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  • Male  (30)
  • American Association for the Advancement of Science (AAAS)  (30)
  • American Meteorological Society (AMS)
  • International Union of Crystallography (IUCr)
  • PANGAEA
  • Wiley-Blackwell
  • 1990-1994  (30)
  • 1980-1984
  • 1993  (30)
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  • American Association for the Advancement of Science (AAAS)  (30)
  • American Meteorological Society (AMS)
  • International Union of Crystallography (IUCr)
  • PANGAEA
  • Wiley-Blackwell
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  • 1990-1994  (30)
  • 1980-1984
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  • 1
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    Genotypic and phenotypic characterization of HIV-1 patients with primary infection (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: Better characterization of human immunodeficiency virus-type 1 (HIV-1) in patients with primary infection has important implications for the development of an acquired immunodeficiency syndrome (AIDS) vaccine because vaccine strategies should target viral isolates with the properties of transmitted viruses. In five HIV-1 seroconverters, the viral phenotype was found to be uniformly macrophage-tropic and non-syncytium-inducing. Furthermore, the viruses were genotypically homogeneous within each patient, but a common signature sequence was not discernible among transmitted viruses. In the two cases where the sexual partners were also studied, the sequences of the transmitted viruses matched best with minor variants in the blood of the transmitters. There was also a stronger pressure to conserve sequences in gp120 than in gp41, nef, and p17, suggesting that a selective mechanism is involved in transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, T -- Mo, H -- Wang, N -- Nam, D S -- Cao, Y -- Koup, R A -- Ho, D D -- AI24030/AI/NIAID NIH HHS/ -- AI25541/AI/NIAID NIH HHS/ -- AI27742/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1179-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, New York University School of Medicine, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356453" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Female ; Gene Products, gag/chemistry/genetics ; Genes, Viral ; Genotype ; Giant Cells/physiology ; HIV Antigens/chemistry/genetics ; HIV Envelope Protein gp120/chemistry/*genetics ; HIV Envelope Protein gp41/chemistry/genetics ; HIV Infections/*microbiology/transmission ; HIV Seropositivity/microbiology ; HIV-1/chemistry/*genetics/*physiology ; Humans ; Macrophages ; Male ; Molecular Sequence Data ; Phenotype ; Sequence Alignment ; Sexual Partners ; *Viral Proteins ; Virus Replication ; gag Gene Products, Human Immunodeficiency Virus
    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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    Effects of oral administration of type II collagen on rheumatoid arthritis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-24
    Description: Rheumatoid arthritis is an inflammatory synovial disease thought to involve T cells reacting to an antigen within the joint. Type II collagen is the major protein in articular cartilage and is a potential autoantigen in this disease. Oral tolerization to autoantigens suppresses animal models of T cell-mediated autoimmune disease, including two models of rheumatoid arthritis. In this randomized, double-blind trial involving 60 patients with severe, active rheumatoid arthritis, a decrease in the number of swollen joints and tender joints occurred in subjects fed chicken type II collagen for 3 months but not in those that received a placebo. Four patients in the collagen group had complete remission of the disease. No side effects were evident. These data demonstrate clinical efficacy of an oral tolerization approach for rheumatoid arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trentham, D E -- Dynesius-Trentham, R A -- Orav, E J -- Combitchi, D -- Lorenzo, C -- Sewell, K L -- Hafler, D A -- Weiner, H L -- AG00294/AG/NIA NIH HHS/ -- MO1 RR01032/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 24;261(5129):1727-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Beth Israel Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8378772" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Adult ; Aged ; Arthritis, Rheumatoid/*drug therapy/immunology ; Autoimmune Diseases/*drug therapy/immunology ; Collagen/*administration & dosage/adverse effects/therapeutic use ; Double-Blind Method ; Female ; Humans ; Immune Tolerance ; Male ; Middle Aged ; Placebo Effect ; T-Lymphocytes/immunology
