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  • Humans  (90)
  • 1995-1999
  • 1990-1994  (90)
  • 1980-1984
  • 1993  (90)
  • 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
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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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    WT1-mediated growth suppression of Wilms tumor cells expressing a WT1 splicing variant (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-24
    Description: A human Wilms tumor cell line (RM1) was developed to test the tumor suppressor activity of WT1, a zinc finger transcription factor that is expressed in the developing human kidney and is mutationally inactivated in a subset of Wilms tumors. Transfection of each of four wild-type WT1 isoforms suppressed the growth of RM1 cells. The endogenous WT1 transcript in these cells was devoid of exon 2 sequences, a splicing alteration that was also detected in varying amounts in all Wilms tumors tested but not in normal kidney. Production of this abnormal transcript, which encodes a functionally altered protein, may represent a distinct mechanism for inactivating WT1 in Wilms tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haber, D A -- Park, S -- Maheswaran, S -- Englert, C -- Re, G G -- Hazen-Martin, D J -- Sens, D A -- Garvin, A J -- CA37887/CA/NCI NIH HHS/ -- CA58596/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 24;262(5142):2057-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Massachusetts General Hospital Cancer Center, Boston 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266105" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Division/genetics ; DNA-Binding Proteins/biosynthesis/*genetics/physiology ; Genes, Wilms Tumor/genetics/*physiology ; Humans ; Mice ; Mice, Nude ; Molecular Sequence Data ; Neoplasm Transplantation ; RNA, Messenger/genetics ; Tumor Cells, Cultured ; WT1 Proteins ; Wilms Tumor/*genetics/*pathology
    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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    Preferential migration of activated CD4+ and CD8+ T cells in response to MIP-1 alpha and MIP-1 beta (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: Recombinant human macrophage inflammatory protein-1 alpha (rhMIP-1 alpha) and rhMIP-1 beta were potent chemoattractants of human T lymphocytes. These rhMIP-1 cytokines attracted only T cells activated by monoclonal antibody to CD3 and did not attract unstimulated lymphocytes. Phenotypic analysis revealed that CD4+ T cells were capable of migrating in response to rhMIP-1 beta, whereas rhMIP-1 alpha induced chemotaxis of predominantly CD8+ T lymphocytes. Activated naive and memory T cells also migrated in response to rhMIP-1 cytokines. Furthermore, these cytokines enhanced the ability of T cells to bind to an endothelial cell monolayer. These results suggest that rhMIP-1 cytokines preferentially recruit specific T cell subsets during the evolution of the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taub, D D -- Conlon, K -- Lloyd, A R -- Oppenheim, J J -- Kelvin, D J -- N01-C0-74102/PHS HHS/ -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick Cancer Research and Development Center (FCRDC), MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7682337" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antibodies, Monoclonal/immunology ; Antigens, CD3/immunology ; Antigens, CD8/analysis ; CD4-Positive T-Lymphocytes/immunology/*physiology ; Cell Adhesion ; Chemokine CCL4 ; Chemokine CCL5 ; *Chemotaxis, Leukocyte ; Clone Cells ; Cytokines/*pharmacology ; Endothelium, Vascular/cytology ; Humans ; Immunologic Memory ; *Lymphocyte Activation ; Lymphokines/pharmacology ; Macrophage Inflammatory Proteins ; Monokines/*pharmacology ; Recombinant Proteins/pharmacology ; T-Lymphocyte Subsets/immunology/physiology ; T-Lymphocytes, Cytotoxic/immunology/*physiology ; T-Lymphocytes, Regulatory/immunology/*physiology ; Umbilical Veins
    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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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
    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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  • 6
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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
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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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    Rapid loss of CD4+ T cells in human-PBL-SCID mice by noncytopathic HIV isolates (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: Human immunodeficiency virus (HIV) isolates differ in cell tropism, replication, pathogenicity, and syncytial induction in vitro. CD4+ T cells were enumerated in severe combined immunodeficient mice transplanted with human peripheral blood leukocytes (hu-PBL-SCID mice) and infected with HIV isolates with different in vitro cytopathicity. Two noncytopathic, macrophage-tropic strains, HIV-1SF162 and HIV-2UC1, induced extensive CD4+ T cell depletion, whereas HIV-1SF33, which is highly cytopathic for T cells in vitro, caused little CD4+ T cell depletion at equivalent virus burden. In vitro cytopathicity assays therefore do not predict CD4 depletion in the hu-PBL-SCID model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosier, D E -- Gulizia, R J -- MacIsaac, P D -- Torbett, B E -- Levy, J A -- AI24499/AI/NIAID NIH HHS/ -- AI29182/AI/NIAID NIH HHS/ -- AI30238/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8097595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *CD4-Positive T-Lymphocytes/immunology/microbiology ; Cytopathogenic Effect, Viral ; HIV Infections/*immunology/microbiology ; HIV-1/*pathogenicity/physiology ; HIV-2/*pathogenicity/physiology ; Humans ; Leukocyte Count ; Lymphopenia/*immunology ; Mice ; Mice, SCID ; Polymerase Chain Reaction ; T-Lymphocyte Subsets/immunology/microbiology ; Virus Replication
