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  • Articles  (57)
  • Latest Papers from Table of Contents or Articles in Press  (57)
  • Mice  (53)
  • Biochemistry and Biotechnology
  • Chemistry
  • 1985-1989
  • 1980-1984  (57)
  • 1970-1974
  • 1984  (37)
  • 1980  (20)
  • Natural Sciences in General  (57)
  • Technology
  • Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
Collection
  • Articles  (57)
Source
Keywords
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Years
  • 1985-1989
  • 1980-1984  (57)
  • 1970-1974
Year
Journal
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  • 1
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    Autoimmunity and increased c-myb transcription (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-30
    Description: A single recessive gene, lpr, induces an autoimmune-lymphoproliferative syndrome in several strains of mice. The lymphoid organs of lpr/lpr mice contained cells with increased amounts of myb RNA, which codes for a protein found in the nucleus. A similar human lymphoproliferative disorder also had an increase in c-myb expression. Mouse T cells induced by mitogens to proliferate did not express large amounts of myb RNA, indicating that marked myb expression is not a general feature of lymphocyte activation and proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mountz, J D -- Steinberg, A D -- Klinman, D M -- Smith, H R -- Mushinski, J F -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1087-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantibodies/*genetics ; Autoimmune Diseases/*genetics ; Female ; *Genes, Recessive ; Lymphocytes/immunology ; Lymphoproliferative Disorders/*genetics ; Mice ; Mice, Inbred Strains ; Nucleic Acid Hybridization ; *Oncogenes ; Species Specificity ; Spleen/immunology ; *Transcription, Genetic
    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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    Hypoxic coordinate regulation of mitochondrial enzymes in mammalian cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: The effect of hypoxic exposure on various mitochondrial enzymes and on cell mitochondrial genomic content was studied in two types of mammalian cells. Hypoxia depressed the activity of six enzymes to the same degree. The kinetics of depression and of recovery during reexposure to normoxia were statistically similar for three marker enzymes. Despite the global and symmetrical decrease in enzyme activities, mitochondrial DNA remained constant. This suggests either symmetrical loss of mitochondrial enzymes from all mitochondria or complete loss of enzymes from a subpopulation of mitochondria with retention of an intact mitochondrial genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, B J -- Robin, E D -- Tapper, D P -- Wong, R J -- Clayton, D A -- 5 R01 HL23701-14/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):707-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320368" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis ; Anaerobiosis ; Animals ; Anoxia/physiopathology ; Citrate (si)-Synthase/genetics/*metabolism ; DNA, Mitochondrial/*genetics ; Electron Transport Complex IV/genetics/*metabolism ; Macrophages/*enzymology ; Mice ; Mitochondria/*enzymology ; Mitochondria, Muscle/*enzymology ; Oxidoreductases/genetics/*metabolism ; Oxo-Acid-Lyases/*metabolism ; Rats
    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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    Mebendazole therapy of parenteral trichinellosis (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-03-14
    Description: Mebendazole was highly effective against the helminth parasite Trichinella spiralis in mice subjected to a 3-day course of treatment during the invasive and encystment phases of experimental trichinellosis. When treatment began either 2 or 4 weeks after the mice were inoculated with parasites, the number of larvae developing in the host musculature was greatly reduced by twice-daily oral administration of 3.125, 6.25, or 12.5 milligrams of mebendazole per kilogram of body weight.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCracken, R O -- Taylor, D D -- New York, N.Y. -- Science. 1980 Mar 14;207(4436):1220-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7355285" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Benzimidazoles/*therapeutic use ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Larva ; Male ; Mebendazole/administration & dosage/*therapeutic use ; Mice ; Muscles/parasitology ; Trichinella/drug effects ; Trichinellosis/*drug therapy
    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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    Genes for growth hormone, chorionic somatommammotropin, and growth hormones-like gene on chromosome 17 in humans (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-07-11
