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Xue-Lian Zhang Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Xinyi Zhao Department of Physiology, School of Medicine, Jinan University, Guangzhou, China

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Yong Wu Department of Physiology, School of Medicine, Jinan University, Guangzhou, China
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Wen-qing Huang Department of Transfusion Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China

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Jun-jiang Chen Department of Physiology, School of Medicine, Jinan University, Guangzhou, China
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Peijie Hu Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Wei Liu Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Yi-Wen Chen Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Jin Hao Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Rong-Rong Xie Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Hsiao Chang Chan Epithelial Cell Biology Research Center, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China

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Ye Chun Ruan Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Hui Chen Cell-Gene Therapy Translational Medicine Research Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China

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Jinghui Guo Department of Physiology, School of Medicine, Jinan University, Guangzhou, China

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of ACE-2, angiotensin(1–7) (Ang(1–7)) and its receptor (MAS-1), which causes vasodilation and therefore counteracts the pressor arm ( 4 ). While the over-activated pressor arm causes a deleterious effect contributing to the end-organ damage in

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Janaína Felix Braga Department of Physiology and Biophysics, National Institute of Science and Technology in Nanobiopharmaceutics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil

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Daniela Ravizzoni Dartora Cardiology Institute of Rio Grande do Sul/University Foundation of Cardiology (IC/FUC), Porto Alegre, Rio Grande do Sul, Brazil

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Natalia Alenina Max-Delbruck Center of Molecular Medicine (MDC), Berlin-Buch, Berlin, Germany

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Michael Bader Cardiology Institute of Rio Grande do Sul/University Foundation of Cardiology (IC/FUC), Porto Alegre, Rio Grande do Sul, Brazil

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Robson Augusto Souza Santos Department of Physiology and Biophysics, National Institute of Science and Technology in Nanobiopharmaceutics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil
Cardiology Institute of Rio Grande do Sul/University Foundation of Cardiology (IC/FUC), Porto Alegre, Rio Grande do Sul, Brazil

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), endothelium ( 12 ), adipose tissue and liver ( 13 ). Moreover, Mas deletion has been reported to have deleterious effects on glucose and lipid metabolism ( 14 ). Although it is now clear, in contrast to ACE/Ang II/AT1R, the ACE2/Ang(1–7)/Mas axis has a

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Xi Wang Department of Obstetrics and Gynaecology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

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Qi Yu Department of Obstetrics and Gynaecology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

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Introduction McCune–Albright syndrome (MAS) is a rare congenital sporadic disorder arising from somatic activating mutations in the GNAS gene. The precise prevalence of MAS is unknown and is estimated to range between 1/100,000 and 1/1

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Sarah J Delforce School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia
Priority Research Centre for Reproductive Sciences, University of Newcastle, Newcastle, New South Wales, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia

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Eugenie R Lumbers School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia
Priority Research Centre for Reproductive Sciences, University of Newcastle, Newcastle, New South Wales, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia

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Celine Corbisier de Meaultsart School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia
Priority Research Centre for Reproductive Sciences, University of Newcastle, Newcastle, New South Wales, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia

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Yu Wang Oregon Health and Science University, Portland, Oregon, USA

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Anthony Proietto Hunter Centre for Gynaecological Cancer, John Hunter Hospital, Newcastle, New South Wales, Australia

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Geoffrey Otton Hunter Centre for Gynaecological Cancer, John Hunter Hospital, Newcastle, New South Wales, Australia

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Jim Scurry Hunter Area Pathology Service, John Hunter Hospital, Newcastle, New South Wales, Australia

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Nicole M Verrills School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Priority Research Centre for Cancer, University of Newcastle, Newcastle, New South Wales, Australia

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Rodney J Scott School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia
Hunter Area Pathology Service, John Hunter Hospital, Newcastle, New South Wales, Australia

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Kirsty G Pringle School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia
Priority Research Centre for Reproductive Sciences, University of Newcastle, Newcastle, New South Wales, Australia
Hunter Medical Research Institute, Newcastle, New South Wales, Australia

