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151. Effects of Whole Body Vibration Plus Diet on Insulin-Resistance in Middle-Aged Obese Subjects

Author: Paolo Sbraccia, Calogero Foti, Monica D’Adamo, Valeria Guglielmi, Davide Lauro, Alfonso Bellia, M. Sallì, Mauro Lombardo, L. Giordani, Massimo Federici, and C. Tirabasso
Subjects: Adult, Blood Glucose, Leptin, Male, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Diet, Reducing, medicine.medical_treatment, Physical Therapy, Sports Therapy and Rehabilitation, Vibration, Settore MED/13 - Endocrinologia, Insulin resistance, Internal medicine, medicine, Humans, Insulin, Whole body vibration, Orthopedics and Sports Medicine, Obesity, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Settore MED/14 - Nefrologia, Anthropometry, Adiponectin, Tumor Necrosis Factor-alpha, business.industry, Middle Aged, medicine.disease, Lipids, Settore MED/34 - Medicina Fisica e Riabilitativa, C-Reactive Protein, Endocrinology, Female, Blood sugar regulation, Insulin Resistance, Sedentary Behavior, business
Abstract: We investigated the early effects of whole body vibration (WBV) added to hypocaloric diet on insulin-resistance and other parameters associated with glucose regulation in sedentary obese individuals. We randomly assigned 34 patients to WBV plus hypocaloric diet (WBV group) or diet alone (CON group) for 8 weeks. Fasting and post-load glucose, insulin, lipids, C-reactive protein, tumor necrosis factor-α, leptin, adiponectin were assessed. Insulin sensitivity index (ISI) was derived from oral-glucose-tolerance test. Body composition was evaluated with dual-energy X-ray absorptiometry. Both groups lost approximately 5% of weight, with greater reduction of body fat in WBV than in CON (-7.1±1.2 Kg vs. -5.3±1.0 Kg, p=0.003). Percent variation of ISI was more pronounced in WBV than in CON group (+35±4% vs. + 22±5%, p=0.002), accompanied by slight improvement in post-load glucose (-1.07±0.02 vs. - 0.12±0.01 mmol/l, p=0.031) but without changes in fasting levels. Adiponectin significantly increased in WBV group compared with CON (p=0.021 for comparison) whereas no differences in leptin and inflammatory markers were observed. In middle-aged sedentary obese subjects, WBV added to hypocaloric diet for 8 weeks improved body composition, insulin-resistance, glucose regulation and adiponectin levels to a greater extent compared with diet alone. Efficacy and feasibility of this approach in the long term need to be ascertained.
Published: 2013
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152. Insulin resistance and atherosclerosis: convergence between metabolic pathways and inflammatory nodes

Author: Robert Stöhr and Massimo Federici
Subjects: Population, Adipose tissue, Inflammation, Biology, Biochemistry, Immune system, Insulin resistance, Diabetes mellitus, medicine, Animals, Humans, Obesity, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, education, Molecular Biology, education.field_of_study, Macrophages, Monocyte, Cell Biology, Atherosclerosis, medicine.disease, Insulin receptor, medicine.anatomical_structure, Immunology, biology.protein, Inflammation Mediators, Insulin Resistance, medicine.symptom, Metabolic Networks and Pathways
Abstract: For some time now it has been known that diabetes and atherosclerosis are chronic inflammatory diseases that are closely associated with one another and often develop together. In both there is an increase in tissue-wide inflammation that is exhibited by the infiltration of immune cells into the adipose tissue and the vascular walls respectively. The monocyte/macrophage populations that are recruited in these seemingly different settings also display a high similarity by exhibiting similar phenotypes in both conditions. In the insulin resistant as well as the atherosclerotic setting there is a distinct switch in the macrophage populations present from an anti-inflammatory (M2) population to an inflammatory (M1) population, which releases cytokines and chemotactic factors with the ability to worsen the local environment and thus aggravate the situation by creating a vicious circle. However, although some discoveries suggest that preventing the development of M1 macrophages reduces inflammation and thereby aggravation of these diseases, there are currently no clear-cut opinions on how to achieve a switch from M2 to M1.
Published: 2013
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153. Pioglitazone improves glucose metabolism and modulates skeletal muscle TIMP-3–TACE dyad in type 2 diabetes mellitus: a randomised, double-blind, placebo-controlled, mechanistic study

Author: Franco Folli, Amalia Gastaldelli, Giuseppe Daniele, Zandra Perez-Cadena, Teresa Vanessa Fiorentino, Subhash Kamath, Paolo Fanti, Alberto Chavez-Velasquez, Francesco Andreozzi, Christopher P. Jenkinson, Devjit Tripathy, Ralph A. DeFronzo, and Massimo Federici
Subjects: Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Population, Type 2 diabetes, ADAM17 Protein, Insulin resistance, Internal medicine, Diabetes mellitus, Plasminogen Activator Inhibitor 1, Diabetes Mellitus, Internal Medicine, medicine, Humans, Hypoglycemic Agents, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Muscle, Skeletal, education, Chemokine CCL2, Tissue Inhibitor of Metalloproteinase-3, education.field_of_study, Glucose tolerance test, Pioglitazone, Adiponectin, medicine.diagnostic_test, Chemokine CX3CL1, Interleukin-6, Tumor Necrosis Factor-alpha, business.industry, Skeletal, Glucose Tolerance Test, Middle Aged, medicine.disease, Metformin, ADAM Proteins, Glucose, Endocrinology, Diabetes Mellitus, Type 2, Female, Thiazolidinediones, Muscle, business, Type 2, medicine.drug
Abstract: Pioglitazone (PIO) is a peroxisome proliferator-activated receptor (PPAR)γ agonist insulin-sensitiser with anti-inflammatory and anti-atherosclerotic effects. Our objective was to evaluate the effect of low-dose PIO (15 mg/day) on glucose metabolism and inflammatory state in obese individuals with type 2 diabetes. A randomised, double-blind, placebo-controlled, mechanistic trial was conducted on 29 patients with type 2 diabetes treated with metformin and/or sulfonylurea. They were randomised to receive PIO or placebo (PLC) for 6 months, in a 1:1 ratio. Participants were allocated to interventions by central office. All study participants, investigators and personnel performing measurements were blinded to group assignment. At baseline and after 6 months patients underwent: (1) OGTT; (2) muscle biopsy to evaluate expression of TNF-α, tissue inhibitor of metalloproteases 3 (TIMP-3) levels, TNF-α converting enzyme (TACE) expression and enzymatic activity; (3) euglycaemic–hyperinsulinaemic clamp; (4) measurement of plasma high-sensitivity C-reactive protein (hsCRP), plasminogen activator inhibitor type-1 (PAI-1), TNF-α, IL-6, monocyte chemotactic protein-1 (MCP-1), adiponectin and fractalkine (FRK). The interventions were PIO 15 mg/day vs placebo and the main outcomes measured were absolute changes in whole-body insulin sensitivity, insulin secretion and inflammatory state. Fifteen participants were randomized to receive PIO and 14 participants were randomized to receive PLC. Eleven participants completed the study in the PIO group and nine participants completed the study in the PLC group and were analysed. Fasting plasma glucose and HbA1c decreased modestly (p
Published: 2013
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154. MicroRNAs in Endothelial Senescence and Atherosclerosis

Author: Viviana Casagrande, Massimo Federici, and Rossella Menghini
Subjects: Genetic Markers, Senescence, Pharmaceutical Science, Inflammation, Disease, Biology, Bioinformatics, Downregulation and upregulation, microRNA, Autophagy, Genetics, medicine, Animals, Humans, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Endothelial dysfunction, Cellular Senescence, Genetics (clinical), Regulation of gene expression, Neovascularization, Pathologic, Settore BIO/12, Gene Expression Profiling, Endothelial Cells, Atherosclerosis, medicine.disease, MicroRNAs, Gene Expression Regulation, Immunology, Molecular Medicine, medicine.symptom, Cardiology and Cardiovascular Medicine, Cell aging
Abstract: Aging is an important risk factor for the development of many cardiovascular diseases as atherosclerosis and is accompanied by the decline of endothelial function. Senescence of endothelial cells has been proposed to be involved in endothelial dysfunction and atherogenesis. Therefore, the study of new target therapies to prevent or reverse this process represents a field of great interest. MicroRNAs (miRNAs), a class of short RNAs, play key roles in various biological processes and in the development of human disease through specific posttranscriptional downregulation of gene expression. In particular, miRNAs that are highly expressed by endothelial cells can be detected in high concentration in human atherosclerotic plaques and in the circulation, suggesting their potential translation to bedside to determine the dysfunction of specific signaling pathways which play a role in coronary artery disease in the individual patient, a path towards a stratified medicine approach for early preventive treatment of disease. Here, we review the most recent advances in the field of atherosclerosis that implicate a role for miRNAs with a special emphasis on endothelial senescence and its involvement in the atherosclerotic process. Finally, we briefly discuss the potential use of miRNAs signatures to map atherosclerosis progression and in particular underlying the relevance of circulating plasma miRNAs that can be used clinically as biomarkers of vascular pathology.
Published: 2013
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155. Regulation of TIMP3 in diabetic nephropathy: a role for microRNAs

Author: Rossella Menghini, Francesca Conserva, Maria Mavilio, Massimo Federici, Michele Cavalera, Loredana Fiorentino, and Loreto Gesualdo
Subjects: medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Biology, Nephropathy, Diabetic nephropathy, Mice, Endocrinology, Fibrosis, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Animals, Humans, Diabetic Nephropathies, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Cells, Cultured, Mice, Knockout, Tissue Inhibitor of Metalloproteinase-3, Kidney, Mesangial cell, Gene Expression Profiling, Glomerular basement membrane, General Medicine, medicine.disease, Mice, Inbred C57BL, MicroRNAs, medicine.anatomical_structure, Gene Expression Regulation, Mesangial Cells, Kidney disease
Abstract: Diabetic nephropathy (DN) is the major cause of chronic kidney disease in developed countries and contributes significantly to increased morbidity and mortality among diabetic patients. Morphologically, DN is characterized by tubulo-interstitial fibrosis, thickening of the glomerular basement membrane and mesangial expansion mainly due to accumulation of extracellular matrix (ECM). ECM turnover is regulated by metalloproteinases and tissue inhibitors of metalloproteinases (TIMPs) activities. In diabetic conditions, TIMP3 expression in kidney is strongly reduced, but the causes of this reduction are still unknown. The aim of this study was to elucidate at least one of these mechanisms which relies on differential expression of TIMP3-targeting microRNAs (miRs) in a hyperglycemic environment either in vitro (MES13 cell line) or in vivo (mouse kidney and human biopsies). Among the TIMP3-targeting miRs, miR-21 and miR-221 were significantly upregulated in kidneys from diabetic mice compared to control littermates, and in a mesangial cell line grown in high glucose conditions. In human samples, only miR-21 expression was increased in kidney biopsies from diabetic patients compared to healthy controls. The expression of miR-217, which targets TIMP3 indirectly through downregulation of SirT1, was also increased in diabetic kidney and MES13 cell line. In agreement with these result, SirT1 expression was reduced in mouse and human diabetic kidneys as well as in MES13 mesangial cell line. TIMP3 deficiency has recently emerged as a hallmark of DN in mouse and human. In this study, we demonstrated that this reduction is due, at least in part, to increased expression of certain TIMP3-targeting miRs in diabetic kidneys compared to healthy controls. Unveiling the post-transcriptional mechanisms responsible for TIMP3 downregulation in hyperglycemic conditions may orient toward the use of this protein as a possible therapeutic target in DN.
Published: 2013
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156. Low FT3: a possible marker of frailty in the elderly

Author: Massimo Federici, Alessia Valentini, Elena Gasbarra, Aldo Bertoli, Maria Assunta Cianfarani, and Umberto Tarantino
Subjects: Gerontology, Male, Thyrotropin, Comorbidity, 030204 cardiovascular system & hematology, Thyroid Function Tests, 0302 clinical medicine, Settore MED/33 - Malattie Apparato Locomotore, FT3, 030212 general & internal medicine, Original Research, Aged, 80 and over, Hip fracture, Frailty, Thyroid, General Medicine, Europe, medicine.anatomical_structure, Ambulatory, Population study, Triiodothyronine, Female, medicine.medical_specialty, Thyroid Hormones, Frail Elderly, NTIS, 03 medical and health sciences, Hip Fracture, Thyroid-stimulating hormone, Internal medicine, medicine, Humans, aging, frailty, hip fracture, Geriatric Assessment, Aged, business.industry, Hip Fractures, RC952-954.6, medicine.disease, Health Surveys, Thyroxine, Ageing, Geriatrics, Sarcopenia, Clinical Interventions in Aging, Observational study, Geriatrics and Gerontology, business, Biomarkers
Abstract: Aldo Bertoli,1 Alessia Valentini,1 Maria Assunta Cianfarani,1 Elena Gasbarra,2 Umberto Tarantino,2 Massimo Federici1 1Department of Systems Medicine, University of Rome “Tor Vergata”, Rome, Italy; 2Department of Orthopaedics and Traumatology, University of Rome “Tor Vergata”, Rome, Italy Introduction: Frailty is associated with a functional decline of multiple physiological systems, of which they may be a cause or consequence. The objective of the study was to evaluate the prevalence of thyroid hormone modifications in elderly frail subjects and its relationship with frailty.Study population and methods: An observational study was carried out at the University Hospital “Tor Vergata” in Rome among ambulatory and hospitalized patients. The study population consisted of 112 elderly subjects: 62 were hospitalized following hip fracture and 50 control subjects were outpatients. Participating patients received a multidimensional geriatric evaluation. The Survey of Health, Ageing and Retirement in Europe Frailty Instrument (SHARE-FI) was used to assess the degree of frailty. Thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) were measured to evaluate thyroid status.Results: FT3, but not FT4, was significantly correlated with Frailty score, both in patients with hip fracture and in patients from the control group. In the entire study population, FT3 under normal limits is effective in discriminating frail/prefrail subjects from nonfrail subjects.Discussion: The reduction in serum concentrations of FT3 is a clear manifestation of stress associated with fractures. Numerous preexisting factors, such as the fracture patients’ nutritional status, sarcopenia, disability and comorbidities, which characterize the condition of frailty and influence its pathogenesis, are strongly correlated with FT3 values, suggesting the existence of latent nonthyroidal illness syndrome (NTIS).Conclusion: We conclude that measuring FT3 can be a useful laboratory parameter in clinical assessment, which can play an important role in identifying vulnerable elderly subjects and in quantifying the condition of frailty. Keywords: FT3, frailty, NTIS, hip fracture, aging
Published: 2017

157. The PDE4 inhibitor roflumilast reduces weight gain by increasing energy expenditure and leads to improved glucose metabolism

Author: Julia, Möllmann, Florian, Kahles, Corinna, Lebherz, Ben, Kappel, Christer, Baeck, Frank, Tacke, Christian, Werner, Massimo, Federici, Nikolaus, Marx, and Michael, Lehrke
Subjects: Cyclopropanes, glucose metabolism, hepatic steatosis, Aminopyridines, Diet, High-Fat, Weight Gain, Cyclic AMP-Dependent Protein Kinases, Mice, Inbred C57BL, mitochondria, Mice, Glucose, energy expenditure, insulin resistance, Liver, Non-alcoholic Fatty Liver Disease, Benzamides, Animals, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Energy Metabolism, Signal Transduction
Abstract: To investigate the metabolic effects of the phosphodiesterase-4 (PDE4) inhibitor roflumilast, a clinically approved anti-inflammatory drug used for the treatment of chronic obstructive pulmonary disease.The metabolic effects of roflumilast were investigated in C57BL/6J mice, fed a high-fat Western-type diet and treated with or without roflumilast for a period of 12 weeks.Roflumilast led to a marked reduction in body weight gain, which became apparent in the second week after treatment initiation and was attributable to a pronounced increase in energy expenditure. Furthermore, roflumilast improved glucose tolerance, reduced insulin resistance and diminished steatohepatitis in mice. Mechanistically, this was associated with hepatic protein kinase A (PKA) and cAMP response element binding protein (CREB) activation, leading to peroxisome proliferator-activated receptor gamma coactivator-1α (PCG-1α)-dependent induction of mitochondrial biogenesis. Consistently, roflumilast increased the cellular respiratory capacity of hepatocytes in a PKA-dependent manner.Roflumilast-dependent PDE4 inhibition is a new target for weight loss strategies, especially in conditions of associated comorbidities such as insulin resistance and non-alcoholic steatohepatitis.
Published: 2017

158. Joint effect of insulin signaling genes on cardiovascular events and on whole body and endothelial insulin resistance

Author: Assunta Pandolfi, Carmine Zoccali, Massimiliano Copetti, Sara Di Silvestre, Agostino Consoli, Luana Mercuri, Roberto Baratta, Giovanni Tripepi, Belinda Spoto, Natalia Di Pietro, Sabrina Prudente, Fabio Pellegrini, Vincenzo Trischitta, Simonetta Bacci, Massimo Federici, Alessandra Testa, Stefano Rizza, Rosa Di Paola, Francesca Mallamaci, Eleonora Morini, Renato Lauro, Alessandro Doria, Yuan Yuan Zhang, Lucia Frittitta, and Lorenzo Malatino
Subjects: Male, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Endothelium, medicine.medical_treatment, Single-nucleotide polymorphism, 030204 cardiovascular system & hematology, Article, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Internal medicine, insulin sensitivity, genetic susceptibility, insulin dependent endothelial function, nonsynonymous polymorphism, medicine, Humans, Insulin, Prospective Studies, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, genes, insulin signaling, Cells, Cultured, 030304 developmental biology, 0303 health sciences, biology, cardiovascular diseases, Endothelial Cells, medicine.disease, 3. Good health, IRS1, Nitric oxide synthase, Insulin receptor, Cross-Sectional Studies, Endocrinology, medicine.anatomical_structure, biology.protein, Female, Endothelium, Vascular, Insulin Resistance, Signal transduction, Cardiology and Cardiovascular Medicine, Signal Transduction
Abstract: Insulin resistance (IR) and cardiovascular disease (CVD) share a common soil. We investigated the combined role of single nucleotide polymorphisms (SNPs) affecting insulin signaling (ENPP1 K121Q, rs1044498; IRS1 G972R, rs1801278; TRIB3 Q84R, rs2295490) on CVD, age at myocardial infarction (MI), in vivo insulin sensitivity and in vitro insulin-stimulated nitric oxide synthase (NOS) activity.1. We first studied, incident cardiovascular events (a composite endpoint comprising myocardial infarction-MI, stroke and cardiovascular death) in 733 patients (2186 person-years, 175 events). 2. In a replication attempt, age at MI was tested in 331 individuals. 3. OGTT-derived insulin sensitivity index (ISI) was assessed in 829 individuals with fasting glucose126 mg/dl. 4. NOS activity was measured in 40 strains of human vein endothelial cells (HUVECs).1. Risk variants jointly predicted cardiovascular events (HR = 1.181; p = 0.0009) and, when added to clinical risk factors, significantly improved survival C-statistics; they also allowed a significantly correct reclassification (by net reclassification index) in the whole sample (135/733 individuals) and, even more, in obese patients (116/204 individuals). 2. Risk variants were jointly associated with age at MI (p = 0.006). 3. A significant association was also observed with ISI (p = 0.02). 4. Finally, risk variants were jointly associated with insulin-stimulated NOS activity in HUVECs (p = 0.009).Insulin signaling genes variants jointly affect cardiovascular disease, very likely by promoting whole body and endothelium-specific insulin resistance. Further studies are needed to address whether their genotyping help identify very high-risk patients who need specific and/or more aggressive preventive strategies.
Published: 2013
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159. Effects of Dipeptidyl Peptidase 4 Inhibitors and Sodium-Glucose Linked coTransporter-2 Inhibitors on cardiovascular events in patients with type 2 diabetes mellitus: A meta-analysis

