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  • Articles  (86)
  • Mice  (86)
  • 1980-1984  (86)
  • 1960-1964
  • 1984  (34)
  • 1983  (32)
  • 1981  (20)
  • 1960
  • Medicine  (86)
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  • Articles  (86)
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  • 1980-1984  (86)
  • 1960-1964
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  • 1
    Publication Date: 1983-11-18
    Description: Hybridoma technology has made it possible to introduce into continuous culture normal antibody-forming cells and to obtain large amounts of the immunoglobulin produced by each of these cells. Examination of the structure of a number of monoclonal antibodies that react with a single antigen has provided new information on the structural basis of the specificity and affinity of antibodies. Comparisons of families of monoclonal antibodies derived from a single germ line gene revealed the importance of somatic mutation in generating antibody diversity. Monoclonal antibodies that react with variable regions of other monoclonals allow the further dissection and modulation of the immune response. Finally, the continued somatic instability of immunoglobulin genes in cultured antibody-forming cells makes it possible to determine the rate of somatic mutation and to generate mutant monoclonal antibodies that may be more effective serological reagents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teillaud, J L -- Desaymard, C -- Giusti, A M -- Haseltine, B -- Pollock, R R -- Yelton, D E -- Zack, D J -- Scharff, M D -- 5T32GM7288/GM/NIGMS NIH HHS/ -- AI05231/AI/NIAID NIH HHS/ -- AI10702/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1983 Nov 18;222(4625):721-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6356353" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/genetics/*immunology ; *Antibody Diversity ; Antibody Specificity ; Genes ; Hybridomas/immunology ; Immunoglobulin Idiotypes/immunology ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Protein Conformation ; Structure-Activity Relationship
    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: 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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    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
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1983-12-09
    Description: Previous studies at this laboratory showed that repeated application of inactivated herpes simplex virus type 2 to the mouse cevix produced premalignant and malignant lesions. In the present study mice were inoculated with inactivated herpes simplex virus type 2 or control solution and Freund's adjuvant by intraperitoneal and subcuaneous routes before exposure of the cervix to inactivated virus. It appears that immunization with inactivated virus conferred a protection against the induction of cervical carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wentz, W B -- Heggie, A D -- Anthony, D D -- Reagan, J W -- CA-31973/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Dec 9;222(4628):1128-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6316503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Herpes Simplex/*complications ; Immunization ; Mice ; Simplexvirus/immunology ; Uterine Cervical Neoplasms/microbiology/pathology/*prevention & control
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  • 5
    Publication Date: 1983-05-06
    Description: A simple and efficient method of covalently coupling the strong chelator diethylenetriaminepentaacetic acid to proteins was developed for radiolabeling immunoglobulin G antibodies. After being coupled and labeled with indium-111, a monoclonal antibody to carcinoembryonic antigen retained its ability to bind to its antigen in vitro and in vivo. In nude mice with a human colorectal xenograft, 41 percent of the injected radioactivity became localized in each gram of xenograft at 24 hours compared with 9 percent for control antibody and 19 percent for radioiodinated antibody to carcinoembryonic antigen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hnatowich, D J -- Layne, W W -- Childs, R L -- Lanteigne, D -- Davis, M A -- Griffin, T W -- Doherty, P W -- 1 RO1 CA26968/CA/NCI NIH HHS/ -- 1 RO1 GM26780/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1983 May 6;220(4597):613-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836304" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies ; Antibodies, Monoclonal/immunology ; Carcinoembryonic Antigen/immunology ; Chromatography, High Pressure Liquid ; Humans ; Immunoglobulin G/immunology ; Isotope Labeling/*methods ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Pentetic Acid
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1983-06-24
    Description: Parenteral injection into mice of a toxic pentapeptide isolated from the cyanobacterium Microcystis aeruginosa induced thrombocytopenia, pulmonary thrombi, and hepatic congestion. The lethality of the toxin was unaffected by several anticoagulants. The acute liver damage that follows injection of the toxin has been attributed to direct action on liver cells but may be due to hypoxemia, heart failure, and shock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slatkin, D N -- Stoner, R D -- Adams, W H -- Kycia, J H -- Siegelman, H W -- New York, N.Y. -- Science. 1983 Jun 24;220(4604):1383-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6407109" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Toxins ; Blood Coagulation Tests ; Cyanobacteria/*metabolism ; Female ; Liver/pathology ; Lung/pathology ; Marine Toxins/*adverse effects ; Mice ; Organ Size/drug effects ; Platelet Count ; Pulmonary Embolism/*chemically induced/microbiology/pathology ; Thrombocytopenia/chemically induced
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  • 7
    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
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  • 8
    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
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  • 9
    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
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  • 10
    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
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