsen, H S -- Fikes, J -- Hilbert, D M -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):260-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Sciences, 9410 Key West Avenue, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398604" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; B-Lymphocyte Subsets/immunology ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Humans ; Immunoglobulins/blood ; Interferon-gamma/pharmacology ; *Lymphocyte Activation ; Membrane Proteins/chemistry/genetics/pharmacology/*physiology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Monocytes/*immunology ; Receptors, Cytokine/metabolism ; Receptors, Tumor Necrosis Factor/metabolism ; Recombinant Proteins/pharmacology ; Sequence Alignment ; Species Specificity ; Tumor Necrosis Factor-alpha/chemistry/genetics/pharmacology/*physiology ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1996-11-29
    Description: Transporter-facilitated uptake of serotonin (5-hydroxytryptamine or 5-HT) has been implicated in anxiety in humans and animal models and is the site of action of widely used uptake-inhibiting antidepressant and antianxiety drugs. Human 5-HT transporter (5-HTT) gene transcription is modulated by a common polymorphism in its upstream regulatory region. The short variant of the polymorphism reduces the transcriptional efficiency of the 5-HTT gene promoter, resulting in decreased 5-HTT expression and 5-HT uptake in lymphoblasts. Association studies in two independent samples totaling 505 individuals revealed that the 5-HTT polymorphism accounts for 3 to 4 percent of total variation and 7 to 9 percent of inherited variance in anxiety-related personality traits in individuals as well as sibships.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lesch, K P -- Bengel, D -- Heils, A -- Sabol, S Z -- Greenberg, B D -- Petri, S -- Benjamin, J -- Muller, C R -- Hamer, D H -- Murphy, D L -- New York, N.Y. -- Science. 1996 Nov 29;274(5292):1527-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Wurzburg, Fuchsleinstrasse 15, 97080 Wurzburg, Germany. kplesch@rzbox.uni-wuerzburg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8929413" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Alleles ; Anxiety Disorders/*genetics ; Carrier Proteins/*genetics ; Cell Line ; Female ; Genetic Markers ; Genotype ; Humans ; Male ; Membrane Glycoproteins/*genetics ; *Membrane Transport Proteins ; Middle Aged ; *Nerve Tissue Proteins ; Neurotic Disorders/*genetics ; Nuclear Family ; Personality Tests ; Phenotype ; *Polymorphism, Genetic ; *Promoter Regions, Genetic ; Serotonin/*metabolism ; Serotonin Plasma Membrane Transport Proteins ; Transfection
    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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  • 4
    Publication Date: 1996-06-28
    Description: Because stimulation of CD4+ lymphocytes leads to activation of human immunodeficiency virus-type 1 (HIV-1) replication, viral spread, and cell death, adoptive CD4+ T cell therapy has not been possible. When antigen and CD28 receptors on cultured T cells were stimulated by monoclonal antibodies (mAbs) to CD3 and CD28 that had been immobilized, there was an increase in the number of polyclonal CD4+ T cells from HIV-infected donors. Activated cells predominantly secreted cytokines associated with T helper cell type 1 function. The HIV-1 viral load declined in the absence of antiretroviral agents. Moreover, CD28 stimulation of CD4+ T cells from uninfected donors rendered these cells highly resistant to HIV-1 infection. Immobilization of CD28 mAb was crucial to the development of HIV resistance, as cells stimulated with soluble CD28 mAb were highly susceptible to HIV infection. The CD28-mediated antiviral effect occurred early in the viral life cycle, before HIV-1 DNA integration. These data may facilitate immune reconstitution and gene therapy approaches in persons with HIV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, B L -- Mosca, J D -- Riley, J L -- Carroll, R G -- Vahey, M T -- Jagodzinski, L L -- Wagner, K F -- Mayers, D L -- Burke, D S -- Weislow, O S -- St Louis, D C -- June, C H -- AI29331/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1939-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Naval Medical Research Institute, Bethesda, Maryland 20889, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658167" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Antigens, CD28/*immunology ; Antigens, CD3/immunology ; CD4 Lymphocyte Count ; CD4-Positive T-Lymphocytes/cytology/*immunology/*virology ; Cell Division ; Cells, Cultured ; Chemokines/metabolism ; Cytokines/metabolism ; HIV Infections/immunology/*virology ; HIV-1/immunology/*physiology ; Humans ; Interleukin-2/pharmacology ; *Lymphocyte Activation ; Phytohemagglutinins/pharmacology ; Virus Integration ; Virus Replication
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  • 5
    Publication Date: 1995-11-10
