Journal articles: 'Fetal heart development'

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J. Patterson, A., and L. Zhang. "Hypoxia and Fetal Heart Development." Current Molecular Medicine 10, no. 7 (October 1, 2010): 653–66. http://dx.doi.org/10.2174/156652410792630643.

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Bae, Soochan, Yuhui Xiao, Guohu Li, Carlos A. Casiano, and Lubo Zhang. "Effect of maternal chronic hypoxic exposure during gestation on apoptosis in fetal rat heart." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (September 2003): H983—H990. http://dx.doi.org/10.1152/ajpheart.00005.2003.

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Chronic hypoxia during pregnancy is one of the most common insults to fetal development. We tested the hypothesis that maternal hypoxia induced apoptosis in the hearts of near-term fetal rats. Pregnant rats were divided into two groups, normoxic control and continuous hypoxic exposure (10.5% O2) from day 15 to 21 of gestation. Hearts were isolated from fetal rats of 21-day gestational age. Maternal hypoxia increased hypoxia-inducible factor-1α protein in fetal hearts. Chronic hypoxia significantly increased the percentage and size of binucleated myocytes and increased apoptotic cells from 1.4 ± 0.14% to 2.7 ± 0.3% in the fetal heart. In addition, the active cleaved form of caspase 3 was significantly increased in the hypoxic heart, which was associated with an increase in caspase 3 activity. There was a significant increase in Fas protein levels in the hypoxic heart. Chronic hypoxia did not change Bax protein levels but significantly decreased Bcl-2 proteins. In addition, chronic hypoxia significantly suppressed expression of heat shock protein 70. However, chronic hypoxia significantly increased expression of the anti-apoptotic protein 14–3-3 θ, among other 14–3-3 isoforms. Chronic hypoxia differentially regulated β-adrenoreceptor (β-AR) subtypes with an increase in β1-AR levels but no changes in β2-AR. The results demonstrate that maternal hypoxia increases apoptosis in fetal rat heart, which may be mediated by an increase in Fas and a decrease in Bcl-2 proteins. Chronic hypoxia-mediated increase in β1-AR and decrease in heat shock proteins may also play an important role in apoptosis in the fetal heart.

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Morrison, J. L., K. J. Botting, J. L. Dyer, S. J. Williams, K. L. Thornburg, and I. C. McMillen. "Restriction of placental function alters heart development in the sheep fetus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 1 (July 2007): R306—R313. http://dx.doi.org/10.1152/ajpregu.00798.2006.

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Placental insufficiency, resulting in restriction of fetal substrate supply, is a major cause of intrauterine growth restriction (IUGR) and increased neonatal morbidity. Fetal adaptations to placental restriction maintain the growth of key organs, including the heart, but the impact of these adaptations on individual cardiomyocytes is unknown. Placental and hence fetal growth restriction was induced in fetal sheep by removing the majority of caruncles in the ewe before mating (placental restriction, PR). Vascular surgery was performed on 13 control and 11 PR fetuses at 110–125 days of gestation (term: 150 ± 3 days). PR fetuses with a mean gestational Po2 < 17 mmHg were defined as hypoxic. At postmortem (<135 or >135 days), fetal hearts were collected, and cardiomyocytes were isolated and fixed. Proliferating cardiomyocytes were counted by immunohistochemistry of Ki67 protein. Cardiomyocytes were stained with methylene blue to visualize the nuclei, and the proportion of mononucleated cells and length and width of cardiomyocytes were measured. PR resulted in chronic fetal hypoxia, IUGR, and elevated plasma cortisol concentrations. Although there was no difference in relative heart weights between control and PR fetuses, there was an increase in the proportion of mononucleated cardiomyocytes in PR fetuses. Whereas mononucleated and binucleated cardiomyocytes were smaller, the relative size of cardiomyocytes when expressed relative to heart weight was larger in PR compared with control fetuses. The increase in the relative proportion of mononucleated cardiomyocytes and the relative sparing of the growth of individual cardiomyocytes in the growth-restricted fetus are adaptations that may have long-term consequences for heart development in postnatal life.

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Arai, Masashi. "Antenatal Glucocorticoid Therapy for Fetal Heart Development." Circulation Journal 74, no. 1 (2010): 47–48. http://dx.doi.org/10.1253/circj.cj-09-0827.

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Strizhakov, A. N., A. M. Rodionova, I. V. Ignatko, and V. A. Zaidenov. "Effect of infection on the development of fetal arrhythmias." Voprosy ginekologii, akušerstva i perinatologii 21, no. 3 (2022): 6–12. http://dx.doi.org/10.20953/1726-1678-2022-3-6-12.

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Objective. To assess the impact of infection on the development of fetal arrhythmias. Patients and methods. The study included 84 pregnant women who were divided into two groups: the study group, which consisted of 44 patients aged 20–42 years (Me 31 ± 0.93 years) with fetal arrhythmia and/or minor heart defects at 21–41 weeks’ gestation (Me 37.41 ± 0.58 weeks), and the comparison group, which enrolled 40 pregnant women without fetal heart defects and with normal fetal heart rate to determine the significance of serological markers of myocarditis. Results. Significant titers of non-specific anti-myocardial antibodies to vascular smooth muscle and endothelium were detected in 14 (31.8%) and 7 (15.9%) fetuses, respectively. “Conditionally positive” titers for anti-smooth muscle antibodies were detected in 3 (6.8%) fetuses and for anti-endothelial cell antibodies in 4 (9%) fetuses. There was no significant increase in specific anti-heart antibody titers in both groups. Conclusion. Hypoxia should be considered as a trigger for fetal arrhythmias. The infectious and inflammatory processes are one of the links in the pathogenesis of fetal arrhythmias. Key words: fetal arrhythmia, intrauterine infection, minor heart defects

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Hofman, Paul L., Kelly Hiatt, Mervin C. Yoder, and Scott A. Rivkees. "A1 adenosine receptors potently regulate heart rate in mammalian embryos." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 4 (October 1, 1997): R1374—R1380. http://dx.doi.org/10.1152/ajpregu.1997.273.4.r1374.

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A1adenosine receptors (A1ARs) have been recently shown to be expressed in rodent embryonic hearts at very early stages of development. To determine the functional significance of fetal cardiac A1AR expression during embryogenesis, murine fetal heart preparations were studied between postconceptual days 9 and 12. Dose-response curves generated using a variety of adenosine agonists revealed that A1AR activation potently regulated fetal heart rates. The A1AR agonist, N 6-cyclopentyladenosine, inhibited heart rates in a dose-dependent manner (half-maximal effective concentration = 3.6 × 10−8 M) and stopped fetal cardiac contractions in 63% of preparations. In contrast, A2a and A2b receptor activation did not alter heart rates, and activation of A3 receptors produced modest declines in heart rates. Endogenous adenosine also acted tonically to suppress fetal heart rates, as demonstrated by the A1AR antagonist 1,3-dipropyl-8-cyclopentylxanthine, increasing heart rates, whereas the adenosine reuptake blocker dipyridamole lowered fetal heart rates. Pertussis toxin treatment blocked A1AR action, showing that A1AR action was G protein mediated. Using drugs that alter cAMP levels and ion channel action, we were able to show that A1AR action involves events mediated by cAMP, ATP-dependent K, L-type calcium, sodium, and chloride channels, and the pacemaker current. These data show that adenosine and A1ARs potently regulate mammalian heart rates via multiple effector systems at very early stages of prenatal development.

