Journal articles: 'Fetal size/growth'

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Harrington, Kevin, and Stuart Campbell. "Fetal size and growth." Current Opinion in Obstetrics and Gynecology 5, no. 2 (April 1993): 186???194. http://dx.doi.org/10.1097/00001703-199304000-00004.

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Kirchengast, Sylvia, and Beda Hartmann. "Association patterns of fetal head dimensions, postcranial body growth and neonatal size." Anthropologischer Anzeiger 77, no. 2 (April 30, 2020): 173–81. http://dx.doi.org/10.1127/anthranz/2020/1137.

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Merialdi, M., L. E. Caulfield, N. Zavaleta, A. Figueroa, K. A. Costigan, F. Dominici, and J. A. Dipietro. "Fetal growth in Peru: comparisons with international fetal size charts and implications for fetal growth assessment." Ultrasound in Obstetrics and Gynecology 26, no. 2 (July 22, 2005): 123–28. http://dx.doi.org/10.1002/uog.1954.

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Spencer, J. A. D., T. C. Chang, S. C. Robson, and S. Gallivan. "Fetal size and growth in Bangladeshi pregnancies." Ultrasound in Obstetrics and Gynecology 5, no. 5 (May 1, 1995): 313–17. http://dx.doi.org/10.1046/j.1469-0705.1995.05050313.x.

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Frusca, T., S. Parolini, A. Dall'Asta, W. A. Hassan, A. Vitulo, A. Gillett, D. Pasupathy, and C. C. Lees. "Fetal size and growth velocity in chronic hypertension." Pregnancy Hypertension 10 (October 2017): 101–6. http://dx.doi.org/10.1016/j.preghy.2017.06.007.

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McCarthy, Elizabeth A., and Susan P. Walker. "International fetal growth standards: one size fits all." Lancet 384, no. 9946 (September 2014): 835–36. http://dx.doi.org/10.1016/s0140-6736(14)61416-1.

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Friedrich, M. J. "International Standards for Newborn Size and Fetal Growth." JAMA 312, no. 15 (October 15, 2014): 1503. http://dx.doi.org/10.1001/jama.2014.13252.

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Keshavarz, Elham, Marjan Rustazade Sheikhyusefi, Ensi Khalili Pouya, Masoumeh Mirzamoradi, Mehdi Khazaei, Yashar Moharamzad, and Morteza Sanei Taheri. "Association Between Fetal Thymus Size and Intrauterine Growth Restriction." Journal of Diagnostic Medical Sonography 38, no. 2 (December 14, 2021): 120–26. http://dx.doi.org/10.1177/87564793211054747.

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Objective: The objective of this study was to evaluate the association between reduced fetal thymus size and intrauterine growth restriction (IUGR). This study was devised to determine the association between thymus size and any abnormal Doppler indices within the fetal umbilical artery (UA), as well as the middle cerebral artery (MCA). Materials and Methods: Forty-six pregnancies between 20 and 38 weeks of gestation with IUGR and 46 normal pregnancies within similar gestational age (GA) range were included. The transverse diameter of fetal thymus was measured. In the IUGR group, the fetal umbilical artery (UA) and middle cerebral artery (MCA) Doppler flow velocities were recorded. Results: The mean GA of fetuses with IUGR (33.5 weeks) was higher than control group (30.3 weeks). To adjust for the effect of GA, analysis of covariance (ANCOVA) was performed. The adjusted mean thymus diameters were 19.02 mm in IUGR and 21.25 within the control group (mean difference = 2.23 mm; P = .02). The mean (±SD) thymus size in 16 fetuses, with abnormal Doppler findings, was significantly lower than in the group with normal Doppler findings, 17.45 (±2.50) vs 22.02 (±5.39) mm; P < .001. Conclusion: IUGR may be associated with reduced fetal thymus size, especially when coupled with abnormal Doppler findings. The thymus size in a group of IUGR fetuses, with abnormal Doppler findings, was smaller than IUGR fetuses, with normal Doppler findings.

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Fulford, A. J. C., S. E. Moore, S. E. Arifeen, L. Å. Persson, L. M. Neufeld, Y. Wagatsuma, and A. M. Prentice. "Disproportionate early fetal growth predicts postnatal thymic size in humans." Journal of Developmental Origins of Health and Disease 4, no. 3 (March 7, 2013): 223–31. http://dx.doi.org/10.1017/s2040174413000044.

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Prenatal events can affect neonatal thymus size and adult immune function. The causal insults are unknown, although fetal nutrient restriction is suspected. We used ultrasound at three time points during pregnancy (14, 19 and 30 weeks) to measure the growth of six fetal dimensions in rural Bangladeshi women participating in the Maternal and Infant Nutrition Interventions, Matlab study. Postnatal ultrasound was used to calculate thymic index (TI) at birth, 2, 6 and 12 m. Of the 3267 women recruited, 2861 participated by providing data at least at one fetal biometry and one TI time point. Patterns of fetal growth were summarized using principal components calculated from fetal dimensionz-scores. Random effects regression, controlling for infant size and season of measurement were used to relate these patterns to TI. We found that smaller leg length relative to head circumference, characteristic of head-sparing growth restriction, was predictive of lower TI. This association was significant at all time points but strongest in earlier pregnancy. Each standard deviation increase in leg–head proportion was associated with an increase in TI of ∼5%. We conclude that growth patterns typical of poor fetal nutrition are associated with poor thymic development. The greater strength of this association in the first trimester is consistent with a period of vulnerability during the early ontogeny of the thymus and suggests that preventative intervention would need to be given in early pregnancy.

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Schwartz, Nadav, Mary Sammel, Hayley Quant, Rita Leite, and Samuel Parry. "379: Early placental size helps predict fetal growth restriction." American Journal of Obstetrics and Gynecology 208, no. 1 (January 2013): S166—S167. http://dx.doi.org/10.1016/j.ajog.2012.10.544.

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Hata, Toshiyuki, and Shu-Yan Dai. "Three-Dimensional Ultrasound in Fetal Size and Growth Assessment." Current Medical Imaging Reviews 4, no. 3 (August 1, 2008): 184–93. http://dx.doi.org/10.2174/157340508785294552.

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Kind, K. L., J. A. Owens, J. S. Robinson, K. J. Quinn, P. A. Grant, P. E. Walton, R. S. Gilmour, and P. C. Owens. "Effect of restriction of placental growth on expression of IGFs in fetal sheep: relationship to fetal growth, circulating IGFs and binding proteins." Journal of Endocrinology 146, no. 1 (July 1995): 23–34. http://dx.doi.org/10.1677/joe.0.1460023.

