Affiliation: Oregon Health and Science University
- Thyroid hormone drives fetal cardiomyocyte maturationNatasha N Chattergoon
Oregon Health and Science University, Portland, OR, USA
FASEB J 26:397-408. 2012..Thyroidectomized fetuses had reduced cell cycle activity and binucleation. These findings support the hypothesis that T(3) is a prime driver of prenatal cardiomyocyte maturation...
- Fetal roots of cardiac diseaseK L Thornburg
Heart Research Center, Oregon Health and Science University, 3181 Sam Jackson Park Road, Portland, Oregon 97239, USA
Heart 91:867-8. 2005
- The role of growth in heart developmentKent L Thornburg
Heart Research Center, Department of Medicine Cardiovascular Medicine, Oregon Health and Science University, Portland, OR 97239 3098, USA
Nestle Nutr Workshop Ser Pediatr Program 61:39-51. 2008..Insults that modify the maturational timeline, final myocyte number, vascularity and endothelial responsiveness in the heart can have effects that persist long after the insult has been ameliorated...
- Contemporary comparative placenta research--an interview with Allen Enders. Interview by Kent L Thornburg and Joan S HuntAllen Enders
Heart Research Center, Portland, Oregon, USA
Int J Dev Biol 54:231-6. 2010..The story of Allen Enders success will be an inspiration to all up and coming placentologists who are destined to discover the exciting ..
- Review: The placenta is a programming agent for cardiovascular diseaseK L Thornburg
Heart Research Center, Oregon Health and Science University, 3303 SW Bond Avenue, CH15H, Portland, OR 97239, USA
Placenta 31:S54-9. 2010..Together these models suggest that the ultimate fitness of the heart is determined by hemodynamic, growth factor, and oxygen/nutrient cues before birth, all of which are influenced, if not regulated by the placenta...
- Nitric oxide and fetal coronary regulationKent L Thornburg
Heart Research Center and Department of Medicine Cardiology, School of Medicine, Oregon Health and Science University, Portland, Oregon 97201, USA
J Card Surg 17:307-16. 2002..However, in the presence of L-NNA and severe hypoxemia, coronary flow does not exceed flows found during adenosine administration...
- Regulation of the cardiomyocyte population in the developing heartKent Thornburg
Heart Research Center, Oregon Health and Science University, Portland, OR 97239 3098, USA
Prog Biophys Mol Biol 106:289-99. 2011..T₃ also suppresses increased mitotic activity of stimulated cardiomyocytes but does so by increasing the cell cycle suppressant, p21, and decreasing the cell cycle activator, cyclin D1...
- Hemodynamic changes in pregnancyK L Thornburg
Department of Physiology and Pharmacology, Informatics and Outcomes Research School of Medicine, Oregon Health Sciences University, Portland 97201, USA
Semin Perinatol 24:11-4. 2000..The complex hormonal environment is changing throughout pregnancy. In summary, under the influence of circulating chemical mediators blood flow is redistributed to the uterus, breast, and kidney...
- Coronary flow regulation in the fetal sheepK L Thornburg
Department of Physiology, Oregon Health Sciences University, Portland, Oregon 97201, USA
Am J Physiol 277:R1249-60. 1999....
- Reduced systolic pressure load decreases cell-cycle activity in the fetal sheep heartP F O'Tierney
Heart Research Center, Oregon Health and Sciences Univ, Portland, OR 97239, USA
Am J Physiol Regul Integr Comp Physiol 299:R573-8. 2010..005) and the left ventricle (P < 0.002) of the enalaprilat-infused fetuses. Thus, we conclude a sustained reduction in systolic pressure load decreases hyperplastic growth in the fetal heart...
- Thyroid hormone inhibits proliferation of fetal cardiac myocytes in vitroN N Chattergoon
Heart Research Center, Oregon Health and Science University, Portland, Oregon 97239 3098, USA
J Endocrinol 192:R1-8. 2007..1) T3 inhibits fetal cardiomyocyte proliferation, while (2) p21 protein levels increase, and (3) cyclin D1 levels decrease. Thus, T3 may be a potent regulator of cardiomyocyte proliferation and maturation in the late gestation fetus...
- 3D computer modeling of human cardiogenesisJ O Pentecost
Congenital Heart Research Center, Oregon Health Sciences University, Portland 97202, USA
Comput Med Imaging Graph 23:45-9. 1999..These innovations in embryo reconstruction not only facilitate medical education, they also serve as new tools for scientific investigation of cardiogenesis and congenital heart disease...
- The effects of anaemia as a programming agent in the fetal heartL Davis
Department of Obstetrics and Gynecology, Oregon Health Sciences University, Portland, OR 97201 3098, USA
J Physiol 565:35-41. 2005..New information on these mechanisms is likely to lead to better prevention of and therapies for adult-onset coronary disease...
- Graphical and stereolithographic models of the developing human heart lumenJ O Pentecost
Oregon Health Sciences University, Congenital Heart Research Center, 3181 SW Sam Jackson Park Road, L464, Portland, OR 97201, USA
Comput Med Imaging Graph 25:459-63. 2001..This novel use of Carnegie collection images and graphical modeling software provides tools for broadening our understanding of normal and aberrant heart formation...
- Augmentation of coronary conductance in adult sheep made anaemic during fetal lifeL Davis
Department of Obstetrics and the Heart Research Center, Oregon Health Sciences University, Portland, OR 97239 3098, USA
J Physiol 547:53-9. 2003..Vascular reactivity of the mesenteric arteries was not different. These data suggest that coronary conductance can be modified in utero by anaemia (high flow and hypoxaemia) and that the remodelled coronary tree persists to adulthood...
