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Che-Pei Kung Department of Internal Medicine, Washington University School of Medicine, St Louis, Missouri, USA

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Maureen E Murphy Department of Internal Medicine, Washington University School of Medicine, St Louis, Missouri, USA

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, activated p53 induces expression of growth-arrest genes, such as CDKN1A/p21 , to facilitate DNA damage repair. When encountering prolonged or catastrophic DNA damage, p53 triggers programmed cell death (apoptosis), primarily by transactivating genes that

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Takahiro Nemoto Department of Physiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan

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Yoshihiko Kakinuma Department of Physiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan

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Tamotsu Shibasaki Department of Physiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan

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, Ehnvall et al . 2004 , Corbett et al . 2006 ). Recent animal studies have indicated that maternal malnutrition-induced impairment of fetal programing of the HPA axis function is associated with adult-onset dysregulation of the axis ( Chadio et al

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Michael A Hahn Hormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, E25, St Leonards, New South Wales 2065, Australia

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Julie McDonnell Hormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, E25, St Leonards, New South Wales 2065, Australia

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Deborah J Marsh Hormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, E25, St Leonards, New South Wales 2065, Australia

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the pathogenicity of exonic HRPT2 mutations. While predictive programs may be useful in giving a preliminary indication of the effect of sequence variants on splicing, functional assays are required to determine the true effects, if any, on splicing

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Isabella Artner Cell and Developmental Biology, Departments of

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Yan Hang Cell and Developmental Biology, Departments of

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Min Guo Cell and Developmental Biology, Departments of

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Guoqiang Gu Cell and Developmental Biology, Departments of

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Roland Stein Cell and Developmental Biology, Departments of
Cell and Developmental Biology, Departments of

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MafA versus MafB, which allow Insulin activation, although not a more general endocrine differentiation program in this chick assay system. Figure 1 MafA, but not MafB, induces insulin expression in chick gut endoderm. Double immunofluorescence

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Junny Chan
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Elizabeth H Rabbitt
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Barbara A Innes
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Judith N Bulmer
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Paul M Stewart
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Mark D Kilby
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Martin Hewison
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similar to decidua where there is close interaction between stromal and non-stromal cells (such as the thymus), glucocorticoids are known to play a key role in modulating programmed cell death ( Wyllie 1980 , Wyllie & Morris 1982 ). Therefore, to assess

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Bruno C Pereira Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, USP, Ribeirão Preto, São Paulo, Brazil

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Alisson L da Rocha Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, USP, Ribeirão Preto, São Paulo, Brazil

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Ana P Pinto Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, USP, Ribeirão Preto, São Paulo, Brazil

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José R Pauli Sport Sciences Course, Faculty of Applied Sciences, State University of Campinas, Limeira, São Paulo, Brazil

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Leandro P de Moura Sport Sciences Course, Faculty of Applied Sciences, State University of Campinas, Limeira, São Paulo, Brazil

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Rania A Mekary Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
Department of Social and Administrative Sciences, MCPHS University, Boston, Massachusetts, USA

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Ellen C de Freitas School of Physical Education and Sport of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil

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Adelino S R da Silva Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, USP, Ribeirão Preto, São Paulo, Brazil
School of Physical Education and Sport of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil

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The main aim of this investigation was to verify the effects of overtraining (OT) on the insulin and inflammatory signaling pathways in mice skeletal muscles. Rodents were divided into control (CT), overtrained by downhill running (OTR/down), overtrained by uphill running (OTR/up), and overtrained by running without inclination (OTR) groups. Rotarod, incremental load, exhaustive, and grip force tests were used to evaluate performance. Thirty-six hours after the grip force test, the extensor digitorum longus (EDL) and soleus were extracted for subsequent protein analyses. The three OT protocols led to similar responses of all performance evaluation tests. The phosphorylation of insulin receptor beta (pIRβ; Tyr), protein kinase B (pAkt; Ser473), and the protein levels of plasma membrane glucose transporter-4 (GLUT4) were lower in the EDL and soleus after the OTR/down protocol and in the soleus after the OTR/up and OTR protocols. While the pIRβ was lower after the OTR/up and OTR protocols, the pAkt was higher after the OTR/up in the EDL. The phosphorylation of IκB kinase alpha and beta (pIKKα/β; Ser180/181), stress-activated protein kinases/Jun amino-terminal kinases (pSAPK-JNK; Thr183/Tyr185), factor nuclear kappa B (pNFκB p65; Ser536), and insulin receptor substrate 1 (pIRS1; Ser307) were higher after the OTR/down protocol, but were not altered after the two other OT protocols. In summary, these data suggest that OT may lead to skeletal muscle insulin signaling pathway impairment, regardless of the predominance of eccentric contractions, although the insulin signal pathway impairment induced in OTR/up and OTR appeared to be muscle fiber-type specific.

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E Oliveira Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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C R Pinheiro Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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A P Santos-Silva Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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I H Trevenzoli Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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Y Abreu-Villaça Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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J F Nogueira Neto Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute
Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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A M Reis Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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M C F Passos Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute
Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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E G Moura Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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P C Lisboa Department of Physiological Sciences, Laboratory of Lipids, Department of Physiology and Biophysics, Department of Applied Nutrition, Roberto Alcantara Gomes Biology Institute

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Nogueira-Neto JF Lisboa PC 2009 Temporal evaluation of body composition, glucose homeostasis and lipid profile of male rats programmed by maternal protein restriction during lactation . Hormone and Metabolic Research 41 866 – 873 . Fraga

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Nadia Schoenmakers University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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Kyriaki S Alatzoglou University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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V Krishna Chatterjee University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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Mehul T Dattani University of Cambridge Metabolic Research Laboratories, Developmental Endocrinology Research Group, Wellcome Trust‐Medical Research Council Institute of Metabolic Science, Addenbrooke's Hospital, Level 4, PO Box 289, Hills Road, Cambridge CB2 0QQ, UK

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deficiencies ( Alatzoglou & Dattani 2009 , Kelberman et al . 2009 ). Since TSH is not elevated in CCH, this entity will evade diagnosis in TSH-based, primary CH screening programs, and patients are at risk of neurodevelopmental delay if severe CCH remains

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Gary A Wittert Freemasons Centre for Male Health and Wellbeing, South Australian Health and Medical Research Institute, and University of Adelaide, Adelaide, South Australia, Australia

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Mathis Grossmann Department of Medicine, The University of Melbourne and Department of Endocrinology Austin Health, Heidelberg, Australia

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Bu B Yeap Medical School, University of Western Australia, and Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, Western Australia, Australia

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David J Handelsman ANZAC Research Institute, University of Sydney and Andrology Department, Concord Hospital, Sydney, New South Wales, Australia

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of Type 2 Diabetes (T4DM) study’. T4DM sought to determine whether treatment with testosterone, on the background of a lifestyle program, would prevent the progression of prediabetes to T2D or reverse newly diagnosed T2D in men aged 50 and over with

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Bishnu Adhikari Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Poultry Science, University of Arkansas, Fayetteville, Arkansas, USA

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Prabhat Khanal Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Institute of Basic Medical Sciences, Faculty of Medicine, The Norwegian Transgenic Centre (NTS), University of Oslo, Oslo, Norway
Faculty of Biosciences and Aquaculture (FBA), Nord University, Steinkjer, Norway

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Mette Olaf Nielsen Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Secretory function of the pancreatic α-cell, in contrast to the pancreatic β-cell, does not appear to be a target of nutritional programming in late foetal life in sheep. Implications of gender differences in glucagon secretory patterns remain to be

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