scholarly journals The effects of intrauterine growth restriction and antenatal glucocorticoids on ovine fetal lung development

2012 ◽  
Vol 71 (6) ◽  
pp. 689-696 ◽  
Author(s):  
Amy E. Sutherland ◽  
Kelly J. Crossley ◽  
Beth J. Allison ◽  
Graham Jenkin ◽  
Euan M. Wallace ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Lung Development ◽  
Fetal Lung ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Fetal Lung Development ◽  
Ovine Fetal

scholarly journals VP38.03: Fetal lung assessment using T2*‐MR in intrauterine growth restriction

2020 ◽  
Vol 56 (S1) ◽  
pp. 223-223
Author(s):  
K. Vellvé ◽  
F. Crovetto ◽  
M. Schabel ◽  
A. Nakaki ◽  
V. Roberts ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Fetal Lung ◽  
Growth Restriction ◽  
Intrauterine Growth

Effects of intrauterine growth restriction on lung liquid dynamics and lung development in fetal sheep

2001 ◽  
Vol 184 (2) ◽  
pp. 209-216 ◽  
Author(s):  
Megan L. Cock ◽  
Cheryl A. Albuquerque ◽  
Belinda J. Joyce ◽  
Stuart B. Hooper ◽  
Richard Harding
Keyword(s):  
Intrauterine Growth Restriction ◽  
Lung Development ◽  
Growth Restriction ◽  
Fetal Sheep ◽  
Intrauterine Growth ◽  
Lung Liquid ◽  
Liquid Dynamics

Effects of intrauterine growth restriction during late pregnancy on the ovine fetal renal function and antioxidant capacity

2021 ◽  
Vol 92 (1) ◽  
Author(s):  
Yang Zi ◽  
Chi Ma ◽  
Huimin Li ◽  
Suting Shen ◽  
Yingchun Liu ◽  
...  
Keyword(s):  
Renal Function ◽  
Antioxidant Capacity ◽  
Intrauterine Growth Restriction ◽  
Late Pregnancy ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Ovine Fetal

4D-5 Intrauterine growth restriction alters fetal lung programming by affecting essential epithelial-mesenchymal signaling pathways

2007 ◽  
Vol 83 ◽  
pp. S68-S69
Author(s):  
A. Karadag ◽  
R. Sakurai ◽  
J. Belperio ◽  
H. Guang ◽  
M. Desai ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Intrauterine Growth Restriction ◽  
Fetal Lung ◽  
Growth Restriction ◽  
Intrauterine Growth

Effects of intrauterine growth restriction during late pregnancy on the cell apoptosis and related gene expression in ovine fetal liver

2017 ◽  
Vol 90 ◽  
pp. 204-209 ◽  
Author(s):  
Yingchun Liu ◽  
Chi Ma ◽  
Hui Li ◽  
Lingyao Li ◽  
Feng Gao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Apoptosis ◽  
Intrauterine Growth Restriction ◽  
Fetal Liver ◽  
Late Pregnancy ◽  
Growth Restriction ◽  
Related Gene ◽  
Intrauterine Growth ◽  
Ovine Fetal

scholarly journals Role of miR-29 in mediating offspring lung phenotype in a rodent model of intrauterine growth restriction

2018 ◽  
Vol 315 (5) ◽  
pp. R1017-R1026 ◽  
Author(s):  
Tsai-Der Chuang ◽  
Reiko Sakurai ◽  
Ming Gong ◽  
Omid Khorram ◽  
Virender K. Rehan
Keyword(s):  
Intrauterine Growth Restriction ◽  
Lung Development ◽  
Molecular Mechanisms ◽  
Vascular Tissue ◽  
Growth Restriction ◽  
Lung Fibroblasts ◽  
Intrauterine Growth ◽  
Maternal Undernutrition ◽  
Ecm Proteins

Considerable epidemiological and experimental evidence supports the concept that the adult chronic lung disease (CLD), is due, at least in part, to aberrations in early lung development in response to an abnormal intrauterine environment; however, the underlying molecular mechanisms remain unknown. We used a well-established rat model of maternal undernutrition (MUN) during pregnancy that results in offspring intrauterine growth restriction (IUGR) and adult CLD to test the hypothesis that in response to MUN, excess maternal glucocorticoids (GCs) program offspring lung development to a CLD phenotype by altering microRNA (miR)-29 expression, which is a key miR in regulating extracellular matrix (ECM) deposition during development and injury-repair. At postnatal day 21 and 5 mo, compared with the control offspring lung, MUN offspring lung miR-29 expression was significantly decreased in conjunction with an elevated expression of multiple downstream target ECM proteins [collagen (COL)1A1, COL3A1, COL4A5, and elastin], at both mRNA and protein levels. Importantly, MUN-induced changes in miR-29 and target gene expressions were at least partially blocked in the lungs of offspring of MUN dams treated with metyrapone, a selective GC synthesis inhibitor. Furthermore, dexamethasone treatment of cultured fetal rat lung fibroblasts significantly induced miR-29 expression along with the suppression of target ECM proteins. These data, along with the previously known role of miR-29 in regulating ECM deposition in vascular tissue in the MUN offspring, suggest miR-29 to be a common mechanistic denominator for the vascular and pulmonary phenotypes in the IUGR offspring, providing a novel potential therapeutic target.

Pathological features of the sequence in pregnant women with delayed fetal growth

2019 ◽  
pp. 50-54
Author(s):  
V.O. Golyanovskiy ◽  
◽  
Ye.O. Didyk ◽  
Keyword(s):  
Pregnant Women ◽  
Intrauterine Growth Restriction ◽  
Normal Development ◽  
Intrauterine Infection ◽  
Normal Pregnancy ◽  
Growth Restriction ◽  
Control Group ◽  
Intrauterine Growth ◽  
Increased Risk ◽  
Infection And Inflammation

Pregnant women with intrauterine growth restriction (IUGR) have an increased risk of adverse perinatal and long-term complications compared with the birth of children with normal body weight. Thus, IUGR is one of the main challenges for the global health system, especially in poor and developing countries. Morpho-functional studies of the placentas help in determining the causes of IUGR, and therefore, timely prevent complications in pregnant women with IUGR. The objective: The purpose of this study is to investigate various morphometric and pathomorphological changes in the placenta, including inflammatory, in cases of IUGR, and to establish a correlation of these results with the etiology and complications for the fetus. Materials and methods. In the current study, 54 placentas of the fetuses with IUGR (the main group) were compared with 50 placentas of the fetuses with normal development (control group). The criteria for the inclusion of IUGR were gestational age more than 30 weeks and all fetuses with a weight less than 10th percentile for this period of pregnancy. The placenta material was studied pathomorphologically with laboratory screening for infection and inflammation. Similarly, the results were determined for placentas of the fetuses with normal development compared to placentas with IUGR. Results. The placenta study showed the presence of calcification in the case of IUGR, as well as in the case of prolonged pregnancy. However, calcification of the placenta in the case of IUGR was more progressive compared with placenta in the normal pregnancy. In addition, the presence of intrauterine infection and inflammation was observed, which could also lead to an adverse outcome for the further progression of pregnancy with IUGR. Conclusion. A comparative macro- and microscopic pathomorphological study of the placentas in the two groups has shown a significant increase in the pathological changes in all the anatomical structures of the fetuses with IUGR. Key words: Intrauterine growth restriction (IUGR), fetal weight, pathomorphological changes of the placenta.

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