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Antipatis, Christos, Cheryl J. Ashworth, George Grant, Richard G. Lea, Susan M. Hay, and William D. Rees. "Effects of maternal vitamin A status on fetal heart and lung: changes in expression of key developmental genes." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 6 (December 1, 1998): L1184—L1191. http://dx.doi.org/10.1152/ajplung.1998.275.6.l1184.

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Vitamin A is required during pregnancy for fetal lung development. These experiments monitored fetal lung morphology in normal and vitamin A-deficient rats. The expression of elastin and the growth arrest-specific gene 6 ( gas6) in fetal and neonatal hearts and lungs was assessed by Northern blotting. In normal-fed rats, elastin and gas6 were expressed in the fetal lung and heart from day 19 of gestation up to day 2 postnatally. Maternal vitamin A deficiency altered fetal lung development. On day 20, the bronchial passageways were less developed and showed reduced staining for elastic fibers, and in the neonates, the relative air space and the size of the sacculi were reduced. In the fetal lung, the mRNAs for elastin and gas6 were reduced to 56 and 68% of the control values, respectively. In the fetal heart, the mRNA for elastin was reduced to 64% of the control value, whereas gas6 was increased twofold. In the neonate, there was no change in elastin expression in the lung or heart, but gas6 expression in the heart was increased twofold. These results suggest that, in the pregnant rat, vitamin A deficiency may retard fetal lung development or influence the differentiation of critical cell lines. The changes in elastin and gas6 expression may be used to identify the cell types affected.

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Salman, Huseyin Enes, and Huseyin Cagatay Yalcin. "Computational Modeling of Blood Flow Hemodynamics for Biomechanical Investigation of Cardiac Development and Disease." Journal of Cardiovascular Development and Disease 8, no. 2 (January 31, 2021): 14. http://dx.doi.org/10.3390/jcdd8020014.

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The heart is the first functional organ in a developing embryo. Cardiac development continues throughout developmental stages while the heart goes through a serious of drastic morphological changes. Previous animal experiments as well as clinical observations showed that disturbed hemodynamics interfere with the development of the heart and leads to the formation of a variety of defects in heart valves, heart chambers, and blood vessels, suggesting that hemodynamics is a governing factor for cardiogenesis, and disturbed hemodynamics is an important source of congenital heart defects. Therefore, there is an interest to image and quantify the flowing blood through a developing heart. Flow measurement in embryonic fetal heart can be performed using advanced techniques such as magnetic resonance imaging (MRI) or echocardiography. Computational fluid dynamics (CFD) modeling is another approach especially useful when the other imaging modalities are not available and in-depth flow assessment is needed. The approach is based on numerically solving relevant physical equations to approximate the flow hemodynamics and tissue behavior. This approach is becoming widely adapted to simulate cardiac flows during the embryonic development. While there are few studies for human fetal cardiac flows, many groups used zebrafish and chicken embryos as useful models for elucidating normal and diseased cardiogenesis. In this paper, we explain the major steps to generate CFD models for simulating cardiac hemodynamics in vivo and summarize the latest findings on chicken and zebrafish embryos as well as human fetal hearts.

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Hahurij, Nathan D., Emmeline E. Calkoen, Monique R. M. Jongbloed, Arno A. W. Roest, Adriana C. Gittenberger-de Groot, Robert E. Poelmann, Marco C. De Ruiter, Conny J. van Munsteren, Paul Steendijk, and Nico A. Blom. "Echocardiographic Assessment of Embryonic and Fetal Mouse Heart Development: A Focus on Haemodynamics and Morphology." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/531324.

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Background. Heart development is a complex process, and abnormal development may result in congenital heart disease (CHD). Currently, studies on animal models mainly focus on cardiac morphology and the availability of hemodynamic data, especially of the right heart half, is limited. Here we aimed to assess the morphological and hemodynamic parameters of normal developing mouse embryos/fetuses by using a high-frequency ultrasound system.Methods. A timed breeding program was initiated with a WT mouse line (Swiss/129Sv background). All recordings were performed transabdominally, in isoflurane sedated pregnant mice, in hearts of sequential developmental stages: 12.5, 14.5, and 17.5 days after conception (n=105).Results. Along development the heart rate increased significantly from 125 ± 9.5 to 219 ± 8.3 beats per minute. Reliable flow measurements could be performed across the developing mitral and tricuspid valves and outflow tract. M-mode measurements could be obtained of all cardiac compartments. An overall increase of cardiac systolic and diastolic function with embryonic/fetal development was observed.Conclusion. High-frequency echocardiography is a promising and useful imaging modality for structural and hemodynamic analysis of embryonic/fetal mouse hearts.

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DiPietro, Janet A., Denice M. Hodgson, Kathleen A. Costigan, Sterling C. Hilton, and Timothy R. B. Johnson. "Development of fetal movement — fetal heart rate coupling from 20 weeks through term." Early Human Development 44, no. 2 (February 1996): 139–51. http://dx.doi.org/10.1016/0378-3782(95)01704-6.

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Chattergoon, Natasha N. "Thyroid hormone signaling and consequences for cardiac development." Journal of Endocrinology 242, no. 1 (July 2019): T145—T160. http://dx.doi.org/10.1530/joe-18-0704.

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The fetal heart undergoes its own growth and maturation stages all while supplying blood and nutrients to the growing fetus and its organs. Immature contractile cardiomyocytes proliferate to rapidly increase and establish cardiomyocyte endowment in the perinatal period. Maturational changes in cellular maturation, size and biochemical capabilities occur, and require, a changing hormonal environment as the fetus prepares itself for the transition to extrauterine life. Thyroid hormone has long been known to be important for neuronal development, but also for fetal size and survival. Fetal circulating 3,5,3′-triiodothyronine (T3) levels surge near term in mammals and are responsible for maturation of several organ systems, including the heart. Growth factors like insulin-like growth factor-1 stimulate proliferation of fetal cardiomyocytes, while thyroid hormone has been shown to inhibit proliferation and drive maturation of the cells. Several cell signaling pathways appear to be involved in this complicated and coordinated process. The aim of this review was to discuss the foundational studies of thyroid hormone physiology and the mechanisms responsible for its actions as we speculate on potential fetal programming effects for cardiovascular health.

