
Perinatal Programming
Beschreibung
Perinatal Programming addresses the environment-dependent setting of fundamental life functions and dispositions for diseases in developmental periods during pregnancy and in early infancy. It provides a new view of the origins of health and diseases. To realize these associations may enable us to prevent diseases for the long term. This book reviews actual state-of-the-art knowledge in the perinatal programming field. The authors are internationally known scientists of this research area.
Rezensionen / Stimmen
Perinatal programming is one of the most powerful ideas in biology and medicine in the 21st century. Compelling evidence indicates that prevention of childhood and adult diseases must begin during fetal life. Epigenomics has the potential to provide a mechanistic understanding of many phenomena underpinning the developmental origins of health and disease. The book is timely, insightful and of great relevance to obstetrics, perinatal medicine and modern biology. Roberto RomeroChief - Perinatology Research BranchProgram Director for Perinatal Research & ObstetricsNational Institute of Child Health and Human Development/National Institutes of Health, USA "Wer in das spannende Gebiet der Perinatalen Programmierung eintauchen möchte, hat mit diesem Buch das richtige Medium gefunden. Das in Englisch geschriebene Werk bietet gebündeltes Fachwissen - für den Einsteig, zur Fortbildung und zum Nachschlagen."Dorothee Hahne in: Ernährung im Fokus 13-07-08Weitere Details
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Inhalt
- Intro
- Foreword
- Abbreviations
- 1 The past and future of perinatal medicine
- 2 Perinatal brain programming and functional teratology
- 3 Experimental models of low birth weight - insight into the developmental programming of metabolic health, aging and immune function
- 3.1 Developmental programming and the metabolic syndrome in humans
- 3.2 The thrifty phenotype hypothesis
- 3.3 Evidence for developmental programming of the metabolic syndrome from animal models
- 3.4 Developmental programming of aging
- 3.5 Developmental programming and immunity
- 3.6 Conclusions
- 4 Cardiovascular consequences of IUGR: Experimental aspects
- 4.1 Intrauterine growth retardation and maternal undernutrition
- 4.2 Long-term cardiovascular consequences of undernutrition: Animal models of programming
- 4.3 The mechanistic basis of cardiovascular programming
- 4.4 Research priorities
- 5 Fetal programming of endocrine function in IUGR offspring depends on the cause of low birth weight: Evidence from animal models and the human FIPS-study
- 5.1 Introduction
- 5.2 Leptin and IGF-1, two key candidate molecules of endocrine programming
- 5.3 Animal models of IUGR
- 5.4 Human IUGR study (FIPS)
- 5.5 Summary
- 6 Intrauterine corticosteroids for lung maturation: Observations of HPA axis function and cardiac autonomic balance in the neonate
- 6.1 Introduction
- 6.2 Vulnerability of the hypothalamic-pituitary-adrenal (HPA) axis
- 6.3 Vulnerability of the sympathetic nervous system
- 6.4 Findings in humans
- 6.5 HPA axis functionality in neonates after intrauterine betamethasone treatment
- 6.6 The cardiac autonomic system after intrauterine betamethasone treatment
- 6.7 Summary
- 7 Feast or Famine: In the fast lane to puberty
- 7.1 Introduction
- 7.2 Animal studies
- 7.3 Conclusions
- 8 Early life origins of diabetes and obesity: General aspects and the thin - fat baby paradigm
- 8.1 Introduction
- 8.2 Nutrition and Diabetes
- 8.3 Maternal nutrition, fetal growth, and future health
- 8.4 Developmental plasticity, programming, teratogenesis, and predictive adaptive response
- 8.5 Birth weight: An exposure, an intermediate variable, or only a marker?