    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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    Mutation of unique region of Bruton's tyrosine kinase in immunodeficient XID mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: The cytoplasmic tyrosine kinase, Bruton's tyrosine kinase (Btk, formerly bpk or atk), is crucial for B cell development. Loss of kinase activity results in the human immunodeficiency, X-linked agammaglobulinemia, characterized by a failure to produce B cells. In the murine X-linked immunodeficiency (XID), B cells are present but respond abnormally to activating signals. The Btk gene, btk, was mapped to the xid region of the mouse X chromosome by interspecific backcross analysis. A single conserved residue within the amino terminal unique region of Btk was mutated in XID mice. This change in xid probably interferes with normal B cell signaling mediated by Btk protein interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rawlings, D J -- Saffran, D C -- Tsukada, S -- Largaespada, D A -- Grimaldi, J C -- Cohen, L -- Mohr, R N -- Bazan, J F -- Howard, M -- Copeland, N G -- AR36834/AR/NIAMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):358-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332901" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology/immunology ; Base Sequence ; Cell Line ; Chromosome Mapping ; Crosses, Genetic ; Exons ; Female ; Genetic Linkage ; Immunologic Deficiency Syndromes/enzymology/*genetics/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Inbred DBA ; Mice, Mutant Strains ; Molecular Sequence Data ; Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; *X Chromosome
    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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    Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-13
    Description: The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles in 42 families with late onset AD. Thus APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corder, E H -- Saunders, A M -- Strittmatter, W J -- Schmechel, D E -- Gaskell, P C -- Small, G W -- Roses, A D -- Haines, J L -- Pericak-Vance, M A -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Joseph and Kathleen Bryan Alzheimer's Disease Research Center, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8346443" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; *Alleles ; Alzheimer Disease/*genetics/metabolism/mortality ; Amyloid beta-Peptides/metabolism ; Apolipoprotein E4 ; Apolipoproteins E/*genetics/physiology ; Female ; *Gene Frequency ; Genotype ; Homozygote ; Humans ; Linkage Disequilibrium ; Male ; Risk Factors ; Survival Rate
    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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    Thymic selection of cytotoxic T cells independent of CD8 alpha-Lck association (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-17
    Description: The CD8 alpha cytoplasmic domain associates with p56lck, a nonreceptor protein-tyrosine kinase. The biological relevance of CD8 alpha-Lck association in T cell development was tested with transgenic mice generated to express a CD8 alpha molecule with two amino acid substitutions in its cytoplasmic domain, which abolishes the association of CD8 alpha with Lck. The CD8 alpha mutant was analyzed in a CD8-/- background and in the context of the transgenic 2C T cell receptor. The development and function of CD8+ T cells in these mice were apparently normal. Thus, CD8 alpha-Lck association is not necessary for positive selection, negative selection, or CD8-dependent cytotoxic function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, I T -- Limmer, A -- Louie, M C -- Bullock, E D -- Fung-Leung, W P -- Mak, T W -- Loh, D Y -- AI 155322-13/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1581-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Genetics, and Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8372352" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/metabolism ; Antigens, CD8/immunology/*metabolism ; *Cytotoxicity, Immunologic ; Female ; Genes, MHC Class I ; Lymphocyte Culture Test, Mixed ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell ; T-Lymphocytes, Cytotoxic/*immunology
    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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    Double-blind pilot trial of oral tolerization with myelin antigens in multiple sclerosis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: Multiple sclerosis (MS) is thought to be an autoimmune disease mediated by T lymphocytes that recognize myelin components of the central nervous system. In a 1-year double-blind study, 30 individuals with relapsing-remitting MS received daily capsules of bovine myelin or a control protein to determine the effect of oral tolerization to myelin antigens on the disease. Six of 15 individuals in the myelin-treated group had at least one major exacerbation; 12 or 15 had an attack in the control group. T cells reactive with myelin basic protein were reduced in the myelin-treated group. No toxicity or side effects were noted. Although conclusions about efficacy cannot be drawn from these data, they open an area of investigation for MS and other autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiner, H L -- Mackin, G A -- Matsui, M -- Orav, E J -- Khoury, S J -- Dawson, D M -- Hafler, D A -- NS23132/NS/NINDS NIH HHS/ -- NS24247/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1321-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7680493" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, Differentiation, T-Lymphocyte/analysis ; Autoantigens/*administration & dosage ; Double-Blind Method ; Female ; HLA-DR2 Antigen/genetics ; Haplotypes ; Humans ; Immune Tolerance ; Male ; Multiple Sclerosis/genetics/*therapy ; Myelin Basic Protein/immunology ; Myelin Sheath/immunology ; Pilot Projects ; T-Lymphocytes/immunology