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van der Pol, Atze, Andres Gil, Herman H. W. Silljé, Jasper Tromp, Ekaterina S. Ovchinnikova, Inge Vreeswijk-Baudoin, Martijn Hoes, et al. "Accumulation of 5-oxoproline in myocardial dysfunction and the protective effects of OPLAH." Science Translational Medicine 9, no. 415 (November 8, 2017): eaam8574. http://dx.doi.org/10.1126/scitranslmed.aam8574.

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In response to heart failure (HF), the heart reacts by repressing adult genes and expressing fetal genes, thereby returning to a more fetal-like gene profile. To identify genes involved in this process, we carried out transcriptional analysis on murine hearts at different stages of development and on hearts from adult mice with HF. Our screen identified Oplah, encoding for 5-oxoprolinase, a member of the γ-glutamyl cycle that functions by scavenging 5-oxoproline. OPLAH depletion occurred as a result of cardiac injury, leading to elevated 5-oxoproline and oxidative stress, whereas OPLAH overexpression improved cardiac function after ischemic injury. In HF patients, we observed elevated plasma 5-oxoproline, which was associated with a worse clinical outcome. Understanding and modulating fetal-like genes in the failing heart may lead to potential diagnostic, prognostic, and therapeutic options in HF.

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ZHOU, JIZI, XINRAN DONG, QIONGJIE ZHOU, HUIJUN WANG, YANYAN QIAN, WEIDONG TIAN, DUAN MA, and XIAOTIAN LI. "microRNA expression profiling of heart tissue during fetal development." International Journal of Molecular Medicine 33, no. 5 (March 7, 2014): 1250–60. http://dx.doi.org/10.3892/ijmm.2014.1691.

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Iruretagoyena, J. I., W. Davis, C. Bird, J. Olsen, R. Radue, A. Teo Broman, C. Kendziorski, et al. "Metabolic gene profile in early human fetal heart development." MHR: Basic science of reproductive medicine 20, no. 7 (March 27, 2014): 690–700. http://dx.doi.org/10.1093/molehr/gau026.

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Hoyer, Dirk, Esther Heinicke, Susann Jaekel, Florian Tetschke, Dania Di Pietro Paolo, Jens Haueisen, Ekkehard Schleußner, and Uwe Schneider. "Indices of fetal development derived from heart rate patterns." Early Human Development 85, no. 6 (June 2009): 379–86. http://dx.doi.org/10.1016/j.earlhumdev.2009.01.002.

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Schmidt, Judy V., and Patricia Robin McCartney. "History and Development of Fetal Heart Assessment: A Composite." Journal of Obstetric, Gynecologic & Neonatal Nursing 29, no. 3 (May 2000): 295–305. http://dx.doi.org/10.1111/j.1552-6909.2000.tb02051.x.

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Lee, C. T., C. A. Brown, S. M. J. Hains, and B. S. Kisilevsky. "Fetal Development: Voice Processing in Normotensive and Hypertensive Pregnancies." Biological Research For Nursing 8, no. 4 (April 2007): 272–82. http://dx.doi.org/10.1177/1099800406298448.

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Recent observation of maternal voice recognition provides evidence of rudimentary memory and learning in healthy term fetuses. However, such higher order auditory processing has not been examined in the presence of maternal hypertension, which is associated with reduced and/or impaired uteroplacental blood flow. In this study, voice processing was examined in 40 fetuses (gestational ages of 33 to 41 weeks) of hypertensive and normotensive women. Fetuses received 2 min of no sound, 2 min of a tape-recorded story read by their mothers or by a female stranger, and 2 min of no sound while fetal heart rate was recorded. Results demonstrated that fetuses in the normotensive group had heart rate accelerations during the playing of their mother's voice, whereas the response occurred in the hypertensive group following maternal voice offset. Across all fetuses, a greater fetal heart rate change was observed when the amniotic fluid index was above compared to below the median (i.e., 150 mm), indicating that amniotic fluid volume may be an independent moderator of fetal auditory sensitivity. It was concluded that differential fetal responding to the mother's voice in pregnancies complicated by maternal hypertension may reflect functional elevation of sensorineural threshold or a delay in auditory system maturation, signifying functional differences during fetal life or subtle differences in the development of the central nervous system.

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Keller, A., J. D. Rouzeau, F. Farhadian, C. Wisnewsky, F. Marotte, N. Lamande, J. L. Samuel, K. Schwartz, M. Lazar, and M. Lucas. "Differential expression of alpha- and beta-enolase genes during rat heart development and hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 6 (December 1, 1995): H1843—H1851. http://dx.doi.org/10.1152/ajpheart.1995.269.6.h1843.

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We have analyzed the transition between isoforms of the glycolytic enzyme enolase (2-phospho-D-glycerate hydrolyase; EC 4.2.1.11) in rat heart during normal and pathological growth. A striking fall in embryonic alpha-enolase gene expression occurs during cardiac development, mostly controlled at pretranslational steps. In fetal and neonatal hearts, muscle-specific beta-enolase gene expression is a minor contributor to total enolase. Control mechanisms of beta-enolase gene expression must include posttranscriptional steps. Aortic stenosis induces a rapid and drastic decrease in beta-enolase transcript level in cardiomyocytes, followed by the fall in beta-subunit level. In contrast, alpha-enolase transcript level is not significantly altered, although the corresponding subunit level increases in nonmuscle cells. We conclude that, like fetal heart, hypertrophic heart is characterized by a high ratio of alpha- to beta-enolase subunit concentrations. This study indicates that the decrease in beta-enolase gene expression may be linked to beneficial energetic changes in contractile properties occurring during cardiac hypertrophy

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Bhavnani, Bhagu R., Goran Enhorning, Laila Ekelund, Duncan Wallace, and Chee Chung Pan. "Maternal diabetes and its effect on biochemical and functional development of rabbit fetal lung." Biochemistry and Cell Biology 66, no. 5 (May 1, 1988): 396–404. http://dx.doi.org/10.1139/o88-048.

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The effect of maternal diabetes on functional and biochemical maturation of the fetal lung was studied in a rabbit model. Pregnancy was initiated only after diabetes had been established. Both the pregnant doe and its fetuses were hyperglycemic. For comparison, the fetal heart and liver were also studied. In the diabetic group, the DNA content was lower in the fetal heart and lung while the protein content was higher in all three tissues. The glycogen levels were higher only in the fetal lung. Glycogen synthase was higher in the fetal lung and heart while phosphorylase activity was higher in all three tissues from the diabetic group. The activities of key enzymes involved in glycolysis were not affected. No difference was observed in the concentration of total phospholipids or in the ability of the airway fluid to reduce surface tension. In contrast, fetal lungs from diabetic does did not expand as well as the controls and retained less air on deflation. These findings suggest that the utilization of glycogen in fetal lungs from the diabetic does was not complete and that the increased incidence of respiratory distress in infants of diabetic mothers may not be due to a lack of surfactant.

