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  • 1
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    The ras oncogenes increase the intrinsic resistance of NIH 3T3 cells to ionizing radiation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-05
    Description: Identification of genes that function to protect cells from radiation damage is an essential step in understanding the molecular mechanisms by which mammalian cells cope with ionizing radiation. The intrinsic radiation resistance (D0) of NIH 3T3 cells was markedly and significantly increased by transformation with ras oncogenes activated by missense mutations. This radiobiologic activity appeared to be a specific consequence of the ras mutations rather than of transformation, since revertant cells that contained functional ras genes (but were no longer phenotypically transformed) retained their increased D0's.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sklar, M D -- CA 41166/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):645-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277276" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/*radiation effects ; Cell Transformation, Neoplastic ; Cells, Cultured ; Clone Cells ; Dose-Response Relationship, Radiation ; *Genes, ras ; Mice ; Mice, Inbred Strains
    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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    Taxonomic differences in the scaling of brain on body weight among mammals (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-30
    Description: Theories for the evolution of brain weight in mammals suggest that closely related species have diverged largely as a result of selection for differences in body weight, but that differences among more distantly related species have arisen due to greater net directional selection on brain weight. This pattern of changing selection causes brain weight to evolve more slowly than body weight among closely related species, such as those in the same genus, than among more distantly related species, such as those from different families or orders; a phenomenon known as the "taxon-level effect." Thus, brain weight differs more for a given difference in body weight as the species compared are more distantly related. An alternative explanation for the taxon-level effect is proposed. Distantly related species are more likely to inhabit different ecological conditions than are more closely related species. Where the taxon-level effect occurs, brain weight appears to have evolved in response to the demands of these different ecological conditions. As a consequence, brain weight differs more among distantly related species, for any given difference in body weight, than among closely related species. This effect, rather than a progressive pattern of changing selection pressures, may account for the taxon-level effect in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pagel, M D -- Harvey, P H -- New York, N.Y. -- Science. 1989 Jun 30;244(4912):1589-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Oxford, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2740904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Artiodactyla/anatomy & histology ; *Biological Evolution ; *Body Weight ; Brain/*anatomy & histology ; Carnivora/anatomy & histology ; Chiroptera/anatomy & histology ; Ecology ; Mammals/*anatomy & histology/classification ; Models, Biological ; Organ Size ; Primates/anatomy & histology ; Regression Analysis ; Rodentia/anatomy & histology ; Selection, Genetic ; Species Specificity ; Statistics 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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  • 3
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    Vaccination against experimental allergic encephalomyelitis with T cell receptor peptides (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-11-03
    Description: Experimental allergic encephalomyelitis (EAE) is an autoimmune disease of the central nervous system mediated by CD4+ T cells reactive with myelin basic protein (MBP). Rats were rendered resistant to the induction of EAE by vaccination with synthetic peptides corresponding to idiotypic determinants of the beta chain VDJ region and J alpha regions of the T cell receptor (TCR) that are conserved among encephalitogenic T cells. These findings demonstrate the utility of TCR peptide vaccination for modulating the activity of autoreactive T cells and represent a general therapeutic approach for T cell-mediated pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howell, M D -- Winters, S T -- Olee, T -- Powell, H C -- Carlo, D J -- Brostoff, S W -- New York, N.Y. -- Science. 1989 Nov 3;246(4930):668-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Response Corporation, San Diego, CA 92121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814489" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Encephalomyelitis, Autoimmune, Experimental/*immunology/prevention & control ; Immunotherapy ; Macromolecular Substances ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Peptides/administration & dosage/chemical synthesis/immunology ; Rats ; Rats, Inbred Lew ; Receptors, Antigen, T-Cell/genetics/*immunology ; Sequence Homology, Nucleic Acid ; *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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  • 4