    Description: A blood donor infected with human immunodeficiency virus-type 1 (HIV-1) and a cohort of six blood or blood product recipients infected from this donor remain free of HIV-1-related disease with stable and normal CD4 lymphocyte counts 10 to 14 years after infection. HIV-1 sequences from either virus isolates or patient peripheral blood mononuclear cells had similar deletions in the nef gene and in the region of overlap of nef and the U3 region of the long terminal repeat (LTR). Full-length sequencing of one isolate genome and amplification of selected HIV-1 genome regions from other cohort members revealed no other abnormalities of obvious functional significance. These data show that survival after HIV infection can be determined by the HIV genome and support the importance of nef or the U3 region of the LTR in determining the pathogenicity of HIV-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deacon, N J -- Tsykin, A -- Solomon, A -- Smith, K -- Ludford-Menting, M -- Hooker, D J -- McPhee, D A -- Greenway, A L -- Ellett, A -- Chatfield, C -- Lawson, V A -- Crowe, S -- Maerz, A -- Sonza, S -- Learmont, J -- Sullivan, J S -- Cunningham, A -- Dwyer, D -- Dowton, D -- Mills, J -- New York, N.Y. -- Science. 1995 Nov 10;270(5238):988-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉AIDS Molecular Biology Unit, Macfarlane Burnet Centre for Medical Research, Fairfield, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7481804" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Base Composition ; Base Sequence ; *Blood Donors ; Blood Transfusion ; CD4 Lymphocyte Count ; Cohort Studies ; Disease Progression ; Female ; Gene Rearrangement ; *Genes, nef ; Genome, Viral ; HIV Infections/immunology/transmission/*virology ; *HIV Long Terminal Repeat ; HIV-1/*genetics/*pathogenicity/physiology ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Multigene Family ; Sequence Deletion ; Virulence ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1981-12-04
    Description: Leucine catabolism is regulated by either of the first two degradative steps: (reversible) transamination to the keto acid or subsequent decarboxylation. A method is described to measure rates of leucine transamination, reamination, and keto acid oxidation. The method is applied directly to humans by infusing the nonradioactive tracer, L-[15N,1-13C]leucine. Leucine transamination was found to be operating several times faster than the keto acid decarboxylation and to be of equal magnitude in adult human males under two different dietary conditions, postabsorptive and fed. These results indicate that decarboxylation, not transamination, is the rate-limiting step in normal human leucine metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matthews, D E -- Bier, D M -- Rennie, M J -- Edwards, R H -- Halliday, D -- Millward, D J -- Clugston, G A -- AM-25994/AM/NIADDK NIH HHS/ -- HD-10667/HD/NICHD NIH HHS/ -- RR-00954/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1981 Dec 4;214(4525):1129-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7302583" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Carbon Isotopes ; Humans ; Kinetics ; Leucine/*metabolism ; Male ; Models, Biological ; Nitrogen Isotopes ; Oxidation-Reduction
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  • 7
    Publication Date: 1999-11-27
    Description: Apoptosis can be triggered by members of the Bcl-2 protein family, such as Bim, that share only the BH3 domain with this family. Gene targeting in mice revealed important physiological roles for Bim. Lymphoid and myeloid cells accumulated, T cell development was perturbed, and most older mice accumulated plasma cells and succumbed to autoimmune kidney disease. Lymphocytes were refractory to apoptotic stimuli such as cytokine deprivation, calcium ion flux, and microtubule perturbation but not to others. Thus, Bim is required for hematopoietic homeostasis and as a barrier to autoimmunity. Moreover, particular death stimuli appear to activate apoptosis through distinct BH3-only proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bouillet, P -- Metcalf, D -- Huang, D C -- Tarlinton, D M -- Kay, T W -- Kontgen, F -- Adams, J M -- Strasser, A -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1735-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Autoimmune Diseases/etiology ; *Autoimmunity ; B-Lymphocytes/physiology ; Carrier Proteins/*physiology ; Cells, Cultured ; Crosses, Genetic ; Female ; Gene Targeting ; Glomerulonephritis/etiology ; Hematopoietic Stem Cells/physiology ; Homeostasis ; Leukocyte Count ; Leukocytes/*physiology ; Male ; *Membrane Proteins ; Mice ; Mice, Transgenic ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2/physiology ; Signal Transduction ; T-Lymphocyte Subsets/physiology
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  • 8
    Publication Date: 1999-04-02