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Ermini, Leonardo, Maurizio Mandalà, Laura Cresti, Sofia Passaponti, Laura Patrussi, Luana Paulesu, Kent Thornburg, and Francesca Ietta. "Fetal Myocardial Expression of GLUT1: Roles of BPA Exposure and Cord Blood Exosomes in a Rat Model." Cells 11, no. 20 (October 11, 2022): 3195. http://dx.doi.org/10.3390/cells11203195.

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Dietary exposure to Bisphenol A (BPA), an industrial chemical present in food containers, affects nutrient metabolism in the myocardium of offspring during intrauterine life. Using a murine model, we observed that fetal hearts from mothers exposed to BPA (2.5 μg/kg/day) for 20 days before mating and for all of the gestation had decreased expression of glucose transporter-1 (GLUT1), the principal sugar transporter in the fetal heart, and increased expression of fatty acid cluster of differentiation 36 transporter (CD36), compared to control fetuses from vehicle-treated mothers. We confirmed the suppression of GLUT1 by exposing fetal heart organotypic cultures to BPA (1 nM) for 48 h but did not detect changes in CD36 compared to controls. During pregnancy, the placenta continuously releases extracellular vesicles such as exosomes into fetal circulation. These vesicles influence the growth and development of fetal organs. When fetal heart cultures were treated with cord blood-derived exosomes isolated from BPA-fed animals, GLUT1 expression was increased by approximately 40%. Based on our results, we speculate that exosomes from cord blood, in particular placenta-derived nanovesicles, could contribute to the stabilization of the fetal heart metabolism by ameliorating the harmful effects of BPA on GLUT1 expression.

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Shimada, Shogo, Christian Robles, Ben M. W. Illigens, Alejandra M. Casar Berazaluce, Pedro J. del Nido, and Ingeborg Friehs. "Distention of the Immature Left Ventricle Triggers Development of Endocardial Fibroelastosis: An Animal Model of Endocardial Fibroelastosis Introducing Morphopathological Features of Evolving Fetal Hypoplastic Left Heart Syndrome." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/462469.

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Background.Endocardial fibroelastosis (EFE), characterized by a diffuse endocardial thickening through collagen and elastin fibers, develops in the human fetal heart restricting growth of the left ventricle (LV). Recent advances in fetal imaging indicate that EFE development is directly associated with a distended, poorly contractile LV in evolving hypoplastic left heart syndrome (HLHS). In this study, we developed an animal model of EFE by introducing this human fetal LV morphopathology to an immature rat heart.Methods and Results.A neonatal donor heart, in which aortic regurgitation (AR) was created, was heterotopically transplanted into a recipient adult rat. AR successfully induced the LV morphology of evolving HLHS in the transplanted donor hearts, which resulted in the development of significant EFE covering the entire LV cavity within two weeks postoperatively. In contrast, posttransplants with a competent aortic valve displayed unloaded LVs with a trace of EFE.Conclusions.We could show that distention of the immature LV in combination with stagnant flow triggers EFE development in this animal model. This model would serve as a robust tool to develop therapeutic strategies to treat EFE while providing insight into its pathogenesis.

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Lock, Mitchell C., Ross L. Tellam, Jack R. T. Darby, Jia Yin Soo, Doug A. Brooks, Christopher K. Macgowan, Joseph B. Selvanayagam, et al. "Differential gene responses 3 days following infarction in the fetal and adolescent sheep heart." Physiological Genomics 52, no. 3 (March 1, 2020): 143–59. http://dx.doi.org/10.1152/physiolgenomics.00092.2019.

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There are critical molecular mechanisms that can be activated to induce myocardial repair, and in humans this is most efficient during fetal development. The timing of heart development in relation to birth and the size/electrophysiology of the heart are similar in humans and sheep, providing a model to investigate the repair capacity of the mammalian heart and how this can be applied to adult heart repair. Myocardial infarction was induced by ligation of the left anterior descending coronary artery in fetal (105 days gestation when cardiomyocytes are proliferative) and adolescent sheep (6 mo of age when all cardiomyocytes have switched to an adult phenotype). An ovine gene microarray was used to compare gene expression in sham and infarcted (remote, border and infarct areas) cardiac tissue from fetal and adolescent hearts. The gene response to myocardial infarction was less pronounced in fetal compared with adolescent sheep hearts and there were unique gene responses at each age. There were also region-specific changes in gene expression between each age, in the infarct tissue, tissue bordering the infarct, and tissue remote from the infarction. In total, there were 880 genes that responded to MI uniquely in the adolescent samples compared with 170 genes in the fetal response, as well as 742 overlap genes that showed concordant direction of change responses to infarction at both ages. In response to myocardial infarction, there were specific changes in genes within pathways of mitochondrial oxidation, muscle contraction, and hematopoietic cell lineages, suggesting that the control of energy utilization and immune function are critical for effective heart repair. The more restricted gene response in the fetus may be an important factor in its enhanced capacity for cardiac repair.

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MEEHAN, Julia, and John M. KENNEDY. "Influence of thyroid hormone on the tissue-specific expression of cytochrome c oxidase isoforms during cardiac development." Biochemical Journal 327, no. 1 (October 1, 1997): 155–60. http://dx.doi.org/10.1042/bj3270155.

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In mammals, cytochrome coxidase (COX) is composed of 13 different protein subunits. In the rat, two nuclear-encoded subunits, COX VIa and VIII, exist as tissue-specific isoforms: heart and liver. Using Northern-blot analysis, the levels of transcripts for the heart and liver isoforms of VIa and VIII were examined in developing rat hearts. The liver isoform was found to be the predominant form of subunit VIa and the exclusive form of VIII in the 18-day fetal hearts. The mRNA levels of the heart isoform of both subunits increased dramatically to reach adult levels by 14 days. Although the levels of the VIa- and VIII-liver isoform mRNAs remained stable throughout early development, their levels decreased by 40 and 36% respectively between the 18-day fetal stage and 18-day neonatal stage. Therefore the up-regulation of the heart isoforms and down-regulation of the liver isoforms appear to be regulated in a co-ordinated manner during development. To determine if thyroid hormone influences the expression of these developmentally regulated isoforms, the RNA was also extracted from the hearts of 2-week-old hypothyroid rats. The results showed that the levels of VIII-heart and VIa-liver COX mRNAs were approx. 40% lower in the hypothyroid hearts, while VIII-liver and VIa-heart COX isoform expression remained unchanged. These data demonstrate that the isoforms of COX subunits VIa and VIII are not co-ordinately regulated by changes in thyroid hormone levels. Therefore we conclude that, although thyroid hormone influences the expression of isoforms, it appears to do so via a different mechanism from that which regulates the developmental transition.