    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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    Sex, violence, and sociobiology (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barash, D P -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):491.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Child ; Child Abuse ; Female ; Humans ; Male ; *Sexual Behavior ; Sexual Behavior, Animal ; Sociology ; *Violence
    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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    Microsatellite instability in cancer of the proximal colon (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: Colorectal tumor DNA was examined for somatic instability at (CA)n repeats on human chromosomes 5q, 15q, 17p, and 18q. Differences between tumor and normal DNA were detected in 25 of the 90 (28 percent) tumors examined. This instability appeared as either a substantial change in repeat length (often heterogeneous in nature) or a minor change (typically two base pairs). Microsatellite instability was significantly correlated with the tumor's location in the proximal colon (P = 0.003), with increased patient survival (P = 0.02), and, inversely, with loss of heterozygosity for chromosomes 5q, 17p, and 18q. These data suggest that some colorectal cancers may arise through a mechanism that does not necessarily involve loss of heterozygosity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thibodeau, S N -- Bren, G -- Schaid, D -- CA-15083-18E8.1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):816-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Mayo Clinic, Rochester, MN 55905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484122" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Chromosomes, Human, Pair 15 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, Pair 5 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Neoplasm/*genetics ; DNA, Satellite/*genetics ; Female ; Heterozygote ; Humans ; Male ; Middle Aged ; *Mutation ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid
    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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    A genetic linkage map of the mouse: current applications and future prospects (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, N G -- Jenkins, N A -- Gilbert, D J -- Eppig, J T -- Maltais, L J -- Miller, J C -- Dietrich, W F -- Weaver, A -- Lincoln, S E -- Steen, R G -- HG00198/HG/NHGRI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):57-66.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Markers ; *Genome ; Human Genome Project ; Humans ; Male ; Mice/*genetics ; Multigene Family ; Muridae/*genetics ; Mutation ; Neoplasms/genetics
    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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    MHC-restricted depletion of human myelin basic protein-reactive T cells by T cell vaccination (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Activated autoreactive T cells are potentially pathogenic and regulated by clonotypic networks. Experimental autoimmune diseases can be treated by inoculation with autoreactive T cells (T cell vaccination). In the present study, patients with multiple sclerosis were inoculated with irradiated myelin basic protein (MBP)-reactive T cells. T cell responses to the inoculates were induced to deplete circulating MBP-reactive T cells in the recipients. Regulatory T cell lines isolated from the recipients inhibited T cells used for vaccination. The cytotoxicity of the CD8+ T cell lines was restricted by major histocompatibility antigens. Thus, clonotypic interactions regulating autoreactive T cells in humans can be induced by T cell vaccination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Medaer, R -- Stinissen, P -- Hafler, D -- Raus, J -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1451-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Multiple Sclerosis Research Unit, Dr. L. Willems Instituut, Diepenbeek, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690157" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Cell Line ; Epitopes/immunology ; Female ; Humans ; *Immunotherapy, Adoptive ; Lymphocyte Activation ; Male ; Middle Aged ; Multiple Sclerosis/immunology/*therapy ; Myelin Basic Protein/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Vaccination
    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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