- 8.6 Role of postnatal growth
- 8.7 Contributions of the Pune Maternal Nutrition Study
- 8.8 Genetics and epigenetics of fetal growth and diabetes-obesity
- 8.9 Conclusion
- 9 The outcome in offspring of obese mothers: Clinical and experimental aspects
- 9.1 Introduction
- 9.2 Associations between obesity in mother and child
- 9.3 Experimental models of maternal obesity
- 9.4 Summary
- 10 Short and long term effects of gestational obesity: Clinical observations
- 10.1 Maternal metabolism in normal pregnancy
- 10.2 Fetal growth and body composition
- 10.3 The child of the obese woman
- 10.4 Maternal factors facilitating fetal fat accretion
- 10.5 Summary
- 11 Emerging role of neuroendocrine programming in obesity
- 11.1 Introduction
- 11.2 Development of hypothalamic neuroendocrine pathways controlling appetite
- 11.3 Animal models of metabolic programming
- 11.4 Assessment of neuroendocrine regulation in metabolically malprogrammed animals
- 11.5 Structural influences of perinatal nutrition on hypothalamic appetite-related networks
- 11.6 Developmental signals influencing the ultimate architecture of neuroendocrine feeding pathways
- 11.7 Perspectives and conclusions
- 12 Genetic influences on the long-term effects of the perinatal environment on energy homeostasis and offspring obesity
- 12.1 Introduction
- 12.2 Neural control of energy homeostasis
- 12.3 Development of neural systems controlling energy homeostasis
- 12.4 Gene x environment interactions in the development of obesity
- 12.5 Summary and conclusions
- 13 Perinatal programming in offspring of diabetic mothers: Clinical data
- 13.1 Introduction
- 13.2 Short-term implications for the offspring
- 13.3 Long-term implications for the offspring
- 13.4 Own studies
- 13.5 Concluding remarks
- 14 Experimental observations on perinatal programming in offspring of diabetic mothers
- 14.1 Introduction
- 14.2 Epidemiological and clinical studies
- 14.3 Animal studies
- 14.4 Conclusions and outlook
- 15 Prenatal infections and long-term mental outcome: Modeling schizophrenia-related dysfunctions using the prenatal PolyI:C model in mice
- 15.1 Introduction
- 15.2 Schizophrenia and animal models
- 15.3 Features and methodology of the mouse prenatal PolyI:C model
- 15.4 Schizophrenia-related phenotypes in the mouse prenatal PolyI:C model
- 15.5 Concluding remarks
- 16 Prenatal programming of cognition and emotion in humans: From birth to age 20
- 16.1 Prenatal maternal anxiety and stress are associated with less favorable developmental outcomes
- 16.2 PMAS is associated with altered fetal, infant, and child neurobehavioral development
- 16.3 PMAS is associated with adolescent emotion and HPA activity: HPA mediates the link between PMAS and adolescent depressed mood
- 16.4 PMAS is associated with adolescent cognition: Neuropsychological, ERP, and fMRI measures reveal evidence for impaired endogenous cognitive control
- 16.5 Conclusion
- 17 Perinatal programming of allergy
- 17.1 Allergy and atopy
- 17.2 Early development of the immune system
- 17.3 Physiology and pathophysiology of early immune reactions
- 17.4 Regulatory T cells
- 17.5 The role of mucosal surfaces
- 17.6 The role of early tolerance induction
- 17.7 Murine models
- 17.8 Human milk
- 17.9 Empirical results
- 17.10 DNA methylation and demethylation
- 18 Perinatal origin of testicular germ cell cancer: Possible involvement of developmental reprogramming
- 18.1 Introduction
- 18.2 Carcinoma in situ testis
- 18.3 Testicular dysgenesis
- 18.4 Perinatal reprogramming of germ cells
- 18.5 Involvement of perinatal reprogramming in the CIS phenotype?
- 18.6 Concluding remarks
- 19 Epigenetic adaptation during early life
- 19.1 DNA methylation patterns and cellular identity
- 19.2 Early life environment and DNA methylation
- 19.3 Reversibility of DNA methylation
- adaptive responsivity of the methylome
- 19.4 Adaptation of the methylome early in life
- 19.5 Epigenetic programming by maternal care in the rat
- 19.6 Signaling cascades leading from maternal care to epigenetic programming
- 19.7 Reversibility of early life DNA methylation programming by maternal care
- 19.8 Epigenetic programming by early life events in humans
- 19.9 Genome-wide and system-wide effects of early life adversity
- 19.10 Prospects
- 20 Toward a unifying concept on perinatal programming: Vegetative imprinting by environment-dependent biocybernetogenesis
- 20.1 Historical and semantic notes
- 20.2 A main current focus: The "small baby syndrome" and the "match-mismatch" hypotheses
- 20.3 An alternative, integrative, and mechanistic hypothesis on perinatal programming
- 20.4 A mechanistic clue: Developmental programming of neuro-endocrine and vegetative regulatory systems
- 20.5 Epigenomic plasticity as a key mechanism in perinatal programming
- 20.6 For example: Fetal and neonatal overnutrition - a paradigm with practical relevance
- 20.7 Intergenerative transmission and prevention of perinatally acquired characteristics
- 20.8 Synopsis
- Author index
- Index
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