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Abstract To determine whether tissue production of the IGFs is altered when fetal growth is retarded, IGF-I and -II mRNAs were measured in tissues of fetal sheep subjected to placental restriction and the relationships between IGF gene expression, circulating IGF protein and fetal growth were examined. The majority of potential placental attachment sites were surgically removed from the uterus of 12 non-pregnant ewes to restrict placental size in a subsequent pregnancy. Blood and tissues were collected at 121 days of gestation (term=150) in 12 fetuses with restricted placental size and eight normal fetuses. IGF-I and IGF-II mRNA was detected by solution hybridization/ribonuclease protection assay in placenta and all fetal tissues studied. IGF-I mRNA was most abundant in skeletal muscle and liver and IGF-II mRNA was highest in kidney and lung. Restriction of placental size reduced fetal weight by 17% and reduced the pO2 (18%) and glucose concentration (23%) of fetal blood. Placental restriction also reduced IGF-I mRNA in fetal muscle (P<0·002), lung (P<0·05) and kidney (P<0·01) but had no significant effect on IGF-II mRNA in any tissue. IGF-I mRNA in fetal liver, kidney and skeletal muscle correlated positively with the concentration of IGF-I protein in fetal blood (P<0·01). There was no relationship between the concentration of IGF-II protein in fetal blood and IGF-II mRNA in any fetal tissue examined. The concentration of IGF-binding protein-3 (IGFBP-3) in fetal arterial blood plasma measured by RIA correlated positively with fetal weight and with plasma IGF-I. This study shows that restriction of placental growth in sheep reduces circulating levels of IGF-I and IGFBP-3 in the sheep fetus and reduces the capacity of the fetus to produce IGF-I at a number of tissue sites. Altered production of IGF-I, but not IGF-II, by fetal tissues may contribute to retarded fetal growth. Journal of Endocrinology (1995) 146, 23–34

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Sferruzzi-Perri, A. N., J. A. Owens, J. S. Robinson, and C. T. Roberts. "273.Insulin-like growth factor treatment of pregnant guinea pigs during early pregnancy promotes fetal growth." Reproduction, Fertility and Development 16, no. 9 (2004): 273. http://dx.doi.org/10.1071/srb04abs273.

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Insulin-like growth factor (IGF)-II is an important regulator of growth in many tissues and is abundantly expressed in the placenta during pregnancy. Gene ablation studies performed in mice have shown that IGF-II deficiency results in both impaired fetal and placental growth, whereas deficiency in IGF-I reduces fetal growth only. Conversely, maternal IGF supplementation in early pregnancy in the guinea pig increases placental and fetal size by mid pregnancy. This study aimed to determine whether these anabolic effects persist into late pregnancy after cessation of treatment. On Day 20 of pregnancy, mothers were anaesthetised and a mini osmotic pump was implanted subcutaneously, to deliver 1mg/kg/day IGF-I (n = 7), IGF-II (n = 9) or vehicle (n = 7) for 17 days. Guinea pigs were killed on Day 62 of pregnancy (term ~67 days). Fetal and placental weights, and maternal and fetal body composition, were measured. Total litter size was unaffected by IGF treatment; however, IGF-II increased the number of viable fetuses by 26% (P = 0.01). After adjusting for the number of viable pups per litter, maternal IGF treatment increased fetal growth by increasing abdominal circumference, crown-rump length and fetal weight (fetal weight: IGF-I 79+/–2.5 g; IGF-II 78+/–2.6 g; vs vehicle 68+/–2.5 g, P = 0.02). IGF treatment did not alter absolute or relative fetal organ weights. IGF-I reduced placental weight by 9% and IGF-II increased it by 9%, but not significantly. IGF-I increased the fetal weight�:�placental weight ratio (19+/–0.9 vs 15+/–0.9, respectively P = 0.043). IGF treatment did not affect maternal weight gain during pregnancy nor net carcass weight; however, IGF-I reduced maternal lung and adipose tissue weights. In conclusion, maternal IGF-II treatment during early pregnancy improved fetal growth into late gestation, possibly by modulating placental efficiency. As poor placental development is implicated in fetal growth restriction, increasing maternal IGF abundance in early to mid pregnancy may be a potential therapeutic approach to placental insufficiency.

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Turner, Steve. "Perinatal Programming of Childhood Asthma: Early Fetal Size, Growth Trajectory during Infancy, and Childhood Asthma Outcomes." Clinical and Developmental Immunology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/962923.

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The “fetal origins hypothesis” or concept of “developmental programming” suggests that faltering fetal growth and subsequent catch-up growth are implicated in the aetiology of cardiovascular disease. Associations between reduced birth weight, rapid postnatal weight gain, and asthma suggest that there are fetal origins to respiratory disease. The present paper first summarises the literature relating birth weight and post natal growth trajectories to asthma outcomes. Second, issues regarding the interpretation of antenatal fetal ultrasound measurements are discussed. Finally, recent reports linking antenatal measurement and growth trajectory to early childhood asthma outcomes are discussed. Understanding the nature and timing of factors which influence antenatal growth may give important insight into the antecedents of early-onset asthma with implications for interventions.

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Gluckman, P. D., P. C. H. Morel, G. R. Ambler, B. H. Breier, H. T. Blair, and S. N. McCutcheon. "ELEVATING MATERNAL INSULIN-LIKE GROWTH FACTOR-I IN MICE AND RATS ALTERS THE PATTERN OF FETAL GROWTH BY REMOVING MATERNAL CONSTRAINT." Journal of Endocrinology 134, no. 1 (July 1992): R1—R3. http://dx.doi.org/10.1677/joe.0.134r001.

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ABSTRACT Fetal growth is normally constrained by maternal factors. This constraint is demonstrated by the usual inverse linear relationship between litter size and mean fetal weight. Cross-breeding experiments between mice of lines selected for high or low plasma insulin-like growth factor (IGF-I) levels suggested that elevations in maternal IGF-I abolish (P <0.01) this constraining effect and reverse the usual positive relationship between fetal and placental size in late gestation. This was confirmed by treating mice and rats throughout pregnancy with IGF-I. In normal mice and in low IGF-I line mice treatment with IGF-I 10μg 8-hourly s.c. from day 1 to 19 of pregnancy) abolished maternal constraint whereas 0.9% (w/v) NaCl treatment did not. In Wistar rats osmotic pumps were implanted to deliver IGF-I (1μg/g body weight per day), bovine GH (bGH; 0.6μg/g body weight per day) or saline from day 1 to 19 of pregnancy. IGF-I therapy but not bGH or saline abolished (P < 0.01) maternal constraint and altered (P <0.01) the relationship between placental and fetal weight. When high or low IGF-I line mice embryos were transplanted into a normal line of mice, the expected negative relationship (P <0.05) between mean fetal weight and litter size was maintained. However the embryos of the high line were heavier (P <0.05) than those from the low line irrespective of fetal number, suggesting a direct role for IGF-I in the regulation of fetal growth. Thus both endogenous and exogenous elevations in maternal IGF-I indirectly promote fetal growth either by altering nutrient delivery to the placenta or by affecting placental function.

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Shcherbakova, Elizaveta A., Alexey N. Baranov, Pavel P. Revako, Natalya G. Istomina, and Gennady M. Burenkov. "Fetal growth restriction: ways to the solution of the problem. A literature review." Journal of obstetrics and women's diseases 71, no. 6 (February 7, 2023): 83–95. http://dx.doi.org/10.17816/jowd61809.