    Description: The human genes for growth hormone (GH), chorionic somatomammotropin (CSH), and a third growth hormone-like gene (GHL) have been located on chromosome 17 in humans. DNA fragments of 2.6, 2.8, and 9.5 kilobase pairs containing GH, CSH, and GHL, respectively, were identified in human genomic DNA, and a 7.5-kilobase DNA fragment related to growth hormone DNA sequences was found in mouse cells. In somatic hybrids of human and mouse cells containing reduced numbers of human chromosomes, but a normal complement of mouse chromosomes, the mouse, 7.5-kolobase DNA fragment was always present, whereas the 2.6-, 2.8-, and 9.5-kilobase human fragments were present only when human chromosome 17 was also present.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Owerbach, D -- Rutter, W J -- Martial, J A -- Baxter, J D -- Shows, T B -- New York, N.Y. -- Science. 1980 Jul 11;209(4453):289-92.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7384802" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; *Chromosomes, Human, 16-18 ; *DNA/metabolism ; *Genes ; Growth Hormone/*biosynthesis ; Humans ; Hybrid Cells/metabolism ; Mice ; Placental Lactogen/*biosynthesis ; Translocation, Genetic
    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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    Immunologic inhibition of ultraviolet radiation-induced tumor suppressor cell activity (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-05-11
    Description: Long-term exposure of C3H mice to ultraviolet radiation resulted in the formation of suppressor T cells that recognize ultraviolet radiation-induced regressor skin cancers as a class before the appearance of overt tumors. Administration of monoclonal antibodies to the product of the I-Jk subregion of the major histocompatibility complex or low doses of cyclophosphamide in vivo inhibited the development or activity of these cells. This activity of the monoclonal antibody was eliminated by adsorption on B10.BR (I-Jk) but not B10.D2 (I-Jd) splenocytes. These findings provide evidence that elements expressing the I-J determinant are important in regulating the host response prior to the overt development of ultraviolet radiation-induced skin cancers and suggest novel therapeutic approaches to malignancies or other diseases involving suppressor T cells in their pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Granstein, R D -- Parrish, J A -- McAuliffe, D J -- Waltenbaugh, C -- Greene, M I -- 1F32 CA07014-102/CA/NCI NIH HHS/ -- AI 18072/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 May 11;224(4649):615-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6231725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Cyclophosphamide/pharmacology ; H-2 Antigens/immunology ; Mice ; Mice, Inbred C3H ; Neoplasms, Experimental/immunology ; Spleen/cytology ; T-Lymphocytes, Regulatory/drug effects/*immunology/radiation effects ; Ultraviolet Rays
    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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    Expression of a retrovirus encoding human HPRT in mice (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-10
    Description: Transmissible retroviruses encoding human hypoxanthine phosphoribosyltransferase (HPRT) were used to infect mouse bone marrow cells in vitro, and the infected cells were transplanted into mice. Both active human HPRT-protein and chronic HPRT-virus production were detected in hematopoietic tissue of the mice, showing transfer of the gene. These results indicate the possible use of retroviruses for somatic cell therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, A D -- Eckner, R J -- Jolly, D J -- Friedmann, T -- Verma, I M -- CA 19562/CA/NCI NIH HHS/ -- GM28223/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 10;225(4662):630-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6377498" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/microbiology ; Bone Marrow Transplantation ; DNA, Recombinant/metabolism ; Hematopoietic Stem Cells/microbiology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Isoenzymes/metabolism ; Lesch-Nyhan Syndrome/genetics/therapy ; Mice ; Nucleic Acid Hybridization ; Rats ; Retroviridae/enzymology/*genetics ; Spleen/microbiology
    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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    Interferon-beta-related DNA is dispersed in the human genome (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-03-23
    Description: Interferon-beta 1 (IFN-beta 1) complementary DNA was used as a hybridization probe to isolate human genomic DNA clones lambda B3 and lambda B4 from a human genomic DNA library. Blot-hybridization procedures and partial nucleotide sequencing revealed that lambda B3 is related to IFN-beta 1 (and more distantly to IFN-alpha 1). Analyses of DNA obtained from a panel of human-rodent somatic cell hybrids that were probed with DNA derived from lambda B3 showed that lambda B3 is on human chromosome 2. Similar experiments indicated that lambda B4 is not on human chromosomes 2, 5, or 9. The finding that DNA related to the IFN-beta 1 gene (and IFN-alpha 1 gene) is dispersed in the human genome raises new questions about the origins of the interferon genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sagar, A D -- Sehgal, P B -- May, L T -- Inouye, M -- Slate, D L -- Shulman, L -- Ruddle, F H -- AI-16262/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 23;223(4642):1312-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6546621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosome Mapping ; Chromosomes, Human/*analysis ; Chromosomes, Human, 1-3 ; Chromosomes, Human, 4-5 ; Chromosomes, Human, 6-12 and X ; Cloning, Molecular ; Cricetinae ; DNA/*analysis ; *Genes ; Humans ; Hybrid Cells ; Interferon Type I/*genetics ; Mice ; Nucleic Acid Hybridization