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receptor (AGTR2) and antagonises AGTR1 activation. Ang I can also be further converted by angiotensin-converting enzyme 2 (ACE2) to Ang(1–7). Ang(1–7) acts upon its receptor Mas. This results in antagonism of Ang II/AGTR1 stimulation, thus inhibiting

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Ming Zhu Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Bingxin Xu Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Meng Wang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Shangyun Liu Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Yue Zhang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Chao Zhang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Introduction The melanocortin receptors (MCRs) belong to α group of rhodopsin G-protein-coupled receptors. Mammalian MCRs consist of five subtypes, generally referred to as MC1R, MC2R, MC3R, MC4R and MC5R. A widely reported function of MC1R is

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Martin Wiegand MRC Biostatistics Unit, School of Clinical Medicine, University of Cambridge, Cambridge, UK

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David J Halsall Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Sarah L Cowan Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Kevin Taylor Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Robert J B Goudie MRC Biostatistics Unit, School of Clinical Medicine, University of Cambridge, Cambridge, UK

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Jacobus Preller Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Mark Gurnell Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK
Wellcome–MRC Institute of Metabolic Science, University of Cambridge and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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activation by converting angiotensin II (AngII) to angiotensin 1–7 (Ang 1–7). Ang 1–7 exerts anti-inflammatory, anti-oxidative and vasodilatory effects via binding to the Mas receptor ( 4 ). AngII binds AngII receptor type 1 which then exerts pro

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M L M Barreto-Chaves Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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N Senger Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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M R Fevereiro Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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A C Parletta Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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A P C Takano Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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participating in Akt and TGF-β activation.Increased levels of Ang-(1–7) prevents the development of T3-induced cardiac hypertrophy by blocking GSK3β/NFATc3 activation via the MAS receptor. AGT, angiotensinogen; Ang I, angiotensin I; Ang II, angiotensin II; Ang

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Abdul K Siraj Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Rong Bu Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Maham Arshad Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Kaleem Iqbal Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Sandeep Kumar Parvathareddy Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Tariq Masoodi Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Laila Omar Ghazwani Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Saif S Al-Sobhi Department of Surgery, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Fouad Al-Dayel Department of Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Khawla S Al-Kuraya Human Cancer Genomic Research, Research Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

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Introduction Thyroid cancer is the most frequently occurring endocrine cancer with an increasing incidence rate worldwide and with a frequency among the younger age group ( 1 , 2 ). It is also the second most common malignancy, after breast

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Dorte Glintborg Department of Endocrinology, Odense University Hospital, Odense, Denmark
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark

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Katrine Hass Rubin OPEN – Odense Patient data Explorative Network, Department of Clinical Research, University of Southern Denmark and Odense University Hospital, Odense, Denmark

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Mads Nybo Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Odense, Denmark

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Bo Abrahamsen OPEN – Odense Patient data Explorative Network, Department of Clinical Research, University of Southern Denmark and Odense University Hospital, Odense, Denmark
Department of Medicine, Holbæk Hospital, Holbæk, Denmark

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Marianne Andersen Department of Endocrinology, Odense University Hospital, Odense, Denmark
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark

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Introduction Polycystic ovary syndrome (PCOS) comprises irregular ovulation, hyperandrogenism, and/or polycystic ovaries when no other etiology can be found ( 1 ). Frank (overt) hypothyroidism is associated with insulin resistance

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Jesper Krogh Department of Endocrinology & Metabolism, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark

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Peter Plomgaard Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Biochemistry, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Ruth Frikke-Schmidt Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Biochemistry, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Sten Velschow Fluisense ApS, Lillerød, Denmark

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Jesper Johannesen Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark
Department of Pediatrics, Copenhagen University Hospital - Herlev & Gentofte, Copenhagen, Denmark

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Linda Maria Hilsted Department of Clinical Biochemistry, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Malene Schrøder Fluisense ApS, Lillerød, Denmark

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Ulla Feldt-Rasmussen Department of Endocrinology & Metabolism, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark

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Introduction In an everyday endocrine setting, the dynamic response of hormones is assessed for the diagnosis and evaluation of several conditions such as adrenal insufficiency ( 1 ), acromegaly ( 2 ), and growth hormone deficiency ( 3

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