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Fetal growth restriction is a condition that is defined as the inability of a fetus to reach its full genetically determined growth potential. The mechanism underlying the pathogenesis is a placental dysfunction in the form of inadequate supply of oxygen and nutrients to the fetus. Clinically, this is reflected by a drop in fetal size percentiles over the course of gestation. Worldwide, fetal growth restriction is a leading cause of stillbirth, neonatal mortality and morbidity in postnatal period. Prenatal identification of fetuses with this pathology significantly reduces the incidence of adverse perinatal outcomes. However, recognizing this pathology is often a hard challenge because fetal growth cannot be assessed using only a few biometric parameters of fetal size and the fetal growth potential is hypothetical. It is also necessary to distinguish between fetal growth restriction and a fetus small for gestational age to determine the correct the management of pregnancy and the timing of delivery. In this article, we present the approaches to the management of pregnancies and deliveries in fetal growth restriction, and we identify directions for further research in this area.

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Ekin, Atalay, Cenk Gezer, Cuneyt Eftal Taner, Ulas Solmaz, Naciye Sinem Gezer, and Mehmet Ozeren. "Prognostic Value of Fetal Thymus Size in Intrauterine Growth Restriction." Journal of Ultrasound in Medicine 35, no. 3 (February 9, 2016): 511–17. http://dx.doi.org/10.7863/ultra.15.05039.

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Miyague, Nelson I., and Alessandro Ghidini. "Effect of fetal growth restriction on ultrasonographically measured cardiac size." Early Human Development 48, no. 1-2 (April 1997): 93–98. http://dx.doi.org/10.1016/s0378-3782(96)01840-3.

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Pedersen, Nina Gros, Francesc Figueras, Karen R. Wøjdemann, Ann Tabor, and Jason Gardosi. "Early Fetal Size and Growth as Predictors of Adverse Outcome." Obstetrics & Gynecology 112, no. 4 (October 2008): 765–71. http://dx.doi.org/10.1097/aog.0b013e318187d034.

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Shields, Beverley M., Beatrice A. Knight, Anita Hill, Andrew T. Hattersley, and Bijay Vaidya. "Fetal Thyroid Hormone Level at Birth Is Associated with Fetal Growth." Journal of Clinical Endocrinology & Metabolism 96, no. 6 (June 1, 2011): E934—E938. http://dx.doi.org/10.1210/jc.2010-2814.

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Context: Thyroid function is known to play an important role in fetal neurological development, but its role in regulating fetal growth is not well established. Overt maternal and fetal thyroid disorders are associated with reduced birth weight. We hypothesized that, even in the absence of overt thyroid dysfunction, maternal and fetal thyroid function influence fetal growth. Aim: In normal, healthy pregnancies, we aimed to assess whether fetal thyroid hormone at birth (as measured in cord blood) is associated with fetal growth. We also aimed to study whether fetal thyroid hormone at birth is associated with maternal thyroid hormone in the third trimester. Methods: In 616 healthy mother-child pairs, TSH, free T4 (FT4), and free T3 (FT3) were measured in mothers at 28 wk gestation and in umbilical cord blood at birth. Birth weight, length, head circumference, and tricep and bicep skinfold thicknesses were measured on the babies. Results: Cord FT4 was associated with birth weight (r = 0.25; P < 0.001), length (r = 0.17; P < 0.001), and sum of skinfolds (r = 0.19; P < 0.001). There were no associations between birth measurements and either cord TSH or cord FT3. Maternal FT4 and cord FT4 were correlated (r = 0.14; P = 0.0004), and there were weaker negative associations between maternal TSH and cord FT4 (r = −0.08; P = 0.04) and FT3 (r = −0.10; P = 0.01). Conclusion: Associations between cord FT4 and birth size suggest that fetal thyroid function may be important in regulating fetal growth, both of skeletal size and fat. The correlation between third-trimester maternal FT4 and cord FT4 supports the belief that maternal T4 crosses the placenta even in late gestation.

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Ashraf Soliman, Shayma Ahmad, Fawzia Alyafei, Nada Alaaraj, and Nada Soliman. "Maternal, placental, and fetal Insulin-Like Growth Factor-I (IGF-1) and IGF Binding proteins (IGFBPs) in Diabetic pregnancies: Effects on fetal growth and birth size." World Journal of Advanced Research and Reviews 17, no. 2 (February 28, 2023): 287–95. http://dx.doi.org/10.30574/wjarr.2023.17.2.0251.

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Introduction: During gestation, IGF1 secretion and availability in the maternal blood and at the maternal-fetal interface is mainly regulated by IGF-binding proteins (IGFBP) such as IGFBP-1 synthesized by the decidua. Data about the interaction between maternal, placental, and fetal IGF1/IGFBP in relation to fetal growth and newborn size during diabetic pregnancy (gestational Diabetes (GDM) and Type 1 DM (T1DM) is not clear. Aim of the study and Methods: We reviewed the research papers published in Pubmed, Google scholar, Research gate, and Scopus in the past 20 years on the relationship between maternal, placental, and fetal/infantile/ IGF1/IGFBP-1 in relation to birth size in pregnancies associated with maternal diabetes. Results: Twenty-eight research papers were selected and reviewed (patients’ number = 1902). In GDM pregnancies, higher maternal IGF1 levels and/or its availability due to lower IGFBP1 levels can increase the size (weight) and functions of the placenta. These include the upregulation of specific placental amino acid transporter isoforms and GLUT-1, stimulation of mTOR signaling which stimulates protein synthesis, increasing mitochondrial functions, and accelerating nutrient transport which significantly contributes to fetal growth and newborn birth size. On the other hand, in pregnant women with T1DM, lower maternal IGF1 is associated with subsequent underweight placenta and lower birthweight.

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Warshaw, Joseph B. "Intrauterine Growth Retardation." Pediatrics In Review 8, no. 4 (October 1, 1986): 107–14. http://dx.doi.org/10.1542/pir.8.4.107.

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Intrauterine growth retardation can result from a variety of environmental and genetic influences on fetal growth. The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Available data suggest that the vast majority of nutritionally growthretarded infants have normal postnatal development without significant difference in IQ or neurologic scores from normal infants. The outcome of infants in whom there is decreased growth potential relates to the condition underlying growth retardation and may, of course, result in later severe handicap. Infants with nutritional intrauterine growth retardation may exhibit decreased fetal size and sparing of brain growth as an adaptive stage in the presence of lower oxygen and substrate availability. Under such conditions, a smaller size may decrease substrate and oxygen needs and improve outcome. All infants with intrauterine growth retardation, however, require follow-up and careful developmental evaluation.

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Ashworth, Cheryl J., Margaret O. Nwagwu, and Harry J. McArdle. "Genotype and fetal size affect maternal–fetal amino acid status and fetal endocrinology in Large White×Landrace and Meishan pigs." Reproduction, Fertility and Development 25, no. 2 (2013): 439. http://dx.doi.org/10.1071/rd12024.

