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Stavroula A Paschou Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Nektaria Papadopoulou-Marketou Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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George P Chrousos Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Christina Kanaka-Gantenbein Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Huntingtin-interacting protein 14 gene is located on chromosome 12 and encodes for a palmitoyl transferase, which is involved in the metabolism and trafficking of proteins met with neurons. Knockdown of the genes in mice revealed increased apoptosis for

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Jia Liu Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China

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Min Liu Department of Radiology, China-Japan Friendship Hospital, Beijing, China

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Zhe Chen Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China

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Yumei Jia Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China

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Guang Wang Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China

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assessing fibrosis of some organs, such as the heart and liver ( 10 , 11 ). Typical thyroid lesions of AIT patients include diffuse lymphocytic infiltration with germinal center formation, fibrosis and apoptosis of thyroid epithelial cells ( 12 ). The

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Zeting Li Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Ling Pei Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Huangmeng Xiao Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Nan Chen Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Fenghua Lai Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Shufang Yue Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Changliu Xu Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Yanbing Li Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Haipeng Xiao Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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Xiaopei Cao Department of Endocrinology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, China

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secreted from pancreatic cells. PANDER has been shown to influence glycolipid metabolism by inducing apoptosis in pancreatic β cells, inhibiting insulin secretion ( 6 , 7 , 8 ), promoting hepatic glucose production, and stimulating lipogenesis ( 9 , 10

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Wenrui Wang Department of Endocrinology, The Second Hospital of Jilin University, Changchun, People’s Republic of China

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Chuan Zhang Department of Endocrinology, The Second Hospital of Jilin University, Changchun, People’s Republic of China

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to β-cell dedifferentiation rather than apoptosis, because the relatively low rate of apoptosis may not fully explain the loss of β-cell mass. β-cell dedifferentiation is characterized by decreased expression of specific genes that maintain the

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Davoud Jafari-Gharabaghlou Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran
Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Mostafa Vaghari-Tabari Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Hajar Oghbaei Department of Physiology, Tabriz University of Medical Sciences, Tabriz, Iran

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Laura Lotz Department of Obstetrics and Gynecology, Erlangen University Hospital, Friedrich-Alexander University of Erlangen–Nürnberg, Erlangen, Germany

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Reza Zarezadeh Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Yeganeh Rastgar Rezaei Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran

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Mahnaz Ranjkesh Medical Radiation Science Research Group (MRSRG), Tabriz University of Medical Sciences, Tabriz, Iran

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Mohammad Nouri Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Department of Reproductive Biology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran

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Amir Fattahi Department of Obstetrics and Gynecology, Erlangen University Hospital, Friedrich-Alexander University of Erlangen–Nürnberg, Erlangen, Germany
Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

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Saba Nikanfar Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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Ralf Dittrich Department of Obstetrics and Gynecology, Erlangen University Hospital, Friedrich-Alexander University of Erlangen–Nürnberg, Erlangen, Germany

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action Ref Leptin Remodeling of the endometrial epithelium (human) Stimulating proliferation and enhancing Fas ligand-induced apoptosis in EECs (39) Repairing endometrial epithelium after embryo implantation (human) ND (39

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Wang-shu Liu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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Ling-yan Hua Department of Ophthalmology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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Su-xiang Zhu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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Feng Xu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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Xue-qin Wang Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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Chun-feng Lu Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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Jian-bin Su Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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Feng Qi Emergency Intensive Care Unit, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China

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apoptosis of cardiomyocytes ( 29 ). In addition, SDF-1 can aggravate cardiac remodeling and worsen cardiac function by enhancing the proliferation of cardiac fibroblasts and collagen production ( 30 ). Correspondingly, plasma SDF-1 levels can serve as a

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Tingting Shu Department of Central Laboratory, Jiangsu Province Official Hospital, Nanjing, Jiangsu, China

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Zhigang Lv Department of Central Laboratory, Jiangsu Province Official Hospital, Nanjing, Jiangsu, China

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Yuchun Xie Department of Central Laboratory, Jiangsu Province Official Hospital, Nanjing, Jiangsu, China

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Junming Tang Department of Clinical Laboratory, Yixing People Hospital, Affiliated Jiangsu University, Yixing, Wuxi, Jiangsu, China

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Xuhua Mao Department of Clinical Laboratory, Yixing People Hospital, Affiliated Jiangsu University, Yixing, Wuxi, Jiangsu, China

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), ( 19 ) which influences the energy supply required for insulin secretion ( 20 ). Moreover, mitochondrial function becomes impaired, which induces endoplasmic reticulum stress response (ER stress), leading to β-cell apoptosis ( 21 , 22 ). In the

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Yusaku Mori Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
Department of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan

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Eunhyoung Ko Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada

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Rudolf Furrer Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada

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Linda C Qu Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada

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Stuart C Wiber Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada

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I George Fantus Departments of Medicine and Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
Division of Endocrinology and Metabolism, Leadership Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, Canada

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Mario Thevis Center for Preventive Doping Research and Institute of Biochemistry, German Sport University Cologne, Cologne, Germany

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Alan Medline Department of Laboratory Medicine & Pathobiology, University of Toronto, Toronto, Ontario, Canada
Department of Pathology, Humber River Regional Hospital, Toronto, Ontario, Canada

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Adria Giacca Departments of Physiology and Medicine, Institute of Medical Science, Banting and Best Diabetes Centre, University of Toronto, Toronto, Ontario, Canada

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the mouse model of the ter Braak et al . paper, loss of p53 function by mutation could have prevented the effect of insulin to inhibit apoptosis via PI3K/Akt-mediated suppression of p53 ( 26 , 37 ). Importantly, in the latter study, carcinosarcoma

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P G Murray Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK
Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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D Hanson Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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T Coulson Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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A Stevens Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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A Whatmore Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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R L Poole Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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D J Mackay Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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G C M Black Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK
Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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P E Clayton Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK
Centre for Paediatrics and Child Health, Faculty of Medicine, Centre for Genetic Medicine, 5th Floor Research, Genetic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK

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perinuclear region (5) . The function of CCDC8 is unknown, but it binds to OBSL1 (3) and is required for p53-mediated apoptosis (6) . The mechanisms leading to the growth impairment seen in 3-M syndrome remain unclear, but are likely to relate to

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Taís S Assmann Endocrine Division, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil
Postgraduation Program in Medical Sciences: Endocrinology, Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil

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Mariana Recamonde-Mendoza Institute of Informatics, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil

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Bianca M De Souza Endocrine Division, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil
Postgraduation Program in Medical Sciences: Endocrinology, Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil

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Daisy Crispim Endocrine Division, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil
Postgraduation Program in Medical Sciences: Endocrinology, Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil

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regulation of various processes, such as cellular differentiation, proliferation, metabolism, aging and apoptosis ( 10 , 12 ). miRNAs are estimated to regulate the expression of more than 60% of protein-coding genes ( 9 ); consequently, changes in their

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