scholarly journals Extrinsic Factors Influencing Fetal Deformations and Intrauterine Growth Restriction

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Wendy Moh ◽  
John M. Graham ◽  
Isha Wadhawan ◽  
Pedro A. Sanchez-Lara

The causes of intrauterine growth restriction (IUGR) are multifactorial with both intrinsic and extrinsic influences. While many studies focus on the intrinsic pathological causes, the possible long-term consequences resulting from extrinsic intrauterine physiological constraints merit additional consideration and further investigation. Infants with IUGR can exhibit early symmetric or late asymmetric growth abnormality patterns depending on the fetal stage of development, of which the latter is most common occurring in 70–80% of growth-restricted infants. Deformation is the consequence of extrinsic biomechanical factors interfering with normal growth, functioning, or positioning of the fetus in utero, typically arising during late gestation. Biomechanical forces play a critical role in the normal morphogenesis of most tissues. The magnitude and direction of force impact the form of the developing fetus, with a specific tissue response depending on its pliability and stage of development. Major uterine constraining factors include primigravida, small maternal size, uterine malformation, uterine fibromata, early pelvic engagement of the fetal head, aberrant fetal position, oligohydramnios, and multifetal gestation. Corrective mechanical forces similar to those that gave rise to the deformation to reshape the deformed structures are often used and should take advantage of the rapid postnatal growth to correct form.

2020 ◽  
Vol 598 (12) ◽  
pp. 2469-2489 ◽  
Author(s):  
Stephanie S. Chassen ◽  
Veronique Ferchaud‐Roucher ◽  
Claire Palmer ◽  
Cun Li ◽  
Thomas Jansson ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Gesessew Kibr

Maternal nutrition is very important for the wellbeing of pregnant women, childbirth, and lactating women, which are crucial and meant for the wellbeing of a mother and newborn baby. This narrative review discusses nutritional malpractices, motivational drivers, and their consequences typically from Ethiopian pregnant women’s context. Different studies (regarding less of study design and type) done among pregnant women (aged 15–49 years) by considering pregnancy-related outcomes and timing of nutritional malpractices were included mostly. Accordingly, taboos of healthy diets, craving for unhealthy foods (sweet, fat, raw, and salty/spicy foods), and nonfood items (soil, coffee residue, stone, and ash) were practiced majorly by the women. The birth difficulty, fetal head plastering, fetus discoloration, fetus burns, abortion, and abdominal cramp are the primary drivers of taboos of healthy diets. Hormonal change and social and nutrient-seeking behavior are the most prevalent drivers to the consumption of unhealthy foods. Additionally, personal interest, flavor, and color of items are important motivators to practice pica. Such pica practice hurts nutrient intake, absorption of iron/zinc, abdominal health, and diarrhea occurrence. Food taboos are high predictors of health disorders, such as intrauterine growth restriction, infection, bleeding, preeclampsia, stillbirth, early birth, low birth weight, retarded development of cognitive, and anemia. Craving and eating unhealthy foods were interconnected with chronic disease development (hypertension, diabetes, heart disease, and cancer), discomforts, preterm labor, preeclampsia, and intrauterine growth restriction in women. Additionally, it is also associated with stillbirth, low birth weight, obesity, birth defect/deficit, hypertension, cancer, diabetes, metabolic syndrome, renal disease, decreased fetal growth, behavioral change, heart failure, and poor cognitive development in the infant. Overall, these nutritional malpractices are significantly associated with many argumentative pregnancies as well as developmental consequences leading to the direction of infant and maternal mortality and morbidity. Therefore, urgent implementation of health and nutrition education programs considering food misconceptions and beliefs regarding pregnancy and use of ground-breaking ways to play down the negative and maximize potential positive dietary effects designed by the government of Ethiopia could also serve as a long-term solution to the problem.


2009 ◽  
Vol 296 (3) ◽  
pp. R681-R692 ◽  
Author(s):  
Michelle E. Schober ◽  
Robert A. McKnight ◽  
Xing Yu ◽  
Christopher W. Callaway ◽  
Xingrao Ke ◽  
...  

Uteroplacental insufficiency (UPI), the major cause of intrauterine growth restriction (IUGR) in developed nations, predisposes to learning impairment. The underlying mechanism is unknown. Neuronal N-methyl-d-aspartate receptors (NMDARs) are critical for synaptogenesis and learning throughout life. We hypothesized that UPI-induced IUGR alters rat hippocampal NMDAR NR2A/NR2B subunit ratio and/or NR1 mRNA isoform expression and synaptic density at day 21 (P21). To test this hypothesis, IUGR was induced by bilateral uterine artery ligation of the late-gestation Sprague-Dawley dam. At P21, hippocampal NMDAR subunit mRNA and protein were measured, as were levels of synaptophysin. Neuronal, synaptic, and glial density in CA1, CA3, and dentate gyrus (DG) was assessed by immunofluorescence. IUGR increased NR1 mRNA isoform NR1-3a and 1-3b expression in both sexes. In P21 males, IUGR increased protein levels of NR1 C2′ and decreased NR1 C2, NR2A, and the NR2A-to-NR2B ratio, whereas in females, IUGR increased NR2B protein. In males, IUGR was associated with decreased myelin basic protein-to-neuronal nuclei ratio in CA1, CA3, and DG. We conclude that IUGR has sex-specific effects and that neither neuronal loss nor decreased synaptic density appears to account for the changes in NMDAR subunits. Rather, it is possible that synaptic NMDAR subunit composition is altered. Our results suggest that apparent recovery in the IUGR hippocampus may be associated with synaptic hyperexcitability. We speculate that the NMDAR plays an important role in IUGR-associated cognitive impairment.