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This study compared maternal plasma amino acid concentrations, placental protein secretion in vitro and fetal body composition and plasma amino acid and hormone concentrations in feto–placental units from the smallest and a normally-sized fetus carried by Large White × Landrace or Meishan gilts on Day 100 of pregnancy. Compared with Large White × Landrace, Meishan placental tissue secreted more protein and Meishan fetuses contained relatively more fat and protein, but less moisture. Fetal plasma concentrations of insulin, triiodothryonine, thyroxine and insulin-like growth factor (IGF)-II were higher in Meishan than Large White × Landrace fetuses. In both breeds, fetal cortisol concentrations were inversely related to fetal size, whereas concentrations of IGF-I were higher in average-sized fetuses. Concentrations of 10 amino acids were higher in Large White × Landrace than Meishan gilts, while glutamine concentrations were higher in Meishan gilts. Concentrations of alanine, aspartic acid, glutamic acid and threonine were higher in Meishan than Large White × Landrace fetuses. Average-sized fetuses had higher concentrations of asparagine, leucine, lysine, phenylalanine, threonine, tyrosine and valine than the smallest fetus. This study revealed novel genotype and fetal size differences in porcine maternal–fetal amino acid status and fetal hormone and metabolite concentrations.

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Lord, Megan G., Sebastian Z. Ramos, Phinnara Has, Kara A. Stoever, David A. Savitz, and Matthew A. Esposito. "Fetal abdominal size and risk of unplanned cesarean in pregnancies complicated by fetal growth restriction." American Journal of Obstetrics and Gynecology 226, no. 1 (January 2022): S464—S465. http://dx.doi.org/10.1016/j.ajog.2021.11.771.

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Owen, Philip, Anthony J. Harrold, and Thomas Farrell. "Fetal size and growth velocity in the prediction of intrapartum caesarean section for fetal distress." BJOG: An International Journal of Obstetrics and Gynaecology 104, no. 4 (April 1997): 445–49. http://dx.doi.org/10.1111/j.1471-0528.1997.tb11496.x.

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Robinson, J., S. Chidzanja, K. Kind, F. Lok, P. Owens, and J. Owens. "Placental control of fetal growth." Reproduction, Fertility and Development 7, no. 3 (1995): 333. http://dx.doi.org/10.1071/rd9950333.

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The placenta exerts its effects on the growth of the fetus from the beginning of pregnancy via metabolic and endocrine mechanisms. To achieve this, the placenta exchanges a wide array of nutrients, endocrine signals, cytokines and growth factors with the mother and the fetus. These exchanges modulate or programme fetal growth and development. This review concentrates on the function and structure of the placenta in humans and in animals, and the effects of experimental perturbation of placental size and function on fetal growth. The consequences for fetal growth of varying the abundance of peptides or, by deleting genes, insulin-like growth factors or cytokines, are also described. Maternal nutritional and hormonal state from as early as the first few days after fertilization, can influence the growth rate of the placenta and the fetus and also the length of gestation. Influences on placental development and their consequences will clearly have an impact on the placental control of fetal growth. Variations in the maternal environment and consequent perturbation of the metabolic and endocrine environment of the placenta and fetus are implicated as being responsible for the associations between prenatal growth of the placenta and its fetus and the subsequent risk of adult disease. The next challenge will be to determine the dominant influences at each stage of fetal and placental growth.

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Henrichs, J., J. J. Schenk, S. J. Roza, M. P. van den Berg, H. G. Schmidt, E. A. P. Steegers, A. Hofman, V. W. V. Jaddoe, F. C. Verhulst, and H. Tiemeier. "Maternal psychological distress and fetal growth trajectories: The Generation R Study." Psychological Medicine 40, no. 4 (August 6, 2009): 633–43. http://dx.doi.org/10.1017/s0033291709990894.

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BackgroundPrevious research suggests, though not consistently, that maternal psychological distress during pregnancy leads to adverse birth outcomes. We investigated whether maternal psychological distress affects fetal growth during the period of mid-pregnancy until birth.MethodPregnant women (n=6313) reported levels of psychological distress using the Brief Symptom Inventory (anxious and depressive symptoms) and the Family Assessment Device (family stress) at 20.6 weeks pregnancy and had fetal ultrasound measurements in mid- and late pregnancy. Estimated fetal weight was calculated using head circumference, abdominal circumference and femur length.ResultsIn mid-pregnancy, maternal distress was not linked to fetal size. In late pregnancy, however, anxious symptoms were related to fetal size after controlling for potential confounders. Anxious symptoms were also associated with a 37.73 g [95% confidence interval (CI) −69.22 to −6.25, p=0.019] lower birth weight. When we related maternal distress to fetal growth curves using multilevel models, more consistent results emerged. Maternal symptoms of anxiety or depression were associated with impaired fetal weight gain and impaired fetal head and abdominal growth. For example, depressive symptoms reduced fetal weight gain by 2.86 g (95% CI −4.48 to −1.23, p<0.001) per week.ConclusionsThe study suggests that, starting in mid-pregnancy, fetal growth can be affected by different aspects of maternal distress. In particular, children of prenatally anxious mothers seem to display impaired fetal growth patterns during pregnancy. Future work should address the biological mechanisms underlying the association of maternal distress with fetal development and focus on the effects of reducing psychological distress in pregnancy.

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Phillips, David I. W., Michael J. Davies, and Jeffrey S. Robinson. "Fetal Growth and the Fetal Origins Hypothesis in Twins — Problems and Perspectives." Twin Research 4, no. 5 (October 1, 2001): 327–31. http://dx.doi.org/10.1375/twin.4.5.327.

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AbstractAlthough there is substantial evidence from studies of singletons that small size at birth is linked with long-term adverse health effects, until recently little was known as to whether these associations extend to twins. A review of published studies suggests that at present there is little consistent evidence that birthsize in twins is associated with increased morbidity or morality. While, these findings may reflect methodological limitations, it is also argued that they arise as a consequence of the substantially different biology of fetal growth in twins.

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Pölzlberger, Eva, Beda Hartmann, Erich Hafner, Ingrid Stümpflein, and Sylvia Kirchengast. "MATERNAL HEIGHT AND PRE-PREGNANCY WEIGHT STATUS ARE ASSOCIATED WITH FETAL GROWTH PATTERNS AND NEWBORN SIZE." Journal of Biosocial Science 49, no. 3 (October 3, 2016): 392–407. http://dx.doi.org/10.1017/s0021932016000493.