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Fisher, Jeffrey W., Stephen R. Channel, Jeffrey S. Eggers, Paula D. Johnson, Kathleen L. MacMahon, Chuck D. Goodyear, Gregory L. Sudberry, D. Alan Warren, John R. Latendresse, and Linda J. Graeter. "Trichloroethylene, Trichloroacetic Acid, and Dichloroacetic Acid: Do They Affect Fetal Rat Heart Development?" International Journal of Toxicology 20, no. 5 (September 2001): 257–67. http://dx.doi.org/10.1080/109158101753252992.

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Trichloroethylene (TCE), trichloroacetic acid (TCA), and dichloroacetic acid (DCA) are commonly found as groundwater contaminants in many regions of the United States. Cardiac birth defects in children have been associated with TCE, and laboratory studies with rodents report an increased incidence of fetal cardiac malformations resulting from maternal exposures to TCE, TCA, and DCA. The objective of this study was to orally treat pregnant CDR(CD) Sprague-Dawley rats with large bolus doses of either TCE (500 mg/kg), TCA (300 mg/kg), or DCA (300 mg/kg) once per day on days 6 through 15 of gestation to determine the effectiveness of these materials to induce cardiac defects in the fetus. All- trans retinoic acid (RA) dissolved in soybean oil was used as a positive control. Soybean oil is commonly used as a dosing vehicle for RA teratology studies and was also used in this study as a dosing vehicle for TCE. Water was used as the dosing vehicle for TCA and DCA. Fetal hearts were examined on gestation day (GD) 21 by an initial in situ, cardiovascular stereomicroscope examination, and then followed by a microscopic dissection and examination of the formalin-fixed heart. The doses selected for TCA and DCA resulted in a modest decrease in maternal weight gain during gestation (3% to 8%). The fetal weights on GD 21 in the TCA and DCA treatment groups were decreased 8% and 9%, respectively, compared to the water control group and 21% in the RA treatment group compared to soybean oil control group. The heart malformation incidence for fetuses from the TCE-, TCA-, and DCA-treated dams did not differ from control values on a per fetus or per litter basis. The rate of heart malformations, on a per fetus basis, ranged from 3% to 5% for TCE, TCA, and DCA treatment groups compared to 6.5% and 2.9% for soybean oil and water control groups. The RA treatment group was significantly higher with 33% of the fetuses displaying heart defects. For TCE, TCA, and DCA treatment groups 42% to 60% of the litters contained at least one fetus with a heart malformation, compared to 52% and 37% of the Utters in the soybean oil and water control groups. For the RA treatment group, 11 of 12 litters contained at least one fetus with a heart malformation. Further research is needed to quantify the spontaneous rates of heart defects for vehicle control rats and to explain the disparity between findings in the present study and other reported findings on the fetal cardiac teratogenicity of TCE, TCA, and DCA.

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Eferl, Robert, Maria Sibilia, Frank Hilberg, Andrea Fuchsbichler, Iris Kufferath, Barbara Guertl, Rainer Zenz, Erwin F. Wagner, and Kurt Zatloukal. "Functions of c-Jun in Liver and Heart Development." Journal of Cell Biology 145, no. 5 (May 31, 1999): 1049–61. http://dx.doi.org/10.1083/jcb.145.5.1049.

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Mice lacking the AP-1 transcription factor c-Jun die around embryonic day E13.0 but little is known about the cell types affected as well as the cause of embryonic lethality. Here we show that a fraction of mutant E13.0 fetal livers exhibits extensive apoptosis of both hematopoietic cells and hepatoblasts, whereas the expression of 15 mRNAs, including those of albumin, keratin 18, hepatocyte nuclear factor 1, β-globin, and erythropoietin, some of which are putative AP-1 target genes, is not affected. Apoptosis of hematopoietic cells in mutant livers is most likely not due to a cell-autonomous defect, since c-jun−/− fetal liver cells are able to reconstitute all hematopoietic compartments of lethally irradiated recipient mice. A developmental analysis of chimeras showed contribution of c-jun−/− ES cell derivatives to fetal, but not to adult livers, suggesting a role of c-Jun in hepatocyte turnover. This is in agreement with the reduced mitotic and increased apoptotic rates found in primary liver cell cultures derived from c-jun−/− fetuses. Furthermore, a novel function for c-Jun was found in heart development. The heart outflow tract of c-jun−/− fetuses show malformations that resemble the human disease of a truncus arteriosus persistens. Therefore, the lethality of c-jun mutant fetuses is most likely due to pleiotropic defects reflecting the diversity of functions of c-Jun in development, such as a role in neural crest cell function, in the maintenance of hepatic hematopoiesis and in the regulation of apoptosis.

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Yan, Jingbin, Birong Liang, Ying Lv, and Yanbin Li. "Monitoring and Analysis of Early Heart Structure of Fetus in Gynecology and Obstetrics Based on Ultrasound Image." Journal of Medical Imaging and Health Informatics 11, no. 3 (March 1, 2021): 973–80. http://dx.doi.org/10.1166/jmihi.2021.3350.

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As the core organ of cardiovascular system, fetal heart plays a very important role. With the development of pregnancy, the early fetal heart rate tends to mature, and the corresponding cardiac function tends to mature and stable. But the fetal heart is very fragile during pregnancy. Various diseases during pregnancy directly lead to fetal heart growth restriction, and even lead to fetal heart function damage. Ultrasound image diagnosis is one of the most important diagnostic methods in medical imaging. It is of great significance to detect the early heart structure of the fetus in gynecology and obstetrics. It can detect the early fetal heart in real time and noninvasively. However, the traditional ultrasonic image detection has many disadvantages in the process of application, such as many noise points, low performance of processing algorithm, which to some extent affects the detection performance of ultrasonic image detection in the detection of fetal heart structure in gynecology and obstetrics. Based on the above problems, this paper proposes an adaptive detection algorithm of superimposed moving image based on ultrasonic image detection, which can accurately extract and analyze fetal heart region when the signal-to-noise ratio of ultrasonic image sequence is low. The average anisotropy algorithm is also proposed innovatively in this paper. In order to predict the structure of fetal heart more accurately, the active heart model combining fetal heart structure and motion information is considered in the actual analysis process. Experiments show that the accuracy error of the algorithm is less than 11 pixels.

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Refaat Kotb, Sally Ahmed, and Amr Shaaban. "Fetal cardiac functional performance and development of diabetic gestations." Obstetrics Gynecology and Reproductive Sciences 1, no. 1 (April 25, 2017): 01–04. http://dx.doi.org/10.31579/2578-8965/002.