    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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    Optical time-of-flight and absorbance imaging of biologic media (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Imaging the interior of living bodies with light may assist in the diagnosis and treatment of a number of clinical problems, which include the early detection of tumors and hypoxic cerebral injury. An existing picosecond time-of-flight and absorbance (TOFA) optical system has been used to image a model biologic system and a rat. Model measurements confirmed TOFA principles in systems with a high degree of photon scattering; rat images, which were constructed from the variable time delays experienced by a fixed fraction of early-arriving transmitted photons, revealed identifiable internal structure. A combination of light-based quantitative measurement and TOFA localization may have applications in continuous, noninvasive monitoring for structural imaging and spatial chemometric analysis in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benaron, D A -- Stevenson, D K -- RR-00081/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1463-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Stanford University School of Medicine, Palo Alto, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8451643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Light ; Models, Theoretical ; Radiation ; Rats ; Spectrophotometry/instrumentation/*methods ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Proliferation of human smooth muscle cells promoted by lipoprotein(a) (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: Elevated blood concentrations of lipoprotein(a) [Lp(a)] and its constituent, apolipoprotein(a) [apo(a)], constitute a major risk factor for atherosclerosis, but their physiological activities remain obscure. Lp(a) and purified apo(a) stimulated the growth of human smooth muscle cells in culture. This effect resulted from inhibition of plasminogen activation, and consequently the activation by plasmin of latent transforming growth factor-beta, which is an inhibitor of smooth muscle cell growth. Because smooth muscle proliferation is one of the hallmarks of atherosclerotic lesions, these results point to a plausible mechanism for the atherogenic activity of Lp(a).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grainger, D J -- Kirschenlohr, H L -- Metcalfe, J C -- Weissberg, P L -- Wade, D P -- Lawn, R M -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins/physiology ; Apoprotein(a) ; Cell Division/drug effects/physiology ; Cells, Cultured ; Fibrinolysin/physiology ; Humans ; Lipoprotein(a)/*physiology ; Muscle, Smooth, Vascular/*cytology/metabolism ; Plasminogen Activators/metabolism ; Rats ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/physiology
    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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  • 10
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    CD19 of B cells as a surrogate kinase insert region to bind phosphatidylinositol 3-kinase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: Antigen receptors on B and T lymphocytes transduce signals by activating nonreceptor protein tyrosine kinases (PTKs). A family of receptor PTKs contains kinase insert regions with the sequence tyrosine-X-X-methionine (where X is any amino acid) that when phosphorylated mediate the binding and activation of phosphatidylinositol 3-kinase (PI 3-kinase). The CD19 membrane protein of B cells enhances activation through membrane immunoglobulin M (mIgM) and was found to contain a functional analog of the kinase insert region. Ligation of mIgM induced phosphorylation of CD19 and association with PI 3-kinase. Thus, CD19 serves as a surrogate kinase insert region for mIgM by providing the means for PI 3-kinase activation by nonreceptor PTKs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuveson, D A -- Carter, R H -- Soltoff, S P -- Fearon, D T -- 5T32GM07309/GM/NIGMS NIH HHS/ -- AI22833/AI/NIAID NIH HHS/ -- AI28191/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 May 14;260(5110):986-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7684160" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, CD/*metabolism ; Antigens, CD19 ; Antigens, Differentiation, B-Lymphocyte/*metabolism ; B-Lymphocytes/*immunology/metabolism ; Base Sequence ; Humans ; Immunoglobulin M/*metabolism ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositols/metabolism ; Phosphorylation ; Phosphotransferases/*metabolism ; Tumor Cells, Cultured ; Tyrosine/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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