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    Autocrine induction of collagenase by serum amyloid A-like and beta 2-microglobulin-like proteins (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-02-03
    Description: Two autocrine proteins of 14 and 12 kilodaltons that induce the synthesis of rabbit fibroblast collagenase were identified. The proteins were purified from serum-free culture medium taken from rabbit synovial fibroblasts stimulated with phorbol myristate acetate. The amino-terminal sequences of the 14- and 12-kilodalton species were approximately 60 to 80 percent homologous with serum amyloid A and beta 2 microglobulin, respectively. The polyacrylamide gel-eluted proteins retained the ability to induce collagenase synthesis in rabbit and human fibroblasts. These autocrine proteins may provide a means to modulate collagenase synthesis in normal remodeling as well as in inflammation and disease states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brinckerhoff, C E -- Mitchell, T I -- Karmilowicz, M J -- Kluve-Beckerman, B -- Benson, M D -- AM-20582/AM/NIADDK NIH HHS/ -- AM-7448/AM/NIADDK NIH HHS/ -- RR-00750/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 3;243(4891):655-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Dartmouth Medical School, Hanover, NH 03756.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536953" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Chromatography, High Pressure Liquid ; DNA Probes ; Enzyme Induction/drug effects ; Fibroblasts/enzymology ; Humans ; Immunosorbent Techniques ; Isoelectric Focusing ; Microbial Collagenase/*biosynthesis ; Molecular Sequence Data ; Nucleic Acid Hybridization ; RNA, Messenger ; Rabbits ; Serum Amyloid A Protein/genetics/isolation & purification/*pharmacology ; Synovial Membrane/*enzymology ; Tetradecanoylphorbol Acetate/pharmacology ; beta 2-Microglobulin/genetics/isolation & purification/*pharmacology
    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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    The role of somatic hypermutation in the generation of antibody diversity (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-09
    Description: The immune system is capable of establishing an enormous repertoire of antibodies before its first contact with antigen. Most antibodies that express germ-line sequences are of relatively low affinity. Once antigen enters the system, it stimulates a somatic mutational mechanism that generates antibodies of higher affinity and selects for the expression of those antibodies to produce a more effective immune response. The details of the mechanism and regulation of somatic hypermutation remain to be elucidated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉French, D L -- Laskov, R -- Scharff, M D -- 5P30CA13330/CA/NCI NIH HHS/ -- AI10702/AI/NIAID NIH HHS/ -- CA39838/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1152-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2658060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Diversity ; Gene Rearrangement ; *Genes, Immunoglobulin ; Humans ; *Mutation
    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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    The regulation of ACTH secretion by IL-1 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lumpkin, M D -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):452-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington, DC 20007.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821618" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/*secretion ; Animals ; Corticotropin-Releasing Hormone/physiology ; Growth Hormone/secretion ; Humans ; Hypothalamus/secretion ; Interleukin-1/*physiology ; Luteinizing Hormone/secretion ; Pituitary Gland, Anterior/*secretion ; Thyrotropin/secretion
    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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    Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-14
    Description: Thousands of pet cats die each year with dilated cardiomyopathy, the cause of which is unknown. Although taurine is present in millimolar concentrations in the myocardium of all mammals, taurine depletion has not previously been associated with a decrease in myocardial function in any species. In this study, low plasma taurine concentrations associated with echocardiographic evidence of myocardial failure were observed in 21 cats fed commercial cat foods and in 2 of 11 cats fed a purified diet containing marginally low concentrations of taurine for 4 years. Oral supplementation of taurine resulted in increased plasma taurine concentrations and was associated with normalization of left ventricular function in both groups of cats. Since myocardial concentrations of taurine are directly related to plasma concentrations and low plasma concentrations were found to be associated with myocardial failure in cats, a direct link between decreased taurine concentration in the myocardium and decreased myocardial mechanical function is proposed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pion, P D -- Kittleson, M D -- Rogers, Q R -- Morris, J G -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):764-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathy, Dilated/diagnosis/etiology/*veterinary ; *Cat Diseases ; Cats ; Dogs ; Echocardiography ; Humans ; Myocardium/metabolism ; Retinal Degeneration/etiology/veterinary ; Taurine/blood/*deficiency/metabolism
