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Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China
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Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China
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–7) (1–10 µM), the protein expression of CFTR was also increased ( Fig. 1B and C ). In addition, the long-term effect of Ang(1–7) in potentiating insulin secretion was abolished by incubating the cells with a selective CFTR inhibitor (CFTRinh-172, 10 µM
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Hyclone (Logan, UT, USA). Antibodies for the detection of Pdx-1 (D59H3), tubulin (2146) and lamin B (13435) were purchased from Cell Signaling Technology (New England Biolabs). The RNeasy Mini Kit was from Qiagen. The Luciferase Assay System was obtained
Department of Endocrinology, Diabetes and Metabolic Diseases, Normandie Univ, UNIROUEN, Rouen University Hospital, Rouen, France
Centre d’Investigation Clinique (CIC-CRB)-INSERM 1404, Rouen University Hospital, Rouen, France
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Department of Endocrinology, Diabetes and Metabolic Diseases, Normandie Univ, UNIROUEN, Rouen University Hospital, Rouen, France
Centre d’Investigation Clinique (CIC-CRB)-INSERM 1404, Rouen University Hospital, Rouen, France
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Department of Endocrinology, Diabetes and Metabolic Diseases, Normandie Univ, UNIROUEN, Rouen University Hospital, Rouen, France
Centre d’Investigation Clinique (CIC-CRB)-INSERM 1404, Rouen University Hospital, Rouen, France
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magnification, it seemed that 26RFa-LI was concentrated in cells of the isthmus and the neck, whereas the surface epithelium cells of the gastric pit and the base of the gland were not immunostained ( Fig. 1A and B ). However, higher magnification revealed
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overexpression and knockdown of PANDER were confirmed by qPCR and Western blot analyses ( Fig. 1A , B , C , D , E and F ). GCG gene expression, the GLP-1 protein in the cells, and the supernatant GLP-1 level were significantly reduced in the PANDER
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
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INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
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INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
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INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
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INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
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-HSD2 immunoreactivities were present in ZF of normal adrenals ( Fig. 2 B). In the adenoma, very intense immunostaining for 17α-OH and 3β-HSD2 was detected in almost all oncocytic cells and heterogeneous immunolabeling was observed in spongiocytic cells
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Department of Neurosurgery, Technical University Munich (TMU), Munich, Germany
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Medizinische Klinik Und Poliklinik III, University Hospital Carl Gustav Carus, Dresden, Germany
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Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
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Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
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72 h treatment ( Fig. 4A ). RGS also caused an increase in caspase3/7 activity in NCI-H295R cells ( P < 0.001) ( Fig. 4B ). At 100 nM, 300 nM, 1000 nM, and 3000 nM, RGS caused a 6.7-, 6.3-, 5.4-, and 5.7-fold increase in caspase 3/7 activity
School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia
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Saint Vincent’s Clinical School, UNSW Sydney, Sydney, Australia
SydPath, Saint Vincent’s Hospital, Sydney, Australia
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Gene & Stem Cell Therapy Program Centenary Institute, The University of Sydney, Camperdown, New South Wales, Australia
Faculty of Medicine & Health, The University of Sydney, Camperdown, New South Wales, Australia
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School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia
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School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia
School of Medicine, University of Wollongong, New South Wales, Australia
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School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia
Department of Head & Neck Surgery, Liverpool Hospital, Liverpool, New South Wales, Australia
Department of Clinical Medicine, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia
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School of Medicine, Western Sydney University, Campbelltown, New South Wales, Australia
South West Sydney Clinical School, UNSW Sydney, Sydney, Australia
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inclusion of additional variables can enhance the predictive capabilities of the current AJCC/UICC TNM staging system. Programmed cell death protein 1 (PD‐1), an inhibitory costimulatory molecule expressed on activated T, B, and NK cells, plays a critical
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European Pancreas Center, Department of General, Visceral and Transplantation Surgery, Heidelberg University Hospital, Heidelberg, Germany
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expression of ATX and STAT3 in BON1 cells transfected with ATX and STAT3 siRNAs was significantly inhibited ( Fig. 2A and B ). The number of invaded BON1 cells on the bottom of the membrane was significantly reduced after transfection with ATX or STAT3
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-hydroxy steroid dehydrogenase 5; HSD3B , 3beta-hydroxysteroid dehydrogenase; PGR , progesterone receptor; TBP, TATA-box-binding protein. Hormone assays Cell supernatants were collected and concentrations of the adipokines leptin (high
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are processed by antigen-presenting cells (such as dendritic cells, macrophages, or B cells). To trigger the activation of a T cell, antigen presentation through the major histocompatibility complex (MHC) and binding to a co-stimulatory protein are