    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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    Chromosome 4 Jt gene controls murine T cell surface I-J expression (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-10
    Description: Data are presented suggesting a resolution to the paradox concerning the murine response subregion I-J, which encodes a suppressor T cell marker. The controversy arose when sequences corresponding to I-J DNA were not found in the central immune response region described by immunogeneticists. New evidence is presented that T cell surface I-J expression results from the action of at least two complementing genes. One gene is within the H-2 region on chromosome 17; the second gene, termed Jt, is on chromosome 4. The two recombinant mouse strains B10.A(3R) and B10.A(5R) originally used to define the I-J subregion apparently differ not within the H-2 region but elsewhere.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayes, C E -- Klyczek, K K -- Krum, D P -- Whitcomb, R M -- Hullett, D A -- Cantor, H -- CA34106/CA/NCI NIH HHS/ -- T 32 CA 09106/CA/NCI NIH HHS/ -- T 32 GM 07215/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):559-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6607530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Surface/*genetics ; Chromosome Mapping ; *Genes ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; Species Specificity ; 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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  • 9
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    Antidepressants cause lethal disruption of membrane function in the human protozoan parasite Leishmania (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-23
    Description: The antidepressant compounds clomipramine and nitroimipramine were cidal to extracellular promastigotes of both human protozoan parasites Leishmania donovani and Leishmania major. Clomipramine also killed amastigotes of both species within murine macrophages with no apparent toxicity to the host cells. Further, amastigotes were more sensitive than promastigotes to clomipramine. Clomipramine (100 micromoles per liter or 0.2 nanomole per 1 X 10(6) cells) inhibited L-proline transport in promastigotes. Synergistic inhibition of L-proline transport was observed with clomipramine after addition of either of the ionophores valinomycin or nigericin. These observations suggest that the cytotoxic effects of clomipramine result from its disruption of the proton electrochemical gradient of the parasite surface membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zilberstein, D -- Dwyer, D M -- New York, N.Y. -- Science. 1984 Nov 23;226(4677):977-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6505677" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/drug effects/physiology/ultrastructure ; Clomipramine/*toxicity ; Humans ; Imipramine/analogs & derivatives/*toxicity ; Leishmania/cytology/*drug effects/physiology ; Mice ; Mice, Inbred BALB C ; Proline/metabolism ; Species Specificity
    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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    1,25-dihydroxyvitamin D3: a novel immunoregulatory hormone (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-29
    Description: The hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], at picomolar concentrations, inhibited the growth-promoting lymphokine interleukin-2, which is produced by human T lymphocytes activated in vitro by the mitogen phytohemagglutinin. Other metabolites of vitamin D3 were less effective than 1,25(OH)2D3 in suppressing interleukin-2; their order of potency corresponded to their respective affinity for the 1,25(OH)2D3 receptor, suggesting that the effect on interleukin-2 was mediated by this specific receptor. The proliferation of mitogen-activated lymphocytes was also inhibited by 1,25(OH)2D3. This effect of the hormone became more pronounced at later stages of the culture. These findings demonstrate that 1,25(OH)2D3 is an immunoregulatory hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsoukas, C D -- Provvedini, D M -- Manolagas, S C -- AM29779/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1438-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6427926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcitriol/*pharmacology ; Cell Division/drug effects ; Cell Line ; Humans ; Immunity, Cellular/*drug effects ; Interleukin-2/antagonists & inhibitors ; Lymphocyte Activation/drug effects ; Lymphocytes/drug effects ; Mice ; Monocytes/drug effects ; Receptors, Immunologic/drug effects ; Receptors, Interleukin-2
    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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