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Objective of research: To reveal and asses probable change in fetal cardiac physiological function of pregestational diabetic gestations. Research design: We performed a prospective research study of 31 gestations between 22 weeks’ gestational age and full term, and who had pregestational diabetes. All diabetic women recruited in the research performed had glycosylated hemoglobin lower than 6.5%. All gestations involved in the research performed had an early sonographic confirmation of fetal gestational age. Doppler study of blood flow via the fetal mitral and tricuspid valves were performed every 4 weeks using a pulsed wave sonographic Doppler machine with a 3.5- or 5-MHz ultrasound transducer. The subsequent parameters were analysed and calculated automatically from the revealed flow velocity waveforms: the peak velocity during the rapid ventricular filling phase (E wave) and during the atrial systole phase (A wave), and the ratio between these obtained velocities (E/A ratio); and the velocity time fundamental of the fetal atrioventricular blood flow (correlated with volume flow). A comparative statistical analysis between the Doppler parameters revealed from fetal examination of diabetic gestations and of normal gestations was performed by using the Mann-Whitney test. Results: Each gestation recruited for the study performed around four to five fetal echocardiographic Sonographic assessments at 22, 26, 30, 34, and 38 weeks’ gestation. The E/A ratio of the mitral and tricuspid valves did not Rise in fetuses of diabetic women during the third trimester and was observed to be statistically significantly higher manner in fetuses of nondiabetic gestations in comparison with fetuses of diabetic gestations at 34 and 38 gestational weeks. Calculated velocity time basic of the mitral and tricuspid valves when multiplied by fetal heart rate was greater, but not statistically significant, in fetuses of nondiabetic gestations when put in comparison with diabetic gestations fetuses at 34 and 38 weeks’ gestational weeks. The E-wave of both the mitral and tricuspid valves rised in both study categories all the way through pregnancy. The A-wave of the mitral and tricuspid valves rised only in diabetic gestation fetuses all over the final gestational trimester and was statistically significant in a greater manner at 34 and 38 gestational weeks compared with fetuses of nondiabetic women. Conclusion: variability in fetal atrioventricular blood flow forms between fetuses of diabetic gestations and normal gestations does not essentially cause variability in fetal functional cardiac compliance.

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Carver, W., R. L. Price, D. S. Raso, L. Terracio, and T. K. Borg. "Distribution of beta-1 integrin in the developing rat heart." Journal of Histochemistry & Cytochemistry 42, no. 2 (February 1994): 167–75. http://dx.doi.org/10.1177/42.2.8288862.

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Cell-cell and cell-matrix interactions play critical roles in various developmental processes including differentiation, proliferation, and migration. Members of the integrin family of cell surface components are important mediators of these cell-extracellular matrix (ECM) contacts or interactions. The ECM provides signals to individual cells essential for development and differentiation and plays essential roles in establishing and maintaining the complex structure of the vertebrate heart. Integrins provide a fundamental link for transduction of developmental signals to cells. Integrin expression by cardiac myocytes is altered during neonatal heart development and disease; however, little is known regarding the spatial and temporal patterns of integrin expression during embryonic and fetal heart development. Essential to understanding the role of integrins in the organization of the heart, the present studies have localized beta-1 integrin protein and mRNA in fetal and neonatal rat hearts. Beta-1 integrin is predominantly found in regions of remodeling (trabeculae) in the early heart (10-13 days of gestation). Later in development (15 days of gestation onward), beta-1 integrin is abundant in regions containing an elaborate ECM, such as the valves. These studies further support the hypothesis that the expressions of integrins and ECM are coordinately regulated in the developing heart.

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Mittra, A. K., and N. K. Choudhary. "DEVELOPMENT OF A WEB-BASED FETAL MONITORING SYSTEM: AN INNOVATIVE APPROACH." Biomedical Engineering: Applications, Basis and Communications 20, no. 01 (February 2008): 27–37. http://dx.doi.org/10.4015/s101623720800057x.

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The well being of the fetal is one of the primary issues in prenatal obstetric care. The assessment of fetal well being is usually practiced by observing the fetal heart rate and monitoring its patterns. Ultrasound based instruments are commonly used for this purpose in hospitals, but they are not suitable for home monitoring applications because of several known reasons. This work is focused around the development of a web-based prototype system for routine fetal home monitoring application. This is helpful in management of complex pregnancies. The presented system is used for recording fetal heart sound in the woman's restful hours at home and makes it available to the physician remotely via the internet. Transmitted data is then processed by an innovative methodology for deriving crucial results of diagnostic importance. After careful examination of these results, status report is electronically e-mailed to the expectant mother for a ready reference and subsequent action. The system has been tested on 20 pregnant women with varied gestation age and pathological conditions. The resultant performance was compared with a standard ultrasound based device commonly used in hospitals. It is found that the developed fetal health care system provides promising result that enables fetal monitoring in low stress, and relaxed home environment. It also supports rapid information flow, and provides quick accessibility to information at the point of decision.

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Barros, L. P. R., A. C. C. Carvalho, M. M. Zamith, E. M. B. Barros, M. Schlosser, and E. R. F. L. Moraes. "Development of an Ultrasound Center for Screening Fetal Heart Malformations." Ultrasound in Medicine & Biology 39, no. 5 (May 2013): S89. http://dx.doi.org/10.1016/j.ultrasmedbio.2013.02.423.

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PILLAI, MARY, and DAVID JAMES. "The Development of Fetal Heart Rate Patterns During Normal Pregnancy." Obstetrics & Gynecology 76, no. 5 (November 1990): 812–16. http://dx.doi.org/10.1097/00006250-199011000-00017.

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Sylwestrzak, Oskar, and Maria Respondek-Liberska. "Echocardiographic Methods of Fetal Heart Size Assessmentheart to Chest Area Ratio and Transversal Heart Diameter." Prenatal Cardiology 8, no. 1 (June 15, 2018): 20–23. http://dx.doi.org/10.1515/pcard-2018-0003.

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Abstract Introduction: Ultrasound assessment of fetal heart size (FHS) is widely used and recommended in many guidelines of fetal echocardiography due to its clinical value. The aim of this study was an analysis of some fetal heart measurements: ratio of heart area to chest area (HA/ CA) and transversal diameter of heart (AP) and their correlation to gestational age. Material and methods: This retrospective study was based on database of records of ultrasound and echocardiographic examinations performed in our unit and included fetuses between 15th and 39th week of gestation with no evidence of heart defect or any abnormality. Results: 609 ultrasound examinations were analyzed. The mean HA/CA was 0,30 ± 0,015, with no statistical difference between female and male (p>0,05), and seemed to be relatively constant with slight increase with advancing gestational age. The AP diameter in whole group correlated with gestational age (r=0,94) and there was no difference related to the fetuses gender. Conclusion: The correlation of AP diameter and relative constancy of HA/CA ratio with gestational age presented in our normograms could be used for monitoring fetal development, but also for fetal cardiomegaly assessment.