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SummaryThe impact of maternal height, pre-pregnancy weight status and gestational weight gain on fetal growth patterns and newborn size was analysed using a dataset of 4261 singleton term births taking place at the Viennese Danube Hospital between 2005 and 2013. Fetal growth patterns were reconstructed from three ultrasound examinations carried out at the 11th/12th, 20th/21th and 32th/33th weeks of gestation. Crown–rump length, biparietal diameter, fronto-occipital diameter, head circumference, abdominal transverse diameter, abdominal anterior–posterior diameter, abdominal circumference and femur length were determined. Birth weight, birth length and head circumference were measured immediately after birth. The vast majority of newborns were of normal weight, i.e. between 2500 and 4000 g. Maternal height showed a just-significant but weak positive association (r=0.03: p=0.039) with crown–rump length at the first trimester and with the majority of fetal parameters at the second trimester (r>0.06; p<0.001) and third trimester (r>0.09; p<0.001). Pre-pregnancy weight status was significantly positively associated with nearly all fetal dimensions at the third trimester (r>0.08; p<0.001). Maternal height (r>0.17; p<0.001) and pre-pregnancy weight status (r>0.13; p<0.001), but also gestational weight gain (r>0.13; p<0.001), were significantly positively associated with newborn size. Some of these associations were quite weak and the statistical significance was mainly due to the large sample size. The association patterns between maternal height and pre-pregnancy weight status with fetal growth patterns (p<0.001), as well as newborn size (p<0.001), were independent of maternal age, nicotine consumption and fetal sex. In general, taller and heavier women gave birth to larger infants. This association between maternal size and fetal growth patterns was detectable from the first trimester onwards.

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Veille, J., R. Hanson, M. Sivakoff, H. Hoen, and M. Ben-Ami. "Fetal Cardiac Size in Normal, Intrauterine Growth Retarded, and Diabetic Pregnancies." American Journal of Perinatology 10, no. 04 (July 1993): 275–79. http://dx.doi.org/10.1055/s-2007-994739.

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O'Gorman, Neil, and Laurent J. Salomon. "Fetal biometry to assess the size and growth of the fetus." Best Practice & Research Clinical Obstetrics & Gynaecology 49 (May 2018): 3–15. http://dx.doi.org/10.1016/j.bpobgyn.2018.02.005.

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Airoldi, J., D. C. Wood, A. Ness, E. Done, V. Berghella, R. J. Librizzi, R. J. Bolognese, and S. Weiner. "P10.27: The size of the ductus venosus in fetal growth restriction." Ultrasound in Obstetrics and Gynecology 26, no. 4 (September 2005): 445. http://dx.doi.org/10.1002/uog.2490.

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Wilson, Roneé E., Hamisu M. Salihu, Maureen W. Groer, Getachew Dagne, Kathleen O’Rourke, and Alfred K. Mbah. "Impact of Maternal Thyroperoxidase Status on Fetal Body and Brain Size." Journal of Thyroid Research 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/872410.

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The obstetric consequences of abnormal thyroid function during pregnancy have been established. Less understood is the influence of maternal thyroid autoantibodies on infant outcomes. The objective of this study was to examine the influence of maternal thyroperoxidase (TPO) status on fetal/infant brain and body growth. Six-hundred thirty-one (631) euthyroid pregnant women were recruited from prenatal clinics in Tampa Bay, Florida, and the surrounding area between November 2007 and December 2010. TPO status was determined during pregnancy and fetal/infant brain and body growth variables were assessed at delivery. Regression analysis revealed maternal that TPO positivity was significantly associated with smaller head circumference, reduced brain weight, and lower brain-to-body ratio among infants born to TPO+ white, non-Hispanic mothers only, distinguishing race/ethnicity as an effect modifier in the relationship. No significant differences were noted in body growth measurements among infants born to TPO positive mothers of any racial/ethnic group. Currently, TPO antibody status is not assessed as part of the standard prenatal care laboratory work-up, but findings from this study suggest that fetal brain growth may be impaired by TPO positivity among certain populations; therefore autoantibody screening among high-risk subgroups may be useful for clinicians to determine whether prenatal thyroid treatment is warranted.

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Ashraf Soliman, Noor Hamed, Fawzia Alyafei, Nada Alaaraj, Shayma Ahmad, Maya Itani, and Nada Soliman. "Insulin like growth factor 1 (IGF-1) and IGF binding proteins in obese pregnant women and their babies: Potential effects on placental function and fetal growth." World Journal of Advanced Research and Reviews 17, no. 2 (February 28, 2023): 093–100. http://dx.doi.org/10.30574/wjarr.2023.17.2.0222.

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Introduction: The placenta expresses significant amounts of insulin and IGF1 receptors at distinct locations on both fetal and maternal surfaces. This makes the IGF1 and the insulin receptor accessible to fetal and/or maternal insulin, IGF1 and IGF2. IGFs are involved in the receptor-mediated regulation of placental growth and transport, and placental angiogenesis. Maternal obesity during gestation mediates significant changes in the metabolism of mothers, placentas as well as fetal growth. Objectives: In obese women. the role of the insulin like growth factor system IGFs, IGF receptors, IGF-binding proteins (IGFBPs) and IGFBP proteases during gestation, and their effect on placental growth and fetal anthropometric changes need further clarification. In this update we reviewed the literature on the detected changes in the maternal and fetal IGFs in relation to placental growth and function and to fetal growth and newborn size in pregnant obese mothers. Eighteen research articles fitted the criteria of this update. Results: Twenty-three research papers were including 2817 pregnant obese and non-obese women (controls) and their babies were selected and reviewed. Results showed that obesity and excessive nutrient intake during gestation increase maternal IGF1and decreases IGBP1. Increased maternal IGF1 and/or its availability due to decreased IGFBP1 can increase the size (weight) and development of the placenta, stimulate mTOR signaling which stimulates protein synthesis, mitochondrial function, and upregulate specific placental amino acid transporter isoforms (amino acids transport), GLUT-1, (glucose transport) and possibly lipid transport to the fetus which can induce fetal IGF1 secretion and lead to overgrowth. Conclusions: In obese women during pregnancy, increased level of IGF1 and/or its availability due to decreased IGFBP1 can increase the size (weight) and development of the placenta, stimulate mTOR signaling which stimulates protein synthesis, mitochondrial function, and upregulate placental transport of amino acids, glucose and possibly fatty acids.

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Heese, Sandra, Kerstin Hammer, Mareike Möllers, Helen A. Köster, Maria K. Falkenberg, Maria Eveslage, Janina Braun, Kathrin Oelmeier de Murcia, Walter Klockenbusch, and Ralf Schmitz. "Adrenal gland size in growth restricted fetuses." Journal of Perinatal Medicine 46, no. 8 (October 25, 2018): 900–904. http://dx.doi.org/10.1515/jpm-2017-0339.

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Abstract Objective To compare the adrenal gland size of fetal growth restricted (FGR) and normal control fetuses. Study design In this prospective study the adrenal gland size of 63 FGR fetuses and 343 normal controls was measured between 20 and 41 weeks of gestation. The total width and the medulla width were measured in a new standardized transversal plane. The cortex width and a calculated ratio of the total and medulla width (adrenal gland ratio) were compared between both groups. Results The mean cortex width and the adrenal gland ratio in FGR fetuses were higher in comparison to the controls (P<0.001; P=0.036, respectively). The cortex width correlated positively with the gestational age (control group: P<0.001; FGR group: P=0.089) whilst the adrenal gland ratio showed no association with the gestational age (control group: P=0.153; FGR group: P=0.314). Conclusion The adrenal gland cortex width and the adrenal gland ratio were increased in FGR fetuses compared to normal fetuses.

