Titlebook: Early Life Origins of Health and Disease; E. Marelyn Wintour,Julie A. Owens Book 2006 The Editor(s) (if applicable) and The Author(s), und

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https://doi.org/10.1007/978-3-663-15733-5ction and a range of adulthood indices of cardiovascular dysfunction and risk. Whilst the emphasis has been on the programming of hypertension, there is also evidence for an impact of the early life environment on later development of vascular endothelial dilator dysfunction and associated risk fact

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https://doi.org/10.1007/978-3-662-33773-8ing epidemic proportions in some sectors of the community and is often found in association with the two most characterised adult onset diseases, hypertension and noninsulin dependent diabetes mellitus. Epidemiological studies in humans have identified various maternal states such as anemia, diabete

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https://doi.org/10.1007/978-3-662-35040-9 exposure of the fetus to elevated levels of glucocorticoids, or exposure at inappropriate times, subtly disturbs normal fetal development. Experimental studies have demonstrated that late gestational exposure to excess glucocorticoids causes programming of a number of organ systems.

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Zur Physiologie und Hygiene der Luftfahrtes. These studies have generally utilized excessive alcohol exposure models, and examined resultant outcomes that are gross and can be measured in the offspring as a fetus or at birth. Very few studies have addressed the possible long term, or programming, effects of prenatal alcohol exposure. Even

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Zur Regelung von Automobilmaschinenew, derive from adverse events in utero, such as maternal nutrition deficiency, infection and hypoxia. The hypothesis was originally derived from neuropathological changes in patients with established schizophrenia that are highly suggestive of impaired neural development occurring around mid-gestat

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