Author: Gianluigi Savarese, Fabiana De Martino, Teresa Losco, Lars H. Lund, Bruno Trimarco, Francesca Ferrazzano, Caterina Marciano, Pasquale Perrone-Filardi, Carmen D'Amore, Santo Dellegrottaglie, Giuseppe M.C. Rosano, Massimo Federici, Savarese, Gianluigi, D'Amore, Carmen, Federici, Massimo, DE MARTINO, Fabiana, Dellegrottaglie, Santo, Marciano, Caterina, Ferrazzano, Francesca, Losco, Teresa, Lund, Lars H., Trimarco, Bruno, Rosano, Giuseppe M. C., and PERRONE FILARDI, Pasquale
Subjects: Blood Glucose, medicine.medical_specialty, 030209 endocrinology & metabolism, Settore MED/11 - Malattie dell'Apparato Cardiovascolare, Outcomes, 030204 cardiovascular system & hematology, Placebo, Cardiovascular, law.invention, Dipeptidyl Peptidase 4 Inhibitors, Settore MED/13 - Endocrinologia, 03 medical and health sciences, 0302 clinical medicine, Sodium-Glucose Transporter 2, Randomized controlled trial, law, Internal medicine, Type 2 diabetes mellitus, medicine, Humans, Myocardial infarction, Sodium-Glucose Transporter 2 Inhibitors, Stroke, Dipeptidyl peptidase-4, Randomized Controlled Trials as Topic, Outcome, Glycemic, Dipeptidyl-Peptidase IV Inhibitors, Sodium-Glucose Linked coTransporter-2 Inhibitor, Sodium-Glucose Linked coTransporter-2 Inhibitors, business.industry, Dipeptidyl Peptidase 4 Inhibitor, Type 2 Diabetes Mellitus, medicine.disease, Type 2 diabetes mellitu, Treatment Outcome, Endocrinology, Diabetes Mellitus, Type 2, Cardiovascular Diseases, Heart failure, Cardiology and Cardiovascular Medicine, business
Abstract: Background Dipeptidyl Peptidase 4 Inhibitors (DPP4-I) and Sodium-Glucose Linked coTransporter-2 Inhibitors (SGLT2-I) improve glycemic control in patients with type 2 diabetes mellitus (DM). However, only few studies were designed to assess the efficacy and safety of these drugs on cardiovascular (CV) events and mortality. The purpose of the current study was to evaluate the effects of DPP4-Is and SGLT2-Is on CV events and mortality by meta-analysis. Methods Randomized trials enrolling more than 200 patients, comparing DPP-4-Is or SGLT2-Is versus placebo or active treatments in patients with DM, and reporting at least one event among all-cause and CV mortality, stroke, myocardial infarction (MI) and new onset of heart failure (HF), were included. Results 157 randomized trials (114 on DPP4-Is and 43 on SGLT2-Is) enrolling 140,470 patients (107,100 in DPP4-I and 33,370 in SGLT2-I studies) were included in the analysis. Compared to control, treatment with DPP4-Is did not affect all-cause (RR: 1.010; 95% CI: 0.935–1.091) and CV (RR: 0.975; CI: 0.887–1.073) mortality as well as risk of MI (RR: 0.915; CI: 0.835–1.002), stroke (RR: 0.933; CI: 0.820–1.062) and HF (RR: 1.083; CI: 0.973–1.205). Treatment with SGLT2-Is significantly reduced the risk of all-cause death by 28% (RR: 0.718; CI: 0.613–0.840), CV death by 33% (RR: 0.668; CI: 0.544–0.821), MI by 20% (RR: 0.803; CI: 0.668–0.965) and HF by 35% (RR: 0.652; CI: 0.517–0.823) without effect on stroke (RR: 1.158; CI: 0.912–1.469). Conclusions DPP4-Is show a safe CV profile as they do not affect mortality and CV events, including HF, in patients with type 2 DM. SGLT2-Is are associated with improved CV outcome and survival in DM patients.
Published: 2016

160. Changes in blood microbiota profiles associated with liver fibrosis in obese patients: A pilot analysis

Author: Jacques Amar, Michael Courtney, José Manuel Fernández-Real, Matteo Serino, Rémy Burcelin, Massimo Federici, Carine Valle, Salah Benyahya, Benjamin Lelouvier, Sandrine Païssé, Maria Rosa Ortiz, Florence Servant, Anne-Claire Brunet, and Josep Puig
Subjects: 0301 basic medicine, Liver Cirrhosis, Male, medicine.medical_specialty, medicine.drug_class, Pilot Projects, Biology, Gastroenterology, 03 medical and health sciences, Liver disease, Feces, Fibrosis, Internal medicine, Nonalcoholic fatty liver disease, medicine, Humans, Obesity, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Ribosomal DNA, Hepatology, Bile acid, Microbiota, Middle Aged, medicine.disease, 3. Good health, 030104 developmental biology, Real-time polymerase chain reaction, Cross-Sectional Studies, Cohort, Biomarker (medicine), Female
Abstract: The early detection of liver fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) is an important clinical need. In view of the suggested role played by bacterial translocation in liver disease and obesity, we sought to investigate the relationship between blood microbiota and liver fibrosis (LF) in European cohorts of patients with severe obesity. We carried out a cross-sectional study of obese patients, well characterized with respect to the severity of the NAFLD, in the cohort FLORINASH. This cohort has been divided into a discovery cohort comprising 50 Spanish patients and then in a validation cohort of 71 Italian patients. Blood bacterial DNA was analyzed both quantitatively by 16S ribosomal DNA (rDNA) quantitative polymerase chain reaction and qualitatively by 16S rDNA targeted metagenomic sequencing and functional metagenome prediction. Spanish plasma bile acid contents were analyzed by liquid chromatography/mass spectrometry. The 16S rDNA concentration was significantly higher in patients of the discovery cohort with LF. By 16S sequencing, we found specific differences in the proportion of several bacterial taxa in both blood and feces that correlate with the presence of LF, thus defining a specific signature of the liver disease. Several secondary/primary bile acid ratios were also decreased with LF in the discovery cohort. We confirmed, in the validation cohort, the correlation between blood 16S rDNA concentration and LF, whereas we did not confirm the specific bacterial taxa signature, despite a similar trend in patients with more-severe fibrosis.Changes in blood microbiota are associated with LF in obese patients. Blood microbiota analysis provides potential biomarkers for the detection of LF in this population. (Hepatology 2016;64:2015-2027).
Published: 2016

161. Overexpression of Tissue Inhibitor of Metalloproteinase 3 in Macrophages Reduces Atherosclerosis in Low-Density Lipoprotein Receptor Knockout Mice

Author: Arianna Marino, Giuseppe Pugliese, Marta Letizia Hribal, Viviana Casagrande, Rossella Menghini, Paolo Gentileschi, Orazio Schillaci, Massimo Federici, Paolo Sbraccia, Valentina Marchetti, Michele Cavalera, Davide Lauro, Stefano Menini, Marta Fabrizi, Ottavia Porzio, and Renato Lauro
Subjects: Male, Pathology, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Stromal cell, Mice, Transgenic, 030204 cardiovascular system & hematology, Biology, metalloproteinases, Settore MED/13 - Endocrinologia, Mice, 03 medical and health sciences, 0302 clinical medicine, atherosclerosis, inflammation, lipotoxicity, macrophages, medicine, Animals, Macrophage, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Promoter Regions, Genetic, Receptor, 030304 developmental biology, Mice, Knockout, Tissue Inhibitor of Metalloproteinase-3, 0303 health sciences, Settore BIO/12, Macrophages, Monocyte, Tissue inhibitor of metalloproteinase, Atherosclerosis, Molecular biology, Up-Regulation, Mice, Inbred C57BL, Disease Models, Animal, medicine.anatomical_structure, Receptors, LDL, Knockout mouse, LDL receptor, Diet, Atherogenic, Cardiology and Cardiovascular Medicine, Lipoprotein
Abstract: Objective— Tissue inhibitor of metalloproteinase 3 (TIMP3) is a stromal protein that inhibits the activity of proteases and receptors. TIMP3 is downregulated in metabolic and inflammatory disorders, such as type 2 diabetes mellitus and atherosclerosis, particularly in regions enriched with monocyte/macrophage cells. To investigate the role of TIMP3 in atherosclerosis, we generated a new mouse model in which Timp3 was overexpressed in the atherosclerotic plaque via a macrophage-specific promoter (MacT3). We elucidated any potential antiatherosclerotic effects of TIMP3, including regulation of monocyte/macrophage recruitment within atherosclerotic plaques, in MacT3 mice crossbred with low-density lipoprotein receptor knockout (LDLR −/− ) mice. Methods and Results— MacT3/LDLR −/− mice had an improvement of atherosclerosis and metabolic parameters compared with LDLR −/− . En face aorta and aortic root examination of MacT3/LDLR −/− mice revealed smaller atherosclerotic plaques with features of stability, such as increased collagen content and decreased necrotic core formation. Atherosclerotic plaques in MacT3/LDLR −/− mice contained fewer T cells and macrophages. Furthermore, TIMP3 overexpression in macrophages resulted in reduced oxidative stress signals, as evidenced by lower lipid peroxidation, protein carbonylation, and nitration in atheromas. Conclusion— Our study confirmed that macrophage-specific overexpression of TIMP3 decreases the inflammatory content and the amplitude of atherosclerotic plaques in mice.
Published: 2012
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162. Decreased IRS2 and TIMP3 Expression in Monocytes From Offspring of Type 2 Diabetic Patients Is Correlated With Insulin Resistance and Increased Intima-Media Thickness

Author: Davide Lauro, Renato Lauro, Iris Cardolini, Alessio Luzi, Francesca Davato, Rossella Menghini, Massimo Federici, Marina Cardellini, Ottavia Porzio, Stefano Rizza, Paolo Gentileschi, Rossella D'Alfonso, Maria Adelaide Marini, and Paolo Sbraccia
Subjects: Adult, Male, medicine.medical_specialty, Complications, Insulin Receptor Substrate Proteins, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Enzyme-Linked Immunosorbent Assay, Type 2 diabetes, 030204 cardiovascular system & hematology, Biology, Carotid Intima-Media Thickness, Polymerase Chain Reaction, Monocytes, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Internal medicine, Internal Medicine, medicine, Humans, Insulin, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, 030304 developmental biology, Tissue Inhibitor of Metalloproteinase-3, 0303 health sciences, Settore BIO/12, Glucose clamp technique, Middle Aged, medicine.disease, Atherosclerosis, IRS2, IRS1, Insulin receptor, Endocrinology, Diabetes Mellitus, Type 2, biology.protein, Glucose Clamp Technique, Female, Insulin Resistance
Abstract: OBJECTIVE In humans, it is unclear if insulin resistance at the monocyte level is associated with atherosclerosis in vivo. Here we have studied first-degree relatives of patients with type 2 diabetes to investigate whether a reduction in components of the insulin signal transduction pathways, such as the insulin receptor (InsR) or InsR substrate 1 or 2 (IRS1 or IRS2), or a reduction in genetic modifiers of insulin action, such as the TIMP3/ADAM17 (tissue inhibitor of metalloproteinase 3/A disintegrin and metalloprotease domain 17) pathway, is associated with evidence of atherosclerosis. RESEARCH DESIGN AND METHODS Insulin sensitivity was analyzed through euglycemic-hyperinsulinemic clamp, and subclinical atherosclerosis was analyzed through intimal medial thickness. Monocytes were isolated through magnetic cell sorting, and mRNA and proteins were extracted and analyzed by quantitative PCR and pathscan enzyme-linked immunosorbent assays, respectively. RESULTS In monocyte cells from human subjects with increased risk for diabetes and atherosclerosis, we found that gene expression, protein levels, and tyrosine phosphorylation of IRS2, but not InsR or IRS1, were decreased. TIMP3 was also reduced, along with insulin resistance, resulting in increased ectodomain shedding activity of the metalloprotease ADAM17. CONCLUSIONS Systemic insulin resistance and subclinical atherosclerosis are associated with decreased IRS2 and TIMP3 expression in circulating monocytes.
Published: 2011

163. Human placental lactogen (hPL-A) activates signaling pathways linked to cell survival and improves insulin secretion in human pancreatic islets

Author: Massimo Federici, Renato Lauro, Barbara Bartolini, Luca Bova, Marco F. Lombardo, Davide Lauro, Fabiana De Angelis, Federico Bertuzzi, Barbara Capuani, Giulia Donadel, and Rita Nano
Subjects: endocrine system, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Cell Survival, MAP Kinase Signaling System, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Settore MED/50 - Scienze Tecniche Mediche Applicate, Apoptosis, Biology, p38 Mitogen-Activated Protein Kinases, Settore MED/13 - Endocrinologia, Mice, Endocrinology, Human placental lactogen, Cell Line, Tumor, Insulin-Secreting Cells, Internal medicine, Insulin Secretion, medicine, Animals, Humans, Insulin, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Extracellular Signal-Regulated MAP Kinases, Insulinoma, Protein kinase B, PI3K/AKT/mTOR pathway, Settore MED/04 - Patologia Generale, Human Growth Hormone, Pancreatic islets, Placental Lactogen, medicine.disease, Prolactin, Rats, Pancreatic Neoplasms, medicine.anatomical_structure, Beta cell, Signal transduction, Proto-Oncogene Proteins c-akt, Research Paper
Abstract: The search for factors either promoting islets proliferation or survival during adult life is a major issue for both type 1 and 2 diabetes mellitus. Among factors with mitogenic activity on pancreatic β-cells, human placental lactogen (hPL) showed stronger activity when compared to the other lactogen hormones: growth hormone (GH) and prolactin (PRL). The aim of the present work is to elucidate the biological and molecular events of hPL isoform A (hPL-A) activity on human cultured islets. We used pure human pancreatic islets and insulinoma cell lines (βTC-1 and RIN, murine and rat respectively) stimulated with hPL-A recombinant protein and we compared hPL-A activity with that of hGH. We showed that hPL-A inhibits apoptosis, both in insulinoma and human islets, by the phosphorylation of AKT protein. Indeed, the antiapoptotic role of hPL-A was mediated by PI3K, p38 and it was independent by PKA, Erk1/2. Compared with hGH, hPL-A modulated at different intervals and/or intensity by the phosphorylation of JAKs/STATs and MAPKinases. Moreover, hPL-A induced PDX-1 intracellular expression, improving beta cell activity and ameliorating insulin secretion in response to high glucose stimulation. Our data support the idea that hPL-A is involved in the regulation of beta cells activity. Importantly, we found that hPL-A can preserve and improve the ability of purified human pancreatic islets cultured to secrete insulin in vitro.
Published: 2011
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164. Galectin-3 ablation protects mice from diet-induced NASH: A major scavenging role for galectin-3 in liver

Author: Iacobini, Carla, Menini, Stefano, Ricci, Carlo, Blasetti Fantauzzi, C., BLASETTI FANTAUZZI, Claudia, Angela, Scipioni, Salvi, Laura, Cordone, Samantha, Francesca, Delucchi, Matteo, Serino, Massimo, Federici, Flavia, Pricci, and Pugliese, Giuseppe
Subjects: CD36 Antigens, Liver Cirrhosis, Galectin 3, Receptor for Advanced Glycation End Products, Apoptosis, Inbred C57BL, medicine.disease_cause, Severity of Illness Index, Mice, Non-alcoholic Fatty Liver Disease, Immunologic, Fibrosis, Receptors, steatosis, Leukocytes, Receptors, Immunologic, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, advanced lipoxidation endproducts, Beta oxidation, Mice, Knockout, Chemistry, Atherogenic, medicine.anatomical_structure, Liver, Galectin-3, Hepatocyte, Female, medicine.symptom, medicine.medical_specialty, Knockout, Inflammation, Internal medicine, medicine, Animals, Gene Silencing, Antigens, Hepatology, fibrosis, Lipid metabolism, inflammation, oxidative stress, Fibroblasts, Lipid Metabolism, medicine.disease, Diet, Mice, Inbred C57BL, Fatty Liver, Antigens, CD36, Diet, Atherogenic, Oxidative Stress, Endocrinology, Steatosis, CD36, Oxidative stress
Abstract: Excess fatty acid oxidation and generation of reactive carbonyls with formation of advanced lipoxidation endproducts (ALEs) is involved in nonalcoholic steatohepatitis (NASH) by triggering inflammation, hepatocyte injury, and fibrosis. This study aimed at verifying the hypothesis that ablation of the ALE-receptor galectin-3 prevents experimental NASH by reducing receptor-mediated ALE clearance and downstream events.Galectin-3-deficient (Lgals3(-/-)) and wild type (Lgals3(+/+)) mice received an atherogenic diet or standard chow for 8 months. Liver tissue was analyzed for morphology, inflammation, cell and matrix turnover, lipid metabolism, ALEs, and ALE-receptors.Steatosis was significantly less pronounced in Lgals3(-/-) than Lgals3(+/+) animals on atherogenic diet. NASH, invariably detected in Lgals3(+/+) mice, was observed, to a lower extent, only in 3/8 Lgals3(-/-) mice, showing less inflammatory, degenerative, and fibrotic phenomena than Lgals3(+/+) mice. This was associated with higher circulating ALE levels and lower tissue ALE accumulation and expression of other ALE-receptors. Up-regulation of hepatic fatty acid synthesis and oxidation, inflammatory cell infiltration, pro-inflammatory cytokines, endoplasmic reticulum stress, hepatocyte apoptosis, myofibroblast transdifferentiation, and impaired Akt phosphorylation were also significantly attenuated in Lgals3(-/-) animals. Galectin-3 silencing in liver endothelial cells resulted in reduced N(ε)-carboxymethyllysine-modified albumin uptake and ALE-receptor expression.Galectin-3 ablation protects from diet-induced NASH by decreasing hepatic ALE accumulation, with attenuation of inflammation, hepatocyte injury, and fibrosis. It also reduced up-regulation of lipid synthesis and oxidation causing less fat deposition, oxidative stress, and possibly insulin resistance. These data suggest that galectin-3 is a major receptor involved in ALE uptake by the liver.
Published: 2011
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165. The ENPP1 Q121 Variant Predicts Major Cardiovascular Events in High-Risk Individuals

Author: Stefano Rizza, Massimiliano Copetti, Davide Mangiacotti, Francesca Mallamaci, Vincenzo Trischitta, Davide Lauro, Fabio Pellegrini, Carmine Zoccali, Yuan Yuan Zhang, Giovanni Tripepi, Renato Lauro, Christine Powers, Massimo Federici, Sabrina Prudente, Giuseppe Di Stolfo, Belinda Spoto, Filippo Aucella, Thomas H. Hauser, Ernest V. Gervino, Alessandra Testa, Rui Xu, Alessandro Doria, Simonetta Bacci, Salvatore De Cosmo, Antonio Pacilli, and Antonio Facciorusso
Subjects: 0303 health sciences, medicine.medical_specialty, Cross-sectional study, business.industry, Endocrinology, Diabetes and Metabolism, Hazard ratio, Type 2 diabetes, 030204 cardiovascular system & hematology, medicine.disease, Obesity, 3. Good health, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Endocrinology, Internal medicine, Internal Medicine, medicine, Myocardial infarction, Prospective cohort study, business, 030304 developmental biology
Abstract: OBJECTIVE Insulin resistance (IR) and cardiovascular disease may share a common genetic background. We investigated the role of IR-associated ENPP1 K121Q polymorphism (rs1044498) on cardiovascular disease in high-risk individuals. RESEARCH DESIGN AND METHODS A prospective study (average follow-up, 37 months) was conducted for major cardiovascular events (myocardial infarction [MI], stroke, cardiovascular death) from the Gargano Heart Study (GHS; n = 330 with type 2 diabetes and coronary artery disease), the Tor Vergata Atherosclerosis Study (TVAS; n = 141 who had MI), and the Cardiovascular Risk Extended Evaluation in Dialysis (CREED) database (n = 266 with end-stage renal disease). Age at MI was investigated in cross-sectional studies of 339 type 2 diabetic patients (n = 169 from Italy, n = 170 from the U.S.). RESULTS Incidence of cardiovascular events per 100 person--years was 4.2 in GHS, 10.8 in TVAS, and 11.7 in CREED. Hazard ratios (HRs) for KQ+QQ versus individuals carrying the K121/K121 genotype (KK) individuals were 1.47 (95% CI 0.80–2.70) in GHS, 2.31 (95% CI 1.22–4.34) in TVAS, and 1.36 (95% CI 0.88–2.10) in CREED, and 1.56 (95% CI 1.15–2.12) in the three cohorts combined. In the 395 diabetic patients, the Q121 variant predicted cardiovascular events among obese but not among nonobese individuals (HR 5.94 vs. 0.62, P = 0.003 for interaction). A similar synergism was observed in cross-sectional studies, with age at MI being 3 years younger in Q121 carriers than in KK homozygotes among obese but not among nonobese patients (P = 0.035 for interaction). CONCLUSIONS The ENPP1 K121Q polymorphism is an independent predictor of major cardiovascular events in high-risk individuals. In type 2 diabetes, this effect is exacerbated by obesity. Future larger studies are needed to confirm our finding.
Published: 2011
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166. Tribute to Professor Guido Pozza, founder and first Editor-in-Chief of Acta Diabetologica

Author: Massimo Federici, Massimo Porta, and Antonio Secchi
Subjects: Diabetes and Metabolism, Settore MED/09 - Medicina Interna, Endocrinology, Endocrinology, Diabetes and Metabolism, Philosophy, Internal Medicine, Editor in chief, Tribute, General Medicine, Classics
Published: 2018
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167. Adiponectin Isoforms in Elderly Patients with or without Coronary Artery Disease