    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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    RNA as an RNA polymerase: net elongation of an RNA primer catalyzed by the Tetrahymena ribozyme (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-18
    Description: A catalytic RNA (ribozyme) derived from an intervening sequence (IVS) RNA of Tetrahymena thermophila will catalyze an RNA polymerization reaction in which pentacytidylic acid (C5) is extended by the successive addition of mononucleotides derived from a guanylyl-(3',5')-nucleotide (GpN). Cytidines or uridines are added to C5 to generate chain lengths of 10 to 11 nucleotides, with longer products being generated at greatly reduced efficiency. The reaction is analogous to that catalyzed by a replicase with C5 acting as the primer, GpNs as the nucleoside triphosphates, and a sequence in the ribozyme providing a template. The demonstration that an RNA enzyme can catalyze net elongation of an RNA primer supports theories of prebiotic RNA self-replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Been, M D -- Cech, T R -- GM28039/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 18;239(4846):1412-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2450400" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalysis ; Esterification ; Guanine Nucleotides/metabolism ; Nucleotides/metabolism ; Oligonucleotides/metabolism ; RNA/*biosynthesis ; RNA Precursors ; RNA Replicase/metabolism ; RNA Splicing ; RNA, Catalytic ; RNA, Ribosomal/*metabolism ; Templates, Genetic ; Tetrahymena/*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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  • 9
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    Subset-specific expression of potassium channels in developing murine T lymphocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-12
    Description: Ion channels were studied in four major subsets of developing murine thymocytes by using patch-clamp recording and cell-surface staining techniques. The expression of three types of voltage-gated potassium channels in thymocytes varies consistently with the cell's developmental state and functional class as defined by cell-surface markers. One class of potassium channel (type n) predominates in immature thymocyte subsets as well as in mature-phenotype CD4+CD8- thymocytes (precursors to helper T lymphocytes), and the average surface density of this channel type correlates with the extent of cell proliferation. Two additional types of potassium channels (types n' and l) are found in the mature CD4-CD8+ thymocyte subset that contains precursors to cytotoxic and suppressor T cells. The subset-specific expression of type n' and l potassium channels suggests their use as additional cell-surface markers with which to identify precursors to the cytotoxic suppressor T cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewis, R S -- Cahalan, M D -- AI21808/AI/NIAID NIH HHS/ -- NS08021/NS/NINDS NIH HHS/ -- NS14609/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):771-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, California College of Medicine, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2448877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Surface/analysis ; Electric Conductivity ; Ion Channels/*physiology ; Membrane Potentials ; Mice ; Phenotype ; T-Lymphocytes/classification/immunology/*physiology
    Print ISSN: 0036-8075
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  • 10
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    Nicotinic antagonists enhance process outgrowth by rat retinal ganglion cells in culture (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: Functional nicotinic cholinergic receptors are found on mammalian retinal ganglion cell neurons in culture. The neurotransmitter acetylcholine (ACh) can be detected in the medium of many of these retinal cultures, after release presumably from the choline acetyltransferase-positive amacrine cells. The postsynaptic effect of endogenous or applied ACh on the ganglion cells can be blocked with specific nicotinic antagonists. Here it is shown that within 24 hours of producing such a pharmacologic blockade, the retinal ganglion cells begin to sprout or regenerate neuronal processes. Thus, the growth-enhancing effect of nicotinic antagonists may be due to the removal of inhibition to growth by tonic levels of ACh present in the culture medium. Since there is a spontaneous leak of ACh in the intact retina, the effects of nicotinic cholinergic drugs on process outgrowth in culture may reflect a normal control mechanism for growth or regeneration of retinal ganglion cell processes that is exerted by ACh in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipton, S A -- Frosch, M P -- Phillips, M D -- Tauck, D L -- Aizenman, E -- EY05477/EY/NEI NIH HHS/ -- EY06087/EY/NEI NIH HHS/ -- NS00879/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1293-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/*pharmacology ; Cells, Cultured ; Mecamylamine/*pharmacology ; Picrotoxin/pharmacology ; Rats ; Receptors, Nicotinic/drug effects/*physiology ; Retina/*cytology ; Retinal Ganglion Cells/*cytology/drug effects ; Tubocurarine/*pharmacology
    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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