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Jin, Danyao, Janet Wilson Rich-Edwards, Chunyi Chen, Yue Huang, Yinping Wang, Xiangrong Xu, Jue Liu, et al. "Gestational Diabetes Mellitus: Predictive Value of Fetal Growth Measurements by Ultrasonography at 22–24 Weeks: A Retrospective Cohort Study of Medical Records." Nutrients 12, no. 12 (November 27, 2020): 3645. http://dx.doi.org/10.3390/nu12123645.

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Early intervention of gestational diabetes mellitus (GDM) is effective in reducing pregnancy disorders. Fetal growth, measured by routine ultrasound scan a few weeks earlier before GDM diagnosis, might be useful to identify women at high risk of GDM. In the study, generalized estimating equations were applied to examine the associations between ultrasonic indicators of abnormal fetal growth at 22–24 weeks and the risk of subsequent GDM diagnosis. Of 44,179 deliveries, 8324 (18.8%) were diagnosed with GDM between 24 and 28 weeks. At 22–24 weeks, fetal head circumference (HC) < 10th, fetal femur length (FL) < 10th, and estimated fetal weight (EFW) < 10th percentile were associated with 13% to 17% increased risks of maternal GDM diagnosis. Small fetal size appeared to be especially predictive of GDM among women who were parous. Fetal growth in the highest decile of abdominal circumference (AC), HC, FL and EFW was not associated with risk of subsequent GDM. The observed mean difference in fetal size across gestation by GDM was small; there was less than 1 mm difference for AC, HC, and FL, and less than 5 g for EFW before 24 weeks. Despite similar mean fetal growth among women who were and were not later diagnosed with GDM, mothers with fetuses in the lowest decile of HC, FL and EFW at 22–24 weeks tended to have higher risk of GDM.

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Halley, Andrew C. "Minimal variation in eutherian brain growth rates during fetal neurogenesis." Proceedings of the Royal Society B: Biological Sciences 284, no. 1854 (May 10, 2017): 20170219. http://dx.doi.org/10.1098/rspb.2017.0219.

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A central question in the evolution of brain development is whether species differ in rates of brain growth during fetal neurogenesis. Studies of neonatal data have found allometric evidence for brain growth rate differences according to physiological variables such as relative metabolism and placental invasiveness, but these findings have not been tested against fetal data directly. Here, we measure rates of exponential brain growth acceleration in 10 eutherian mammals, two marsupials, and two birds. Eutherian brain acceleration exhibits minimal variation relative to body and visceral organ growth, varies independently of correlated growth patterns in other organs, and is unrelated to proposed physiological constraints such as metabolic rate or placental invasiveness. Brain growth rates in two birds overlap with eutherian variation, while marsupial brain growth is exceptionally slow. Peak brain growth velocity is linked in time with forebrain myelination and eye opening, reliably separates altricial species born before it from precocial species born afterwards, and is an excellent predictor of adult brain size ( r 2 = 0.98). Species with faster body growth exhibit larger relative brain size in early ontogeny, while brain growth is unrelated to allometric measures. These findings indicate a surprising conservation of brain growth rates during fetal neurogenesis in eutherian mammals, clarify sources of variation in neonatal brain size, and suggest that slow body growth rates cause species to be more encephalized at birth.

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Bale, Laurie K., and Cheryl A. Conover. "Disruption of insulin-like growth factor-II imprinting during embryonic development rescues the dwarf phenotype of mice null for pregnancy-associated plasma protein-A." Journal of Endocrinology 186, no. 2 (August 2005): 325–31. http://dx.doi.org/10.1677/joe.1.06259.

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Pregnancy-associated plasma protein-A (PAPP-A), an insulin-like growth factor-binding protein (IGFBP) protease, increases insulin-like growth factor (IGF) activity through cleavage of inhibitory IGFBP-4 and the consequent release of IGF peptide for receptor activation. Mice homozygous for targeted disruption of the PAPP-A gene are born as proportional dwarfs and exhibit retarded bone ossification during fetal development. Phenotype and in vitro data support a model in which decreased IGF-II bioavailability during embryogenesis results in growth retardation and reduction in overall body size. To test the hypothesis that an increase in IGF-II during embryogenesis would overcome the growth deficiencies, PAPP-A-null mice were crossed with ΔH19 mutant mice, which have increased IGF-II expression and fetal overgrowth due to disruption of IgfII imprinting. ΔH19 mutant mice were 126% and PAPP-A-null mice were 74% the size of controls at birth. These size differences were evident at embryonic day 16.5. Importantly, double mutants were indistinguishable from controls both in terms of size and skeletal development. Body size programmed during embryo development persisted post-natally. Thus, disruption of IgfII imprinting and consequent elevation in IGF-II during fetal development was associated with rescue of the dwarf phenotype and ossification defects of PAPP-A-null mice. These data provide strong genetic evidence that PAPP-A plays an essential role in determining IGF-II bioavailability for optimal fetal growth and development.

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Owens, J. A., K. L. Kind, F. Carbone, J. S. Robinson, and P. C. Owens. "Circulating insulin-like growth factors-I and -II and substrates in fetal sheep following restriction of placental growth." Journal of Endocrinology 140, no. 1 (January 1994): 5–13. http://dx.doi.org/10.1677/joe.0.1400005.

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Abstract To determine the relationship between placental delivery of oxygen and glucose, circulating insulin-like growth factors (IGFs) and fetal growth, the effect of variable restriction of placental growth was determined in sheep in late gestation. Arterial blood was obtained via indwelling catheters at 120 and 127 days of gestation, prior to necropsy at 130 days to measure fetal and placental weights. Plasma was acidified and subjected to size-exclusion high-performance liquid chromatography at pH 2·8 to dissociate and separate IGFs from their binding proteins. The acid-dissociated IGF fraction was analysed by sensitive and highly specific radioligand assays for IGF-I and IGF-II, previously defined using ovine IGFs. Fetal weight and blood pO2 and glucose at 120 and 127 days of gestation correlated positively with placental weight. Plasma IGF-I was positively associated with fetal weight and fetal liver weight, and with blood pO2 and glucose at both ages. Plasma IGF-II levels also correlated positively with fetal weight, fetal liver weight and with blood glucose and pO2, but only at 127 days of gestation. In the most severely growth-retarded fetal sheep, blood glucose and pO2 and plasma IGF-I were significantly reduced when compared with normal fetuses at 120 days. All decreased further by 127 days of gestation as did plasma IGF-II in severely growth-retarded fetal sheep compared with normal fetuses. These observations are consistent with the hypothesis that both IGF-I and IGF-II are chronically regulated by oxygen and nutrition in utero and mediate part of the influence of placental supply of substrate over fetal growth. Journal of Endocrinology (1994) 140, 5–13

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Talmor, Alon, Anneleen Daemen, Edile Murdoch, Hannah Missfelder-Lobos, Dirk Timmerman, Tom Bourne, Dino A. Giussani, and Christoph Lees. "Defining the relationship between fetal Doppler indices, abdominal circumference and growth rate in severe fetal growth restriction using functional linear discriminant analysis." Journal of The Royal Society Interface 10, no. 88 (November 6, 2013): 20130376. http://dx.doi.org/10.1098/rsif.2013.0376.

