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      Biological Effects of Exposure to a Radiofrequency Electromagnetic Field on the Placental Barrier in Pregnant Rats

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          Abstract

          The placenta protects the fetus against excessive stress‐associated maternal cortisol during pregnancy. We studied whether exposure to radiofrequency electromagnetic field (RF‐EMF) radiation during pregnancy can cause changes in dams and their placentas. Pregnant Sprague–Dawley rats were divided into cage‐control, sham‐exposed, and RF‐exposed groups. They were exposed to RF‐EMF signals at a whole‐body specific absorption rate of 4 W/kg for 8 h/day from gestational Day 1 to 19. Levels of cortisol in the blood, adrenal gland, and placenta were measured by enzyme‐linked immunosorbent assay. Levels of adrenocorticotropic hormone and corticotropin‐releasing hormone were monitored in maternal blood. Expression levels of placental 11β‐hydroxysteroid dehydrogenase type 2 ( 11β‐HSD2) messenger RNA (mRNA) were measured by reverse transcription polymerase chain reaction. Morphological changes in the placenta were analyzed using hematoxylin and eosin staining. Fetal parts of the placenta were measured using Zen 2.3 blue edition software. Maternal cortisol in circulating blood (RF: 230 ± 24.6 ng/ml and Sham: 156 ± 8.3 ng/ml) and the adrenal gland (RF: 58.3 ± 4.5 ng/ml and Sham: 30 ± 3.8 ng/ml) was significantly increased in the RF‐exposed group ( P < 0.05). Placental cortisol was stably maintained, and the level of placental 11β‐HSD2 mRNA expression was not changed in the RF‐exposed group. RF‐EMF exposure during pregnancy caused a significant elevation of cortisol levels in circulating blood; however, no changes in the placental barrier were observed in pregnant rats. Bioelectromagnetics. © 2021 Bioelectromagnetics Society

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          Fetal origins of adult disease.

          Dr. David Barker first popularized the concept of fetal origins of adult disease (FOAD). Since its inception, FOAD has received considerable attention. The FOAD hypothesis holds that events during early development have a profound impact on one's risk for development of future adult disease. Low birth weight, a surrogate marker of poor fetal growth and nutrition, is linked to coronary artery disease, hypertension, obesity, and insulin resistance. Clues originally arose from large 20th century, European birth registries. Today, large, diverse human cohorts and various animal models have extensively replicated these original observations. This review focuses on the pathogenesis related to FOAD and examines Dr. David Barker's landmark studies, along with additional human and animal model data. Implications of the FOAD extend beyond the low birth weight population and include babies exposed to stress, both nutritional and nonnutritional, during different critical periods of development, which ultimately result in a disease state. By understanding FOAD, 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. Copyright © 2011 Mosby, Inc. All rights reserved.
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            Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems.

            Stress-related variation in the intrauterine milieu may impact brain development and emergent function, with long-term implications in terms of susceptibility for affective disorders. Studies in animals suggest limbic regions in the developing brain are particularly sensitive to exposure to the stress hormone cortisol. However, the nature, magnitude, and time course of these effects have not yet been adequately characterized in humans. A prospective, longitudinal study was conducted in 65 normal, healthy mother-child dyads to examine the association of maternal cortisol in early, mid-, and late gestation with subsequent measures at approximately 7 y age of child amygdala and hippocampus volume and affective problems. After accounting for the effects of potential confounding pre- and postnatal factors, higher maternal cortisol levels in earlier but not later gestation was associated with a larger right amygdala volume in girls (a 1 SD increase in cortisol was associated with a 6.4% increase in right amygdala volume), but not in boys. Moreover, higher maternal cortisol levels in early gestation was associated with more affective problems in girls, and this association was mediated, in part, by amygdala volume. No association between maternal cortisol in pregnancy and child hippocampus volume was observed in either sex. The current findings represent, to the best of our knowledge, the first report linking maternal stress hormone levels in human pregnancy with subsequent child amygdala volume and affect. The results underscore the importance of the intrauterine environment and suggest the origins of neuropsychiatric disorders may have their foundations early in life.
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              Mechanisms of disease: glucocorticoids, their placental metabolism and fetal 'programming' of adult pathophysiology.