Author: Massimo Federici, Fabrizio Gigli, Barbara Micchelini, Renato Lauro, Stefano Rizza, Angelica Galli, and Davide Lauro
Subjects: medicine.medical_specialty, Waist, Adiponectin, business.industry, Renal function, medicine.disease, Brain natriuretic peptide, Coronary artery disease, Endocrinology, Internal medicine, Diabetes mellitus, Cardiology, Medicine, cardiovascular diseases, Myocardial infarction, Geriatrics and Gerontology, business, Coronary atherosclerosis
Abstract: OBJECTIVES: To study the distribution of adiponectin isoforms in a group of very old patients. DESIGN: Cross-sectional. SETTING: Geriatric ambulatory clinic of the Department of Medicine at Policlinico “Tor Vergata.” PARTICIPANTS: One hundred eight elderly adults (mean age 85.0±3.2) with or without a history of a previous myocardial infarction as proof of established coronary artery disease (CAD) at least 3 months before entry into the study. Accordingly, subjects were divided into CAD positive (CAD+, n=50) and CAD negative (CAD−, n=58). MEASUREMENT: Assessment of adiponectin isoforms along with metabolic, lipid, and inflammatory profiles. RESULTS: CAD+ subjects had significantly higher levels of total adiponectin (Tot-Ad) and low-molecular-weight adiponectin (LMW-Ad) than CAD− subjects (P=.008 for both). LMW-Ad and high-sensitivity C-reactive protein were positively correlated, even after adjustment for waist circumference, sex, glomerular filtration rate, and presence of diabetes mellitus (correlation coefficient (r)=0.25, P=.05). This association was not confirmed when CAD+ subjects were analyzed alone. A positive association was found in CAD+ subjects between brain natriuretic peptide (BNP), high-molecular-weight adiponectin (HMW-Ad), and Tot-Ad (r=0.798 and r=0.795, P
Published: 2010
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168. Metabolic syndrome and risk of pulmonary involvement

Author: Paola Rogliani, Davide Lauro, Marco Mura, Angelica Galli, Cesare Saltini, Mario Cazzola, Massimo Federici, and Giacomo Curradi
Subjects: Male, Pulmonary and Respiratory Medicine, medicine.medical_specialty, Settore MED/09 - Medicina Interna, HDL, Settore MED/10 - Malattie dell'Apparato Respiratorio, Settore MED/50 - Scienze Tecniche Mediche Applicate, Population, Blood sugar, Blood lipids, FEV1/FVC ratio, Insulin resistance, Airflow limitation, Risk Factors, Forced Expiratory Volume, Internal medicine, Diabetes Mellitus, medicine, Humans, HDL-C, Pulmonary involvement, education, Abdominal obesity, Metabolic Syndrome, education.field_of_study, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, business.industry, Metabolic Syndrome X, Cholesterol, HDL, Metabolic disorder, Middle Aged, respiratory system, Prognosis, medicine.disease, respiratory tract diseases, Cholesterol, Endocrinology, Diabetes Mellitus, Type 2, Spirometry, Cardiology, Female, medicine.symptom, Metabolic syndrome, business, Type 2, circulatory and respiratory physiology
Abstract: Metabolic syndrome (MS) is a complex disorder recognized clinically by the findings of abdominal obesity, elevated triglycerides, atherogenic dyslipidaemia, elevated blood pressure, high blood glucose and/or insulin resistance. It is associated with a pro-thrombotic and a pro-inflammatory state. A growing body of evidence suggests that individuals in the community with moderate airflow limitation may have co-existing systemic inflammation with this background. Therefore, we examined a population of 237 patients with metabolic disorder for the concomitant presence of functional pulmonary involvement, as assessed by FEV(1) and FVC impairment. Criteria for the identification of the MS included 3 or more of the following: waist circumference: (102 cm in men,88 cm in women), triglycerides levels (or =150 mg/dl), high-density lipoprotein cholesterol levels (40 mg/dl in men,50 mg/dl in women), blood pressure (or =135/or =85 mmHg), and fasting glucose levels (100 mg/dl). 119 subjects were diagnosed MS. Non-smokers patients suffering from MS presented lower spirometric values, with a trend to ventilatory restrictive more than obstructive pattern. Also in smokers patients with MS there was a trend to harmonic decrease in FEV(1) and FVC but not in FEV(1)/FVC ratio, although the changes did not reach statistical significance. Mainly abdominal circumference, and also insulin resistance were retained as independent predictors of both FEV(1) and FVC changes. However, HDL-C was the strongest predictor of FEV(1) and FVC changes, with an inverse association.
Published: 2010
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169. MicroRNA 217 Modulates Endothelial Cell Senescence via Silent Information Regulator 1

Author: Giuseppe Novelli, Gerry Melino, Renato Lauro, Viviana Casagrande, Francesca Amati, Rossella Menghini, Eugenio Martelli, Massimo Federici, Marina Cardellini, Alessandro Terrinoni, Mariuca Vasa-Nicotera, and Arnaldo Ippoliti
Subjects: Senescence, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Angiogenesis, Regulator, SirT1 protein, FOXO1, Biology, Umbilical vein, Cell Line, endothelial cells, aging, atherosclerosis, microRNAs, Sirtuin 1, Physiology (medical), Internal medicine, microRNA, medicine, Humans, Sirtuins, Cellular Senescence, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, Settore BIO/12, Cell biology, Vascular endothelial growth factor B, Endothelial stem cell, Endocrinology, Cardiology and Cardiovascular Medicine
Abstract: Background— Aging is a major risk factor for the development of atherosclerosis and coronary artery disease. Through a microarray approach, we have identified a microRNA ( miR-217 ) that is progressively expressed in endothelial cells with aging. miR-217 regulates the expression of silent information regulator 1 (SirT1), a major regulator of longevity and metabolic disorders that is progressively reduced in multiple tissues during aging. Methods and Results— miR-217 inhibits SirT1 expression through a miR-217 –binding site within the 3′-UTR of SirT1. In young human umbilical vein endothelial cells, human aortic endothelial cells, and human coronary artery endothelial cells, miR-217 induces a premature senescence-like phenotype and leads to an impairment in angiogenesis via inhibition of SirT1 and modulation of FoxO1 (forkhead box O1) and endothelial nitric oxide synthase acetylation. Conversely, inhibition of miR-217 in old endothelial cells ultimately reduces senescence and increases angiogenic activity via an increase in SirT1. miR-217 is expressed in human atherosclerotic lesions and is negatively correlated with SirT1 expression and with FoxO1 acetylation status. Conclusions— Our data pinpoint miR-217 as an endogenous inhibitor of SirT1, which promotes endothelial senescence and is potentially amenable to therapeutic manipulation for prevention of endothelial dysfunction in metabolic disorders.
Published: 2009
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170. 'The Linosa Study': Epidemiological and heritability data of the metabolic syndrome in a Caucasian genetic isolate

Author: Paolo Sbraccia, Renato Lauro, Giuseppe Novelli, Alfonso Bellia, Giovam Battista Rini, Massimo Federici, Gaspare Cusumano, G. Di Fede, Emiliano Giardina, Manfredi Tesauro, Davide Lauro, Bellia, A, Giardina, E, Lauro, D, Tesauro, M, Di Fede, G, Cusumano, G, Federici, M, Rini, GB, Novelli, G, Lauro, R, and Sbraccia, P
Subjects: Blood Glucose, Male, Settore MED/09 - Medicina Interna, Genetic Linkage, Endocrinology, Diabetes and Metabolism, Prevalence, Medicine (miscellaneous), Settore MED/13 - Endocrinologia, Young Adult, Age Factors, Metabolic Syndrome X, Cholesterol, HDL, Hypertriglyceridemia, Sex Factors, Humans, Aged, Italy, Smoking, European Continental Ancestry Group, Adult, Middle Aged, Insulin Resistance, Adolescent, Female, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Metabolic Syndrome, education.field_of_study, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, Nutrition and Dietetics, Cholesterol, Cardiology and Cardiovascular Medicine, Genetic isolate, medicine.medical_specialty, Waist, HDL, Population, Biology, White People, Insulin resistance, Internal medicine, medicine, education, nutritional and metabolic diseases, metabolic syndrome,Heritability,Insulin resistance,Metabolic syndrome,Obesity, Heritability, medicine.disease, Obesity, Endocrinology, Settore MED/03 - Genetica Medica, Metabolic syndrome, Demography
Abstract: Background and aims Growing evidence suggests that the metabolic syndrome (MetS) has both a genetic and environmental basis. To evaluate the possibility of a further genetic analysis, we estimated prevalence rates and heritabilities for the MetS and its individual traits in the adult population of Linosa, a small and isolated Italian Island in the southern-central part of the Mediterranean Sea. Methods and results The Linosa Study (LiS) group consisted of 293 Caucasian native subjects from 51 families (123 parents; 170 offsprings). The MetS was defined according to NCEP/ATP III criteria and the following prevalence rates were calculated: hyperglycaemia 20.3%; central obesity 34.9%; hypertension 43.4%; hypertriglyceridaemia 29.9%; "low HDL" 56.6%; MetS 29.9%. Waist circumference was significantly related to all the quantitative parameters included in the NCEP/ATP III MetS definition. The MetS showed a heritability of 27% ( p =0.0012) and among its individual components, treated as continuous and discrete traits, heritability ranged from 10% for blood glucose to 54% for HDL-cholesterol. Among MetS subtypes, the clustering of central obesity, hypertriglyceridaemia and "Iow HDL" had the highest heritability (31%; p Conclusion These data showed high prevalence rates for the MetS and its related traits in an isolated and small Caucasian population. The appreciable heritability estimates for the MetS and some of its components/clusters in the LiS population might support the observation of genetic factors underlying the pathogenesis of the MetS and encourage further analysis to identify new susceptibility genes.
Published: 2009
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171. Impaired regulation of the TNF-α converting enzyme/tissue inhibitor of metalloproteinase 3 proteolytic system in skeletal muscle of obese type 2 diabetic patients: a new mechanism of insulin resistance in humans

Author: J. J. Wewer, Franco Folli, R. M. Jhingan, D. Smokler, Alberto O. Chavez, Victoria E. Centonze, Christopher P. Jenkinson, R. Khokka, Devjit Tripathy, Sara M. Reyna, Nicolas Musi, A. Barrentine, S. Kamath, Adriana Monroy, Massimo Federici, Ralph A. DeFronzo, M. Veerasamy, and Dawn K. Coletta
Subjects: Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Blotting, Western, Enzyme-Linked Immunosorbent Assay, Type 2 diabetes, ADAM17 Protein, Biology, Matrix metalloproteinase, Article, Insulin resistance, Diabetes mellitus, Internal medicine, Receptors, Diabetes Mellitus, Internal Medicine, medicine, Humans, Muscle, Skeletal, Tissue Inhibitor of Metalloproteinase-3, Receptors, Interleukin-6, ADAM Proteins, Diabetes Mellitus, Type 2, Gene Expression Regulation, Insulin Resistance, Female, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, Interleukin-6, Blotting, Insulin, Skeletal muscle, Skeletal, Tissue inhibitor of metalloproteinase, medicine.disease, medicine.anatomical_structure, Endocrinology, Enzyme inhibitor, biology.protein, Muscle, Western, Type 2
Abstract: TNF-alpha levels are increased in obesity and type 2 diabetes. The regulation of TNF-alpha converting enzyme (TACE) and its inhibitor, tissue inhibitor of metalloproteinase 3 (TIMP3), in human type 2 diabetes is unknown.We examined TACE/TIMP3 regulation: (1) in lean and obese normal glucose tolerant (NGT) individuals and in type 2 diabetes patients; (2) following 6 h of lipid/saline infusion in NGT individuals; and (3) in cultured human myotubes from lean NGT individuals incubated with palmitate. Insulin sensitivity was assessed by a euglycaemic clamp and TACE/TIMP3 was evaluated by confocal microscopy, RT-PCR, western blotting and an in vitro activity assay. Circulating TNF-alpha, TNF-alpha-receptor 1 (TNFR1), TNF-alpha-receptor 2 (TNFR2), IL-6 receptor (IL-6R), vascular cell adhesion molecule (VCAM) and intercellular adhesion molecule (ICAM) levels were evaluated.TIMP3 levels were reduced and TACE enzymatic activity was increased in type 2 diabetes skeletal muscle. TACE expression, and TACE, TNF-alpha, TNFR1 and IL-6R levels were increased in type 2 diabetes, and positively correlated with insulin resistance. A 6 h lipid infusion into NGT individuals decreased insulin-stimulated glucose metabolism by 25% with increased TACE, decreased expression of the gene encoding TIMP3 and increased IL-6R release. Palmitate induced a dramatic reduction of TIMP3 and increased the TACE/TIMP3 ratio in cultured myotubes.TACE activity was increased in skeletal muscle of obese type 2 diabetes patients and in lipid-induced insulin resistance. We propose that dysregulation of membrane proteolysis by TACE/TIMP3 of TNF-alpha and IL-6R is an important factor for the development of skeletal muscle insulin resistance in obese type 2 diabetes patients by a novel autocrine/paracrine mechanism.
Published: 2009
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172. Adiponectin isoforms are not associated with the severity of coronary atherosclerosis but with undiagnosed diabetes in patients affected by stable CAD

Author: Marina Cardellini, Alessia Savo, Francesco Romeo, Massimo Federici, Fabrizio Clementi, Ottavia Porzio, Gaetano Chiricolo, Matteo Serino, Stefano Rizza, and Renato Lauro
Subjects: Male, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Endocrinology, Diabetes and Metabolism, Medicine (miscellaneous), Coronary Artery Disease, Type 2 diabetes, Coronary Angiography, Impaired glucose tolerance, Coronary artery disease, Electrocardiography, Internal medicine, Diabetes mellitus, Glucose Tolerance Test, Regression Analysis, Humans, Tomography, X-Ray Computed, Aged, Protein Isoforms, Diabetes Mellitus, Type 2, Adiponectin, Middle Aged, Female, Diabetes Mellitus, Medicine, cardiovascular diseases, Myocardial infarction, Risk factor, Tomography, Coronary atherosclerosis, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, Nutrition and Dietetics, business.industry, nutritional and metabolic diseases, medicine.disease, X-Ray Computed, Cardiology, Cardiology and Cardiovascular Medicine, business, Type 2
Abstract: Background and aims Total adiponectin is emerging as an independent risk factor for cardiovascular diseases, but the role of adiponectin isoforms in coronary artery disease (CAD) is still unknown. We investigated the role of adiponectin isoforms with respect to the severity of coronary disease and to the presence of undiagnosed diabetes in patients with CAD. Methods and results We recruited 205 CAD patients, all living in the central area of Italy, with a history of a previous myocardial infarction but apparently not affected by type 2 diabetes (DM2). We compared the CAD patients to a control population ( n =100) matched for age, sex, BMI and cardiovascular risk factors, but without overt diabetes and cardiovascular disease. In all patients we measured Total Adiponectin (Tot-Ad) and its isoforms, metabolic, pro- and anti-inflammatory markers and we performed an oral glucose tolerance test (OGTT). CAD patients underwent a coronary angiography and/or coronary multi-slice computed tomography. Based on the severity of CAD they were divided into mono-vessel versus multi-vessel patients. Tot-Ad levels and its isoforms were comparable in patients with mono-vessel versus multi-vessel CAD. After the OGTT, in CAD patients, the results showed that 19% of patients were affected by unknown DM2, 36.1% by unknown impaired glucose tolerance (IGT), and only 43.9% were truly normoglycemic (NGT). Low levels of high molecular weight-adiponectin (HMW-Ad) were significantly associated with undiagnosed IGT or DM2 status ( p Conclusions In our cohort of CAD patients, Tot-Ad and its isoforms do not correlate with severity of CAD, but with undiagnosed defects of glucose metabolism.
Published: 2009
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173. Transgenic mice overexpressing human G972R IRS-1 show impaired insulin action and insulin secretion

Author: Renato Lauro, Fatima Bosch, Giorgio Sesti, Anna Pujol, Roberta Amoruso, Davide Lauro, Massimo Federici, D. Barcaroli, F. Tornei, Rossella Menghini, and Marta Letizia Hribal
Subjects: Male, Settore MED/09 - Medicina Interna, medicine.medical_treatment, Adipose tissue, Transgenic, Settore MED/13 - Endocrinologia, Mice, insulin resistance, Insulin Secretion, Glucose homeostasis, Insulin, Glucose tolerance test, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, medicine.diagnostic_test, Settore BIO/12, Skeletal, Articles, Adipose Tissue, Liver, Molecular Medicine, Muscle, Signal Transduction, medicine.medical_specialty, Insulin Receptor Substrate Proteins, Normal diet, Mice, Transgenic, Carbohydrate metabolism, Biology, insulin signalling, Arginine, Mouse model, Insulin resistance, Adipokines, Internal medicine, medicine, Animals, Humans, Hypoglycemic Agents, Muscle, Skeletal, Cell Biology, Glucose Tolerance Test, medicine.disease, Liver Glycogen, Glucose, Insulin Resistance, Amino Acid Substitution, Endocrinology, glucose intolerance
Abstract: Molecular scanning of human insulin receptor substrate (Irs) genes revealed a single lrs1 prevalent variant, a glycine to arginine change at codon 972 (G972R); previous in vitro studies had demonstrated that the presence of this variant results in an impaired activation of the insulin signalling pathway, while human studies gave controversial results regarding its role in the pathogenesis of insulin resistance and related diseases. To address in vivo impact of this IRS-1 variant on whole body glucose homeostasis and insulin signalling, we have generated transgenic mice overexpressing it (Tg972) and evaluated insulin action in the liver, skeletal muscle and adipose tissue and assessed glucose homeostasis both under a normal diet and a high-fat diet. We found that Tg972 mice developed age-related glucose and insulin intolerance and hyperglycaemia, with insulin levels comparatively low. Glucose utilization and insulin signalling were impaired in all key insulin target tissues in Tg972 mice. There were no differences in pancreatic morphology between Tg972 and wild-type mice, however when insulin secretion was evaluated in isolated islets, it was significantly reduced in Tg972 mice islets at any glucose concentration tested. Under a high-fat diet, Tg972 mice had increased body and adipose tissue weight, and were more prone to develop diet-induced glucose and insulin intolerance. So, we believe that Tg972 mice may represent a useful model to elucidate the interaction between genetic and environmental factors in insulin resistance pathogenesis. Furthermore, they may become an important tool to test novel tailored therapies.
Published: 2008