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Quijada, Pearl, Michael A. Trembley, and Eric M. Small. "The Role of the Epicardium During Heart Development and Repair." Circulation Research 126, no. 3 (January 31, 2020): 377–94. http://dx.doi.org/10.1161/circresaha.119.315857.

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The heart is lined by a single layer of mesothelial cells called the epicardium that provides important cellular contributions for embryonic heart formation. The epicardium harbors a population of progenitor cells that undergo epithelial-to-mesenchymal transition displaying characteristic conversion of planar epithelial cells into multipolar and invasive mesenchymal cells before differentiating into nonmyocyte cardiac lineages, such as vascular smooth muscle cells, pericytes, and fibroblasts. The epicardium is also a source of paracrine cues that are essential for fetal cardiac growth, coronary vessel patterning, and regenerative heart repair. Although the epicardium becomes dormant after birth, cardiac injury reactivates developmental gene programs that stimulate epithelial-to-mesenchymal transition; however, it is not clear how the epicardium contributes to disease progression or repair in the adult. In this review, we will summarize the molecular mechanisms that control epicardium-derived progenitor cell migration, and the functional contributions of the epicardium to heart formation and cardiomyopathy. Future perspectives will be presented to highlight emerging therapeutic strategies aimed at harnessing the regenerative potential of the fetal epicardium for cardiac repair.

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Johansson, Bertil, Erik Wedenberg, and Björn Westin. "Fetal heart rate response to acoustic stimulation in relation to fetal development and hearing impairment." Acta Obstetricia et Gynecologica Scandinavica 71, no. 8 (January 1992): 610–15. http://dx.doi.org/10.3109/00016349209006229.

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Nijhuis, Ilse J. M., and Judith ten Hof. "Development of fetal heart rate and behavior: indirect measures to assess the fetal nervous system." European Journal of Obstetrics & Gynecology and Reproductive Biology 87, no. 1 (November 1999): 1–2. http://dx.doi.org/10.1016/s0301-2115(99)00143-8.

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Bora, Rishabh, and Neharika Malhotra Bora. "Fetal Origin of Adult Disease." Donald School Journal of Ultrasound in Obstetrics and Gynecology 8, no. 2 (2014): 164–77. http://dx.doi.org/10.5005/jp-journals-10009-1352.

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ABSTRACT Fetal origins of adult disease, a concept first popularized by Dr David Barker, has subsequently led to many studies which have provided the evidence that certain diseases do have links pointing to fetal origins—adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which result in increased disease risk in adulthood. Links that are well-established are—reduced birth weight and increased risk of coronary heart disease, hypertension and stroke in adulthood. The concept of a fetal origin of adult disease have been extended well-beyond coronary heart disease and being a risk factor for coronary heart disease, and now includes investigations of the development of the central nervous system, early origins of adult mental health and cognitive function. By understanding fetal origin of adult disease, health care professionals and policy makers will make this issue a high health care priority and implement preventive measures and treatment for those at higher risk for chronic diseases. How to cite this article Malhotra N, Malhotra J, Bora NM, Bora R, Malhotra K. Fetal Origin of Adult Disease. Donald School J Ultrasound Obstet Gynecol 2014;8(2):164-177.

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Mayor, Reina S., Katelyn E. Finch, Jordan Zehr, Eugenia Morselli, Michael D. Neinast, Aaron P. Frank, Lisa D. Hahner, et al. "Maternal high-fat diet is associated with impaired fetal lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 4 (August 15, 2015): L360—L368. http://dx.doi.org/10.1152/ajplung.00105.2015.

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Maternal nutrition has a profound long-term impact on infant health. Poor maternal nutrition influences placental development and fetal growth, resulting in low birth weight, which is strongly associated with the risk of developing chronic diseases, including heart disease, hypertension, asthma, and type 2 diabetes, later in life. Few studies have delineated the mechanisms by which maternal nutrition affects fetal lung development. Here, we report that maternal exposure to a diet high in fat (HFD) causes placental inflammation, resulting in placental insufficiency, fetal growth restriction (FGR), and inhibition of fetal lung development. Notably, pre- and postnatal exposure to maternal HFD also results in persistent alveolar simplification in the postnatal period. Our novel findings provide a strong association between maternal diet and fetal lung development.

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Izzo, Antonella, Rosanna Manco, Tiziana de Cristofaro, Ferdinando Bonfiglio, Rita Cicatiello, Nunzia Mollo, Marco De Martino, et al. "Overexpression of Chromosome 21 miRNAs May Affect Mitochondrial Function in the Hearts of Down Syndrome Fetuses." International Journal of Genomics 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/8737649.

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Dosage-dependent upregulation of most of chromosome 21 (Hsa21) genes has been demonstrated in heart tissues of fetuses with Down syndrome (DS). Also miRNAs might play important roles in the cardiac phenotype as they are highly expressed in the heart and regulate cardiac development. Five Hsa21 miRNAs have been well studied in the past: miR-99a-5p, miR-125b-2-5p, let-7c-5p, miR-155-5p, and miR-802-5p but few information is available about their expression in trisomic tissues. In this study, we evaluated the expression of these miRNAs in heart tissues from DS fetuses, showing that miR-99a-5p, miR-155-5p, and let-7c-5p were overexpressed in trisomic hearts. To investigate their role, predicted targets were obtained from different databases and cross-validated using the gene expression profiling dataset we previously generated for fetal hearts. Eighty-five targets of let-7c-5p, 33 of miR-155-5p, and 10 of miR-99a-5p were expressed in fetal heart and downregulated in trisomic hearts. As nuclear encoded mitochondrial genes were found downregulated in trisomic hearts and mitochondrial dysfunction is a hallmark of DS phenotypes, we put special attention to let-7c-5p and miR-155-5p targets downregulated in DS fetal hearts and involved in mitochondrial function. The let-7c-5p predicted target SLC25A4/ANT1 was identified as a possible candidate for both mitochondrial and cardiac anomalies.

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Osuala, Kingsley, Candice N. Baker, Ha-Long Nguyen, Celines Martinez, David Weinshenker, and Steven N. Ebert. "Physiological and genomic consequences of adrenergic deficiency during embryonic/fetal development in mice: impact on retinoic acid metabolism." Physiological Genomics 44, no. 19 (October 1, 2012): 934–47. http://dx.doi.org/10.1152/physiolgenomics.00180.2011.