              Epidemiological evidence suggests that an adverse prenatal environment permanently 'programs' physiology and increases the risk of cardiovascular, metabolic, neuroendocrine and psychiatric disorders in adulthood. Prenatal stress or exposure to excess glucocorticoids might provide the link between fetal maturation and adult pathophysiology. In a variety of animal models, prenatal stress, glucocorticoid exposure and inhibition (or knockout of) 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2)--the fetoplacental barrier to maternal glucocorticoids--reduce birth weight and cause increases in adult blood pressure, glucose levels, hypothalamic-pituitary-adrenal (HPA) axis activity and anxiety-related behaviors. In humans, mutations in the gene that encodes 11beta- hydroxysteroid dehydrogenase type 2 are associated with low birth weight. Babies with low birth weight have higher plasma cortisol levels throughout life, which indicates HPA-axis programming. In human pregnancy, severe maternal stress affects the offspring's HPA axis and is associated with neuropsychiatric disorders; moreover, maternal glucocorticoid therapy alters offspring brain function. The molecular mechanisms that underlie prenatal programming might reflect permanent changes in the expression of specific transcription factors, including the glucocorticoid receptor; tissue specific effects reflect modification of one or more of the multiple alternative first exons or promoters of the glucocorticoid receptor gene. Intriguingly, some of these effects seem to be inherited by subsequent generations that are unexposed to exogenous glucocorticoids at any point in their lifespan from fertilization, which implies that these epigenetic effects persist.
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                Author and article information

                Contributors
                yhahn@ajou.ac.kr
                Journal
                Bioelectromagnetics
                Bioelectromagnetics
                10.1002/(ISSN)1521-186X
                BEM
                Bioelectromagnetics
                John Wiley and Sons Inc. (Hoboken )
                0197-8462
                1521-186X
                01 February 2021
                April 2021
                : 42
                : 3 ( doiID: 10.1002/bem.v42.3 )
                : 191-199
                Affiliations
                [ 1 ] Department of Neurosurgery Ajou University School of Medicine Suwon Republic of Korea
                [ 2 ] Radio Technology Research Department Electronics and Telecommunications Research Institute Daejeon Republic of Korea
                [ 3 ] Department of Radio Sciences and Engineering, College of Engineering Chungnam National University Daejeon Republic of Korea
                [ 4 ] School of Electrical and Computer Engineering Chungbuk National University Cheongju Republic of Korea
                [ 5 ] Neuroscience Graduate Program, Department of Biomedical Sciences Graduate School of Ajou University Suwon Republic of Korea
                Author notes
                [*] [* ]Correspondence to: Young Hwan Ahn, Department of Neurosurgery, Ajou University School of Medicine, Suwon 442‐721, Republic of Korea.

                E‐mail: yhahn@ 123456ajou.ac.kr

                Author information
                https://orcid.org/0000-0002-4734-5589
                https://orcid.org/0000-0003-2652-7524
                https://orcid.org/0000-0003-3185-6939
                https://orcid.org/0000-0001-8109-2055
                http://orcid.org/0000-0002-4734-5589
                Article
                BEM22322
                10.1002/bem.22322
                8048814
                33527465
                b1218a17-5f1f-45f9-9081-0388ce94bf8e
                © 2021 The Authors. Bioelectromagnetics published by Wiley Periodicals LLC on behalf of Bioelectromagnetics Society

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 27 October 2020
                : 05 May 2020
                : 30 December 2020
                Page count
                Figures: 3, Tables: 1, Pages: 9, Words: 5370
                Funding
                Funded by: The ICT R&D program of MSIT/IITP
                Award ID: 2019‐0‐00102
                Award ID: A Study on Public Health and Safety
                Funded by: The National Research Foundation of Korea (NRF) funded by the Ministry of Education
                Award ID: Basic Science Research Program/NRF‐2018R1A6A3A110
                Categories
                Research Article
                Research Articles
                Custom metadata
                2.0
                April 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.2 mode:remove_FC converted:15.04.2021

                rf‐emf,pregnancy,hypothalamic–pituitary–adrenal axis,cortisol,placenta

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