174. Erratum

Author: Sascha Martens, Masashi Narita, Rajkumar Cheluvappa, Kevin A. Roth, Ta Yuan Chang, Kartik Venkatachalam, Chang-Shen Lin, Sharon G. Adler, Flaminia Pavone, Dianwen Ju, Michelle A. Ozbun, Michael R. Duchen, Shu Feng Zhou, Wei-Guo Zhu, Aaron Di Antonio, Defeng Wu, Taixing Cui, Xu Guang Guo, Zhiping Xie, Lorena García Nannig, Eloy Bejarano, Stéphane D. Lemaire, Petro Starokadomskyy, Hyung Ryong Kim, Mario Pinar, Rebecca T. Marquez, Zvenyslava Husak, Anthony R. White, Joanna Poulton, Antonis S. Zervos, Shweta Sharma, Jochen Walter, Nicholas T. Ktistakis, Christopher H.K. Cheng, Sunhee Lee, Yuen Li Chung, Howard O. Fearnhead, Young J. Oh, Ivano Amelio, Guillermo A. Blanco, Jan Simak, Junfang Wu, Yingying Lu, Mary Kate McBrayer, Soo Han Bae, Ichizo Nishino, Hong-Ming Hu, Benjamin R. Underwood, Tomonori Kimura, Zexian Liu, Savithrama P. Dinesh-Kumar, Qian Yang, Andreas Kern, Hsing Jien Kung, Jan B. Parys, Cam Patterson, Celine Perier, Toshiro Okazaki, Daisuke Koya, Avinash Sonawane, Cédric Cleyrat, Robert I. Richards, Kai Y. Soo, Rodrigo Mora-Rodriguez, Gigi N.C. Chiu, Moon Moo Kim, Vladimir N. Uversky, Shengfang Ge, Matthew T. V. Chan, Irene Kyrmizi, Lara Gibellini, Ángela M. Valverde, Erik Norberg, Fan Zhang, Jan C. Koch, Alec C. Kimmelman, Jingfang Ju, Jie Bai, Lei Duan, Paulina Ordonez, Shuwen Liu, Wolfdieter Springer, Eric Deutsch, Elena Ortona, Jose M. Seguí-Simarro, Vinay Choubey, Leonidas Stefanis, Robert G. Hawley, Claudia Bincoletto, Xian-Hui He, Zhifen Yang, Thomas M. Durcan, Martine Biard-Piechaczyk, Kui Lin, Hongming Pan, Konstantinos Kambas, Cristina Muñoz-Pinedo, Marta Magariños, Yoshinori Takahashi, Adrienne M. Gorman, Philippe Gailly, Takahiko Akematsu, Justine D. Mintern, Liang Xu, Tetsuo Shioi, Luis M. Botana, Yule Liu, Yong Yeon Cho, Jinzhi Lei, Eung Kweon Kim, Alakananda Basu, Vikash Kumar Dubey, Candelaria Gomez-Manzano, Avital Eisenberg-Lerner, Chuan-Ming Xie, Wenjie Dai, Pedro Gonzalez-Alegre, Maria Condello, Zheng-Hong Qin, Zhi-Min Yuan, Catherine Andreadi, Anna Rita Migliaccio, Chong Liu, Michaël Boyer-Guittaut, Melanie Denizot, Esperanza Arias, Greet Van den Berghe, Guomei Tang, Timothy P. Devarenne, Xianyong Sheng, Louis R. Lapierre, J. Wade Harper, Zuzana Storchova, Aileen R. Ariosa, Sug Hyung Lee, Qi Zeng, Godefridus J. Peters, Daniela L. Papademetrio, Alexandre Arcaro, Zhiyuan Yao, Pablo Iribarren, Mario Chiariello, Maria Rosaria Torrisi, Parimal Karmakar, Yong Huang, Sebastiano Sciarretta, Nathalie Andrieu-Abadie, László Fésüs, Patricia Boya, Ruediger Rudolf, Leonor Miller-Fleming, Vasilis J. Promponas, Juan Segura-Aguilar, Paula Daza, Shiow Ju Lee, Songshu Meng, Paul K. Herman, Ludwig Eichinger, Ye-Guang Chen, Kay F. Macleod, Thomas Simmet, Cristina Corral-Ramos, Claudio Brancolini, Jun Ren, Ying Jiang, Benoît Derrien, Xiao Fang Yu, Qing Zhong, Zong Wan Mao, Xingcong Ren, Armando A. Genazzani, Marina Pierdominici, Sanbing Shen, Sandra Moreno, Hana Algül, Maurizio Renna, Ricardo Sánchez-Prieto, Ashok K. Saluja, Yasuo Uchiyama, Pope L. Moseley, Victor E. Dosenko, Chun-Feng Liu, Bakhos A. Tannous, Efthimios Sivridis, Baharia Mograbi, Michiko Shintani, Amanda S. Bess, Rodrigo Portes Ureshino, Avnika A. Ruparelia, Paul Hofman, Eric Chevet, Martha M. Monick, Hong Gang Wang, Daping Fan, Jorge Moscat, Giuseppe Matarese, Consiglia Pacelli, Young Seok Cho, Miriam Cnop, Stefan Böckler, Nikolai V. Gorbunov, Christina J. Sigurdson, Hang T.T. Nguyen, Aurélie François, Katarina Kågedal, Sam Gandy, Silvia Campello, Alain Bruhat, Filomena Fiorito, Hua Feng, Man Tian Mi, Gian Maria Fimia, Masaki Tanaka, Guofei Zhou, José L. Crespo, Heinz Jungbluth, Anna Chiara Nascimbeni, Arianne L. Theiss, Svetlana Dokudovskaya, Mar Lorente, Sergio Lavandero, Yu Xia Zhao, Fangming Lin, Yuchen Feng, Gad Galili, Silvia Cetrullo, Paula I. Moreira, Dhyan Chandra, Dimitrios J. Stravopodis, Roberta A. Gottlieb, Gregory A. Taylor, Longping Wen, Faqiang Li, Marco Sardiello, Umesh K. Jinwal, Francesca Belleudi, Lan Tan, Livia Di Renzo, Tamas Korcsmaros, Xinbing Sui, Douglas R. Green, Guillermo Mazzolini, Hervé Le Stunff, Kelly S. Doran, Mary E. Choi, Carlos S. Subauste, Natalia Rodriguez-Muela, Nicholas J. Talbot, Marta Palmieri, Sonia Hernández-Tiedra, Ligia C. Gomes, Irving M. Shapiro, Makoto Ubukata, Mario P. Tschan, Baris Bingol, Benjamin Loos, Terry Kwok, Luca M. Neri, Sreejayan Nair, Michele Wolfe Bianchi, Ralf Erdmann, Alexander Greenhough, Neeraj Vij, Jeong Hun Kim, Satoaki Matoba, Bo Liu, George R. Beck, Michael Moore, Vrajesh V. Parekh, Kyle A. Bauckman, Li-Lin Du, Mikihiro Fujiya, Yan G. Zhao, Renaud Legouis, Jiangwei Zhang, Kailiang Jia, Nadezda Apostolova, Sehamuddin Galadari, Khosrow Adeli, Ming Yong Zhang, Carmela Fusco, Angel Ortega, Anna Pensalfini, Zsuzsanna Szatmári, Marco Tafani, Isabella Ceccherini, Anne Hamacher-Brady, Kuen Jer Tsai, Anita C. Truttmann, Franco Fortunato, Keisuke Miyazawa, Chunhai Fan, Berge A. Minassian, Jian Zhang, Frank A. Anania, Heesun Cheong, Amal O. Amer, Ing Swie Goping, Won-Ki Huh, Anita Solhaug, Joan Cl ria, Laurent Le Cam, Seungmin Hwang, Karen L. Wright, Antonella De Matteis, Troy T. Rohn, Ivana Bjedov, Subbiah Pugazhenthi, Hal E. Broxmeyer, Xue Yuan Bai, Koenraad Norga, Minnie M. Sarwal, Daniel F. Schorderet, Ioannis P. Nezis, Mei Qing Wang, Jun Hee Lee, Yong J. Lee, David A. Tumbarello, Fernando Macian, Joern Dengjel, Dmitry V. Bulavin, Andrew J. Halayko, Ben Berkhout, Aseem Pandey, Santosh Kesari, Karin Przyklenk, Elena V. Tchetina, Matthew L. Albert, Laura Segatori, Joel N. Meyer, Mustapha Rouis, Éva Margittai, Ashish Jain, David Hahn, Thomas Vaccari, Lori R. Covey, Ghanshyam Swarup, Kuo Yang Huang, Gennaro Napolitano, Sam W. Lee, Seong Who Kim, Alberto Anel, Vladimir V. Rogov, Laura A. Carleton, Amine Belaid, Byoung Kuk Jang, Sheng-Han Kuo, Patricia L. Yeyati, Jae U. Jung, Teresa Zoladek, Sabrina Di Bartolomeo, Clémence Richetta, Peixin Yang, Daniela Trisciuoglio, Hye Seung Jung, Katsumi Higaki, Eui-Bae Jeung, Ivan Topisirovic, Isabella Caniggia, Susan E. Logue, Issidora S. Papassideri, Lynda A. Morrison, Caihong Wang, Graeme Sargent, Beth Levine, Mingxiang Ye, David M. Sabatini, Consuelo Amantini, Julio A. Aguirre-Ghiso, Lawrence H. Boise, Patricia Silvia Romano, Sean T. Sweeney, Takayuki Tsukuba, Reinhard Dechant, Benoit Barbeau, Marta Martinez-Vicente, Kuo How Huang, Edésio José Tenório de Melo, Faustino Mollinedo, José M. Fuentes, Joaquín Jordán, Dong-Hyung Cho, Dexian Zheng, Jeroen J.M. 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Gisou van der Goot, Xinfeng Liu, Alexandru Almasan, Akiko Maeda, Yu Qiu, Yaohua Wu, Annie Sittler, Wen-Xing Ding, Wenhua Zhu, Hung-Jen Liu, Moisés Martínez-Velázquez, Jeffery S. Cox, Seung Yong Yoon, Concepcio Marin, Wilian A. Silveira, Fulvio Chiacchiera, W. Douglas Fairlie, Jian Xin Gao, Shuilong Leng, Nathan R. Brady, Josef M. Penninger, Puran Singh Sijwali, Florian Gruber, Tibor Vellai, Jiunn-Liang Ko, Laura Korhonen, Slimane Ait-Si-Ali, Hirokazu Arimoto, Alberto M. Martelli, Teresa L. M. Thurston, Chuanshan Xu, Kathrin Pallauf, Eduardo Couve, Shweta Saran, Lionel Blanc, Maylin Almonte-Beceril, Yong-Keun Jung, Lena Lavie, Junsoo Park, Camilla Palumbo, Claire H. Mitchell, Sophie Pattingre, Guillermo Velasco, Steve S.-L. Chen, Xiu-Fen Ming, Xin Qi, Vania Gelmetti, Nicolas Dupont, Soraya S. Smaili, Chinnaswamy Jagannath, Uta Dahmen, Daolin Tang, Rodrigo Franco, John H. Kehrl, Xiaonan Dong, Carsten Sachse, Jeff Kuret, Genzou Takemura, Supawadee Sukseree, Joëlle Botti, W. Haung Yu, Aurelia Lugea, Scott J. Bultman, Divaker Choubey, Frank A. Sinicrope, You-Wen He, Jian Wu, Yoshitaka Isaka, Geert Bultynck, Giuseppe Merla, Luigi Maiuri, Sonia Melino, Hannelore Maes, Daniele Lettieri Barbato, Ian G. Ganley, Zhihong Yang, Daniel Hofius, Kimberly McCall, Peiwen Chen, Istvan Lekli, Alicia Rosello, Eric Ghigo, Atsushi Kuno, Iman Tavassoly, Chris Albanese, Agustín Aranda, Salvatore Pepe, Hong Jiang, Henri Batoko, Giovanna Elvira Granato, Vincent Zecchini, Stephen E. Girardin, Maria T. Diaz-Meco, Philippe Marambaud, G. Amadoro, Sangeeta Khare, Christelle Koechlin-Ramonatxo, Emery H. Bresnick, Christian Behl, Mikio Nishimura, Julien Puyal, Wenjie Guo, Hsinyu Lee, Carolyn M. Sue, Derrick Gibbings, Alina Maloyan, Philippe Pierre, Serge N. Manié, Gerry Melino, Elizabeth A. Woodcock, Roberto Ciarcia, Liwen Jiang, Michael C. Kruer, Vladimir Trajkovic, Yunjiao Zhang, Nina Raben, Beata Pajak, Michael J. Ragusa, Riccardo Autelli, Kelly Jean Thomas, Suzana Gispert, Wei Li Zhao, Cheol Hyeon Kim, Pothana Saikumar, Arsenio Fernández-López, Juliano Machado, Valentina Iovane, Cai Ping Tan, Carmine Settembre, Neelam Azad, Yohta Shimada, Shivendra V. Singh, Hai Rao, Hirosato Mashima, Michael T. Stang, Yasuhito Sakuraba, Gemma Fabriàs, Tuck Wah Soong, Didac Carmona-Gutierrez, Ilse Vanhorebeek, F. Javier Oliver, Mondira Kundu, Alfonso Schiavi, Dan Lindholm, José L. Revuelta, Jason S. King, Susana Castro-Obregón, Paul Digard, Hua Zhu, Komal Raina, Yun Dai, Ruben K. Dagda, Nuria Martinez-Lopez, Andrea A. Gust, Lucia Notterpek, Robert Clarke, Manon E. Wildenberg, Mingzhou Chen, Leticia Reyes, Laura Berliocchi, John J. McMahon, Hongzhuan Chen, E.M. Nolte, Stefan W. Ryter, Fulvio Reggiori, Jiefei Geng, Michael A. Mandell, John H. Fingert, Holger Prokisch, Marina Jendrach, Søren R. Paludan, Elizabeth P. Henske, Ricardo Gargini, Wei-Xing Zong, Susmita Kaushik, Michael Overholtzer, Paul W. Sylvester, Daniel E. Voth, Canhua Huang, Andrea Boman, Gérard Lizard, Rut Valdor, Marc Flajolet, Graham S. Taylor, Nicola Di Daniele, Leonardo H. Travassos, Ying Yang, Anumantha G. Kanthasamy, Hasan Mukhtar, Yuhua Zhu, Noor Gammoh, Ignacio Vega-Naredo, Victoria Ryabovol, Sara W. Bird, Gang Min Hur, Qun-Ying Lei, Fan Yi, Laura Caberlotto, Maria F. Galindo, Bilal Piperdi, Leonidas C. Platanias, P. Hande Özdinler, Régis Delage-Mourroux, Julio Madrigal-Matute, Xu Liu, Nagio Takigawa, Aurora Pujol, Marta Margeta, Hee Jeong Kong, Christian Behrends, Michael Thumm, Shirley Luckhart, Emilio Clementi, John W. Steele, Liliana Schaefer, Philip L. Lorenzi, Chao-Yu Miao, She Min Lu, Jane E. Ishmael, Jin Hyoung Kim, V. Izzo, Yanming Wang, Balindiwe J.N. Sishi, Vincent Galy, Andras Perl, Shouqing Luo, Giovanni Vitale, Yongsheng Che, Rodrigo Troncoso, Liu Yang, Thomas J. Begley, Sebastien G. Bouret, Elizete Rizzo, James M. Piret, Junjun Wang, Herman P. Spaink, Thomas S. Jacques, Robin F. B. 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Tait, Aimee L. Edinger, Jeffrey P. MacKeigan, Paul A. Ney, Mireia Niso-Santano, Valeria Crippa, Andreas S. Reichert, Isabelle Dugail, Jon D. Lane, Farida V. Minibayeva, Gianluca Tettamanti, Scott Pattison, Péter Lõrincz, Kamal Chowdhury, Ulrich E. Schaible, Maria Agnello, Paolo Pinton, Niels Jessen, Lei Guo, Kwang-Huei Lin, David N. Zacks, Ying Jan Wang, Simone Fulda, John J. Lemasters, Andrea Viale, Anna Maria Marconi, Valerie Askanas, Yoshitaka Nagai, François M. Vallette, Joan K. Heath, Srinivasan Dasarathy, Soo-Youl Kim, Günter U. Höglinger, Tamara Kravic-Stevovic, Iraide Alloza, Tiago F. Outeiro, Ana Serrano-Puebla, Elena A. Minina, Terrence M. Donohue, Ming Guo, Alexandra Giatromanolaki, Abdel Halim Harrath, Ken Sato, Anne Elisabeth Theron, Usha P. Andley, Claudio Cardinali, Maija Pesonen, Penny E. Lovat, Chanhee Kang, Sabah N. A. Hussain, Lisa A. Brennan, Jose A. Tapia, Christoph Becker, Huixin Yu, Pei-Yu Wang, Bertrand Joseph, Zhen Yan, Georgia Minakaki, Ricardo Escalante, Ralph A. Nixon, Katsuhiko Asanuma, M. Helena Vasconcelos, David J. Reiner, Shengkan Jin, David Dávila, Theo Rein, Balakrishna L. Lokeshwar, Antonio Miranda-Vizuete, Carl Ward, Vito Turk, Frederick D. Quinn, Katja Köhler, Masaru Harada, Kathleen Boesze-Battaglia, Fraser P. Coxon, Paulo R. Jannig, Miguel A. Peñalva, Manjula Kalia, Marco Corazzari, Chunjuan Song, Xianghua Yan, Lilach Toker, Benjamin Pineda, Vanessa Ginet, Ye Xu, Chun Jung Chen, Roberto Towns, Amy A. Kiger, Rajagopal Ramesh, Maria Rita Rippo, Joseph A. Hill, Boris Zhivotovsky, Peter Speck, Ya Hua, Peter J. Roach, Fabio Penna, Kasper M.A. Rouschop, Jeng-Jer Shieh, Maria Angeles Mena, Mei Zhao, Sonia Rocha, Xin Wen, Sylvain Lefort, Michael Scharl, Ramnik J. Xavier, Alan Cheng, Marion Bouchecareilh, Stella Y. Lee, Maria Xilouri, Qi Chen, Claudia Spies, Pengfei Ge, Natascia Ventura, Luca Galluzzi, Yau Hung Chen, Jing Pu Zhang, Diego Albani, Dingzhong Tang, Nikolai Engedal, Stefania Meschini, Maria Lyngaas Torgersen, Shibu M. Poulose, Jean-Paul Decuypere, Ziheng Xu, Jocelyn Laporte, Thierry Arnould, Albert Haas, Ida J. van der Klei, Agustín Hernández, Dong Wook Shin, Per E. Stromhaug, Valentín Ceña, Ugo Pagnini, Karolina Pakos-Zebrucka, Blagovesta Popova, Lisa M Lindqvist, Sangita C. Sinha, Yuguang Shi, Zvonimir Marelja, Robin Candau, Xin Wang, Evelina Gatti, Olatz Pampliega, Michael P. Lisanti, Elena Tamagno, Mei Lan Tan, Gary Warnes, Zdena Palková, Shigeomi Shimizu, Ingo Schmitz, Tino Kurz, Soledad Matus, Gopal Chakrabarti, Joseph J.Y. Sung, Beáta G. Vértessy, Giuliana Cassinelli, Giovanni Benard, Yin Chen, Emma Colucci-Guyon, Craig Blackstone, Lizhi Cao, Sebastian Schuck, Qingqiu Gong, Theocharis Panaretakis, Jayoung Choi, Sven R. Carlsson, Libuše Váchová, Raymond Chuen-Chung Chang, Yang Liu, Zheng Dong, Qinghua Shi, Hélène Duez, Tiziana Bachetti, Axel H. Schönthal, Sumit Sahni, Bo Wang, Naomichi Matsumoto, Markus Rehm, Liliana Torosantucci, Toren Finkel, Yi Hsin Tseng, Hsiang Cheng Chi, Fang Lin, Tony George Jacob, Ju-Xian Song, Alessandro Fanzani, Marc Tatar, Paola Costelli, Rubén Gómez-Sánchez, Yunfei Wen, Juha J. Hulmi, Francesca V. Mariani, Min Zeng, Chiung Chyi Shen, Carine Michiels, Yan Burelle, Andreas L. Serra, Goran Petrovski, Kwang Woon Kim, Paula Ludovico, Darius Ebrahimi-Fakhari, Yee Joo Tan, Luisa De Martino, Alvaro Glavic, Pierre Lapaquette, Edmund B. Rucker, Andreas Mayer, Shigeko Yamashiro, Scott K. Powers, Robert M. Gogal, Ebru Goncu, Yuichiro J. Suzuki, Anna Maria Giammarioli, Claudio Hetz, Eric H. Baehrecke, Cheryl L. Walker, Cinzia Lanzi, Deepti S. 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Kumar, Deok Ryong Kim, Jianjie Ma, Sang Won Suh, Guido Kroemer, Klára Megyeri, Michael N. Sack, Heinrich Taegtmeyer, Gilles Pagès, Gabriella Marfe, Gregg L. Semenza, Karine G. Le Roch, Marisa Brini, Marina Bouché, Oliver Kepp, Vinay V. Eapen, J. David Beckham, Stephan T. Stern, Xudong Zhang, Marcello Pinti, Xiangnan Zhang, Jae Keun Lee, Ana Coto-Montes, Assaf Rudich, Laura D. Attardi, Debabrata Ghosh, Philip Rosenstiel, Sébastien Besteiro, Maria Rosa Sarrias, R. Andres Floto, Xiao Ming Yin, Nicholas W. Lukacs, Hermann Pavenstädt, Matias Simons, Hitoshi Nakatogawa, Sandro Alves, Krisztina Takács-Vellai, Masato Koike, Debasish Sinha, Shoji Notomi, Faraj Terro, Maria Carmela Roccheri, Santiago Ambrosio, K. Ulrich Bayer, Yumin Li, Terje Johansen, Christian Kuhn, Yee Shin Lin, David C. Rubinsztein, Ziwei Qu, Ronit Shiri-Sverdlov, Emmanuel T. Akporiaye, Galila Agam, Hui Ling Chiang, Seung-Jae Lee, Yu Xue, Francesca Giampieri, Markus Damme, Tassula Proikas-Cezanne, Tianwei Lin, Marc Kantorow, Guang-Chao Chen, Qiangrong Liang, Claudia Manzoni, Joan S. Steffan, Emilio Boada-Romero, Damien Freyssenet, Sepp D. Kohlwein, Maria D. Barrachina, Yulin Liao, Jiankang Chen, Erika Isono, Hugo Seca, Mei Wang, Taras Y. Nazarko, Yannick Bailly, Nadya V. Koshkina, Tapas K. Maiti, Bärbel Rohrer, Karin Nowikovsky, James H. Hurley, Gerald W. Dorn, Nils C. Gassen, Kazuhiro Nagata, Eiki Kominami, A. Ivana Scovassi, Ana Maria Cuervo, Adi Kimchi, Minghua Yang, Sylviane Muller, Life Sciences Institute and Department of Molecular, Cellular, and Developmental Biology and Biological Chemistry, University of Michigan [Ann Arbor], University of Michigan System-University of Michigan System, Defense in Plant-Pathogen Interactions [Nagoya, Japan], Nagoya University-Graduate School of Bioagricultural Sciences [Nagoya, Japan], Facultad de Quimica [Santiago], Pontificia Universidad Católica de Chile (UC), Institute of Cancer Sciences [Glasgow, UK] (CR-UK Beatson Institute), University of Glasgow, Cell Death Research & Therapy (CDRT) Lab, Université Catholique de Louvain, Harvard University Statistics Department, Harvard University [Cambridge], Centre épigénétique et destin cellulaire (EDC (UMR_7216)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Conway Institute of Biomolecular and Biomedical Research and School of Chemical and Bioprocess Engineering, University College Dublin [Dublin] (UCD), Immunobiologie des Cellules dendritiques, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Biochemistry and Molecular Biology, Thomas Jefferson University-Sidney Kimmel Cancer Center, Jefferson (Philadelphia University + Thomas Jefferson University)-Jefferson (Philadelphia University + Thomas Jefferson University), Centro de Estudios Farmacológicos y Botánicos [Buenos Aires] (CEFYBO), Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET)-Facultad de Medicina [Buenos Aires], Universidad de Buenos Aires [Buenos Aires] (UBA)-Universidad de Buenos Aires [Buenos Aires] (UBA), Thérapie génique, Génomique et Epigénomique (U 1169), Université Paris-Saclay-Institut National de la Santé et de la Recherche Médicale (INSERM)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Sud - Paris 11 (UP11), Department of Experimental Medicine and Public Health, University of Camerino, MRC Toxicology Unit, University of Leicester, Génomique Fonctionnelle des Tumeurs Solides (U1162), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Departamento de Bioquímica y Biología Molecular y Celular, University of Zaragoza - Universidad de Zaragoza [Zaragoza], Department of Pharmaco-Biology, Università della Calabria [Arcavacata di Rende] (Unical), Department of Molecular Genetics [Rehovot, Israël], Weizmann Institute of Science, Fondation Universitaire Notre Dame de la Paix (FUNDP), Facultés Universitaires Notre-Dame de la Paix, Département Advanced Research And Techniques For Multidimensional Imaging Systems (ARTEMIS), Institut Mines-Télécom [Paris] (IMT)-Télécom SudParis (TSP), USC Neuromuscular Center, Department of Neurology, University of Southern California (USC), Centre méditérannéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Giannina Gaslini Institute, Department of Molecular Pharmacology, Albert Einstein College of Medicine, Department of Cancer Biology, University of Massachusetts Medical School [Worcester] (UMASS), University of Massachusetts System (UMASS)-University of Massachusetts System (UMASS), Institut des Sciences de l'Evolution de Montpellier (UMR ISEM), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École pratique des hautes études (EPHE)-Université de Montpellier (UM)-Institut de recherche pour le développement [IRD] : UR226-Centre National de la Recherche Scientifique (CNRS), Inner Mongolia Agricultural University (IMAU), Franche-Comté Électronique Mécanique, Thermique et Optique - Sciences et Technologies (UMR 6174) (FEMTO-ST), Université de Franche-Comté (UFC)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Mécanique et des Microtechniques (ENSMM)-Université de Technologie de Belfort-Montbeliard (UTBM), Indian Institute of Science [Bangalore] (IISc Bangalore), Politecnico di Milano [Milan] (POLIMI), Département des Sciences Biologiques [Montréal], Université du Québec à Montréal (UQAM), Laboratory of Molecular Biology, Scientific Institute E. Medea, Université Catholique de Louvain (UCL), Univ Ancona, Politecn Marche, University of Toronto, Munich Cluster for systems neurology [Munich] (SyNergy), Technische Universität München [München] (TUM)-Ludwig-Maximilians-Universität München (LMU), Institut de Recherche sur le Cancer et le Vieillissement (IRCAN), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA), Department of Clinical and Molecular Medicine, Università degli Studi di Roma 'La Sapienza' [Rome]-Réseau International des Instituts Pasteur (RIIP)-Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP), Physiopathologie du système nerveux central - Institut François Magendie, Université Bordeaux Segalen - Bordeaux 2-IFR8-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'Hémato-Cancérologie Expérimentale, CRP-Santé, Dpt of Neuroscience and Brain Technologies [Genova], NeuroEngineering & bio-arTificial Synergic SystemS Laboratory [Genova] (NetS3 Lab), Istituto Italiano di Tecnologia (IIT)-Istituto Italiano di Tecnologia (IIT), Center for Infection and Immunity Amsterdam (CINIMA), Laboratoire de biogenèse membranaire (LBM), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), Centre de résonance magnétique biologique et médicale (CRMBM), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Centre National de la Recherche Scientifique (CNRS), Régulation de l'expression génétique (REG), Département de Biologie - ENS Paris, École normale supérieure - Paris (ENS Paris)-École normale supérieure - Paris (ENS Paris)-Centre National de la Recherche Scientifique (CNRS), Dynamique des interactions membranaires normales et pathologiques (DIMNP), Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Intégrative de la Cellule (I2BC), Université Paris-Sud - Paris 11 (UP11)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS)-Université Paris-Saclay, Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Department of Microbiology and Immunology, Stanford University School of Medicine [CA, USA], Institut de Myologie, Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Association française contre les myopathies (AFM-Téléthon)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Department of Dermatology, Brigham and Women's Hospital [Boston], San Raffaele Scientific Institute, Milan, Italy, Laboratory of Molecular Neuroembryology, University of Rome 'Tor Vergeta'-Clinical and Behavioral Neurology - Neuroscienze e riabilitazione, IRCCS Fondazione Santa Lucia [Roma]-Dulbecco Telethon Institute, Department of Pharmacology, Universidade de Santiago de Compostela, Glycobiologie et signalisation cellulaire, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Complexo Hospitalario Universitario A Coruña, Mécanismes moléculaires de l'angiogénèse, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), University of Florida [Gainesville], Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer (JPArc - U1172 Inserm), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université Lille 2 - Faculté de Médecine, Centro de Investigaciones Biológicas (CSIC), Consejo Superior de Investigaciones Científicas [Spain] (CSIC), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (HOTE GREFFON), Université de Franche-Comté (UFC)-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Infection bactérienne, inflammation, et carcinogenèse digestive, Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre des Sciences du Goût et de l'Alimentation [Dijon] (CSGA), Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS), Universita degli Studi di Padova, University of British Columbia (UBC), University of Edinburgh, Unité de Nutrition Humaine - Clermont Auvergne (UNH), Institut National de la Recherche Agronomique (INRA)-Université Clermont Auvergne (UCA), Australian Regenerative Medicine Institute, Monash University, Clayton, 3800, VIC, Australia, Faculty of Engineering and Natural Sciences, Sabanci University [Istanbul], Department of Biological Sciences [Stanford], Stanford University [Stanford], Université de Montréal (UdeM), Department of Human Genetics, Department of Psychiatry, University of Michigan System-University of Michigan System-Molecular and Behavioral Neuroscience Institute, Centre for Computational and Systems Biology (COSBI), Department of Computer Science [Tsukuba], Graduate School of Systems and Information Engineering [Tsukuba], University of Tsukuba-University of Tsukuba, Institut de biochimie et génétique cellulaires (IBGC), University of Western Ontario (UWO), Genetics, Dynamique Musculaire et Métabolisme (DMEM), Institut National de la Recherche Agronomique (INRA)-Université de Montpellier (UM), Department of Biochemistry and Biophysics, University of Naples Federico II, Lund University [Lund], Institute of Molecular Biosciences, Karl-Franzens University Graz, (IMB), Karl-Franzens-Universität Graz, Polytechnic University of Marche, Centre de Recherche en Cancérologie de Marseille (CRCM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Cell Biology, Physiology and Immunology, Research Unit on BioActive Molecules, Departamento de Química Orgánica Biológica, Instituto de Investigaciones Quimicas y Ambientales de Barcelona, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Physiopathologie et thérapie du muscle strié, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR14-Institut National de la Santé et de la Recherche Médicale (INSERM), The Buck Institute for Age Research, University of Pisa - Università di Pisa, Laboratorio di Genetica Molecolare, Istituto Gaslini, Universidad de Castilla-La Mancha (UCLM), Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, University of Crete [Heraklion] (UOC), Division of Molecular and Cellular Pathology [Birmingham], Department of Medical Research, Taichung Veterans General Hospital, Modélisation et Simulation Numérique en Mécanique et Génie des Procédés (MSNMGP), Université de la Méditerranée - Aix-Marseille 2-Université Paul Cézanne - Aix-Marseille 3-Université de Provence - Aix-Marseille 1-Centre National de la Recherche Scientifique (CNRS), University of Queensland [Brisbane], Dept of Mathematics, Purdue University, Purdue University [West Lafayette], Virologie et Pathologie Humaine (VirPath), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de chimie de coordination (LCC), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut de Chimie de Toulouse (ICT-FR 2599), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Zhejiang University, Équipe Micro et nanosystèmes HyperFréquences Fluidiques (LAAS-MH2F), Laboratoire d'analyse et d'architecture des systèmes (LAAS), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse 1 Capitole (UT1)-Université Toulouse - Jean Jaurès (UT2J)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse 1 Capitole (UT1)-Université Toulouse - Jean Jaurès (UT2J), King Abdullah University of Science and Technology (KAUST), Southern University of Science and Technology of China (SUSTech), OASE, National University of Tainan, Taiwan (OASE), National Taiwan University [Taiwan] (NTU), Weifang Bureau of Land Resources [Weifang], Department of cardiology [Guy's and St. Thomas ' hospitals] [London], Guy's and St Thomas' Hospital [London]-Guy's Hospital [London], University of Pennsylvania [Philadelphia], CRLCC Eugène Marquis (CRLCC), Emory University School of Medicine, Emory University [Atlanta, GA], Korea University, Cytokines et Immunologie des Tumeurs Humaines (U753), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Pharmacology [Tartu, Estonie], Institute of Biomedicine and Translational Medicine [Tartu, Estonie], University of Tartu-University of Tartu, Max-Planck-Institut für Biophysikalische Chemie - Max Planck Institute for Biophysical Chemistry [Göttingen], Max-Planck-Gesellschaft, University of Pittsburgh (PITT), Pennsylvania Commonwealth System of Higher Education (PCSHE), University of Cincinnati (UC), Réponses immunes : régulation et développement, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Experimental Medicine, Oxford University, University of Oxford [Oxford], Division of regenerative Medicine, San Raffaele Scientific Institute, The University of New Mexico [Albuquerque], Université Libre de Bruxelles [Bruxelles] (ULB), Macrophages et Développement de l'Immunité, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health [Baltimore], Johns Hopkins University (JHU)-Johns Hopkins University (JHU), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [APHP]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Dipartimento di Scienze Biomediche, Università degli Studi di Modena e Reggio Emilia (UNIMORE), Department of Experimental Medicine and Oncology, University of Turin, Institut de Génomique Fonctionnelle (IGF), Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), CNV, University of Valparaiso, Institut Gustave Roussy (IGR), Universidad Autonoma de Madrid (UAM), Cell Signalling & Proteomics Group [Londres, Royayme-Uni], Barts Cancer Institute [Londres, Royayme-Uni], Queen Mary University of London (QMUL)-Queen Mary University of London (QMUL), Department of General, Visceral and Vascular Surgery [Jena], Friedrich-Schiller-Universität Jena, Department of Biomedical Engineering, The University of Texas at Austin, University of Texas at Austin, Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte - Clermont Auvergne (M2iSH), Institut National de la Recherche Agronomique (INRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Clermont Auvergne (UCA)-Centre de Recherche en Nutrition Humaine d'Auvergne (CRNH d'Auvergne), Fondazione Santa Lucia (IRCCS), Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Jacques Monod (IJM (UMR_7592)), Institute of Biological, Environmental and Rural Sciences (IBERS), Aberystwyth University, Department of Biology, Johns Hopkins University (JHU), Neurogenetics Group, Instituto de Investigación en Recursos Cinegéticos (IREC), Laboratório de Ultraestrutura Celular Hertha Meyer (IBCCF), Universidade Federal do Rio de Janeiro [Rio de Janeiro] (UFRJ), Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology in Zürich [Zürich] (ETH Zürich), Molecular and Cellular Biology, Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), National University of Ireland [Galway] (NUI Galway), Institut des Maladies Neurodégénératives [Bordeaux] (IMN), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), Freiburg Institute for Advanced Studies-LifeNet, Albert-Ludwigs-Universität Freiburg, Groupe de Recherche en Immunopathologies et maladies infectueuses (GRI), Université de La Réunion (UR)-Centre hospitalier Félix-Guyon [Saint-Denis, La Réunion], Brunel University London [Uxbridge], Unité Propre de Recherche 2357, Institution de Biologie Moléculaire des Plantes, Radiothérapie moléculaire (UMR 1030), Department of Chemistry, University of Kentucky, Universidad de Córdoba [Cordoba], Institut Pasteur, Fondation Cenci Bolognetti - Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Università degli Studi di Roma 'La Sapienza' [Rome], Facultad de Ciencias Químicas y Farmacéuticas, Centro de Estudios Moleculares de la Célula, Biochemistry and Molecular Biology, Goethe-University Frankfurt am Main, Department of Biological and Environmental Sciences and Technologies (DiSTeBA), Università del Salento, Institut Bergonié - Département de médecine, Université Bordeaux Segalen - Bordeaux 2-Centre régional de lutte contre le cancer [CRLCC], Institut National Polytechnique de Lorraine (INPL), Récepteurs nucléaires, maladies cardiovasculaires et diabète (EGID), Université de Lille, Droit et Santé-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Institute of cardiometabolism and nutrition (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [APHP]-Sorbonne Université (SU), Institut de recherches sur la catalyse et l'environnement de Lyon (IRCELYON), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Laboratoire de signalisation moléculaire et neurodégénerescence, Université Louis Pasteur - Strasbourg I-IFR37-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Européen de Chimie et Biologie (IECB), Centre National de la Recherche Scientifique (CNRS)-Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM), Trafic membranaire et Division cellulaire, Landesbetrieb Hessisches Landeslabor, Hematology-Oncology Division, Perelman School of Medicine, University of Pennsylvania [Philadelphia]-University of Pennsylvania [Philadelphia], University of Pavia, Instituto de Investigaciones Biotecnológicas [San Martín] (IIB-INTECH), Universidad Nacional de San Martin (UNSAM)-Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET), University of Helsinki, School of Physics and Astronomy [Exeter], University of Exeter, Department of Biomedicinal Chemistry (CSIC), Institut de Química Avançada de Catalunya, Laboratory of Vascular Pathology (IDI-IRCCS), Istituto Dermopatico dell'Immacolata, Peking University [Beijing], MRC Centre for Developmental Neurobiology, University of Brescia, Immunobiologie fondamentale et clinique, Université de Lyon-Université de Lyon-IFR128-Institut National de la Santé et de la Recherche Médicale (INSERM), CIC régional épidémiologie clinique/essais cliniques - Ile de la Réunion (CIC-EC), University of Rome 'Tor Vergeta', Universidad de Oviedo [Oviedo], Laboratoire des signaux et systèmes (L2S), Université Paris-Sud - Paris 11 (UP11)-CentraleSupélec-Centre National de la Recherche Scientifique (CNRS), Dulbecco Telethon Institute/Department of Biology, Istituto Nazionale di Malattie Infettive 'Lazzaro Spallanzani' (INMI), Rockefeller University [New York], The Babraham Institute, Kansas State University, McGill University, Service d'Anatomie et Cytologie Pathologique [Rouen], CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU), Laboratoire Interuniversitaire de Biologie de la Motricité (LIBM ), Université de Lyon-Université de Lyon-Université Jean Monnet [Saint-Étienne] (UJM)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry]), Department of Medicine [New York], Icahn School of Medicine at Mount Sinai [New York] (MSSM), ATOS Origin, Department of Developmental Biology and Neurosciences, Graduate School of Life Sciences-Tohoku University [Sendai], Goethe-University, Goethe-Universität Frankfurt am Main, Institute of physiological chemistry, Hannover Medical School [Hannover] (MHH), Department of Physiology, Department of Plant and Environmental Sciences, Apoptose, cancer et immunité (U848), Laboratoire de Biologie du Développement (LBD), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Departments of Neurology and Psychiatry, Alzheimer's Disease Research Center, Institute of Experimental Immunology - IEI [Zürich, Switzerland], Université de Zurich [Switzerland], Digital Enterprise Research Institute (DERI-NUIG), Spanish National Research Council (CSIC), Cell Death Research and Therapy Unit [Leuven, Belgium] ( Department of Cellular and Molecular Medicine), Centre d'Immunologie de Marseille - Luminy (CIML), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Signaling in Oncogenesis, Angiogenesis and Permeability - SOAP (CRCINA - Département ONCO - Equipe 15), Centre de recherche de Cancérologie et d'Immunologie / Nantes - Angers (CRCINA), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Department of Medicine [San Francisco], University of California [San Francisco] (UCSF), University of California-University of California, Fondazione Santa Lucia [IRCCS], Clinical and Behavioral Neurology [IRCCS Santa Lucia], Institut de biologie moléculaire des plantes (IBMP), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes (URMITE), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR48, INSB-INSB-Centre National de la Recherche Scientifique (CNRS), Department of Anatomy, Histology, Forensic Medicine and Orthopedic, N.A., Division of Pharmacology and Chemotherapy, Department of Internal Medicine, Pathogénie Microbienne Moléculaire, University of Chile [Santiago], Université de Montpellier (UM), Faculdade de Ciências Farmacêuticas de Ribeirão Preto [São Paulo], Universidade de São Paulo (USP), Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas (CIBERNED), Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1), Catalan Institute of Oncology, Department of Cell Biology, National Institute for Basic Biology [Okazaki], Instituto de Bioquímica Vegetal y Fotosíntesis (IBVF), Universidad de Sevilla-Centro de Investigaciones Científicas Isla de la Cartuja, The Adams Super Center for Brain Studies, Tel Aviv University [Tel Aviv], Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Collège de France (CdF)-Centre National de la Recherche Scientifique (CNRS), Department of Pharmacology and biochemistry, Virginia Commonwealth University (VCU), Department of Immunology, St Jude Children's Research Hospital, Department of Biology and Biotechnologies 'Charles Darwin', Lettres, Idées, Savoir (LIS), Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institute of Biological Chemistry and Nutrition, University of Hohenheim, China Seismological Bureau, Massachusetts Institute of Technology (MIT), Rosenstiel Basic Medical Sciences Research Center [Waltham], Brandeis University, Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA), Meakins-Christie Laboratories, Sanford Burnham Medical Research Institute, La Jolla, National Institute of Advanced Industrial Science and Technology (AIST), ORIENT ET MÉDITERRANÉE : Textes, Archéologie, Histoire (OM), Université Panthéon-Sorbonne (UP1)-École pratique des hautes études (EPHE)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), David Geffen School of Medicine [Los Angeles], University of California [Los Angeles] (UCLA), Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Centro de Investigacion y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Biochemistry and Molecular Biology I, Department of Immunology and Infectious Diseases, Harvard School of Public Health, aDepartment of Plant Biology, Uppsala BioCenter, Swedish University of Agricultural Sciences (SLU), Philipps University of Marburg, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Renal Division, University Medical Center Freiburg, Freiburg, Germany, Rural Health Academic Centre, University of Melbourne-Rural Clinical School, Department of Pathology, University of Veterinary and Animal Sciences, Dipartimento di Scienze della Vita [Modena, Italy], Stress Cellulaire, Université de la Méditerranée - Aix-Marseille 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Pathology, Anatomy & Cell Biology [Philadelphia, Pennsylvania, USA], Thomas Jefferson University, Department of Molecular Neuroscience, Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas, Centro de Investigación en Bioquímica Clínica e Inmunología (CONICET), Universidad Nacional de Córdoba, Córdoba, Argentina, Neuroinflammation Unit, Biotech Research and Innovation Centre-University of Copenhagen = Københavns Universitet (KU), Mathematics and Computing in Automatic Control and Optimization for the User (MIAOU), Inria Sophia Antipolis - Méditerranée (CRISAM), Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria), Centre de Recherche des Cordeliers (CRC), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Danish Cancer Society, Institute of Cancer Biology, UCL-Institute of Child Health (ICH), Institute of Child Health-Great Ormond Street Hospital for Children [London] (GOSH), Division of Renal Diseases and Hypertension, University of Colorado [Boulder], Institut de biologie et chimie des protéines [Lyon] (IBCP), Joslin Diabetes Center, Universität Ulm - Ulm University [Ulm, Allemagne], Qingdao Institute of Marine Geology, China Geological Survey, Qingdao 266071, China, Université Paris Diderot - Paris 7 (UPD7), Institute of Software, Chinese Academy of Sciences [Beijing] (CAS), Metabolic Engineering Group, Departamento de Microbiologia y Genetica, Edificio Departamental, Campus Miguel de Unamuno, Universidad de Salamanca, University of Minnesota [Twin Cities], University of Minnesota System, Department of Cellular and Molecular Physiology, Yale University School of Medicine, The Arctic University of Norway, Department of Biological Sciences, The Open University [Milton Keynes] (OU), Summit Analytical, CALRG, Institute of Educational Technology, Institute for Neurologic Disabilities Research, Faculty of Health Sciences-University of Pretoria [South Africa], Department of Paediatric Neurology, Guy's and St Thomas' Hospital [London]-Evelina Children's Hospital, Physiologie des Adaptations Nutritionnelles [UMR_A1280] (PhAN), Institut National de la Recherche Agronomique (INRA)-Université de Nantes (UN), Dana-Farber Cancer Institute and the Department of Cell Biology, Harward Medical School, Translational Health Science and Technology Institute [Faridabad] (THSTI), Department of Biomedical Sciences of Cells and Systems, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands, School of Reliability and Systems Engineering [Beijing], Beihang University, Oxford Centre for Integrative Systems Biology, Center for Membrane and Cell Physiology [Charlottesville, VA, USA] (School of Medicine), University of Virginia [Charlottesville], Apoptose, cancer et immunité (Equipe labellisée Ligue contre le cancer - CRC - Inserm U1138), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), St James's University Hospital, Leeds Teaching Hospitals NHS Trust, Karlsruher Institut für Technologie (KIT), Faculty of Pharmaceutical Sciences, Hokkaido University, École normale supérieure - Paris (ENS Paris), School of Electrical Engineering [Seoul] (Korea University), Department of Mathematics and Statistics [Guelph], University of Guelph, Department of Molecular Genetics, Department of Genetics [Stanford, CA, États-Unis], Institute of Immunology, University Hospital Schleswig-Holstein, Arizona Respiratory Center, Okazaki Institute for Integrative Bioscience, ToxAlim (ToxAlim), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), Newcastle University [Newcastle], JRC Institute for Transuranium Elements [Karlsruhe] (ITU ), European Commission - Joint Research Centre [Karlsruhe] (JRC), Department of Neuroscience, University of Texas Southwestern Medical Center [Dallas], Centre de génétique et de physiologie moléculaire et cellulaire (CGPhiMC), Laboratory of Functional Neurogenomics [Tuebingen, Germany], University of Tuebingen-Center of Neurology and Hertie-Institute for Clinical Brain Research [Tuebingen, Germany], Indian Institute of Technology Bombay (IIT Bombay), European Organization for Nuclear Research (CERN), Harvard Medical School [Boston] (HMS), Indian School of Mines, Department of Computer Science [UIUC] (UIUC), University of Illinois at Urbana-Champaign [Urbana], University of Illinois System-University of Illinois System, Centre for Cancer Biology, Hanson Institute, Adelaide, University of California [San Diego] (UC San Diego), University of California, Centre d’Infection et d’Immunité de Lille (CIIL) - U1019 - UMR 8204 (CIIL), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre National de la Recherche Scientifique (CNRS), Department of Biochemistry, University of Bristol, Organisation Nucléaire et Oncogenèse, Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), FONDAP Center CEMC Estudios Moleculares de la Célula, Unité de Biologie Fonctionnelle et Adaptative (BFA (UMR_8251 / U1133)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), Centre d'infectiologie Necker-Pasteur [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Chungnam National Univesity School of Medicine, Taejon, Korea, Chungnam National Univesity School of Medicine, Micro & Nanobiotechnologies, Institut des Sciences Analytiques (ISA), Centre National de la Recherche Scientifique (CNRS)-Université de Lyon-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-École normale supérieure - Lyon (ENS Lyon)-Centre National de la Recherche Scientifique (CNRS)-Université de Lyon-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-École normale supérieure - Lyon (ENS Lyon), Centre de Recherche en Cancérologie de Lyon (CRCL), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de génétique moléculaire (CGM), Université Paris-Sud - Paris 11 (UP11)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Center for Applied Mathematics, Tsinghua University [Beijing], University of Connecticut School of Medicine, University of Connecticut (UCONN), Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes (LBMCE), Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Microenvironnement et Physiopathologie de la Differenciation, Division of Nephrology and Hypertension, Mayo Clinic, Beatson Institute for Cancer Research, Beatson institute for cancer research, Howard Hughes Medical Institute, Howard Hugues Medical Institute, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Institute of Computing Technology [Beijing] (ICT), Chinese Academy of Sciences [Changchun Branch] (CAS), School of Electronics and Computer Science (ECS), University of Southampton, Third Hospital, Department of Anesthesiology, Cognitive Interaction Technology [Bielefeld] (CITEC), Universität Bielefeld = Bielefeld University, Procédés, Matériaux et Energie Solaire (PROMES), Université de Perpignan Via Domitia (UPVD)-Centre National de la Recherche Scientifique (CNRS), Faculty of Pharmacy- University of Coimbra, National Neuroscience Institute, Key Laboratory of Molecular Virology & Immunology (LMVI), Institut Pasteur de Shanghai, Académie des Sciences de Chine - Chinese Academy of Sciences (IPS-CAS), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Coll Life Sci, Beijing Normal University, Delft University of Technology (TU Delft), Christian-Albrechts-Universität zu Kiel (CAU), Department of Molecular Pathology and Microbiology, Center for Applied Proteomics and Molecular Medicine-George Mason University [Fairfax], Sidney Kimmel Cancer Center, Jefferson (Philadelphia University + Thomas Jefferson University), Institut des Sciences Chimiques de Rennes (ISCR), Institut National des Sciences Appliquées - Rennes (INSA Rennes), Institut National des Sciences Appliquées (INSA)-Université de Rennes (UNIV-RENNES)-Institut National des Sciences Appliquées (INSA)-Université de Rennes (UNIV-RENNES)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Rennes-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES), Department of Chemistry, University of Pittsburgh, University of Pittsburg, Tianjin University of Science and Technology (TUST), Hunan University of Science and Technology [Xiangtan], Laboratoire de Génie Civil et Génie Mécanique (LGCGM), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National des Sciences Appliquées - Rennes (INSA Rennes), Institut National des Sciences Appliquées (INSA)-Université de Rennes (UNIV-RENNES)-Institut National des Sciences Appliquées (INSA), China Agricultural University (CAU), Acad Disaster Reduct and Emergency Management, Minist Civil Affairs, Minist Educ, Beijing, Peoples R China, affiliation inconnue, Département Technologie des Polymères et Composites & Ingénierie Mécanique (TPCIM), École des Mines de Douai (Mines Douai EMD), Institut Mines-Télécom [Paris] (IMT)-Institut Mines-Télécom [Paris] (IMT)-Ministère de l'Economie, des Finances et de l'Industrie, MOE Key Laboratory of Bioinformatics, Centre for Plant Biology, School of Life Sciences, Laboratoire d'Informatique Gaspard-Monge (ligm), Université Paris-Est Marne-la-Vallée (UPEM)-École des Ponts ParisTech (ENPC)-ESIEE Paris-Fédération de Recherche Bézout-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Biochimie Moléculaire et Cellulaire (LBMC), Université de Bourgogne (UB), Center for International Blood and Marrow Transplant Research (CIBMTR), Emory University [Atlanta, GA]-Medical College of Wisconsin, Centre de biophysique moléculaire (CBM), Université d'Orléans (UO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Illman Cancer Center, Pennsylvania Commonwealth System of Higher Education (PCSHE)-Pennsylvania Commonwealth System of Higher Education (PCSHE), Ingénierie des Matériaux Polymères (IMP), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Jean Monnet [Saint-Étienne] (UJM)-Centre National de la Recherche Scientifique (CNRS), Université Côte d'Azur (UCA), Department of Medical Microbiology and Immunology, University of California [Davis] (UC Davis), School of Health Sciences, University of Minho [Braga], Équipe Calcul Distribué et Asynchronisme (LAAS-CDA), University of California [Riverside] (UCR), Ohio State University [Columbus] (OSU), Laboratory of Systems Biology, Van Andel Institute [Grand Rapids], Division of Genetics and Cell Biology, National Center for Gender-Specific Medicine, Istituto Superiore di Sanità, Oregon Health and Science University [Portland] (OHSU), Dendrite Differenciation Group [DZNE - Bonn], German Research Center for Neurodegenerative Diseases - Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Equipe 12, Génétique moléculaire, signalisation et cancer (GMSC), Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre de Recherche en Cancérologie de Lyon (CRCL), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), University Medical Center [Utrecht], Institut d'Investigacions Biomèdiques August Pi I Sunyer [Barcelona, Spain] (Hospital Clinic ), Department of Genetics, Trinity College Dublin, Fisiopatologia de los procesos inflamatorios, Vall d'Hebron Research Institute, Institució Catalana de Recerca i Estudis Avançats (ICREA), Department of Human Genetics, Nagasaki University, Transduction du signal et oncogénèse, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Curie, Center for Experimental and Molecular Medicine, Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA)-University of Amsterdam [Amsterdam] (UvA), Department of medical Biochemistry, University of Amsterdam [Amsterdam] (UvA), IDI-IRCCS Biochemistry Laboratory, Università degli Studi di Roma Tor Vergata [Roma], Program Against Cancer Therapeutic Resistance/Metabolism & Cancer Group [Catalonia, Spain] (ProCURE), Catalan Institute of Oncology-Girona (ICO-Girona), Instituto de Tecnologia Química e Biológica António Xavier (ITQB), Universidade Nova de Lisboa (NOVA), Medical Genetics Unit, IRCCS Casa Sollievo della Sofferenza Hospital, CNR, Consiglio Nazionale delle Ricerche (CNR), Biochimie et Physiologie Moléculaire des Plantes (BPMP), Université de Montpellier (UM)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro)-Institut National de la Recherche Agronomique (INRA)-Centre National de la Recherche Scientifique (CNRS), Laboratory for Developmental Neurobiology, RIKEN Brain Science Institute, The Hospital for sick children [Toronto] (SickKids), Universidad de Sevilla, Immunité muqueuse et vaccination, Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR50-Université Nice Sophia Antipolis (... - 2019) (UNS), DIMS, University of Trento [Trento], Laboratoire de Biologie Moléculaire de la Cellule (LBMC), Department of Cellular and Molecular Medicine [Madrid, Spain], Laboratory of Cell Death and Cancer Therapy [Madrid, Spain], Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas (CSIC) -Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas (CSIC), Plymouth Marine Laboratory, Prospect Place, The Hoe, Plymouth PL1 3HD, UK, Centre d'Immunologie et de Maladies Infectieuses (CIMI), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Dpt. of Cancer & Cell Biology, Interactions Bactéries-Cellules (UIBC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris]-Institut National de la Recherche Agronomique (INRA), Max planck Institute for Biology of Ageing [Cologne], Euromov (EuroMov), Wellcome Trust Centre for Molecular Parasitology [Glasgow, UK], University of Glasgow- Institute of Infection, Immunity and Inflammation [Glasgow, UK], Immunologie et chimie thérapeutiques (ICT), Cancéropôle du Grand Est-Centre National de la Recherche Scientifique (CNRS), UMR 1599, Centre National de la Recherche Scientifique (CNRS), EA 4100, Histoire culturelle et sociale de l'art (HiCSA), Université Panthéon-Sorbonne (UP1)-Université Panthéon-Sorbonne (UP1), Centre for Astrophysics and Supercomputing (Centre for Astrophysics and Supercomputing), Swinburne University of Technology [Melbourne], Department of Cellular and Physiological Sciences [Vancouver, BC, Canada] (Life Sciences Institute), University of British Columbia (UBC)-Life Sciences Institute [Vancouver, BC, Canada], School of Pharmacy, Department of Experimental Medicine, Dept. Neurosciences, Department of Internal Medicine, Radboud University Medical Center [Nijmegen], Institute of Medical Genetics and Applied Genomics, Radiation Physics, School of Life Science, Department of Basic Biology, The Graduate University for Advanced Studies, CIBER de Enfermedades Neurodegenerativas (CIBERNED), Doshisha University, National Cancer Research Center [Tokyo, Japan], University of Washington [Seattle], Department of Experimental Neurodegeneration [Göttingen, Germany], University Medical Center Göttingen (UMG), Cibles moléculaires et thérapeutiques de la maladie d'Alzheimer (CIMoTHeMA), Université de Poitiers, Laboratoire de Probabilités et Modèles Aléatoires (LPMA), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), BioCeV-Institute of Microbiology, Médecine Personnalisée, Pharmacogénomique, Optimisation Thérapeutique (MEPPOT - U1147), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Istituto di chimica biologica, Università degli Studi di Verona, Département Image et Traitement Information (ITI), Institut Mines-Télécom [Paris] (IMT)-Université européenne de Bretagne - European University of Brittany (UEB)-Télécom Bretagne, Department of Cell Biology and Biophysics, Università degli Studi di Firenze [Firenze], Cell Immunity in Cancer, Inflammation and infection Group [Zaragoza, Spain] (Biomedical Research Center), Nanoscience Institute of Aragon - INA [Zaragoza, Spain]-Fundación Agencia Aragonesa para la Investigación y el Desarrollo - ARAID [Zaragoza, Spain]-University of Zaragoza - Universidad de Zaragoza [Zaragoza], Department of Pediatrics, Università degli studi di Napoli Federico II, Transfert de Genes a Visee Therapeutique Dans les Cellules Souches, Developpement Normal et Pathologique du Système Immunitaire, Signalisation et physiopathologie des cellules épithéliales, Facultad de Medicina, Universidad de Santiago de Chile [Santiago] (USACH), Departamento de Farmacobiología, Cinvestav-Sede Sur, Centre de recherche Croissance et signalisation (UMR_S 845), College of Life Sciences, Central China Normal University, Institute of Molecular Biotechnology, Austrian Academy of Sciences (OeAW), Laboratory of Cardiac Surgical Research, Monash University [Clayton], Universidade do Minho, Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Neurodegenerative Diseases Research Group (CIBERNED), Vall d'Hebron Research Institute-Center for Networked Biomedical Research on Neurodegenerative Diseases, Barcelona, Department of medicine, Syracuse, NY, USA, State University of New York (SUNY), National University of Singapore (NUS)-Yong Loo Lin School of Medicine-Graduate School for Integrative Sciences and Engineering, McGill University Health Center [Montreal] (MUHC), National Institute for Infectious Diseases, Transporteurs en Imagerie et Radiothérapie en Oncologie (TIRO - UMR E4320), Service Hospitalier Frédéric Joliot (SHFJ), Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-UMR E4320 (TIRO-MATOs), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Nice Sophia Antipolis (... - 2019) (UNS), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Biomedical Sciences, Department of Genetics of Eukaryotic Microorganisms, Georg-August-University [Göttingen]-Institute of Microbiology and Genetics, Sterol metabolism and therapeutic innovations in oncology, Institut Claudius Regaud, CRLCC Institut Claudius Regaud-CRLCC Institut Claudius Regaud-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Department of Molecular, Cellular and Developmental Biology, Señalización Celular 4, Institute of integrative biology (Liverpool), University of Liverpool, Department of Human Biology, University of Cape Town, National Institute of Diabetes and Digestive and Kidney Diseases [Bethesda], Department of Molecular Biology, Eberhard Karls Universität Tübingen, Technical University of Munich (TUM), Biophysics and Bioinformatics Laboratory, Department of Cell Biology and Morphology, Université de Lausanne (UNIL), Shenyang Institute of Automation, the Chinese Academy of Sciences (SIA), Key Laboratory of Thermo-Fluid Science and Engineering of Ministry of Education, Xi'an Jiaotong University (Xjtu), Dipartimento di Biologia, Mechanics laboratory , UniversityAmar Telidji, 3000 Laghouat, Algéria., Mechanics laboratory , University Amar Telidji, sans affiliation, Service d'hépatologie [Hôpital Beaujon], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), University of Waterloo, Waterloo, ON, Canada, Institute of Cell Biology and Immunology, University of Stuttgart, Chaperones Research Group, Institute of Biosciences and Technology [Houston, TX, États-Unis] (IBT), Texas A&M Health Science Center [Houston, TX, États-Unis] (TAMHSC), Texas A&M University Health Science Center-Texas A&M University Health Science Center, Aquatic and Crop Resource Development, National Research Council of Canada (NRC), Cibles thérapeutiques, formulation et expertise pré-clinique du médicament (CITHEFOR), Université de Lorraine (UL), Dipartimento di Scienze Cliniche e Molecolari, Università Politecnica delle Marche [Ancona] (UNIVPM), Department of Biochemistry and Molecular Biology [Indianapolis, IN, USA], Indiana University School of Medicine, Indiana University System-Indiana University System, Wellcome Trust Centre for Gene Regulation and Expression, College of Life Sciences, University of Dundee, iMed.UL, Faculty of Pharmacy, University of Lisbon, CESAM & Biology Department, Universidade de Aveiro, Celullar and Molecular Medicine, Università degli Studi di Perugia (UNIPG), Institute of Clinical Molecular Biology, Kiel University, Apoptose et Système Immunitaire (ASI), Vieillissement Cellulaire Intégré et Inflammation (VCII), Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing (B2A), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Department of Mathematical Sciences [Aalborg], Aalborg University [Denmark] (AAU), Cambridge Institute for Medical Research (CIMR), University of Cambridge [UK] (CAM), Biozentrum, University of Basel (Unibas), Structural and Computational Biology Unit, European Molecular Biology Laboratory [Grenoble] (EMBL), Rutgers New Jersey Medical School (NJMS), Rutgers University System (Rutgers), Université de Perpignan Via Domitia (UPVD), Universidad Pablo de Olavide [Sevilla] (UPO), Department of Neurosciences, Agronomes et Vétérinaires Sans Frontières (AVSF), AVSF, Department of Mathematics [Gakushuin], Gakushuin University, Department of Internal Medicine [Münster, Germany], University of Münster, Neurogenetics laboratory, University Medicine Goettingen, Institut de biologie structurale (IBS - UMR 5075), Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes (UGA)-Centre National de la Recherche Scientifique (CNRS), Université d'Uruguay, Laboratoire de Biologie Cellulaire et Moléculaire du Contrôle de la Prolifération (LBCMCP), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Institute for Conservation & Improvement of Valentian Agrodiversity (COMAV), Universitat Politecnica de Valencia (UPV), ICBM, University of Chile [Santiago]-Faculty of Medicine, Nutrition, Métabolisme, Aquaculture (NuMéA), Institut National de la Recherche Agronomique (INRA)-Université de Pau et des Pays de l'Adour (UPPA), Department of Cell Biology, Baltimore, Johns Hopkins University School of Medicine, Baylor College of Medicine (BCM), Baylor University, University of Minnesota Medical School, Beijing Candid soft Technology Co. Ltd, Nanjing University of Information Science and Technology, Department of Hepatobiliary and Pancreatic Surgery [Maebashi, Japan], Gunma University Graduate Schoolof Medicine [Maebashi, Japan], Department of Molecular Genetics [Maastricht, The Netherlands], Maastricht University [The Netherlands], Institute of Cell Biology and Genetic Engineering, National Academy of Sciences of Ukraine (NASU), Institute of Pharmacology of Natural Products and Clinical Pharmacology, Institute of Pharmacology, University of Bern, Imagine - Institut des maladies génétiques (IMAGINE - U1163), Wilmer Eye Institute, Mayo Clinic and Mayo College of Medicine, Rochester, Institute of Biochemistry and Biophysics, Polska Akademia Nauk (PAN)-Sciences, Department of Electrical and Computer Engineering [Waterloo] (ECE), University of Waterloo [Waterloo], Department of Chemistry and Toxicology, Norwegian Veterinary Institute, Department of Gynecologic Oncology, The University of Texas M.D. Anderson Cancer Center [Houston], University of Minho, Friedrich Miescher Laboratory (FML), Charité - Universitätsmedizin Berlin / Charite - University Medicine Berlin, Department of Biomedical Sciences and Biotechnologies, Brescia University, Department of Physiological Chemistry [Bochum], Ruhr-Universität Bochum [Bochum], University of Oslo (UiO), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Facultés Universitaires Notre Dame de la Paix (FUNDP), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), École pratique des hautes études (EPHE)-Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Institut de recherche pour le développement [IRD] : UR226, Université du Québec à Montréal = University of Québec in Montréal (UQAM), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Association française contre les myopathies (AFM-Téléthon)-Sorbonne Université (SU), Université Lille 2 - Faculté de Médecine -Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Université de Franche-Comté (UFC), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon), Institut de Chimie de Toulouse (ICT-FR 2599), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Université Toulouse 1 Capitole (UT1)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Toulouse - Jean Jaurès (UT2J)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Toulouse 1 Capitole (UT1)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Université Fédérale Toulouse Midi-Pyrénées, Université libre de Bruxelles (ULB), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Universidade Federal do Rio de Janeiro (UFRJ), Institut Bergonié [Bordeaux], UNICANCER, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Trafic membranaire et Division cellulaire - Membrane Traffic and Cell Division, Centre National de la Recherche Scientifique (CNRS)-CentraleSupélec-Université Paris-Sud - Paris 11 (UP11), McGill University = Université McGill [Montréal, Canada], Service d'Anatomie et Cytologie Pathologique [CHU Rouen], Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Signaling in Oncogenesis, Angiogenesis and Permeability (CRCINA-ÉQUIPE 15), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), Universidad de Chile = University of Chile [Santiago] (UCHILE), Centro de Investigacion Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III (ISC), Université Montpellier 1 (UM1)-CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS), Université Panthéon-Sorbonne (UP1)-École pratique des hautes études (EPHE)-Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Collège de France (CdF (institution)), Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Great Ormond Street Hospital for Children [London] (GOSH)-Institute of Child Health, Hokkaido University [Sapporo, Japan], Université Paris sciences et lettres (PSL), Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université de Lyon-Université de Lyon, Centre d’Infection et d’Immunité de Lille (CIIL) - INSERM U1019 - UMR 9017 (CIIL), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Organisation Nucléaire et Oncogenèse - Nuclear Organization and Oncogenesis, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon], Centre National de la Recherche Scientifique (CNRS)-Institut de biologie physico-chimique (IBPC (FR_550)), Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU), The Beatson Institute for Cancer Research, Beijing Normal University (BNU), Institut National des Sciences Appliquées (INSA)-Université de Rennes (UNIV-RENNES)-Institut National des Sciences Appliquées (INSA)-Ecole Nationale Supérieure de Chimie de Rennes-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Fédération de Recherche Bézout-ESIEE Paris-École des Ponts ParisTech (ENPC)-Université Paris-Est Marne-la-Vallée (UPEM), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA), Université de Lyon-Université de Lyon-Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Université de Lyon-Université de Lyon-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre Léon Bérard [Lyon], Vall d’Hebron Research Institute (VHIR), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Universidade Nova de Lisboa = NOVA University of Lisboa (NOVA), Université de Montpellier (UM)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro)-Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro)-Institut National de la Recherche Agronomique (INRA)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Doshisha University [Kyoto], Université européenne de Bretagne - European University of Brittany (UEB)-Télécom Bretagne-Institut Mines-Télécom [Paris] (IMT), Università degli Studi di Firenze = University of Florence [Firenze], University of Zaragoza - Universidad de Zaragoza [Zaragoza]-Nanoscience Institute of Aragon - INA [Zaragoza, Spain]-Fundación Agencia Aragonesa para la Investigación y el Desarrollo - ARAID [Zaragoza, Spain], Central China Normal University [Wuhan, China], Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-UMR E4320 (TIRO-MATOs), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut Claudius Regaud, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de biologie structurale [1992-2019] (IBS - UMR 5075 [1992-2019]), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre de Biologie Intégrative (CBI), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Nanjing University of Information Science and Technology (NUIST), Facultad de Medicina [Buenos Aires], Universidad de Buenos Aires [Buenos Aires] (UBA)-Universidad de Buenos Aires [Buenos Aires] (UBA)-Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET), Université de Technologie de Belfort-Montbeliard (UTBM)-Ecole Nationale Supérieure de Mécanique et des Microtechniques (ENSMM)-Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Clermont Auvergne (UCA)-Institut National de la Recherche Agronomique (INRA), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET)-Universidad Nacional de San Martin (UNSAM), Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet [Saint-Étienne] (UJM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, George Mason University [Fairfax]-Center for Applied Proteomics and Molecular Medicine, Institut National de la Recherche Agronomique (INRA)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro)-Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro), Institute of Infection, Immunity and Inflammation [Glasgow, UK]-University of Glasgow, Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7)-Université Pierre et Marie Curie - Paris 6 (UPMC), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Université Paris-Sud - Paris 11 (UP11)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB), Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-CHU Rouen, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre Léon Bérard [Lyon]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), and Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Subjects: 0301 basic medicine, Settore BIO/06, biology, Cell Biology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, biology.organism_classification, Cell biology, Interpretation (model theory), 03 medical and health sciences, Arama, 030104 developmental biology, Molecular Biology, Humanities, ComputingMilieux_MISCELLANEOUS
Abstract: Author(s): Klionsky, DJ; Abdelmohsen, K; Abe, A; Abedin, MJ; Abeliovich, H; Arozena, AA; Adachi, H; Adams, CM; Adams, PD; Adeli, K; Adhihetty, PJ; Adler, SG; Agam, G; Agarwal, R; Aghi, MK; Agnello, M; Agostinis, P; Aguilar, PV; Aguirre-Ghiso, J; Airoldi, EM; Ait-Si-Ali, S; Akematsu, T; Akporiaye, ET; Al-Rubeai, M; Albaiceta, GM; Albanese, C; Albani, D; Albert, ML; Aldudo, J; Algul, H; Alirezaei, M; Alloza, I; Almasan, A; Almonte-Beceril, M; Alnemri, ES; Alonso, C; Altan-Bonnet, N; Altieri, DC; Alvarez, S; Alvarez-Erviti, L; Alves, S; Amadoro, G; Amano, A; Amantini, C; Ambrosio, S; Amelio, I; Amer, AO; Amessou, M; Amon, A; An, Z; Anania, FA; Andersen, SU; Andley, UP; Andreadi, CK; Andrieu-Abadie, N; Anel, A; Ann, DK; Anoopkumar-Dukie, S; Antonioli, M; Aoki, H; Apostolova, N; Aquila, S; Aquilano, K; Araki, K; Arama, E; Aranda, A; Araya, J; Arcaro, A; Arias, E; Arimoto, H; Ariosa, AR; Armstrong, JL; Arnould, T; Arsov, I; Asanuma, K; Askanas, V; Asselin, E; Atarashi, R; Atherton, SS; Atkin, JD; Attardi, LD; Auberger, P; Auburger, G; Aurelian, L; Autelli, R
Published: 2016
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175. Do we need research on reporting on diabetes research?