    Description: Human mesenchymal stem cells are thought to be multipotent cells, which are present in adult marrow, that can replicate as undifferentiated cells and that have the potential to differentiate to lineages of mesenchymal tissues, including bone, cartilage, fat, tendon, muscle, and marrow stroma. Cells that have the characteristics of human mesenchymal stem cells were isolated from marrow aspirates of volunteer donors. These cells displayed a stable phenotype and remained as a monolayer in vitro. These adult stem cells could be induced to differentiate exclusively into the adipocytic, chondrocytic, or osteocytic lineages. Individual stem cells were identified that, when expanded to colonies, retained their multilineage potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pittenger, M F -- Mackay, A M -- Beck, S C -- Jaiswal, R K -- Douglas, R -- Mosca, J D -- Moorman, M A -- Simonetti, D W -- Craig, S -- Marshak, D R -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):143-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Osiris Therapeutics, 2001 Aliceanna Street, Baltimore, MD 21231-3043, USA. mpittenger@osiristx.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102814" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*cytology ; Adult ; Apoptosis ; Bone Marrow Cells/cytology ; Cell Differentiation ; Cell Division ; *Cell Lineage ; Cell Separation ; Cells, Cultured ; Chondrocytes/*cytology ; Fibroblasts/cytology ; Flow Cytometry ; Humans ; Mesoderm/*cytology ; Middle Aged ; Osteocytes/*cytology ; Phenotype ; Stem Cells/*cytology
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  • 9
    Publication Date: 1997-10-10
    Description: Substance P is released in the spinal cord in response to painful stimuli, but its role in nociceptive signaling remains unclear. When a conjugate of substance P and the ribosome-inactivating protein saporin was infused into the spinal cord, it was internalized and cytotoxic to lamina I spinal cord neurons that express the substance P receptor. This treatment left responses to mild noxious stimuli unchanged, but markedly attenuated responses to highly noxious stimuli and mechanical and thermal hyperalgesia. Thus, lamina I spinal cord neurons that express the substance P receptor play a pivotal role in the transmission of highly noxious stimuli and the maintenance of hyperalgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantyh, P W -- Rogers, S D -- Honore, P -- Allen, B J -- Ghilardi, J R -- Li, J -- Daughters, R S -- Lappi, D A -- Wiley, R G -- Simone, D A -- MH56368/MH/NIMH NIH HHS/ -- NS23970/NS/NINDS NIH HHS/ -- NS31223/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):275-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory (151), Veterans Administration Medical Center, Minneapolis, MN 55417, USA. manty001@maroon.tc.umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin ; Cell Membrane/metabolism ; Cells, Cultured ; Fluorescent Antibody Technique ; Hyperalgesia/physiopathology/*therapy ; *Immunotoxins ; Injections, Spinal ; *N-Glycosyl Hydrolases ; Neurons/cytology/*metabolism ; Pain/physiopathology ; *Pain Management ; Pain Measurement ; Plant Proteins/metabolism/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/biosynthesis/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Signal Transduction ; Spinal Cord/*cytology/metabolism ; Substance P/*metabolism/pharmacology
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  • 10
    Publication Date: 1995-08-18
    Description: A candidate gene for the chromosome 1 Alzheimer's disease (AD) locus was identified (STM2). The predicted amino acid sequence for STM2 is homologous to that of the recently cloned chromosome 14 AD gene (S182). A point mutation in STM2, resulting in the substitution of an isoleucine for an asparagine (N141l), was identified in affected people from Volga German AD kindreds. This N141l mutation occurs at an amino acid residue that is conserved in human S182 and in the mouse S182 homolog. The presence of missense mutations in AD subjects in two highly similar genes strongly supports the hypothesis that mutations in both are pathogenic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy-Lahad, E -- Wasco, W -- Poorkaj, P -- Romano, D M -- Oshima, J -- Pettingell, W H -- Yu, C E -- Jondro, P D -- Schmidt, S D -- Wang, K -- AG0513C/AG/NIA NIH HHS/ -- R01-AG11762/AG/NIA NIH HHS/ -- R01-AG11899/AG/NIA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Aug 18;269(5226):973-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geriatric Research Education, and Clinical Center (182B), Veterans Affairs Medical Center, Seattle, WA 98108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7638622" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Alzheimer Disease/ethnology/*genetics ; Amino Acid Sequence ; Base Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 1/*genetics ; Cloning, Molecular ; DNA, Complementary/genetics ; Female ; Gene Expression ; Germany/ethnology ; Humans ; Lod Score ; Male ; Membrane Proteins/chemistry/*genetics ; Middle Aged ; Molecular Sequence Data ; Mutation ; Pedigree ; Point Mutation ; Presenilin-2
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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