Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Unit and Chair of Endocrinology and Metabolism, Center for Genomic Research, Department of Clinical Sciences and Community Health, Endocrine Unit, Azienda USL of Modena, NOCSAE, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Pietro Giardini 1355, 41126 Modena, Italy
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Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy, with a steadily increasing incidence in the last few decades worldwide. The predisposition to developing this carcinoma by the heterozygous state of rs2910164 within the precursor of the miR-146a has been reported, but recently not confirmed. Interestingly, on the same chromosome, almost 50 kb separate the pre-miR-146a from the pituitary tumor-transforming gene 1 (PTTG1), a proto-oncogene involved in several tumors, including thyroid cancers. In this study, we analyzed, using a case–control design, the genetic association between PTC and the genomic region encompassing pre-miR-146a rs2910164 and PTTG1 rs1862391 and rs2910202. We enrolled 307 affected patients and 206 healthy controls. The possible presence of thyroid nodules in controls was excluded by ultrasonography. All the cases were submitted to single-nucleotide polymorphism (SNP) genotyping of pre-miR-146a and PTTG1, and risk association analyses were carried out. The genotypic and allelic frequencies of pre-miR-146a rs2910164 were not statistically different in the patients and controls, and this SNP was not in linkage disequilibrium with the investigated PTTG1 SNPs. Consistently, meta-analyses, the first including all the affected cases published to date, did not confirm the previously reported association of the heterozygous CG genotype with PTC. The PTTG1 SNPs exhibited the same allelic frequency in the patients and controls and were not associated with the disease. In conclusion, in a well-selected Italian population, neither pre-miR-146a rs2910164 nor PTTG1 rs1862391 and rs2910202 were found to be associated with the risk of developing PTC.
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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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(Catalog# CRL11605™, ATCC) and grown in RPMI1640 medium (Catalog# 11875101, Thermo Fisher Scientific) with 10% fetal bovine serum (Catalog# 16000044, Thermo Fisher Scientific), 100 IU/mL penicillin and 100 µg/mL streptomycin. ELISA measurement of
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, glucose levels were analyzed using a glucose meter (Roche Diagnostics). An ultra-sensitive mouse insulin ELISA kit (ALP CO Diagnostics) was used to measure insulin levels. Pathological investigation First, animals were anesthetized by ether, then
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method defined by Chinard and was reported as μmol/mL ( 26 ). Arginine decarboxylase, ornithine decarboxylase and agmatinase levels were determined by ELISA kit according to the manufacturer’s protocol (Cusabio Biotech, Wuhan, China) and expressed as pg
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Center for Biochemistry, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany
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Center for Biochemistry, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany
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Center for Biochemistry, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany
Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany
Cologne Center for Musculoskeletal Biomechanics (CCMB), Cologne, Germany
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umbilical blood ( 14 ). Since there is an urgent need for a reliable and sensitive method to determine plasma asprosin levels ( 15 ), our laboratory took the initiative to develop a functional and dependable asprosin ELISA ( 16 ). Here, we set out to test
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
South West Sydney Clinical School, UNSW Sydney, Sydney, 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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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
Centre for Oncology Education and Research Translation (CONCERT), Liverpool, New South Wales, 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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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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healthy controls were collected in the same manner. Healthy controls were defined as volunteers with no active medical conditions. sPD-L1 ELISAs Soluble PD-L1 (sPD-L1) was quantified using a commercially available ELISA (PDCD1LG1 ELISA kit, USCN
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. Figure 2 Factors affecting hepcidin level, constituting the exclusion criteria of our study. The level of hepcidin was measured by the Hepcidin 25 (bioactive) hs ELISA, a highly sensitive enzyme immunoassay for the quantitative in vitro
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< 0.01; ns, not significant. (F–I) The level of Fe 2+ , the content of MDA, the level of ROS, and the content of GSH in NEDD4L-OE GCs was analyzed by ELISA ( n = 3) * P < 0.05, ** P < 0.01. Multiple modes of programmed cell death are
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from Promega. Insulin ELISA kits were purchased from Merodia (Uppsala, Sweden). Hepcidin ELISA kits were purchased from Uscn (Wuhan, China). Cells and cell culture The mouse insulinoma cell line, MIN6 was purchased from the American Type Culture
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Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada
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of CMKLR1 receptor activation (expressed as chemerin 157 equivalents) in each sample was interpolated based on its luciferase/β-galactosidase activity. Total chemerin measurements Total chemerin was quantified using a human pan-chemerin ELISA