Author: Massimo Porta, Massimo Federici, Antonio Secchi, Porta, Massimo, Federici, Massimo, and Secchi, Antonio
Subjects: medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, media_common.quotation_subject, Endocrinology, Internal Medicine, Scientific Misconduct, 030209 endocrinology & metabolism, 030204 cardiovascular system & hematology, League, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Diabetes Mellitus, Heaven, Humans, Quality (business), Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Scientific misconduct, media_common, Publishing, Impact factor, business.industry, Diabetes Mellitu, General Medicine, Public relations, Country of origin, Publish or perish, Democracy, Diabetes and Metabolism, Research Design, Epidemiologic Research Design, business, Human
Abstract: Two years ago we celebrated Acta Diabetologica’s fiftieth anniversary [1] and then proceeded to bring in a number of changes to help it meet the challenges that await diabetes research, and the reporting of diabetes research, in the next 50 years. The Advisory Board was enlarged to members from all over the world, and we take this opportunity to thank them for accepting an additional burden to their already busy schedules. Secondly, we strived to maintain the shortest possible processing times for submitted manuscripts, and the latest statistics testify that we are managing to do so. Third, we worked to manage a consistent backlog of online first published articles. This was meant to meet authors’ reasonable expectations to have their own articles included in a published issue. This policy might have contributed to the fluctuation of the impact factor although we are fully aware that selecting high-quality papers will be the only valuable strategy to have it rise again. Indeed, as Editors, we were happy to see the quality of submitted manuscripts steadily improving over the past two years and feel confident that bibliometric indexes will eventually reward our efforts to make Acta Diabetologica more and more of an outstanding journal. With a historical perspective on the past 50 years, we open this first issue of 2016 with a report on the 100 most cited papers of all times in the field of diabetes research [2]. Though not revealing major surprises, the report confirms that randomized controlled clinical trials, headed by the DCCT and UKPDS, and position statements/guidelines, remain most popular among research workers. However, interestingly and perhaps refreshingly, some ‘‘classical’’ pathophysiology milestones also sit high in the premier league. Pathophysiology lays the foundations, but final answers on diagnosis and treatment can only come from intervention studies, with all the caveats that still surround the translation of trials to the real world. Also the country of origin of top papers, headed by the USA, and the journals in which they were published, sadly Acta Diabetologica is not among them, reserve few surprises, confirming the quality of knowledge produced in areas with a strong tradition in diabetes research. Indeed, even if citations are not necessarily synonymous with quality, we can assume that the equivalence holds true at least in the Heaven of the top 100. For lesser reports, or top 100 to be, selection for publication remains based upon time-honored peer review, a process fraught with shortcomings except that, as someone said about democracy, any alternative is worse. A novel set of trials and tribulations has emerged recently when a number of papers were retracted because authors were found to have suggested themselves (under false names and addresses) and/or complacent friends as reviewers. Subsequent investigations revealed even more sophisticated rings of fraudulent agencies that, for a fee, provide authors with both fabricated articles and friendly reviewers [3]. Sadly, the drive to publish or perish has turned research from the & Massimo Porta massimo.porta@unito.it
Published: 2016

