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  • 1
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    New York : Oxford University Press
    Keywords: Philosophie, Dictionnaires anglais. ; Philosophy, Dictionaries.
    Pages: ix, 418 p.
    ISBN: 0-585-11072-7
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  • 2
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    St. Louis, Mo. : Saunders Elsevier
    Call number: C020:114
    Keywords: Pregnancy / physiology ; Fetus / Physiology ; Infant, Newborn / physiology
    Pages: xv, 777 p. : ill.
    Edition: 3rd ed.
    ISBN: 9781416029441
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    C020:114 departmental collection or stack – please contact the library
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  • 3
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    Cold Spring Harbor, N.Y. : Cold Spring Harbor Laboratory Press
    Call number: C050:63
    Keywords: Telomere / physiology ; Aging / genetics ; Neoplasms / genetics
    Description / Table of Contents: A history of telomere biology / E.H. Blackburn -- The telomerase ribonucleoprotein particle / G. Cristofari and J. Lingner -- Telomerase biochemistry and biogenesis / J.-L. Chen and C.W. Greider -- Telomerase and human cancer / J.W. Shay and W.E. Wright -- Modeling cancer and aging in the telomerase-deficient mouse / K.-K. Wong, S. Chang, and R.A. DePinho -- Telomerase deficiency and human disease / I. Dokal and T. Vulliamy -- Telomerase-independent maintenance of mammalian telomeres / A.A. Neumann and R.R. Reddel -- Telomerase-independent telomere maintenance in yeast / M.J. McEachern and J.E. Haber -- Meiotic telomeres / H. Scherthan -- Telomere position effect: silencing near the end / M.A. Mondoux and V.A. Zakian -- The structural biology of telomeres / D. Rhodes -- Budding yeast telomeres / V. Lundblad -- Mammalian telomeres / T. de Lange -- Drosophila telomeres / S. Pimpinelli -- Ciliate telomeres / C. Price -- Fission yeast telomeres / J.P. Cooper and Y. Hiraoka -- Plant telomeres / D.E. Shippen
    Pages: viii, 576 p. : ill.
    Edition: 2nd ed.
    ISBN: 9780879697341
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  • 4
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    Oxford [England : IRL Press at Oxford University Press
    Call number: H0701:6
    Keywords: Nucleic Acids
    Notes: Includes index.
    Pages: xv, 528 p.
    Edition: 2nd ed.
    ISBN: 019963534X
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    H0701:6 departmental collection or stack – please contact the library
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 102 (1993), S. 0 
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract The model represents a System Dynamics approach to the solution of a reaction-diffusion problem involving biogeochemical processes in a stratified marine sediment. The major reactants and products are represented, their interactions described by Michelis Menton-like equations and their movements controlled by diffusion equations. The model is truly dynamic: all reaction-and diffusion rates of all specified species are predicted by the model in space and time. In order to simplify the output, a steady-state situation is examined where the variation in oxygen, nitrate and ammonium concentrations, and the rates of nitrification and denitrification are seen in relation to different levels of organic matter mineralization. Nitrogen and carbon budgets are also presented. The modelling environment, Cellmatic, was designed to run models with high spatial and temporal structure. Cellmatic is easy to use for simulating any model with these characteristics.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 102 (1993), S. 0 
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract A reaction diffusion model was used to simulate the mineralization processes in an Arctic sediment. The simulation and the actual sediment were compared in relation to profiles of O2, NO3 and NH4+. The site of particulate organic matter (POM) degradation was the single most important factor in fitting the simulation profiles to those of the sediment. It was deduced that most POM degradation occurred close to the sediment surface. When a reasonably good simulation had been obtained, the sensitivity of the model to changes in other parameters was investigated. Increases in POM degradation in the upper sediment resulted in increases in concentration of NH4+ and NO3−, but further increases in POM degradation created anoxic conditions below 3 mm, resulting in decreases in NO3− concentrations. The model was relatively intensive to changes in POM degradation in the lower sediment layers; increases led to more anoxic conditions and to less NO3−. Increases in the C/N ratio of the POM in the lower sediment layers had little effect; increases in C/N in the upper layers led to a decrease in NH4+ and NO3−. The model was sensitive to changes in the first order rate constant for nitrification, but not for denitrification. Decreases in the Km for O2 of the nitrifying bacteria had no effect on the profiles.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 100 (1992), S. 0 
