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JC Osgerby, DC Wathes, D Howard, and TS Gadd

Modifications in maternal nutrition during pregnancy can significantly disrupt fetal growth and subsequent post-natal health and survival. This study investigated the effects of undernutrition on fetal growth and the potential mechanisms involved. Tissue from pregnant ewes (n=27) was investigated on days 45, 90 and 135 of gestation (term = approximately 150 days). The thoracic girth (P<0.05) was greater in fetuses from nutrient restricted ewes on day 45 and there was also a trend towards an increased gut weight (P<0.08). By day 90, the fetal brain and thymus weight were lighter in underfed than in well-fed animals whilst the weight of the fetal ovaries was heavier (P<0.05). On day 135 the fetal heart, pancreas, thymus, gut and kidney weights were lighter in undernourished ewes (P<0.05). When expressed as a percentage of fetal body weight, significance was retained in the heart, pancreas and thymus (P<0.05). Bone growth was also affected. At day 90 the fetal femur and metatarsal were longer in underfed mothers (P<0.05). In contrast, the fetal humerus and scapula were shorter in underfed than in well-fed animals on day 135 (P<0.05) when the weight of the semitendinosus muscle (P<0.05) was also reduced. The fall in fetal glucose (P<0.1), insulin (P<0.01) and IGF-I (P<0.01) levels in underfed ewes on day 135 may have compromised fetal growth. Fetal plasma IGF binding protein-2 also increased between days 90 and 135 in underfed ewes (P<0.03), whilst levels were unaltered in well-fed animals. Although maternal and fetal plasma IGF-I levels increased with gestation (P<0.01) and the placentome morphology altered in all ewes (P<0.05), the fall in placental mass (P<0.05), amniotic and allantoic glucose concentrations (P<0.05) and maternal plasma glucose and insulin levels (P<0.05) in underfed ewes in late gestation may have compromised fetal substrate delivery. These perturbations in fetal development may have significant implications on adult health and carcass conformation, raising important health and economic issues in medical and agricultural sectors.

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TR Regnault, RJ Orbus, FC Battaglia, RB Wilkening, and RV Anthony

Pregnant ewes were exposed chronically to thermoneutral (TN; 20+/-2 degrees C, 30% relative humidity; n=8) or hyperthermic (HT; 40+/-2 degrees C 12 h/day, 35+/-2 degrees C 12 h/day, 30% relative humidity, n=6) environments between days 37 and 93 of pregnancy. Ewes were killed following 56 days of exposure to either environment (days in treatment (dit)), corresponding to 93+/-1 day post coitus (dpc). Maternal core body temperatures (CBT) in HT ewes were significantly elevated above the TN ewes (HT; 39.86+/-0.1 degrees C vs TN; 39.20+/-0.1 degrees C; P<0.001). Both groups of animals displayed circadian CBT, though HT ewes had elevated amplitudes (HT; 0.181+/-0.002 degrees C vs TN; 0.091+/-0.002 degrees C; P<0.001) and increased phase shift constants (HT; 2100 h vs TN; 1800 h; P<0.001). Ewes exposed to chronic heat stress had significantly reduced progesterone and ovine placental lactogen (oPL) concentrations from 72 and 62 dpc respectively (P<0.05), corresponding to approximately 30 dit. However, when compared with the TN ewes, HT cotyledonary tissue oPL mRNA and protein concentrations were not significantly different (P>0.1). Prolactin concentrations rose immediately upon entry into the HT environment, reaching concentrations approximately four times that of TN ewes, a level maintained throughout the study (HT; 216.31+/-32.82 vs TN; 54. 40+/-10.0; P<0.0001). Despite similar feed intakes and euglycemia in both groups of ewes, HT fetal body weights were significantly reduced when compared with TN fetuses (HT; 514.6+/-48.7 vs TN; 703. 4+/-44.8; P<0.05), while placental weights (HT; 363.6+/-63.3 vs TN; 571.2+/-95.9) were not significantly affected by 56 days of heat exposure. Furthermore, the relationship between body weight and fetal length, the ponderal index, was significantly reduced in HT fetuses (HT; 3.01+/-0.13 vs TN; 3.57+/-0.18; P<0.05). HT fetal liver weights were also significantly reduced (HT; 27.31+/-4.73 vs TN; 45.16+/-6.16; P<0.05) and as a result, the brain/liver weight ratio was increased. This study demonstrates that chronic heat exposure lowers circulating placental hormone concentrations. The observation that PL mRNA and protein contents are similar across the two treatments, suggests that reduced hormone concentrations are the result of impaired trophoblast cell development, specifically trophoblast migration. Furthermore, the impact of heat exposure during maximal placental growth is great enough to restrict early fetal development, even before the fetal maximal growth phase (100 dpc-term). These data highlight that intrauterine growth retardation (IUGR) may result primarily from placental trophoblast cell dysfunction, and secondarily from later reduced placental size.

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Pablo Mendez, Iñigo Azcoitia, and Luis Miguel Garcia-Segura

Introduction The nervous system is a target for the ovarian hormone oestradiol. This hormone regulates brain development and function, acting on neurons, synapses and glial cells ( Chowen et al. 2000 , McEwen 2002 ). For many

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C H J Verhoelst, V M Darras, S A Roelens, G M Artykbaeva, and S Van der Geyten

Introduction It is well established that thyroid hormones play a crucial role in vertebrate development in general and in brain development and maturation in particular. The impact of thyroid hormones (THS) on the development of the

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Jirapas Sripetchwandee, Hiranya Pintana, Piangkwan Sa-nguanmoo, Chiraphat Boonnag, Wasana Pratchayasakul, Nipon Chattipakorn, and Siriporn C Chattipakorn

C ). However, both serum and brain MDA levels in female rats were higher than in male. These findings indicate that females are more vulnerable to the development of a severity in oxidative stress than males ( Figs 1 and 2 ). Figure 2 Effects

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Volker Hartenstein

derivative which has profound effects on larval growth, metamorphosis, egg development, and sexual behavior ( Veelaert et al. 1998 , Vullings et al. 1999 , Gilbert et al. 2000 ). The pars lateralis in the brain via its projections to the CA is the

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E Nieves-Martinez, W E Sonntag, A Wilson, A Donahue, D P Molina, J Brunso-Bechtold, and M M Nicolle

, which begins around PD28. Brain development continues through adolescence to young adulthood (PD63–70) ( McCutcheon & Marinelli 2009 ). Because of the high density of GH and IGF1 receptors in the hippocampus ( Adem et al . 1989 , Lai et al . 1993

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Bruce S McEwen, Jason D Gray, and Carla Nasca

The stress response and development of allostatic load. The perception of stress is influenced by one's experiences, genetics, and behavior. When the brain perceives an experience as stressful, physiologic and behavioral responses are initiated

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Nathanael J Yates, Dijana Tesic, Kirk W Feindel, Jeremy T Smith, Michael W Clarke, Celeste Wale, Rachael C Crew, Michaela D Wharfe, Andrew J O Whitehouse, and Caitlin S Wyrwoll

development and function likely means that vitamin D deficiency associates with many other neuropsychiatric outcomes. We have recently shown that vitamin D deficiency in mice increases placental glucocorticoid transfer and increases fetal brain

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Tabata M Bohlen, Thais T Zampieri, Isadora C Furigo, Pryscila D S Teixeira, Edward O List, John J Kopchick, Jose Donato Jr, and Renata Frazao

Introduction Puberty is a complex phenomenon modulated by genetic, epigenetic, environmental, nutritional and hormonal factors. Both the onset and proper development of sexual maturation depend on augmented sex steroid levels, and the ability