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M Fraser, GA Braems and Challis JR

Responsiveness of the fetal sheep adrenal gland to adrenocorticotrophin (ACTH) increases in late pregnancy, resulting in increased glucocorticoid production. Development of this responsiveness is an important determinant of fetal hypothalamic-pituitary-adrenal function and depends, in part, on the potential for ACTH binding to adrenal tissue. In the present study, we have examined the developmental pattern of ACTH receptor (ACTH-R) expression during the latter half of pregnancy and in neonatal and adult life. As hypoxaemia induces increases in cortisol and ACTH secretion, in addition to increasing fetal adrenal responsiveness, a further aim of this study was to investigate whether hypoxaemia was associated with altered expression of the ACTH-R gene. Whole adrenal glands were removed from fetal sheep, lambs and adult sheep at different stages of development for measurement of ACTH-R mRNA. Moderate hypoxaemia was induced for 48 h beginning on days 124-128, or on days 132-134 of gestation, by decreasing the maternal fractional inspired oxygen. ACTH-R mRNA was detected by northern blotting using a cDNA cloned in our laboratory and by in situ hybridisation. ACTH-R mRNA (3.6 kb major transcript) was detected in adrenal tissue at day 63 of gestation. Its relative abundance increased significantly (P<0.05) between days 126-128 and 140-141 of pregnancy, increased further with the onset of spontaneous labour, and remained increased in newborn lambs at 7 h-7 days after birth. ACTH-R mRNA levels then decreased in adrenal tissue from lambs and adult sheep (P<0.05). Hypoxaemia for 48 h significantly increased ACTH-R mRNA expression in adrenals of the older fetuses (days 134-136) compared with that in controls (P<0.05), but was without effect in younger fetuses. We conclude that levels of ACTH-R mRNA in the fetal adrenal gland increase as term approaches, coincident with the endogenous prepartum surge in plasma ACTH and cortisol. Sustained hypoxaemia resulted in an upregulation of mRNA encoding for ACTH-R, but only in older fetuses and in association with a sustained increase in plasma cortisol. These results are consistent with cortisol, ACTH, or both, contributing to increased fetal adrenal responsiveness, by increasing expression of fetal adrenal receptors for ACTH.

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K S Wilson, C S Tucker, E A S Al-Dujaili, M C Holmes, P W F Hadoke, C J Kenyon and M A Denvir

, results from controls of the dexamethasone group were not different from the controls in the hypoxia and GR morpholino group which were not exposed to ethanol. Previous work involving a dose-ranging study (1–200μM) established 100µM dexamethasone as the

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B Shan, C Schaaf, A Schmidt, K Lucia, M Buchfelder, M Losa, D Kuhlen, J Kreutzer, M J Perone, E Arzt, G K Stalla and U Renner

oxygen and nutrients to the tumour cells and to remove intratumoural waste products ( Turner et al . 2000 , Carmeliet 2003 ). Tumour neovascularisation is induced by intratumoural hypoxia, which leads to an increase in hypoxia inducible factor 1α (HIF1A

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Toshiaki Ishizuka, Takashi Hinata and Yasuhiro Watanabe

postischemic neovascularization by 1.5-fold as compared to those from untreated diabetic mice ( Ebrahimian et al . 2006 ). The effects of hyperglycemia or hypoxia have been associated with increased levels of reactive oxygen species (ROS; Waypa et al . 2001

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Hershel Raff and Lauren Jacobson

Introduction Hypoxia is a common neonatal stress leading to significant short-term distress and long-term complications ( Frankel & Stevenson 1987 , Friedman & Fahey 1993 , Low et al. 1993 , Rubaltelli et al. 1998

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Nicholas J Bernier, Sarah L Alderman and Erin N Bristow

relative importance of the POA and the CNSS as sites of CRF and UI expression in this species. We then investigated the impact of two environmental stressors, elevated ammonia levels and hypoxia, and two social stressors, isolation and subordination on the

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Xiaojiong Du, Sirong He, Yaowen Jiang, Lingling Wei and Weiming Hu

islets are exceptionally susceptible to ischemia–reperfusion injury ( Sklavos et al . 2010 ). Hypoxia–reoxygenation is the leading cause of β-cell death during islet preparation, implantation, and revascularization, with the highest percentage of islet

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Elisabete A Forsberg, Ileana R Botusan, Jing Wang, Verena Peters, Ishrath Ansurudeen, Kerstin Brismar and Sergiu Bogdan Catrina

transcriptional level ( Brismar et al . 1994 , Powell et al . 1995 ). Other factors, including hypoxia, pro-inflammatory cytokines, cAMP, glucocorticoids and oxidative stress stimulate the synthesis of IGFBP1 ( Mesotten et al . 2002 ). Hypoxia inducible factor

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Linda Vignozzi, Annamaria Morelli, Erica Sarchielli, Paolo Comeglio, Sandra Filippi, Ilaria Cellai, Elena Maneschi, Sergio Serni, Mauro Gacci, Marco Carini, Marie-Pierre Piccinni, Farid Saad, Luciano Adorini, Gabriella B Vannelli and Mario Maggi

after background subtraction using Adobe Photoshop 6.0 Software (Adobe Systems). Hypoxia detection in rabbit prostate Tissue oxygenation has been analyzed as described previously ( Vignozzi et al . 2006 , 2008 , 2009 , Morelli et al . 2010 a

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Sheree D Martin and Sean L McGee

adequately remodel, resulting in adipose tissue hypoxia ( Ye et al . 2007 ). The lipid storage capacity of individual adipocytes can also be challenged, which similar to lipotoxicity in other tissues, initiates a cellular inflammatory response and in some