- Angiotensin II stimulates hyperplasia but not hypertrophy in immature ovine cardiomyocytesN C Sundgren
Department of Physiology, Oregon Health and Science University, Portland, USA
J Physiol 548:881-91. 2003....
- Cortisol stimulates cell cycle activity in the cardiomyocyte of the sheep fetusG D Giraud
Heart Research Center, Oregon Health and Science University, Portland, Oregon 97239-3098, USA
Endocrinology 147:3643-9. 2006..Thus, increases in fetal heart mass associated with subpressor doses of cortisol are due to cardiomyocyte proliferation and not hypertrophic growth...
- Anaemia stimulates aquaporin 1 expression in the fetal sheep heartS Jonker
Departments of Physiology and Pharmacology, Obstetrics, Medicine (Cardiology, and Heart Research Center, Oregon Health and Science University, Portland, OR 97239, USA
Exp Physiol 88:691-8. 2003..05). Expression of AQP1 in all groups was greatest in the microvascular endothelium. These data suggest that AQP1 plays an important role in the physiological accommodation to fetal anaemia...
- Placental insufficiency decreases cell cycle activity and terminal maturation in fetal sheep cardiomyocytesSamantha Louey
Heart Research Center, Oregon Health and Science University, Portland, OR 97239 3098, USA
J Physiol 580:639-48. 2007..05). It is concluded that in the absence of fetal arterial hypertension, placental insufficiency is associated with substantially depressed growth of the heart through suppressed proliferation and maturation of cardiomyocytes...
- Myocyte enlargement, differentiation, and proliferation kinetics in the fetal sheep heartSonnet S Jonker
Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, USA
J Appl Physiol 102:1130-42. 2007..These data on normal cardiac growth may enable a more detailed understanding of the consequences of experimental and pathological interventions in prenatal life...
- Sequential growth of fetal sheep cardiac myocytes in response to simultaneous arterial and venous hypertensionSonnet S Jonker
Heart Research Center, Oregon Health and Science University, Portland, Oregon, USA
Am J Physiol Regul Integr Comp Physiol 292:R913-9. 2007..This study highlights unique fetal adaptations of the myocardium and the importance of experimental duration when interpreting fetal cardiac growth data...
- Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytesNathan C Sundgren
Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, Oregon 97239, USA
Am J Physiol Regul Integr Comp Physiol 285:R1481-9. 2003....
- Identification, genomic organization and mRNA expression of CRELD1, the founding member of a unique family of matricellular proteinsPaul A Rupp
Department of Molecular and Medical Genetics, Oregon Health and Science University, Portland, OR 97201, USA
Gene 293:47-57. 2002..The CRELD1 gene is deleted in the human cytogenetic disorder 3p- syndrome and is in the region of loss of heterozygosity for several types of cancer. A potential role for this protein in these disorders is discussed...
- Effect of in utero and early-life conditions on adult health and diseasePeter D Gluckman
Liggins Institute, University of Auckland, and National Research Centre for Growth and Development, Auckland, New Zealand
N Engl J Med 359:61-73. 2008
- Sarcoplasmic reticulum Ca2+ release channel ryanodine receptor (RyR2) plays a crucial role in aconitine-induced arrhythmiasMin Fu
School of Medicine and Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, People s Republic of China
Biochem Pharmacol 75:2147-56. 2008..The present study demonstrates a potential method for preventing aconitine-induced arrhythmias by inhibiting Ca(2+) leakage through the sarcoplasmic reticulum RyR(2) channel...
- Fetal anemia leads to augmented contractile response to hypoxic stress in adulthoodCraig S Broberg
Division of Maternal-Fetal Medicine, Medical Research Bldg, L-458, 3181 SW Sam Jackson Park Rd, Portland, OR 97201-3098, USA
Am J Physiol Regul Integr Comp Physiol 285:R649-55. 2003..03). We conclude that in sheep, perinatal anemia can alter cardiac responses to hypoxic stress in the adult long after restoration of normocythemia...
- A possible link between the pubertal growth of girls and breast cancer in their daughtersDavid J P Barker
Heart Research Center, Oregon Health and Science University, Portland, OR, USA
Am J Hum Biol 20:127-31. 2008....
- Meeting report on the 3rd International Congress on Developmental Origins of Health and Disease (DOHaD)Matthew W Gillman
Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care, Boston, MA 02215, USA
Pediatr Res 61:625-9. 2007..Improving the environment to which an individual is exposed during development may be as important as any other public health effort to enhance population health world wide...
- Hypoxia and cardiac programmingKent L Thornburg
J Soc Gynecol Investig 10:251. 2003
- Modeling cardiogenesis: the challenges and promises of 3D reconstructionJeffrey O Pentecost
Department of Medical Informatics and Outcomes Research, Oregon Health and Science University, Portland, Oregon 97201, USA
Curr Top Dev Biol 56:115-43. 2003
- The prenatal environment and later cardiovascular diseaseSamantha Louey
Heart Research Center, Oregon Health and Science University, Portland, Oregon, 97239-3098, USA
Early Hum Dev 81:745-51. 2005..Thus, adults most vulnerable for coronary artery disease may have experienced rapid weight gain in childhood and now have dyslipidemias and depressed endothelial function...
- Thyroid regulation of cardiomyocyte maturationKENT L R THORNBURG; Fiscal Year: 2010..Low cardiomyocyte numbers could lead to a myocardium that is disadvantaged for the work it will perform in extrauterine life. ..