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract Processes involved in the C, N, S, and O cycles in a marine sediment were stimulated for a situation where most organic degradation occured in the top 2 mm and NO3− was not present in the overlying water. The effect of increasing organic loading was examined (degradation of C ? 7 to 107 mmol m−2 d−1). Increasing organic loading had the following results: (1) ? 50% of the dissolved organic nitrogen was lost by diffusion in all treatments; (2) the proportion of NH4++; flux increased, the proportion of nitrification increased slightly and then decreased; and (3) the proportion of NO3− of NO3− efflux.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 13 (2001), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Chronic pain and depressive illness are debilitating disease states that are variably resistant to currently available therapeutic agents. Animal models of chronic pain are associated with activation of the hypothalamo-pituitary-adrenal (HPA) axis, upon which chronic pain acts as an inescapable stressor. Inescapable stress is also associated with ‘depressive-like’ symptoms in experimental animals. Based on reports of the comorbidity between chronic pain and depressive illness in human patients, it is possible that these disease states are linked, via chronic stress-induced HPA dysfunction. Here, we discuss the possible involvement of the HPA axis in the aetiology of both chronic pain and clinical depression, and suggest a strategy for the development of novel pharmacotherapies.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1527-3458
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Retigabine [D23129; N-(2-amino-4-(4-fluorobenzylamino)-phenyl)carbamic acid ethyl ester] is an antiepileptic drug with a recently described novel mechanism of action that involves opening of neuronal KV7.2–7.5 (formerly KCNQ2-5) voltage-activated K+ channels. These channels (primarily KV7.2/7.3) enable generation of the M-current, a subthreshold K+ current that serves to stabilize the membrane potential and control neuronal excitability. In this regard, retigabine has been shown to have a broad-spectrum of activity in animal models of electrically-induced (amygdala-kindling, maximal electroshock) and chemically-induced (pentylenetetrazole, picrotoxin, NMDA) epileptic seizures. These encouraging results suggest that retigabine may also prove useful in the treatment of other diseases associated with neuronal hyperexcitability. Neuropathic pain conditions are characterized by pathological changes in sensory pathways, which favor action potential generation and enhanced pain transmission. Although sometimes difficult to treat with conventional analgesics, antiepileptics can relieve some symptoms of neuropathic pain. A number of recent studies have reported that retigabine can relieve pain-like behaviors (hyperalgesia and allodynia) in animal models of neuropathic pain. Neuronal activation within several key structures within the CNS can also be observed in various animal models of anxiety. Moreover, amygdala-kindled rats, which have a lowered threshold for neuronal activation, also display enhanced anxiety-like responses. Retigabine dose-dependently reduces unconditioned anxiety-like behaviors when assessed in the mouse marble burying test and zero maze. Early clinical studies have indicated that retigabine is rapidly absorbed and distributed, and is resistant to first pass metabolism. Tolerability is good in humans when titrated up to its therapeutic dose range (600-1200 mg/day). No tolerance, dependence or withdrawal potential has been reported, although adverse effects can include mild dizziness, headache, nausea and somnolence. Thus, retigabine may prove to be useful in the treatment of a diverse range of disease states in which neuronal hyperexcitability is a common underlying factor.
    Type of Medium: Electronic Resource
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  • 10
    Keywords: INTERVENTION ; BREAST-CANCER ; STRESS ; LYMPHOCYTES ; SKELETAL-MUSCLE ; POSTMENOPAUSAL WOMEN ; PHYSICAL-ACTIVITY ; OXIDATIVE DNA-DAMAGE ; alkaline comet assay ; WEIGHT-LOSS
    Abstract: INTRODUCTION: Maintenance of normal weight and higher levels of physical activity are associated with a reduced risk of several types of cancer. As genomic instability is regarded as a hallmark of cancer development, one proposed mechanism is improvement of DNA repair function. We investigated links between dietary weight loss, exercise, and strand break rejoining in an ancillary study to a randomized-controlled trial. METHODS: Overweight/obese postmenopausal women (n=439) were randomized to: a) reduced-calorie weight-loss diet ("diet" n=118); b) moderate-to-vigorous intensity aerobic exercise ("exercise" n=117); c) a combination ("diet+exercise" n=117); or d) control (n=87). The reduced-calorie diet had a 10% weight-loss goal. The exercise intervention consisted of 45 minutes of moderate-to-vigorous aerobic activity 5 days/week for 12 months. DNA repair capacity was measured in a subset of 226 women at baseline and 12 months, from cryopreserved peripheral mononuclear cells using the Comet assay. Anthropometric and body composition measures were performed at baseline and 12 months. RESULTS: DNA repair capacity did not change significantly with any of the 12 month interventions compared to control; there were also no significant changes when stratified by changes in body composition or aerobic fitness (VO2max). At baseline, DNA repair capacity was positively associated with weight, BMI, and fat mass (r=0.20, p=0.003; r=0.19, p=0.004; r=0.13, p=0.04, respectively) and inversely with lean body mass (r=-0.14, p=0.04). CONCLUSION: In conclusion, DNA repair capacity did not change with dietary weight loss or exercise interventions in postmenopausal women within a period of 12 months. Other assays that capture different facets of DNA repair function may be needed.
    Type of Publication: Journal article published
    PubMed ID: 25160845
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