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  • Cell & Developmental Biology  (2)
  • Birds -- Conservation -- America.  (1)
  • 1995-1999  (1)
  • 1980-1984  (2)
  • 1940-1944
  • 1
    Online Resource
    Online Resource
    Oxford :Oxford University Press, Incorporated,
    Keywords: Birds -- Conservation -- America. ; Birds -- Migration -- America. ; Birds -- Ecology -- America. ; Birds -- Habitat -- America. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (506 pages)
    Edition: 1st ed.
    ISBN: 9780195359176
    DDC: 598.252/5/097
    Language: English
    Note: Intro -- Contents -- Introduction: Importance of Knowledge and its Application in Neotropical Migratory Birds -- PART I: POPULATION TRENDS -- 1 Population Trends from the North American Breeding Bird Survey -- 2 The Strength of Inferences about Causes of Trends in Populations -- PART II: TEMPORAL PERSPECTIVES ON POPULATION LIMITATION AND HABITAT USE -- 3 When and How are Populations Limited? The Roles of Insect Outbreaks, Fire, and Other Natural Perturbations -- 4 Summer versus Winter Limitation of Populations: What are the Issues and What is the Evidence? -- 5 Habitat Requirements During Migration: Important Link in Conservation -- 6 Habitat Use and Conservation in the Neotropics -- PART III: FOREST MANAGEMENT -- 7 Impacts of Silviculture: Overview and Management Recommendations -- 8 Effects of Silvicultural Treatments in the Rocky Mountains -- 9 Silviculture in Central and Southeastern Oak Pine Forests -- PART IV: GENERAL HUMAN EFFECTS -- 10 Effects of Agricultural Practices and Farmland Structures -- 11 An Assessment of Potential Hazards of Pesticides and Environmental Contaminants -- 12 Livestock Grazing Effects in Western North America -- PART V: SCALE PERSPECTIVES -- 13 Habitat Fragmentation in the Temperate Zone -- 14 A Landscape Ecology Perspective for Research, Conservation, and Management -- 15 Ecology and Behavior of Cowbirds and their Impact on Host Populations -- 16 Single-Species versus Multiple-Species Approaches for Management -- 17 Summary: Model Organisms for Advancing Understanding of Ecology and Land Management -- Index -- A -- B -- C -- D -- E -- F -- G -- H -- I -- K -- L -- M -- N -- O -- P -- R -- S -- T -- W.
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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 109 (1981), S. 289-297 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: GH pituitary cells have been widely utilized for studies of hormone response mechanisms. Studies reported here were motivated by the desirability of isolating characterized GH clones defective in cyclic AMP synthesis or action. Spontaneously occurring GH1 cell variants resistant to the growthinhibitory effects of cyclic AMP analogs were isolated. Characterization of four variants showed that these were deficient in adenosine kinase and had acquired resistance to the cytotoxic effects of purine nucleoside derivatives formed in the culture medium. A second-stage selection was undertaken with mutagenized adenosine kinase-deficient cells. One 8 Br cAMP-resistant variant was found to have normal cyclic AMP-dependent protein kinase activity but exhibited altered adenylate cyclase activity. Activation of cyclase activity by fluoride, guanyl nucleotides, cholera toxin, and hormone (VIP) was subnormal in the variant. Mndependent cyclase activity was also subnormal, suggesting that the 8 Br cAMP-resistant variant may have a deficiency in the catalytic moiety of adenylate cyclase.Surprisingly, adenosine 3′ :5′ -monophosphate and 5′ -monophosphate derivatives were found to be equally potent in growth-inhibiting adenosine kinasedeficient cells. Cross-resistance to 8 Br AMP was observed in the 8 Br cAMP-resistant variant. We conclude that cyclic AMP derivatives inhibit growth of GH cells by an unanticipated mechanism that is, nonetheless, related to endogenous cyclic AMP synthesis.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 103 (1980), S. 489-502 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Previous studies (J. Biol. Chem, 253: 99-105, 1978) showed that thyrotropin-releasing hormone (TRH) acutely stimulated uridine uptake in pituitary cell (GH4C1) cultures. Studies on the role of protein synthesis in this response to TRH led to the finding that an inhibitor of ribosomal translation, cycloheximide, also stimulated uridine uptake acutely. Studies reported here attempt to determine the mechanism of cycloheximide action and whether cycloheximide and hormone stimulation of uridine uptake occurred by similar pathways. The experiments presented indicate that: (1) seven inhibitors of ribosomal translation stimulated uridine uptake; (2) in contrast, inhibition of protein synthesis at tRNA aminoacylation resulted in reduced rates of uridine uptake; (3) inhibition of tRNA aminoacylation blocked cycloheximide but not TRH stimulation of uptake; (4) cycloheximide stimulation of uptake was restricted to amino acid-depleted cultures; (5) amino acid supplementation stimulated uridine uptake with a time-course identical to that of cycloheximide; (6) cycloheximide and amino acid supplementation promoted reacylation of cellular tRNAs in amino acid-depleted cultures; and (7) cycloheximide stimulation of uridine uptake resulted from enhanced nucleoside phosphorylation rather than increased uridine transport. We conclude that cycloheximide and amino acid stimulation of uridine phosphorylation may be mediated through a common pathway involving the extent of amino-acylation of cellular tRNAs. Furthermore, cycloheximide and TRH stimulate uridine phosphorylation by pathways that are distinguishable. It is apparent that not all cellular effects of cycloheximde can be attributed solely to inhibition of the synthesis of proteins.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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