2004 ◽  
Vol 191 (6) ◽  
pp. S132
Author(s):  
Philippe Deruelle ◽  
Iva Gueorguieva ◽  
Berengere Sicot De Jenlis ◽  
Sophie Jaillard ◽  
Jacques Weill ◽  
...  

Endocrinology ◽  
2013 ◽  
Vol 154 (7) ◽  
pp. 2365-2373 ◽  
Author(s):  
Cun Li ◽  
Emma Ramahi ◽  
Mark J. Nijland ◽  
Jaeyhek Choi ◽  
Dean A. Myers ◽  
...  

Abstract Intrauterine growth restriction (IUGR) is an important fetal developmental problem resulting from 2 broad causes: maternal undernutrition and/or decreased fetal nutrient delivery to the fetus via placental insufficiency. IUGR is often accompanied by up-regulation of the hypothalamo-pituitary-adrenal axis (HPAA). Sheep studies show fetal HPAA autonomy in late gestation. We hypothesized that IUGR, resulting from poor fetal nutrient delivery, up-regulates the fetal baboon HPAA in late gestation, driven by hypothalamo-pituitary glucocorticoid receptor (GR) insensitivity and decreased fetal leptin in peripheral plasma. Maternal baboons were fed as ad libitum controls or nutrient restricted to produce IUGR (fed 70% of the control diet) from 0.16 to 0.9 gestation. Peripheral ACTH, cortisol, and leptin were measured by immunoassays. CRH, arginine vasopressin (AVP), GR, leptin receptor (ObRb), and pro-opiomelanocortin peptide expression were determined immunohistochemically. IUGR fetal peripheral cortisol and ACTH, but not leptin, were increased (P < .05). IUGR increased CRH peptide expression, but not AVP, in the fetal hypothalamic paraventricular nucleus (PVN) and median eminence (P < .05). PVN ObRb peptide expression, but not GR, was decreased (P < .05) with IUGR. ObRb and pro-opiomelanocortin were robustly expressed in the anterior pituitary gland, but ∼1% of cells showed colocalization. We conclude that (1) CRH, not AVP, is the major releasing hormone driving ACTH and cortisol secretion during primate IUGR, (2) fetal HPAA activation was aided by GR insensitivity and decreased ObRb expression in the PVN, and (3) the anterior pituitary is not a site for ObRb effects on the HPAA.


2007 ◽  
Vol 293 (3) ◽  
pp. R1267-R1273 ◽  
Author(s):  
Vladislava Zohdi ◽  
Karen M. Moritz ◽  
Kristen J. Bubb ◽  
Megan L. Cock ◽  
Nigel Wreford ◽  
...  

Previous studies have shown that intrauterine growth restriction (IUGR) can impair nephrogenesis, but uncertainties remain about the importance of the gestational timing of the insult and the effects on the renal renin-angiotensin system (RAS). We therefore hypothesized that induction of IUGR during late gestation alters the RAS, and this is associated with a decrease in nephron endowment. Our aims were to determine the effects of IUGR induced during the later stages of nephrogenesis on 1) nephron number; 2) mRNA expression of angiotensin AT1 and AT2 receptors, angiotensinogen, and renin genes in the kidney; and 3) the size of maculae densae. IUGR was induced in fetal sheep ( n = 7) by umbilical-placental embolization from 110 to 130 days of the ∼147-day gestation; saline-infused fetuses served as controls ( n = 7). Samples of cortex from the left kidney were frozen, and the right kidney was perfusion fixed. Total kidney volume, nephron number, renal corpuscle volume, total maculae densae volume, and the volume of macula densa per glomerulus were stereologically estimated. mRNA expression of AT1 and AT2 receptors, angiotensinogen, and renin in the renal cortex was determined. In IUGR fetuses at 130 days, body and kidney weights were significantly reduced and nephron number was reduced by 24%. There was no difference in renin, angiotensinogen, or AT1 and AT2 receptor mRNA expression levels in the IUGR kidneys compared with controls. We conclude that fetal growth restriction late in nephrogenesis can lead to a marked reduction in nephron endowment but does not affect renal corpuscle or macula densa size, or renal RAS gene expression.


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