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Adrenergic hormones are essential for early heart development. To gain insight into understanding how these hormones influence heart development, we evaluated genomic expression changes in embryonic hearts from adrenergic-deficient and wild-type control mice. To perform this study, we used a mouse model with targeted disruption of the Dopamine β-hydroxylase ( Dbh) gene, whose product is responsible for enzymatic conversion of dopamine into norepinephrine. Embryos homozygous for the null allele ( Dbh −/−) die from heart failure beginning as early as embryonic day 10.5 (E10.5). To assess underlying causes of heart failure, we isolated hearts from Dbh −/− and Dbh +/+ embryos prior to manifestation of the phenotype and examined gene expression changes using genomic Affymetrix 430A 2.0 arrays, which enabled simultaneous evaluation of >22,000 genes. We found that only 22 expressed genes showed a significant twofold or greater change, representing ∼0.1% of the total genes analyzed. More than half of these genes are associated with either metabolism (31%) or signal transduction (22%). Remarkably, several of the altered genes encode for proteins that are directly involved in retinoic acid (RA) biosynthesis and transport. Subsequent evaluation showed that RA concentrations were significantly elevated by an average of ∼3-fold in adrenergic-deficient ( Dbh −/−) embryos compared with controls, thereby suggesting that RA may be an important downstream mediator of adrenergic action during embryonic heart development.

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Franco, Diego, Carlos Garcia-Padilla, Jorge N. Dominguez, Estefania Lozano-Velasco, and Amelia Aranega. "Cardiac Development: A Glimpse on Its Translational Contributions." Hearts 2, no. 1 (February 4, 2021): 87–118. http://dx.doi.org/10.3390/hearts2010008.

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Cardiac development is a complex developmental process that is initiated soon after gastrulation, as two sets of precardiac mesodermal precursors are symmetrically located and subsequently fused at the embryonic midline forming the cardiac straight tube. Thereafter, the cardiac straight tube invariably bends to the right, configuring the first sign of morphological left–right asymmetry and soon thereafter the atrial and ventricular chambers are formed, expanded and progressively septated. As a consequence of all these morphogenetic processes, the fetal heart acquired a four-chambered structure having distinct inlet and outlet connections and a specialized conduction system capable of directing the electrical impulse within the fully formed heart. Over the last decades, our understanding of the morphogenetic, cellular, and molecular pathways involved in cardiac development has exponentially grown. Multiples aspects of the initial discoveries during heart formation has served as guiding tools to understand the etiology of cardiac congenital anomalies and adult cardiac pathology, as well as to enlighten novels approaches to heal the damaged heart. In this review we provide an overview of the complex cellular and molecular pathways driving heart morphogenesis and how those discoveries have provided new roads into the genetic, clinical and therapeutic management of the diseased hearts.

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Donofrio, Mary T., Adré J. duPlessis, and Catherine Limperopoulos. "Impact of congenital heart disease on fetal brain development and injury." Current Opinion in Pediatrics 23, no. 5 (October 2011): 502–11. http://dx.doi.org/10.1097/mop.0b013e32834aa583.

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Mittra, A. K., N. K. Choudhary, and A. S. Zadgaonkar. "Development of Adaptive Noise Reducer for Fetal Heart Sound Signal Conditioning." i-manager's Journal on Future Engineering and Technology 3, no. 2 (January 15, 2008): 28–34. http://dx.doi.org/10.26634/jfet.3.2.663.

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Takano, M., and A. Noma. "Development of muscarinic potassium current in fetal and neonatal rat heart." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (March 1, 1997): H1188—H1195. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1188.

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Single atrial myocytes were isolated from fetal, neonatal, and adult rat hearts. The muscarinic K+ current activated by rapid application of acetylcholine (ACh) and adenosine (Ado) was recorded under the whole cell voltage clamp. The current density (pA/pF) of ACh-induced K+ current increased from gestation day 12 to the maximum on neonatal day 20 and decreased in the adult myocytes due to greater increase of the membrane capacitance. The development of Ado-induced K+ current followed a similar time course except for a remarkable decrease after neonatal day 10. No significant change was found in single-channel properties during the development. Receptor subtypes were M2 and A1 receptors for ACh and Ado, respectively. In the dose-response relationship, the half-maximal concentration for ACh-induced current markedly decreased with age, from 1.44 (fetus) to 0.17 microM (adult), whereas that for Ado increased from 0.45 (fetus) to 0.99 microM (adult). These changes of the muscarinic K+ current were discussed in relation to the functional development of cardiac myocytes and underlying mechanisms.

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Cameron, Vicky A., and Leigh J. Ellmers. "Minireview: Natriuretic Peptides during Development of the Fetal Heart and Circulation." Endocrinology 144, no. 6 (June 1, 2003): 2191–94. http://dx.doi.org/10.1210/en.2003-0127.

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Inoue, Hiromasa, Masato Nakatome, Masaru Terada, Mizuki Mizuno, Reiko Ono, Morio Iino, Yukiko Ino, Yoshiaki Ogura, Hisanaga Kuroki, and Ryoji Matoba. "Maternal methamphetamine administration during pregnancy influences on fetal rat heart development." Life Sciences 74, no. 12 (February 2004): 1529–40. http://dx.doi.org/10.1016/j.lfs.2003.08.016.

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Gierałtowski, Jan, Dirk Hoyer, Florian Tetschke, Samuel Nowack, Uwe Schneider, and Jan Żebrowski. "Development of multiscale complexity and multifractality of fetal heart rate variability." Autonomic Neuroscience 178, no. 1-2 (November 2013): 29–36. http://dx.doi.org/10.1016/j.autneu.2013.01.009.

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Schmidt, Judy V. "The Development of AWHONN’s Fetal Heart Monitoring Principles and Practices Workshop." Journal of Obstetric, Gynecologic & Neonatal Nursing 29, no. 5 (September 2000): 509–15. http://dx.doi.org/10.1111/j.1552-6909.2000.tb02772.x.

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Iruretagoyena, J. Igor, Wayne Davis, Christina Kendziorski, Cynthia Bird, Rebecca Radue, Aimee Teo Bromar, Sandra Spliinter-Bondurant, Thaddeus Golos, Ian Bird, and Dinesh Shah. "412: Human fetal heart development during the first and second trimester." American Journal of Obstetrics and Gynecology 206, no. 1 (January 2012): S191—S192. http://dx.doi.org/10.1016/j.ajog.2011.10.430.

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Kinnear, Caroline, Maruti Haranal, Patrick Shannon, Edgar Jaeggi, David Chitayat, and Seema Mital. "Abnormal fetal cerebral and vascular development in hypoplastic left heart syndrome." Prenatal Diagnosis 39, no. 1 (December 27, 2018): 38–44. http://dx.doi.org/10.1002/pd.5395.

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Kim, Kyu Nam, Young-Sun Park, and Jeong-Kyu Hoh. "Sex-related differences in the development of fetal heart rate dynamics." Early Human Development 93 (February 2016): 47–55. http://dx.doi.org/10.1016/j.earlhumdev.2015.12.005.

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Journal articles on the topic 'Fetal heart development'

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