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  • 1
    Keywords: Medicine ; Oncology ; Human Genetics ; Medical genetics ; Biomedicine ; Human Genetics ; Cancer Research ; Gene Function ; Springer eBooks
    Abstract: Exposure to environmental toxicants is associated with changes in DNA methylation and gene expression profiles that together can contribute to increased disease susceptibility. The chapters in this volume, Environmental Epigenomics in Health and Disease - Epigenetics and Disease Origins, address a wide range of environmental exposures, such as airborne particulates, cocaine, radiation, tobacco smoke, and xenoestrogens. Particular emphasis is placed on the consequences of environmental exposures during development on epigenetic reprogramming that influences adult disease pathogenesis. Health outcomes associated with these exposures include autoimmune disorders, neurodevelopmental disorders, and cancer. Importantly, dietary supplements and drugs can modify the epigenetic effects induced by these agents, thereby reducing their toxicological impact. The overall purpose of this volume and its companion, Environmental Epigenomics in Health and Disease - Epigenetics and Complex Diseases, is to give readers an overview of how environmental exposures during early development can influence disease formation by disrupting epigenetic processes and developmental programming
    Pages: : digital.
    ISBN: 9783642233807
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  • 2
    Keywords: Medicine ; Oncology ; Human Genetics ; Neurosciences ; Biomedicine ; Human Genetics ; Cancer Research ; Neurosciences ; Springer eBooks
    Description / Table of Contents: Preface -- Epigenetic programming of the brain -- Epigenetics and maternal brain evolution -- Social environment and DNA methylation:℗ A mechanism for linking nurture and nature -- Sex differences in epigenetic programming of brain differentiation: Implications for mental health and disease -- Epigenetics and neurological disorders -- Phenotypic plasticity, pleiotropy, and the growth-first theory of imprinting -- The imprinted brain: How genes set the balance between autism and psychosis -- Epigenetics at the interface of genetics and environmental factors in autism -- Epigenomic and non-coding℗ RNA regulation in addictive processes -- Epigenetic therapies in neurological diseases -- Epigenetics, nutrition, diabetes, and obesity -- Nutrition, histone epigenetic marks, and disease -- Chromatin switching and gene dynamics associated with type 2 diabetes -- Developmental epigenetic programming in diabetes and obesity -- Epigenetics and cancer -- Developmental reprogramming by environmental estrogens: How early life exposures affect cancer risk in adulthood.-℗ Human cancer epigenetics -- Epigenetics and the law -- Legal and ethical implications of epigenetics -- Subject index.℗
    Abstract: The capacity of the epigenome to interpret both internal and external stimuli and alter expression programs is a critical component in normal development, aging, and disease pathogenesis. In the past decade, we have witnessed an explosion of unprecedented research on and support for epigenetics, epigenomics, and their interface with human health and disease. In this volume, Environmental Epigenomics in Health and Disease - Epigenetics and Complex Diseases, a number of leading investigators in the field of epigenetics discuss patterns of epigenomic modifications in normal cells, and how environmentally-induced changes in them are associated with disease pathogenesis. The authors comprehensively review the epigenetic adaptations that occur in human embryonic stem cells, as well as in differentiating cells and organs such as the brain when exposed to environmental factors, and discuss the legal and ethical implications of such alterations. The overall purpose of this volume and its companion, Environmental Epigenomics in Health and Disease - Epigenetics and Disease Origins, is to give readers an overview of how environmental exposures during early development can influence disease formation by disrupting epigenetic programming
    Pages: : digital.
    ISBN: 9783642368271
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Mammalian genome 10 (1999), S. 74-77 
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Keywords: phenobarbital ; protein kinase C ; EGF ; TGF-B1 ; tumor promotion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Phenobarbital (PB) added to the medium of cultured rat hepatocytes alters epidermal growth factor (EGF) dependent mitogenesis in a biphasic manner; PB concentrations〈1.5 mM are growth stimulatory but higher concentrations significantly inhibit normal hepatocyte proliferation. In contrast, the growth of putative preneoplastic cells is inhibited less by high concentrations of PB. Mechanistic studies designed to test the ability of PB to alter the early events of EGF signal transduction demonstrate that PB neither competes with EGF for binding to the EGF receptor nor alters EGF-induced receptor down-regulation. However, pretreatment with PB (〉1 mM) results in a transient inhibition of EGF binding to hepatocytes. The kinetics of this effect are similar to those obtained when hepatocytes are exposed to the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), a skin tumor promoter and activator of Ca2+/phospholipid-dependent protein kinase C. However, several observations suggest that distinct mechanisms mediate the responses to these two tumor promoters. First, the inhibitory effects of PB and TPA on EGF binding are additive. Also down-regulation of EGF receptors in response to TPA occurs with hepatocytes, A431 epidermal carcinoma cells, HepG2 hepatoma cells, and rat liver epithelial cells, but only hepatocytes are sensitive to PB. Furthermore, translocation of protein kinase C to the membrane occurs in hepatocytes treated with TPA but not in those treated with PB. The chronic treatment of rats with PB further sensitizes hepatocytes to EGF receptor downregulation by inin vitro PB while desensitizing them to EGF receptor down-regulation by TPA. This latter effect is correlated with a decreased ability of TPA to induce translocation of protein kinase C to the membrane. PB significantly increases the intracellular concentration of TGF-β1 in periportal hepatocytes but not in putative preneoplastic cells. TGF-β1 may therefore have an important function in regulating early stages of cell cycle progression in proliferating hepatocytes.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Adult rat hepatocytes were grown in serum-free medium containing 0.05-4 mM Ca+ + and 40 ng/ml EGF. After 48 hours of cultivation the mitotic index and the percentage of second division metaphases were determined. The results demonstrated a maximum proliferation response to EGF at a Ca+ + concentration of 0.4 mM. With lower and higher external Ca+ + concentrations the fraction of cells undergoing more than one cell division decreased. At lower Ca+ + concentrations this decrease appears to result from a reduced viability. In contrast, the low response to EGF at higher Ca+ + concentrations - especially in the physiological range - may reflect the influence of Ca+ + on the state of hepatocyte differentiation.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Using total RNA from human HCCs exhibiting LOH at the M6P/IGF2R locus7, we screened for correspnding mutations in the remaining allele using Ambion's Mismatch Detect™ assay. In one HCC, reverse transcription polymerase chain reaction (RT-PCR) amplification of the region flanked by the primers ...
    Type of Medium: Electronic Resource
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