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  • Life and Medical Sciences  (2)
  • Mice  (2)
  • RFLP  (2)
  • 1995-1999  (6)
  • 1925-1929
  • 1
    Publication Date: 1999-01-29
    Description: A carbapenem antibiotic, L-786,392, was designed so that the side chain that provides high-affinity binding to the penicillin-binding proteins responsible for bacterial resistance was also the structural basis for ameliorating immunopathology. Expulsion of the side chain upon opening of the beta-lactam ring retained antibacterial activity while safely expelling the immunodominant epitope. L-786,392 was well tolerated in animal safety studies and had significant in vitro and in vivo activities against methicillin- and vancomycin-resistant Staphylococci and vancomycin-resistant Enterococci.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosen, H -- Hajdu, R -- Silver, L -- Kropp, H -- Dorso, K -- Kohler, J -- Sundelof, J G -- Huber, J -- Hammond, G G -- Jackson, J J -- Gill, C J -- Thompson, R -- Pelak, B A -- Epstein-Toney, J H -- Lankas, G -- Wilkening, R R -- Wildonger, K J -- Blizzard, T A -- DiNinno, F P -- Ratcliffe, R W -- Heck, J V -- Kozarich, J W -- Hammond, M L -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):703-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Research Laboratories, Rahway, NJ 07065, USA. hugh_rosen@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/blood ; *Bacterial Proteins ; Carbapenems/chemistry/*immunology/metabolism/*pharmacology/toxicity ; Carrier Proteins/metabolism ; Dipeptidases/metabolism ; *Drug Design ; Drug Resistance, Microbial ; Drug Resistance, Multiple ; Enterococcus/drug effects ; Erythrocytes/immunology ; Haptens ; *Hexosyltransferases ; Humans ; Immunodominant Epitopes ; Immunoglobulin G/blood ; Lactams/chemical synthesis/chemistry/metabolism/*pharmacology ; Lymphocyte Activation ; Macaca mulatta ; Mice ; Mice, Inbred DBA ; Microbial Sensitivity Tests ; Muramoylpentapeptide Carboxypeptidase/metabolism ; Penicillin-Binding Proteins ; *Peptidyl Transferases ; Staphylococcal Infections/drug therapy ; Staphylococcus/drug effects ; Thiazoles/chemical synthesis/chemistry/metabolism/*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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  • 2
    Publication Date: 1997-05-02
    Description: Mutations in the tumor suppressor gene PATCHED (PTC) are found in human patients with the basal cell nevus syndrome, a disease causing developmental defects and tumors, including basal cell carcinomas. Gene regulatory relationships defined in the fruit fly Drosophila suggest that overproduction of Sonic hedgehog (SHH), the ligand for PTC, will mimic loss of ptc function. It is shown here that transgenic mice overexpressing SHH in the skin develop many features of basal cell nevus syndrome, demonstrating that SHH is sufficient to induce basal cell carcinomas in mice. These data suggest that SHH may have a role in human tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oro, A E -- Higgins, K M -- Hu, Z -- Bonifas, J M -- Epstein, E H Jr -- Scott, M P -- AR39959/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1997 May 2;276(5313):817-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Dermatology, Stanford University School of Medicine, Stanford, CA 94305-5427, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basal Cell Nevus Syndrome/*genetics/metabolism/pathology ; Carcinoma, Basal Cell/*genetics/metabolism/pathology ; Embryo, Mammalian ; *Gene Expression Regulation, Neoplastic ; Hedgehog Proteins ; Humans ; Intracellular Signaling Peptides and Proteins ; Keratinocytes/metabolism ; Male ; Membrane Proteins/genetics/metabolism ; Mice ; Mice, SCID ; Mice, Transgenic ; Mutation ; Neoplasm Transplantation ; Protein Biosynthesis ; Proteins/*genetics/metabolism ; Receptors, Cell Surface ; Skin/pathology ; Skin Neoplasms/*genetics/metabolism/pathology ; Skin Transplantation ; *Trans-Activators
    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
    Electronic Resource
    Electronic Resource
    Springer
    Theoretical and applied genetics 92 (1996), S. 448-454 
    ISSN: 1432-2242
    Keywords: Key words  Wheat ; Salt tolerance ; Homoeologous recombination ; QTL ; RFLP ; Genetic marker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract   In saline environments, bread wheat, Triticum aestivum L. (genomes AABBDD), accumulates less Na+ and more K+ in expanding and young leaves than durum wheat, T. turgidum L. (genomes AABB). Higher K+/Na+ ratios in leaves of bread wheat correlate with its higher salt tolerance. Chromosome 4D from bread wheat was shown in previous work to play an important role in the control of this trait and was recombined with chromosome 4B in the absence of the Ph1 locus. A population of plants disomic for 4D/4B recombined chromosomes in the genetic background of T. turgidum was developed to investigate the genetic control of K+/Na+ discrimination by chromosome 4D. Evidence was obtained that the trait is controlled by a single locus, designated Kna1, in the long arm of chromosome 4D. In the present work, K+/Na+ discrimination was determined for additional families with 4D/4B chromosomes. The concentrations of Na+ and K+/Na+ ratios in the youngest leaf blades clustered in two nonoverlapping classes, and all recombinant families could be unequivocally assigned to Kna1 and kna1 classes. The Kna1 locus scored this way was mapped on a short region in the 4DL arm and was completely linked to Xwg199, Xabc305, Xbcd402, Xpsr567, and Xpsr375; it was also mapped as a quantitative trait. The results of the QTL analysis, based on the K+/Na+ ratios in the young leaves of greenhouse-grown plants and flag leaves of field-grown plants, agreed with the position of Kna1 determined as a qualitative trait. Several aspects of gene introgression by manipulation of the Ph1 locus are discussed.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Theoretical and applied genetics 92 (1996), S. 448-454 
    ISSN: 1432-2242
    Keywords: Wheat ; Salt tolerance ; Homoeologous recombination ; QTL ; RFLP ; Genetic marker
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In saline environments, bread wheat, Triticum aestivum L. (genomes AABBDD), accumulates less Na+ and more K+ in expanding and young leaves than durum wheat, T. turgidum L. (genomes AABB). Higher K+/Na+ ratios in leaves of bread wheat correlate with its higher salt tolerance. Chromosome 4D from bread wheat was shown in previous work to play an important role in the control of this trait and was recombined with chromosome 4B in the absence of the Ph1 locus. A population of plants disomic for 4D/4B recombined chromosomes in the genetic background of T. turgidum was developed to investigate the genetic control of K+/Na+ discrimination by chromosome 4D. Evidence was obtained that the trait is controlled by a single locus, designated Kna1, in the long arm of chromosome 4D. In the present work, K+/Na+ discrimination was determined for additional families with 4D/4B chromosomes. The concentrations of Na+ and K+/Na+ ratios in the youngest leaf blades clustered in two nonoverlapping classes, and all recombinant families could be unequivocally assigned to Kna1 and kna1 classes. The Kna1 locus scored this way was mapped on a short region in the 4DL arm and was completely linked to Xwg199, Xabc305, Xbcd.402, Xpsr567, and Xpsr375; it was also mapped as a quantitative trait. The results of the QTL analysis, based on the K+/Na+ ratios in the young leaves of greenhousegrown plants and flag leaves of field-grown plants, agreed with the position of Knal determined as a qualitative trait. Several aspects of gene introgression by manipulation of the Ph1 locus are discussed.
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  • 5
    ISSN: 0730-2312
    Keywords: nuclear bodies ; promyelocytic leukemia protein ; herpes simplex virus ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The promyelocytic leukemia protien fused to the retinoic acid receptor in t(15;17) acute promyelocytic leukemia, the primary biliary cirrhosis autoantigen, Sp100, as well as the incompletely charterized protien NDP55, are co-localized in specific immunohistochemically defined nuclear domains (ND10), which are potential equyivalents of ultrastructurally defined nuclear bodies. We investigated whether the distribution of these proteins depends on environmental conditions and whether ND10 correlate with nuclear bodies. Certain nuclear bodies and ND10 react in a similar bodies, which herpes simplex virus infection or heat shock modify both. Redistribution of ND10-associated proteins to hundreds of small sites throughout the chromatin was inducible by stress in the form of heat shock and exposure to Cd++ ions. The change of distribution was rapid and independent of proteins synthesis, and thus not part of the classical heat shock response. The very rapid redistribution of these proteins after heat shock, together with the development of ND10 upon interferon actication, raises the possibility that ND10 represent storage sites of certain matrix proteins readily accessible throughout the chromatin in response to stress or other effectors that induce global nuclear changes. © 1995 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    BioEssays 18 (1996), S. 1025-1027 
    ISSN: 0265-9247
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Werner syndrome is a rare autosomal recessive disorder that mimics some of the characteristics of aging. The gene for this disorder has recently been identified as a helicase of the recQ subclass(1). Other phenotypically distinctive disorders caused by different helicase mutations include Bloom syndrome, Cockayne syndrome, xeroderma pigmentosum and trichothiodystrophy. Possible mechanisms by which helicases might produce the variable phenotypes are discussed. These include altered nucleotide excision repair and RNA polymerase II-mediated transcription. The discovery of the helicase defect in Werner syndrome provides a road map for future study of its unique pathogenesis and conceivable, but unproved, relationship to the aging process.
    Type of Medium: Electronic Resource
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