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SUMMARY:Heart Disease Link to Fetal Hypoxia and Oxidative Stress - Profess
 or Dino Giussani - Department of Physiology\, Development and Neuroscience
 \, Cambridge
DTSTART:20151022T150000Z
DTEND:20151022T160000Z
UID:TALK60471@talks.cam.ac.uk
CONTACT:Alaa
DESCRIPTION:The quality of the intrauterine environment interacts with our
  genetic makeup to shape the risk of developing disease in later life.  Fe
 tal hypoxia is a common complication of pregnancy.  It programmes cardiac 
 and endothelial dysfunction in the offspring in adult life. However\, the 
 mechanisms via which this occurs remain elusive\, precluding the identific
 ation of potential therapy. Using an integrative approach in large and sma
 ll animal species at the in vivo\, isolated organ\, cellular and molecular
  levels\, we proposed the hypothesis that oxidative stress in the fetal he
 art and vasculature underlies the mechanism via which prenatal hypoxia pro
 grammes cardiovascular dysfunction in later life. We show that development
 al hypoxia independent of changes in maternal nutrition not only promotes 
 fetal growth restriction or alters the trajectory of fetal growth\, but it
  also induces changes in the cardiovascular\, metabolic and endocrine syst
 ems of the adult offspring\, which are normally associated with disease st
 ates during ageing (Camm et al. FASEB 25(1):420\, 2011\; Giussani et al. P
 LoS One 7(2):e31017\, 2012). Treatment with antioxidants\, such as vitamin
  C\, melatonin or allopurinol of animal pregnancies complicated with reduc
 ed oxygen delivery to the fetus prevents the alterations in fetal growth\,
  and the cardiovascular\, metabolic and endocrine dysfunction in the fetal
  and adult offspring.  Our latest work shows the intergenerational inherit
 ance of cardiovascular disease risk induced by chronic fetal hypoxia via t
 he paternal line.  Further\, we show the intergenerational transmission of
  cardio-protection via the maternal mitochondria.    Differential transmis
 sion of advantageous and detrimental traits onto offspring via either pare
 ntal linage may provide a mechanism driving natural selection and successf
 ul environmental adaptation from generation to generation.  Combined\, the
  work offers both insight into mechanisms and possible therapeutic targets
  for clinical intervention against the early origin of disease in risky pr
 egnancy across generations.
LOCATION:Hodgkin Huxley Seminar Room\, Physiology Building\, Downing Site
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