Talk:Fetal programming: Difference between revisions

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imported>Anthony.Sebastian
(Attn: Gareth Leng)
imported>Anthony.Sebastian
(add a note for future reference in further developing the article)
 
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::I welcome your collaboration with either project. [[User:Anthony.Sebastian|Anthony.Sebastian]] 21:09, 30 April 2013 (UTC)
::I welcome your collaboration with either project. [[User:Anthony.Sebastian|Anthony.Sebastian]] 21:09, 30 April 2013 (UTC)
==Sebastian note==
Journal of Developmental Origins of Health and Disease (2013), 4(5), 328–337.
& Cambridge University Press and the International Society for Developmental Origins of Health and
Disease 2013 doi:10.1017/S204017441300010X
REVIEW
'''Developmental programming of cardiovascular disease by prenatal hypoxia'''
D. A. Giussani1* and S. T. Davidge2
1Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK
2Departments of Obstetrics &  Gynecology and Physiology, Women and Children’s Health Research
Institute, University of Alberta, Edmonton, Canada
It is now recognized that the quality of the fetal environment during early development is
important in programming cardiovascular health and disease in later life. Fetal hypoxia is one of
the most common consequences of complicated pregnancies worldwide. However, in contrast to the
extensive research effort on pregnancy affected by maternal nutrition or maternal stress, the
contribution of pregnancy affected by fetal chronic hypoxia to developmental programming is only
recently becoming delineated and established. This review discusses the increasing body of evidence
supporting the programming of cardiac susceptibility to ischaemia and reperfusion (I/R) injury, of
endothelial dysfunction in peripheral resistance circulations, and of indices of the metabolic
syndrome in adult offspring of hypoxic pregnancy. An additional focus of the review is the
identification of plausible mechanisms and the implementation of maternal and early life
interventions to protect against adverse programming.
Received 3 January 2013; Revised 20 February 2013; Accepted 14 April 2013; First published online
18 April 2013
Key words:  cardiovascular dysfunction, fetal hypoxia, interventions, metabolic syndrome, treatment
==New topic==

Latest revision as of 16:22, 8 June 2018

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 Definition Refers to adaptations made by a fetus in response to adverse or beneficial intrauterine environments, adaptations targeting the fetus’s survival, adaptations that affect fetal structure and function during the highly plastic period of embryonic/fetal development, adaptations that persist after birth and that influence the structural, metabolic and physiological characteristics of the individual throughout life, which system characteristics can predispose the individual in later life to maladaptations in response to environmental conditions differing from those to which the fetus had adapted. [d] [e]
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 Talk Archive none  English language variant American English

DOHaD researcher, Michael Meaney

- You might want to take a look at Michael Meaney's work - he's arguably the biggest name in this field in rat work - see e.g. http://www.ncbi.nlm.nih.gov/pubmed/21420958 and

Hackman DA, Farah MJ, Meaney MJ (2010) Socioeconomic status and the brain: mechanistic insights from human and animal research. Nat Rev Neurosci11:651-9 "Human brain development occurs within a socioeconomic context and childhood socioeconomic status (SES) influences neural development--particularly of the systems that subserve language and executive function. Research in humans and in animal models has implicated prenatal factors, parent-child interactions and cognitive stimulation in the home environment in the effects of SES on neural development. These findings provide a unique opportunity for understanding how environmental factors can lead to individual differences in brain development, and for improving the programmes and policies that are designed to alleviate SES-related disparities in mental health and academic achievement."Gareth Leng 14:03, 30 April 2013 (UTC)

Thanks, Gareth. I grabbed 60 references from PubMed with must-read-inducing titles, planning to study one-a-day. I started Fetal programming as a writing-to-learn exercise, and plan to start the parent topic, Developmental origins of health and disease, sometime soon. Much of Meaney's work will apply there, too, as he has extensively studied post-natal programming by maternal and parental care.
Biology never ceases to amaze.
I welcome your collaboration with either project. Anthony.Sebastian 21:09, 30 April 2013 (UTC)

Sebastian note

Journal of Developmental Origins of Health and Disease (2013), 4(5), 328–337. & Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2013 doi:10.1017/S204017441300010X


REVIEW Developmental programming of cardiovascular disease by prenatal hypoxia

D. A. Giussani1* and S. T. Davidge2 1Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK 2Departments of Obstetrics & Gynecology and Physiology, Women and Children’s Health Research Institute, University of Alberta, Edmonton, Canada

It is now recognized that the quality of the fetal environment during early development is important in programming cardiovascular health and disease in later life. Fetal hypoxia is one of the most common consequences of complicated pregnancies worldwide. However, in contrast to the extensive research effort on pregnancy affected by maternal nutrition or maternal stress, the contribution of pregnancy affected by fetal chronic hypoxia to developmental programming is only recently becoming delineated and established. This review discusses the increasing body of evidence supporting the programming of cardiac susceptibility to ischaemia and reperfusion (I/R) injury, of endothelial dysfunction in peripheral resistance circulations, and of indices of the metabolic syndrome in adult offspring of hypoxic pregnancy. An additional focus of the review is the identification of plausible mechanisms and the implementation of maternal and early life interventions to protect against adverse programming.

Received 3 January 2013; Revised 20 February 2013; Accepted 14 April 2013; First published online 18 April 2013

Key words: cardiovascular dysfunction, fetal hypoxia, interventions, metabolic syndrome, treatment

New topic