176. Microdialysis and proteomics of subcutaneous interstitial fluid reveals increased galectin-1 in type 2 diabetes patients

Author: Maria J. Pereira, Per-Anders Jansson, Jan W. Eriksson, Martin Schmelz, Emanuel Fryk, Lena Strindberg, Fredrik H. Nystrom, Massimo Federici, Nikolaus Marx, Jan Borén, Jeanna Perman Sundelin, and Per-Arne Svensson
Subjects: Adult, Male, 0301 basic medicine, Proteomics, medicine.medical_specialty, Microdialysis, Settore MED/09 - Medicina Interna, Galectin 1, Endocrinology, Diabetes and Metabolism, food.diet, Adipose tissue, Galectin-1, Obesity, 030209 endocrinology & metabolism, Type 2 diabetes, Biology, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, food, Insulin resistance, Interstitial fluid, Internal medicine, medicine, Humans, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Aged, Extracellular Fluid, Middle Aged, medicine.disease, Very low calorie diet, 030104 developmental biology, Diabetes Mellitus, Type 2
Abstract: To identify a potential therapeutic target for type 2 diabetes by comparing the subcutaneous interstitial fluid from type 2 diabetes patients and healthy men.Proteomics was performed on the interstitial fluid of subcutaneous adipose tissue obtained by microdialysis from 7 type 2 diabetes patients and 8 healthy participants. 851 proteins were detected, of which 36 (including galectin-1) showed significantly altered expression in type 2 diabetes. We also measured galectin-1 expression in: (1) adipocytes isolated from adipose tissue biopsies from these participants; (2) subcutaneous adipose tissue of 24 obese participants before, during and after 16weeks on a very low calorie diet (VLCD); and (3) adipocytes isolated from 6 healthy young participants after 4weeks on a diet and lifestyle intervention to promote weight gain. We also determined the effect of galectin-1 on glucose uptake in human adipose tissue.Galectin-1 protein levels were elevated in subcutaneous dialysates from type 2 diabetes compared with healthy controls (p0.05). In agreement, galectin-1 mRNA expression was increased in adipocytes from the type 2 diabetes patients (p0.05). Furthermore, galectin-1 mRNA expression was decreased in adipose tissue after VLCD (p0.05) and increased by overfeeding (p0.05). Co-incubation of isolated human adipocytes with galectin-1 reduced glucose uptake (p0.05) but this was independent of the insulin signal.Proteomics of the interstitial fluid in subcutaneous adipose tissue in vivo identified a novel adipokine, galectin-1, with a potential role in the pathophysiology of type 2 diabetes.
Published: 2016

177. Inflammation and macrophage infiltration in adipose tissue: A link between diabetes and atherosclerosis

Author: Rossella Menghini, Massimo Federici, and Renato Lauro
Subjects: medicine.medical_specialty, Adipose tissue macrophages, medicine.medical_treatment, Adipose tissue, Inflammation, General Medicine, Biology, medicine.disease, Insulin resistance, Cytokine, Endocrinology, Adipogenesis, Internal medicine, Diabetes mellitus, medicine, Macrophage, medicine.symptom
Abstract: Obesity is associated with macrophage infiltration of adipose tissue, resulting in the development of insulin resistance and cardiovascular diseases. MCP-1 is involved in monocyte recruitment to both early atherosclerotic lesion and adipose tissue. We recently described two possible mechanisms upstream MCP-1 activation. The first involved insulin dependent phosphorylation of GATA2, a transcription factor crucial for adipogenesis and inflammatory program. In the second we showed that an increased expression of several inflammation markers, including MCP-1 in metabolic and vascular tissues might due to a deregulation of TNF-alpha Converting Enzyme (TACE). GATA-2 and TACE could be new targets in the treatment of obesity related inflammation and its complications.
Published: 2007
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178. Vascular, metabolic, and inflammatory abnormalities in normoglycemic offspring of patients with type 2 diabetes mellitus

Author: Carmine Cardillo, Julio A. Panza, Davide Lauro, Angelo Scuteri, Roberto Leo, Micaela Iantorno, Massimo Federici, Michael J. Quon, Umberto Campia, Giulio Cesare Cocciolillo, Mario Turriziani, A. Fusco, Renato Lauro, Manfredi Tesauro, and Stefano Rizza
Subjects: Adult, Male, medicine.medical_specialty, Tumor Necrosis Factor-alpha, Intercellular Adhesion Molecule-1, Humans, Brachial Artery, Interleukin-1beta, Vascular Cell Adhesion Molecule-1, C-Reactive Protein, Inflammation, Diabetes Mellitus, Type 2, Insulin Resistance, Female, Settore MED/09 - Medicina Interna, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Settore MED/50 - Scienze Tecniche Mediche Applicate, Type 2 diabetes, Settore MED/13 - Endocrinologia, Endocrinology, Insulin resistance, Internal medicine, Diabetes mellitus, Diabetes Mellitus, medicine, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Endothelial dysfunction, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, Adiponectin, business.industry, Insulin, Quantitative insulin sensitivity check index, Type 2 Diabetes Mellitus, medicine.disease, business, Type 2
Abstract: Endothelial dysfunction, insulin resistance, and elevated levels of circulating proinflammatory markers are among the earliest detectable abnormalities in people at risk for atherosclerosis. Accelerated atherosclerosis is a leading contributor to morbidity and mortality in type 2 diabetes mellitus, a complex genetic disorder. Therefore, we hypothesized that normoglycemic offspring of patients with type 2 diabetes mellitus (NOPD) may have impaired vascular and metabolic function related to an enhanced proinflammatory state. We compared NOPD (n = 51) with matched healthy control subjects without family history of diabetes (n = 35). Flow- and nitroglycerin-mediated brachial artery vasodilation were assessed by ultrasound to evaluate endothelium-dependent and -independent vascular function. Each subject also underwent an oral glucose tolerance test to evaluate metabolic function. Fasting levels of plasma adiponectin and circulating markers of inflammation (high-sensitivity C-reactive protein, CD40 ligand, interleukin 1beta, tumor necrosis factor alpha, vascular cell adhesion molecule 1, and intracellular adhesion molecule) were measured. Both NOPD and the control group had fasting glucose and insulin levels well within the reference range. However, results from oral glucose tolerance test and quantitative insulin sensitivity check index revealed that NOPD were insulin resistant with significantly impaired flow- and nitroglycerin-mediated dilation compared with the control group. Adiponectin levels were lower, whereas many circulating markers of inflammation were higher, in NOPD compared with the control group. Normoglycemic offspring of patients with type 2 diabetes mellitus have impaired vascular and metabolic function accompanied by an enhanced proinflammatory state that may contribute to their increased risk of diabetes and its vascular complications.
Published: 2007
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179. Carotid artery intima-media thickness is associated with insulin-mediated glucose disposal in nondiabetic normotensive offspring of type 2 diabetic patients

Author: Maria Adelaide Marini, Giorgio Sesti, Francesco Perticone, Massimo Federici, Simona Frontoni, Francesco Andreozzi, Marina Cardellini, Davide Lauro, and Marta Letizia Hribal
Subjects: Adult, Blood Glucose, Male, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Carotid Artery, Common, Physiology, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Settore MED/50 - Scienze Tecniche Mediche Applicate, Blood Pressure, Type 2 diabetes, Settore MED/13 - Endocrinologia, Impaired glucose tolerance, Insulin resistance, Physiology (medical), Diabetes mellitus, Internal medicine, Diabetes Mellitus, medicine, Humans, Insulin, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Ultrasonography, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, Atherosclerosis, Glucose, Diabetic Angiopathies, Diabetes Mellitus, Type 2, Glucose Clamp Technique, Middle Aged, Tunica Media, Insulin Resistance, Metabolism, Female, Adult Children, business.industry, Glucose clamp technique, medicine.disease, Impaired fasting glucose, Common, Endocrinology, Blood pressure, Carotid Artery, business, Type 2
Abstract: The aim of this study was to investigate whether insulin resistance is independently associated with early manifestations of atherosclerosis. To this end, 176 normotensive offspring of type 2 diabetic patients were subjected to euglycemic hyperinsulinemic clamp to assess insulin sensitivity. Early atherosclerosis was studied by ultrasonography of the common carotid artery. Of the total 176 subjects, 145 were glucose tolerant, 18 had impaired fasting glucose, and 13 had impaired glucose tolerance. Univariate correlations showed that age, body mass index, waist, blood pressure, 2-h postchallenge glucose, fasting insulin, triglycerides, interleukin-6, fibrinogen, and white blood cell count were significantly correlated with carotid intima-media thickness (IMT), whereas HDL cholesterol and glucose disposal showed a negative correlation. A stepwise multivariate regression analysis including sex, age, waist circumference, smoking status, systolic blood pressure, diastolic blood pressure, triglyceride, HDL cholesterol, 2-h postchallenge glucose, plasma IL-6, fibrinogen, white blood cell count, insulin-stimulated glucose disposal, and fasting insulin showed that the four variables that remained significantly associated with carotid IMT were waist circumference, insulin-stimulated glucose disposal, white blood cell count, and diastolic blood pressure, accounting for 33.7% of its variation. These findings support the concept that insulin sensitivity, rather than plasma insulin levels, is associated with early atherosclerosis in nondiabetic normotensive offspring of type 2 diabetic patients.
Published: 2007
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180. Serum- and Glucocorticoid-Inducible Kinase 1 Delay the Onset of Endothelial Senescence by Directly Interacting with Human Telomerase Reverse Transcriptase

Author: Paola Rogliani, Giuseppe Sconocchia, Barbara Capuani, Giulia Donadel, Massimo Federici, David Della-Morte, Donatella Pastore, Paolo Sbraccia, Katia Basello, Roberto Arriga, Francesca Pacifici, Andrea Coppola, Francesca Ferrelli, Alfonso Bellia, Marco F. Lombardo, and Davide Lauro
Subjects: 0301 basic medicine, Senescence, Aging, Telomerase, Settore MED/09 - Medicina Interna, Biology, Protein Serine-Threonine Kinases, medicine.disease_cause, Models, Biological, Umbilical vein, Settore MED/13 - Endocrinologia, Immediate-Early Proteins, 03 medical and health sciences, 0302 clinical medicine, medicine, Human Umbilical Vein Endothelial Cells, Humans, Telomerase reverse transcriptase, Cellular Senescence, Settore MED/04 - Patologia Generale, chemistry.chemical_classification, Reactive oxygen species, Kinase, SGK, Signaling, Oxidative Stress, 030104 developmental biology, chemistry, 030220 oncology & carcinogenesis, SGK1, Cancer research, Geriatrics and Gerontology, Reactive Oxygen Species, Oxidative stress, Protein Binding
Abstract: Endothelial senescence is characteristic of vascular aging. Serum- and glucocorticoid-inducible kinase (SGK)1 belongs to a family of serine/threonine kinases regulated by various external stimuli. SGK1 has been shown to be protective against reactive oxygen species (ROS) production and to be involved in processes regulating aging. However, data on the direct relationship between SGK1 and senescence are sparse. In the present study, we sought to investigate the role of SGK1 in cellular aging by using human umbilical vein endothelial cells (HUVECs) infected with different constructs. Senescence was measured at different cellular stages by senescence-associated β-galactosidase (SA-β-gal) activity, human telomerase reverse transcriptase (hTERT) activity, p21 protein levels, and ROS production. HUVECs over-expressing full-length SGK1 (wild-type SGK1 [SGK1WT]) showed a decrease in SA-β-gal and p21 expression and a corresponding increase in hTERT activity in the early stages of aging. Moreover, SGK1WT presented lower levels of ROS production. A direct interaction between SGK1WT and hTERT was also shown by co-immunoprecipitation. The SGK1Δ60 isoform, lacking the amino-terminal 60 amino acids, did not show interaction with hTERT, suggesting a pivotal role of this protein site for the SGK1 anti-aging function. The results from this study may be of particular importance, because SGK1WT over-expression by activating telomerase and reducing ROS levels may delay the processes of endothelial senescence.
Published: 2015
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181. Oral hypoglycemic agents and the heart failure conundrum: Lessons from and for outcome trials

