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  • Book
    Sisko Anttila, Paolo Boffetta, editors.
    Summary: This up-to-date review of the literature on the epidemiology and pathology of work-related cancers also includes sensitive diagnostic questionnaires and data on the risk ratios of differing cancers in relation to a variety of occupations and lifestyle factors.

    Contents:
    Intro
    Foreword
    A Cartography of Occupational Cancer Prevention
    References
    Preface
    Acknowledgments
    Contents
    1: Historical Overview of Occupational Cancer Research
    Early Discoveries
    How Evidence Has Been Accumulated on Selected Associations
    Sources of Evidence on Risk to Humans Due to Chemicals
    Epidemiology
    Animal Experimentation
    Short-Term Tests and Structure-Activity Relationships
    Listing Occupational Carcinogens
    IARC Monographs
    Definite and Probable Occupational Risk Factors for Cancer
    The Evolution of Knowledge
    Interpreting the Lists Illustrative Examples and Controversies
    Polycyclic Aromatic Hydrocarbons (PAHs)
    Diesel and Gasoline Engine Emissions
    Asbestos
    Cadmium and Cadmium Compounds
    Styrene
    1,3-Butadiene
    Vinyl Chloride
    Radium and Radon
    Some Methodological Considerations
    Industry-Based Studies
    Community-Based Case-Control Studies
    Some Trends in Epidemiologic Research on Occupational Cancer
    Continued Importance of Research on Occupational Cancer
    References
    2: Genetics, Epigenetics, and Environmental Interactions
    Genetics and Heritability
    Phenotype Versus Genotype Epigenetics
    DNA Methylation
    Histone Modifications
    Non-coding RNA
    microRNA
    Long Non-coding RNA
    Bringing Together the Concepts of Genetics, Epigenetics, and Phenotype
    Gene-Environment Interactions
    Xenobiotic Metabolism and Excretion
    Phase I Polymorphisms and Cancer
    Phase II Polymorphisms and Cancer
    Other Polymorphisms and Cancer
    Population Stratification
    Gene-Gene Interactions
    Genome-Wide Association Studies (GWAS)
    Epigenetics and Environmental/Occupational Exposure
    Summary
    References 3: Mechanisms of Environmental and Occupational Carcinogenesis
    Environmental and Occupational Carcinogenesis
    Field Cancerization and Expanding Fields
    Environmental and Occupational Sources of DNA Damage
    Physical Carcinogens
    Chemical Carcinogenesis
    Endogenous Mechanisms Activated by Exogenous Exposures
    DNA Repair
    Direct Reversal Repair
    Base Excision Repair
    Nucleotide Excision Repair
    Mismatch Repair
    Interstrand Cross-Link Repair
    Double-Strand DNA Break Repair
    DNA Damage Tolerance
    Apoptosis
    Genetic Mutations
    Epigenetics and Cancer DNA Methylation and Cancer
    Environmental and Occupational Epigenetic Effectors
    Histone Modification
    CpG Methylation and Point Mutations
    Somatic Mutations in Epigenetic Regulators
    Inflammation and Reactive Oxygen Species
    Endocrine Disruption
    References
    4: Head and Neck Cancers
    Introduction
    Descriptive Epidemiology
    Nasopharynx Cancer
    Nonoccupational Risk Factors
    Occupational Risk Factors
    Oral and Pharyngeal Cancers
    Occupations and Agents with Less Than Sufficient Evidence
    Formaldehyde
    Wood Dust and Wood Industry Work
    Digital Access Springer 2020
  • Article
    Toyota T, Abe K, Kudo M.
    Acta Diabetol Lat. 1977 Sep-Dec;14(5-6):250-6.
    In order to determine whether both insulin and C-peptide have an inhibitory action on insulin secretion, the isolated rat pancreas was perfused with exogenous rat insulin or synthetic rat C-peptide in the presence of high or low concentration of glucose. In the presence of 2.8 mM glucose, exogenous rat insulin (4 or 10 ng/ml) and C-peptide 1 and 2 (100 ng/ml) show no effect on the insulin levels in the outflow from the perfused pancreas. However, the insulin response to 16.7 mM glucose decreased in the presence of exogenous rat insulin or synthetic rat C-peptide, showing a biphasic pattern of glucose-induced insulin release. When rat insulin or C-peptide were added at 20 min and removed at 40 min while the isolated pancreas was exposed to a 60-min glucose infusion (16.7 mM), glucose-induced insulin secretion decreased during the infusion of rat insulin or C-peptide. The present study clearly showed that exogenous rat insulin and synthetic rat C-peptide 1 and 2 inhibited glucose-induced insulin secretion. Although the suppressive mechanisms of the exogenous insulin and the C-peptide on insulin release are not yet proved, the inhibitory process is considered to be related to cyclic AMP in the pancreatic B-cell.
    Digital Access Access Options