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The relationship between Doppler measurements, size and growth rate in fetal growth restriction has not been defined. We used functional linear discriminant analysis (FLDA) to investigate these parameters taking account of the difficulties inherent in exploring relationships between repeated observations from a small number of cases. In 40 fetuses with severe growth restriction, serial abdominal circumference (AC), umbilical, middle cerebral artery (MCA) and ductus venosus Doppler pulsatility index measurements were recorded. In 11 singleton fetuses with normal growth, umbilical artery pulsatility index only was measured. Data were expressed as z -scores in relation to gestation and analysed longitudinally using FLDA. In severe growth restriction, the Spearman correlation coefficients between umbilical artery pulsatility index and AC z -score, MCA pulsatility index and AC z -score and ductus venosus pulsatility index z -score and AC z -score were, respectively: −0.36, p = 4.4 × 10 −7 ; 0.70, p = 1.1 × 10 −17 and −0.50, p = 8.1 × 10 −4 . No relationship was seen between Doppler parameters and growth rate. There was no relationship between umbilical artery pulsatility index and AC nor growth rate in normally grown fetuses. In severe fetal growth restriction, Doppler changes are related to absolute fetal AC size, not growth rate.

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Jeckel, K. M., A. C. Boyarko, G. J. Bouma, Q. A. Winger, and R. V. Anthony. "Chorionic somatomammotropin impacts early fetal growth and placental gene expression." Journal of Endocrinology 237, no. 3 (June 2018): 301–10. http://dx.doi.org/10.1530/joe-18-0093.

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Several developmental windows, including placentation, must be negotiated to establish and maintain pregnancy. Impaired placental function can lead to preeclampsia and/or intrauterine growth restriction (IUGR), resulting in increased infant mortality and morbidity. It has been hypothesized that chorionic somatomammotropin (CSH) plays a significant role in fetal development, potentially by modifying maternal and fetal metabolism. Recently, using lentiviral-mediated in vivo RNA interference in sheep, we demonstrated significant reductions in near-term (135 days of gestation; dGA) fetal and placental size, and altered fetal liver gene expression, resulting from CSH deficiency. We sought to examine the impact of CSH deficiency on fetal and placental size earlier in gestation (50 dGA), and to examine placental gene expression at 50 and 135 dGA. At 50 dGA, CSH-deficient pregnancies exhibited a 41% reduction (P ≤ 0.05) in uterine vein concentrations of CSH, and significant (P ≤ 0.05) reductions (≈21%) in both fetal body and liver weights. Placentae harvested at 50 and 135 dGA exhibited reductions in IGF1 and IGF2 mRNA concentrations, along with reductions in SLC2A1 and SLC2A3 mRNA. By contrast, mRNA concentrations for various members of the System A, System L and System y+ amino acid transporter families were not significantly impacted. The IUGR observed at the end of the first-third of gestation indicates that the near-term IUGR reported previously, began early in gestation, and may have in part resulted from deficits in the paracrine action of CSH within the placenta. These results provide further compelling evidence for the importance of CSH in the progression and outcome of pregnancy.

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Vatnick, I., and A. W. Bell. "Ontogeny of fetal hepatic and placental growth and metabolism in sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 3 (September 1, 1992): R619—R623. http://dx.doi.org/10.1152/ajpregu.1992.263.3.r619.

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Ontogeny of fetal hepatic and placental growth and in vitro oxygen consumption (VO2) was investigated in fetal lambs at 75, 100, and 136 days postconception. Fetal hepatic relative weight and placental absolute and relative weights declined during this period. Oxygen consumption per gram dry weight of fetal liver and maternal placenta declined between mid and late gestation while fetal placental VO2 was unchanged. Estimated VO2 of the whole placenta did not change while the estimated total hepatic VO2 increased more than threefold between 75 and 136 days. Total hepatic VO2 was highly correlated with total placental VO2 at 136 days (r = 0.84). The results suggest that the placenta reaches its maximum growth and metabolic capacity before 100 days and possibly at or before midgestation. Changes in hepatic weight-specific total VO2, in addition to the declining relative size of the fetal liver, must contribute to the progressive decline in metabolic rate of the whole fetus during the second half of pregnancy. Correlations between placental and fetal liver weights and metabolic rates suggest the possibility of placental regulation of fetal hepatic growth and metabolism.

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Swanson, A. M., V. Mehta, K. Ofir, M. Rowe, C. Rossi, Y. Ginsberg, H. Griffin, et al. "The use of ultrasound to assess fetal growth in a guinea pig model of fetal growth restriction." Laboratory Animals 51, no. 2 (July 9, 2016): 181–90. http://dx.doi.org/10.1177/0023677216637506.

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Fetal growth restriction (FGR) is a common and potentially severe pregnancy complication. Currently there is no treatment available. The guinea pig is an attractive model of human pregnancy as placentation is morphologically very similar between the species. Nutrient restriction of the dam creates growth-restricted fetuses while leaving an intact uteroplacental circulation, vital for evaluating novel therapies for FGR. Growth-restricted fetuses were generated by feeding Dunkin Hartley guinea pig dams 70% of ad libitum intake from four weeks before and throughout pregnancy. The effect of maternal nutrient restriction (MNR) on dams and fetuses was carefully monitored, and ultrasound measurements of pups collected. There was no difference in maternal weight at conception, however by five weeks post conception MNR dams were significantly lighter ( P < 0.05). MNR resulted in significantly smaller pup size from 0.6–0.66 gestation. Ultrasound is a powerful non-invasive tool for assessing the effect of therapeutic interventions on fetal growth, allowing longitudinal measurement of fetuses. This model and method yield data applicable to the human condition without the need for animal sacrifice and will be useful in the translation of therapies for FGR into the clinic.

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Kitterman, Joseph A. "Physiological factors in fetal lung growth." Canadian Journal of Physiology and Pharmacology 66, no. 8 (August 1, 1988): 1122–28. http://dx.doi.org/10.1139/y88-184.

