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Tracey A Quinn, Udani Ratnayake, Margie Castillo-Melendez, Karen M Moritz, Hayley Dickinson, and David W Walker

) activity and modify the development of several organ systems, particularly the brain. One outcome of maternal physical or psychological illness during pregnancy is an increased risk of neurodevelopmental alterations in the fetus, which can lead to several

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Hongyu Su, Xueyi Chen, Yueming Zhang, Linglu Qi, Yun He, Juanxiu Lv, Yingying Zhang, Xiang Li, Jiaqi Tang, and Zhice Xu

encephalopathy and hypoxic-ischaemic encephalopathy . Early Human Development 329 – 338 . ( https://doi.org/10.1016/j.earlhumdev.2010.05.010 ) Li B Concepcion K Meng X Zhang L 2017 Brain-immune interactions in perinatal hypoxic-ischemic brain

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David R Grattan

and development, endocrinology and metabolism, brain and behaviour, reproduction and immune regulation and protection. The breadth of potential functions is astounding and difficult to conceptualise into a theoretical framework. Many of the reported

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Jia Fang Wang and David J Hill

tissues, and high levels of N-MYC are expressed during development in the fetal brain, kidney, and within neuroblasts migrating from the neural crest. However, little expression of this gene is found in adult tissues. Targeted expression of human N

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Tianru Jin

through binding to its receptor, which is expressed in the brain, pancreas, small and large intestines, kidney, and more importantly liver and adipose tissues ( Jelinek et al . 1993 , Campos et al . 1994 , Burcelin et al . 1996 , Christophe 1996

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Edra London, Michelle Bloyd, and Constantine A Stratakis

)−/− Embryonically lethal Huang et al. (2002) Prkaca+/−:Prkacb(β1)−/− Defects in neural tube development Huang et al. (2002) Prkaca−/−:Prkacb(β1)−+/− Gestationally lethal; all pups had neural tube development defects, some had exencephaly

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Maureen J Charron and Patricia M Vuguin

, 2013 , Rodgers 2012 , Cyphert et al . 2014 ). Binding sites for glucagon have been identified in liver, kidney, intestinal smooth muscle, brain, adipose tissue, heart, pancreatic islet β-cells, and placenta ( Ouhilal et al . 2012 ). Gcgr gene

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P Fu, P-J Shen, C-X Zhao, D J Scott, C S Samuel, J D Wade, G W Tregear, R A D Bathgate, and A L Gundlach

6 after birth in ovarian theca and luteal cells, with a likely involvement in follicle development ( Balvers et al. 1998 ). In adult women, INSL3 is detected in ovarian theca cells of large antral follicles and in the corpora lutea during the

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D Sampson, MR Pickard, AK Sinha, IM Evans, AJ Leonard, and RP Ekins

Maternal thyroid hormone (TH) crosses the placenta and is postulated to regulate fetal brain development. However, TH-dependent stages of fetal brain development remain to be characterised. We have therefore compared the levels of several neuronal and glial cytoskeletal proteins in fetal brains from normal (N) and partially thyroidectomised (TX) rat dams by immunoblotting. Pregnancies were studied both before and after the onset of fetal TH secretion, which occurs at 17.5 days gestation (dg) in the rat. Maternal hypothyroidism disrupted fetal growth, so that fetal body and brain weights were reduced near term. Vimentin expression was unaffected, however, indicating normal acquisition of neuronal and glial precursor cells. Fetal brain levels of glial fibrillary acidic protein (GFAP) were reduced at 21 dg, suggesting delayed astrocytic differentiation, although regression analysis demonstrated appropriate GFAP levels for brain weight. Levels of alpha-internexin, the earliest neurofilament protein expressed in fetal brain were reduced at 16 dg in TX dams, but increased at 21 dg. The ontogeny of neurofilament-L was also perturbed in these pregnancies, with deficient levels apparent at both 16 and 21 dg. These effects on neuronal cytoskeletal proteins were unrelated to fetal brain growth retardation. These findings confirm that maternal hypothyroidism disrupts early fetal brain development. Early disturbances in neuronal differentiation are not corrected by the onset of fetal TH secretion. Such disturbances may contribute to the neurological damage observed in children born to hypothyroxinaemic mothers.

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Jie Xu, Amaury Jean-Marie Bekaert, Joëlle Dupont, Sarah Rouve, Isabella Annesi-Maesano, C Daniel De Magalhaes Filho, Laurent Kappeler, and Martin Holzenberger

. 2000 , 2003 ), IGF-1R +/− and brain-specific IGF-1 receptor knockout (bIGF1RKO +/− ) mutants ( Holzenberger et al . 2003 , Kappeler et al . 2008 ), and several insulin receptor substrate knockouts ( Taguchi et al . 2007 , Selman et al . 2008