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Adequate pulmonary function at birth depends upon a mature surfactant system and lungs of normal size. Surfactant is controlled primarily by hormonal factors, especially from the hypophysis, adrenal, and thyroid; but these have little influence on fetal lung growth. In contrast, current data indicate that lung growth is determined by the following physical factors that permit the lungs to express their inherent growth potential. (a) Adequate intrathoracic space: lesions that decrease intrathoracic space impede lung growth, apparently by physical compression. (b) Adequate amount of amniotic fluid: oligohydramnios retards lung growth, possibly by lung compression or by affecting fetal breathing movements or the volume of fluid within the potential airways and airspaces. (c) Fetal breathing movements of normal incidence and amplitude: fetal breathing movements stimulate lung growth, possibly by stretching the pulmonary tissue, and do not affect mean pulmonary blood flow but do induce small changes in phasic flow; these changes are probably too slight to influence lung growth. (d) Normal balance of volumes and pressures within the potential airways and airspaces: in the fetus, tracheal pressure > amniotic pressure > pleural pressure. This differential produces a distending pressure which may promote lung growth. Disturbing the normal pressure relationships alters the volume of fluid in the lungs and distorts lung growth, which is stimulated by distending the lungs and is impeded by decreasing lung fluid volume. The mechanisms by which these factors affect lung growth remain to be defined. Fetal lung growth also depends on at least a small amount of blood flow through the pulmonary arteries. Although a modest reduction in flow (to 85% of control) does not affect lung growth, total obstruction of the pulmonary artery impairs lung growth. Thus, bronchial blood flow alone is insufficient to supply the nutritional demands of the growing fetal lung.

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Bernstein, Ira M., Gregory Mohs, Mark Rucquoi, and Gary J. Badger. "Case for Hybrid “Fetal Growth Curves”: A Populatiori-Based Estimation of Normal Fetal Size Across Gestational Age." Journal of Maternal-Fetal and Neonatal Medicine 5, no. 3 (January 1996): 124–27. http://dx.doi.org/10.3109/14767059609025411.

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Bernstein, Ira M., Gregory Mohs, Mark Rucquoi, and Gary J. Badger. "Case for hybrid ?fetal growth curves?: A population-based estimation of normal fetal size across gestational age." Journal of Maternal-Fetal Medicine 5, no. 3 (May 1996): 124–27. http://dx.doi.org/10.1002/(sici)1520-6661(199605/06)5:3<124::aid-mfm5>3.0.co;2-o.

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Greenwood, Paul L., Ramona M. Slepetis, and Alan W. Bell. "Influences on fetal and placental weights during mid to late gestation in prolific ewes well nourished throughout pregnancy." Reproduction, Fertility and Development 12, no. 4 (2000): 149. http://dx.doi.org/10.1071/rd00053.

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This study investigated associations between fetal and placental weights from 85 to 130 days gestation in 49 fetuses from 21 ewes of a prolific genotype used as an experimental model of intrauterine growth retardation. The proportion of variation in fetal weight explained by placental weight increased from zero at 85 days to 91% (residual standard deviation (RSD) = 260 g) at 130 days. Overall, stage of pregnancy plus placental weight accounted for 96% of fetal weight variation (RSD = 212 g). Litter size and number of fetuses per uterine horn also influnced individual fetal weights. Gestational age, litter size, placental weight per ewe, and liveweight and condition score of ewes during early to mid gestation (initial LW and CS) explained 99.5% of the variation in fetal weight per ewe (RSD = 236 g). Most variation (86%) in placental weight was explained by stage of pregnancy, litter size, number of placentomes, and initial LW and CS (RSD = 53 g). Placental weight per ewe was influenced by stage of pregancy, litter size and initial ewe LW and CS (R 2 = 0.97; RSD = 89 g). The association of fetal and placental weights with initial ewe LW was positive, and with initial CS was negative. The results show that in the absence of overt nutritional restriction of pregnant ewes, fetal and placental weights are tightly coupled during late gestation and ewe fatness during early pregnancy is inversely related to placental and fetal weights. They demonstrate that placental weight explains most of the variation in fetal weight in the present intrauterine growth retardation model.

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Murotsuki, J., J. R. Challis, V. K. Han, L. J. Fraher, and R. Gagnon. "Chronic fetal placental embolization and hypoxemia cause hypertension and myocardial hypertrophy in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 1 (January 1, 1997): R201—R207. http://dx.doi.org/10.1152/ajpregu.1997.272.1.r201.

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To examine the cardiovascular effects on the fetus of an elevated umbilical vascular resistance resulting in fetal hypoxemia, we embolized the fetal side of the placenta in pregnant sheep and measured cardiovascular and hormonal changes and cellular growth in fetal heart. Chronically catheterized fetal sheep were embolized (n = 6) for 21 days between 0.74 and 0.88 of gestation into the descending aorta until arterial oxygen content was decreased by 40-50% of the preembolization value. Control animals (n = 6) received saline only. During embolization, fetuses became chronically hypoxemic (P < 0.001) and hypertensive (P < 0.001), with a progressive increase in umbilical artery resistance index (P < 0.001). There was also an increase in fetal plasma norepinephrine throughout the study period (P < 0.05). On day 21 of embolization, fetuses showed asymmetrical growth restriction, increased heart weight (P < 0.01), and increase in right and left ventricular wall thickness (P < 0.05) compared with control animals. The protein-to-DNA ratio, an index of cell size, increased in the right ventricular myocardium in the embolized group (P < 0.001), suggesting myocardial cell hypertrophy. We conclude that, during chronic placental damage leading to fetal hypoxemia with an increase in umbilical artery resistance index, fetuses developed arterial hypertension and asymmetrical growth restriction and that increases in afterload to the heart and plasma norepinephrine likely caused fetal myocardial hypertrophy.

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Bloomfield, Frank H., Pierre L. van Zijl, Michael K. Bauer, and Jane E. Harding. "A chronic low dose infusion of insulin-like growth factor I alters placental function but does not affect fetal growth." Reproduction, Fertility and Development 14, no. 7 (2002): 393. http://dx.doi.org/10.1071/rd02022.

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Knowledge of the anabolic effects of insulin-like growth factor I (IGF-I) on fetal growth and feto–placental metabolism are derived from studies using large doses of IGF-I. Low doses of enteral IGF-I have trophic effects on the fetal gut, but there are no data on the effects of systemic low doses of IGF-I on fetal growth and feto–placental metabolism. We therefore compared the effects of a chronic infusion of low dose IGF-I (50�μg�day–1, n = 7) with vehicle-infused controls (n = 7) on fetal growth, metabolism and placental transfer capacity in the chronically instrumented late gestation ovine fetus (121–132 days of gestation; term = 145 days). Insulin-like growth factor I infusion did not affect fetal growth or the size of individual organs, including liver, spleen and bone. Placental morphology was altered, and placental clearances of 3-O-[methyl-3H]D-glucose (a non-metabolizable glucose analogue) and [methyl14C]aminoisobutyric acid (a non-metabolizable analogue of amino acids utilizing the system A transporter), were reduced in IGF-I-treated fetuses (P<0.05 v. control). However, fetal and placental metabolite uptake was not significantly different between groups. We conclude that, despite altering placental transfer capacity and morphology, a chronic low dose infusion of IGF-I does not alter fetal growth or metabolism.

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Reeves, Shane, and Ira Bernstein. "Effects of maternal tobacco-smoke exposure on fetal growth and neonatal size." Expert Review of Obstetrics & Gynecology 3, no. 6 (November 2008): 719–30. http://dx.doi.org/10.1586/17474108.3.6.719.

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Journal articles on the topic 'Fetal size/growth'

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