Author: Nikolaus Marx, Massimo Federici, and Ben Arpad Kappel
Subjects: Blood Glucose, medicine.medical_specialty, TECOS, Endocrinology, Diabetes and Metabolism, Medicine (miscellaneous), Administration, Oral, Settore MED/11 - Malattie dell'Apparato Cardiovascolare, Adamantane, Type 2 diabetes, Saxagliptin, Pharmacology, chemistry.chemical_compound, Cardiovascular safety, Risk Factors, Internal medicine, Diabetes mellitus, medicine, Clinical endpoint, Humans, Hypoglycemic Agents, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Risk factor, Heart Failure, Clinical Trials as Topic, Dipeptidyl-Peptidase IV Inhibitors, Nutrition and Dietetics, business.industry, Oral antidiabetic agents, Sitagliptin Phosphate, Dipeptides, Cardiovascular disease, medicine.disease, Metformin, chemistry, Diabetes Mellitus, Type 2, Cardiovascular Diseases, Sitagliptin, Heart failure, Thiazolidinediones, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract: Aim Type 2 diabetes is not only an independent risk factor for cardiovascular (CV) disease but is also associated with a greater incidence of heart failure (HF). The aim of this review is to examine the effects of oral antidiabetic drugs on CV disease and HF. Data synthesis Trials of anti-diabetic agents are now designed to assess CV safety, but frequently HF is not included as a primary endpoint. However, HF in patients with diabetes is more frequent than other CV events and seems to be underestimated. A burning question is therefore if the most used trial design to monitor CV safety, i.e. non-inferiority, allows clinical translation of trial findings. Available data further suggest that the CV effects of anti-diabetic drugs may be rather class-specific and are only partly due to their glucose-lowering actions. Metformin, recommended as first line in most guidelines, shows positive CV effects while other classes like thiazolidinediones may precipitate HF. Experimental results on the relatively novel dipeptidyl peptidase IV (DPP IV) inhibitors imply CV protective effects, but the non-inferiority trials published to date show an overall neutral CV outcome and a potential increase in HF by saxagliptin. However, results on sitagliptin of the recently released TECOS indicate that HF is not a class-dependent effect of DPP IV inhibitors. Conclusion Further basic research and long-term outcome studies to clarify the effects of antidiabetic agents on CV and HF are required so that we can select the optimal antidiabetic therapy for our patients.
Published: 2015

182. Timp3 deficiency in insulin receptor-haploinsufficient mice promotes diabetes and vascular inflammation via increased TNF

Author: Stefano Rizza, Marta Letizia Hribal, Domenico Accili, Rama Khokha, Alessandro Mauriello, Hiroko Kanno, Matteo Serino, Ottavia Porzio, David C. Lee, Renato Lauro, Giorgio Sesti, Paolo Sbraccia, Valentina Marchetti, Veronica Cunsolo, David Smookler, Susan W. Sunnarborg, Massimo Federici, Rossella Menghini, and Davide Lauro
Subjects: Settore MED/09 - Medicina Interna, Time Factors, medicine.medical_treatment, Messenger, Type 2 diabetes, Inbred C57BL, Transgenic, Mice, Hyperinsulinemia, Homeostasis, Insulin, insulin receptor, Phosphorylation, RNA, Small Interfering, Promoter Regions, Genetic, tissue inhibitor of metalloproteinase 3, Glucose tolerance test, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, medicine.diagnostic_test, Reverse Transcriptase Polymerase Chain Reaction, Muscles, article, vascular disease, Skeletal, General Medicine, enzyme activity, priority journal, Liver, hyperinsulinemia, mouse strain, Muscle, Electrophoresis, Polyacrylamide Gel, wild type, Promoter Regions (Genetics), medicine.symptom, Glycogen, Receptor, Research Article, Protein Binding, Signal Transduction, Electrophoresis, Heterozygote, medicine.medical_specialty, animal experiment, Genetic Vectors, Mice, Transgenic, Inflammation, Deoxyglucose, Biology, Small Interfering, animal tissue, transforming growth factor alpha, Hyperinsulinism, Diabetes mellitus, Internal medicine, Diabetes Mellitus, medicine, Animals, controlled study, RNA, Messenger, Muscle, Skeletal, mouse, Tissue Inhibitor of Metalloproteinase-3, Analysis of Variance, nonhuman, Polyacrylamide Gel, Tumor Necrosis Factor-alpha, animal model, diabetes mellitus, glucose intolerance, hyperglycemia, inflammation, nucleotide sequence, Gene Expression Profiling, Glucose, Glucose Tolerance Test, Hyperglycemia, Mice, Inbred C57BL, Receptor, Insulin, RNA, nutritional and metabolic diseases, medicine.disease, Insulin receptor, Endocrinology, biology.protein
Abstract: Activation of inflammatory pathways may contribute to the beginning and the progression of both atherosclerosis and type 2 diabetes. Here we report a novel interaction between insulin action and control of inflammation, resulting in glucose intolerance and vascular inflammation and amenable to therapeutic modulation. In insulin receptor heterozygous (Insr+/-) mice, we identified the deficiency of tissue inhibitor of metalloproteinase 3 (Timp3, an inhibitor of both TNF-alpha-converting enzyme [TACE] and MMPs) as a common bond between glucose intolerance and vascular inflammation. Among Insr+/- mice, those that develop diabetes have reduced Timp3 and increased TACE activity. Unchecked TACE activity causes an increase in levels of soluble TNF-alpha, which subsequently promotes diabetes and vascular inflammation. Double heterozygous Insr+/-Timp3+/- mice develop mild hyperglycemia and hyperinsulinemia at 3 months and overt glucose intolerance and hyperinsulinemia at 6 months. A therapeutic role for Timp3/TACE modulation is supported by the observation that pharmacological inhibition of TACE led to marked reduction of hyperglycemia and vascular inflammation in Insr+/- diabetic mice, as well as by the observation of increased insulin sensitivity in Tace+/- mice compared with WT mice. Our results suggest that an interplay between reduced insulin action and unchecked TACE activity promotes diabetes and vascular inflammation.
Published: 2005
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183. Phosphorylation of GATA2 by Akt Increases Adipose Tissue Differentiation and Reduces Adipose Tissue–Related Inflammation

Author: Marina Cardellini, Alessandro Mauriello, Davide Lauro, Massimo Federici, Marta Letizia Hribal, Rossella Menghini, Renato Lauro, Paolo Sbraccia, and Valentina Marchetti
Subjects: medicine.medical_specialty, Arteriosclerosis, medicine.medical_treatment, Active Transport, Cell Nucleus, Adipose tissue, Inflammation, Settore MED/08 - Anatomia Patologica, Protein Serine-Threonine Kinases, Biology, Proinflammatory cytokine, Phosphatidylinositol 3-Kinases, Insulin resistance, Proto-Oncogene Proteins, Physiology (medical), Internal medicine, medicine, Humans, Insulin, Obesity, Phosphorylation, DNA-Binding Proteins, Proto-Oncogene Proteins c-akt, Cell Differentiation, GATA2 Transcription Factor, Protein-Serine-Threonine Kinases, Adipose Tissue, Transcription Factors, Phosphoproteins, Signal Transduction, Protein kinase B, Cell Nucleus, medicine.disease, Active Transport, Endocrinology, Adipogenesis, medicine.symptom, Cardiology and Cardiovascular Medicine
Abstract: Background— Obesity-related inflammation is emerging as a major cause of insulin resistance and cardiovascular diseases. GATA2 transcription factor is an inhibitor of adipogenesis and an activator of vascular cells. We hypothesized that GATA2 activity is controlled by insulin during adipogenesis, linking metabolic homeostasis and inflammation. Methods and Results— We show that insulin induces GATA2 phosphorylation on serine 401 in a PI-3K/Akt–dependent manner. Insulin-dependent phosphorylation of serine 401 impairs GATA2 translocation to the nucleus and its DNA binding activity. A GATA2 mutant not phosphorylable by Akt (GATA2 S401A ) acts similarly to wild-type GATA2. In contrast, a GATA2 mutant that mimics Akt phosphorylation (GATA2 S401D ) is restrained in the cytoplasm. Cultured preadipocytes bearing GATA2 S401A do not convert to adipocytes and express high levels of inflammatory cytokines like monocyte chemotactic protein-1 (MCP-1). On the contrary, GATA2 S401D preadipocytes differentiate to adipocytes. When GATA2 S401A preadipocytes are injected in mice fed a high-fat diet, they do not differentiate adequately into adipocytes, maintaining the expression of inflammatory markers like MCP-1. In contrast, injection of GATA2 S401D preadipocytes in mice fed a high-fat diet results in development of adipocytes and no expression of inflammatory markers. Conclusions— GATA2 could be a new target in the prevention and treatment of obesity-related inflammation and its complications.
Published: 2005
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184. Plasma Concentration of IGF-I Is Independently Associated With Insulin Sensitivity in Subjects With Different Degrees of Glucose Tolerance

Author: Raffaele Maio, Marina Cardellini, Elena Succurro, Giorgio Sesti, Maria Adelaide Marini, Renato Lauro, Francesco Perticone, Massimo Federici, Marco Vatrano, and Angela Sciacqua
Subjects: Blood Glucose, Male, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Endocrinology, Diabetes and Metabolism, Blood Pressure, Body Mass Index, Impaired glucose tolerance, chemistry.chemical_compound, Insulin resistance, Reference Values, Diabetes mellitus, Internal medicine, Glucose Intolerance, Diabetes Mellitus, Internal Medicine, medicine, Humans, Insulin, Body Size, Insulin-Like Growth Factor I, Metabolic Syndrome, Advanced and Specialized Nursing, Glucose tolerance test, Settore M-EDF/01 - Metodi e Didattiche delle Attivita' Motorie, medicine.diagnostic_test, Triglyceride, business.industry, Metabolic Syndrome X, Glucose Tolerance Test, Lipids, Diabetes Mellitus, Type 2, Middle Aged, Insulin Resistance, Biological Markers, Female, Stepwise regression, medicine.disease, Blood pressure, Endocrinology, chemistry, business, Body mass index, Biomarkers, Type 2
Abstract: OBJECTIVE—We studied the relationships between plasma IGF-I concentrations and insulin sensitivity in subjects with various degrees of glucose tolerance. RESEARCH DESIGN AND METHODS—A total of 357 nondiabetic subjects, 54 subjects with impaired glucose tolerance and 98 newly diagnosed type 2 diabetic subjects, were consecutively recruited, and anthropometric and biochemical characteristics were collected. RESULTS—IGF-I concentrations were negatively correlated with age, BMI, waist-to-hip ratio, triglyceride levels, and systolic and diastolic blood pressure. IGF-I concentrations were positively correlated with HDL cholesterol and homeostasis model assessment of insulin sensitivity (HOMA-S). The correlations remained significant after adjusting for sex, age, and BMI. Correlations for HOMA-S with these metabolic and anthropometric variables were of a similar degree and direction to those for IGF-I concentrations. Stepwise linear regression analysis in a model, which included well-known modulators of insulin sensitivity such as sex, age, BMI, glucose tolerance status, family history of diabetes, waist-to-hip ratio, systolic and diastolic blood pressure, HDL cholesterol, and triglyceride levels, revealed that IGF-I concentrations were independently associated with insulin sensitivity accounting for 10.8% of its variation (P < 0.0001). IGF-I concentrations were significantly lower in subjects with World Health Organization (WHO)-defined metabolic syndrome compared with subjects without metabolic syndrome (P < 0.0001). Logistic regression analysis showed that each unit increase in log-transformed IGF-I concentrations was associated with a 90.5% reduction in the risk of WHO-defined metabolic syndrome. CONCLUSIONS—These data indicate that IGF-I has the characteristics to be a marker for the insulin resistance syndrome. This suggests that low IGF-I levels may be a useful marker for identifying subjects at risk for cardiovascular disease.
Published: 2005
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185. Transgenic mice with dominant negative PKC-theta in skeletal muscle: A new model of insulin resistance and obesity

Author: Renato Lauro, Elisabetta Mattei, A. Buongiorno, L. Tatangelo, Andrea Giaccari, S. Morelli, M.I. Senni, C. Serra, Marina Bouché, E. Segratella, C. Tiveron, Massimo Federici, M. Pascuccio, and Mario Molinaro
Subjects: Genetically modified mouse, medicine.medical_specialty, Physiology, Insulin, medicine.medical_treatment, Clinical Biochemistry, Skeletal muscle, Cell Biology, Biology, medicine.disease, Endocrinology, Insulin resistance, medicine.anatomical_structure, Internal medicine, medicine, Hyperinsulinemia, Protein kinase B, Protein kinase C, PI3K/AKT/mTOR pathway
Abstract: Protein kinase C theta (PKC-theta) is the PKC isoform predominantly expressed in skeletal muscle, and it is supposed to mediate many signals necessary for muscle histogenesis and homeostasis, such as TGFbeta, nerve-dependent signals and insulin. To study the role of PKC-theta in these mechanisms we generated transgenic mice expressing a "kinase dead" mutant form of PKC-theta (PKC-thetaK/R), working as "dominant negative," specifically in skeletal muscle. These mice are viable and fertile, however, by the 6-7 months of age, they gain weight, mainly due to visceral fat deposition. Before the onset of obesity (4 months of age), they already show increased fasting and fed insulin levels and reduced insulin-sensitivity, as measured by ipITT, but normal glucose tolerance, as measured by ipGTT. After the 6-7 months of age, transgenic mice develop hyperinsulinemia in the fasting and fed state. The ipGTT revealed in the transgenic mice both hyperglycemia and hyperinsulinemia. At the molecular level, impaired activation of the IR/IRS/PI3K pathway and a significant decrease both in the levels and in insulin-stimulated activation of the serine/threonine kinase Akt were observed. Taken together these data demonstrate that over-expression of dominant negative PKC-theta in skeletal muscle causes obesity associated to insulin resistance, as demonstrated by defective receptor and post-receptorial activation of signaling cascade. (C) 2003 Wiley-Liss, Inc.
Published: 2003
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186. Low Molecular Weight Adiponectin Increases the Mortality Risk in Very Old Patients

Author: Giovanni Di Cola, Maria Paola Canale, Massimo Federici, Marina Cardellini, Pasquale Morabito, Daniele Romanello, Stefano Rizza, and Alessio Farcomeni
Subjects: medicine.medical_specialty, Settore MED/09 - Medicina Interna, Short Communication, 030209 endocrinology & metabolism, 030204 cardiovascular system & hematology, Pathology and Forensic Medicine, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Internal medicine, medicine, Myocardial infarction, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Cardiovascular mortality, Old patients, adiponectin, Adiponectin, business.industry, Mortality rate, aging, isoforms, Mean age, Cell Biology, medicine.disease, mortality, Endocrinology, Biomarker (medicine), adiponectin, isoforms, mortality, aging, Neurology (clinical), Geriatrics and Gerontology, business
Abstract: Despite its beneficial role on insulin resistance and atherosclerosis, adiponectin has been frequently reported as an independent positive predictor of cardiovascular mortality. Very few information is available regarding adiponectin isoforms and mortality, in particular in advanced aging. Baseline serum levels of Total Adiponectin and its circulating isoforms (HMW-, MMW-, LMW-Adiponectin) were measured in 97 old patients (mean age: 79 years). Patients were followed up for all-cause mortality (study end-point) for an average of 76.4 ± 37.3 months. A positive association was observed for LMW-Ad and all-cause mortality (HR: 1.13, 95% CI: 1.05-1,22, p: 0.002). After multivariate adjustment for age, sex and a previous history of myocardial infarction, higher levels of LMW-Ad were significantly associated with all-cause mortality (HR: 1.11, 95% CI: 1.02-1.21; p: 0.017). Interestingly neither total adiponectin neither the other two circulating isoforms (MMW- and HMW-Ad) showed any significant association with the study end-point. Our data suggest that the association between high serum adiponectin levels and increased mortality rate in elderly is contingent to an unbalanced circulating levels of adiponectin isoforms. The present results support the hypothesis that high levels of Low Molecular Weight adiponectin are a biomarker for mortality risk in very old patients.
Published: 2018
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187. Pharmacologic Inhibition of the NLRP3 Inflammasome Preserves Cardiac Function after Ischemic and Nonischemic Injury in the Mouse

Author: Kai Liu, Eleonora Mezzaroma, Carlo Marchetti, Fadi N Salloum, Shijun Zhang, Stefano Toldo, Adolfo G Mauro, Salvatore Carbone, Matthew S. Halquist, Benjamin W. Van Tassell, Andrea Nordio, Massimo Federici, Anindita Das, Antonio Abbate, Jeremy E. Chojnacki, and Ankit A. Zalavadia
Subjects: Cardiac function curve, Male, Inflammatory response, Sterile inflammation, Myocardial Ischemia, caspase-1, acute myocardial infarction, Myocardial Reperfusion Injury, Article, Mice, NLRP3, inflammasome, NLR Family, Pyrin Domain-Containing 3 Protein, Medicine, Animals, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Pharmacology, Mice, Inbred ICR, integumentary system, business.industry, Inflammasome, inflammation, Cardiology and Cardiovascular Medicine, Doxorubicin, Immunology, business, Carrier Proteins, medicine.drug
Abstract: Sterile inflammation resulting from myocardial injury activates the NLRP3 inflammasome and amplifies the inflammatory response mediating further damage.We used 2 experimental models of ischemic injury (acute myocardial infarction [AMI] with and without reperfusion) and a model of nonischemic injury due to doxorubicin 10 mg/kg to determine whether the NLRP3 inflammasome preserved cardiac function after injury.Treatment with the NLRP3 inflammasome inhibitor in the reperfused AMI model caused a significant reduction in infarct size measured at pathology or as serum cardiac troponin I level (-56% and -82%, respectively, both P0.001) and preserved left ventricular fractional shortening (LVFS, 31 ± 2 vs. vehicle 26% ± 1%, P = 0.003). In the non-reperfused AMI model, treatment with the NLRP3 inhibitor significantly limited LV systolic dysfunction at 7 days (LVFS of 20 ± 2 vs. 14% ± 1%, P = 0.002), without a significant effect on infarct size. In the doxorubicin model, a significant increase in myocardial interstitial fibrosis and a decline in systolic function were seen in vehicle-treated mice, whereas treatment with the NLRP3 inhibitor significantly reduced fibrosis (-80%, P = 0.001) and preserved systolic function (LVFS 35 ± 2 vs. vehicle 27% ± 2%, P = 0.017).Pharmacological inhibition of the NLRP3 inflammasome limits cell death and LV systolic dysfunction after ischemic and nonischemic injury in the mouse.
Published: 2015

188. FoxO1 regulates asymmetric dimethylarginine via downregulation of dimethylaminohydrolase 1 in human endothelial cells and subjects with atherosclerosis

Author: Arnaldo Ippoliti, Marta Fabrizi, Lucia Anemona, Francesca Davato, Rainer H. Böger, Iris Cardolini, Marina Cardellini, Monica Morelli, Alessandro Mauriello, Marta Ballanti, Viviana Casagrande, Isabel Bernges, Edzard Schwedhelm, Rossella Menghini, Massimo Federici, and Robert Stoehr
Subjects: Carotid Artery Diseases, endocrine system, medicine.medical_specialty, Endothelium, Down-Regulation, Settore MED/08, FOXO1, Biology, Arginine, Transfection, digestive system, Gas Chromatography-Mass Spectrometry, Gene Expression Regulation, Enzymologic, Green fluorescent protein, Amidohydrolases, Endothelial activation, chemistry.chemical_compound, Downregulation and upregulation, Internal medicine, medicine, Human Umbilical Vein Endothelial Cells, Humans, Metabolomics, ADMA, Atherosclerosis, Biomarker, FoxO1, Endothelial dysfunction, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Cells, Cultured, Forkhead Box Protein O1, Wild type, food and beverages, nutritional and metabolic diseases, Forkhead Transcription Factors, medicine.disease, Cell biology, medicine.anatomical_structure, Endocrinology, chemistry, Mutation, Cardiology and Cardiovascular Medicine, Asymmetric dimethylarginine, hormones, hormone substitutes, and hormone antagonists, Chromatography, Liquid, Signal Transduction
Abstract: The O subfamily of forkhead (FoxO) 1 is a pivotal element in the regulation of endothelial activation. Compartmentalization and activity of FoxO1 is regulated by post translational modifications, but the implication in endothelial dysfunction and atherosclerosis remain controversial. Our aim was to identify FoxO1 related metabolic signatures in endothelial cells.Using metabolomics in human umbilical endothelial cells (HUVECs) overexpressing the wild type FoxO1 (FoxO1-WT), the acetylation defective mutant (FoxO1-KR), the unphosphorylated nuclear localized mutant (FoxO1-ADA) and the Green Fluorescent Protein (GFP) control vector, we identify metabolic pathways differentially affected by the different FoxO1 localization and activity. Among metabolites, asymmetric dimethylarginine (ADMA) was increased in FoxO1-ADA compared with FoxO1-WT and FoxO1-KR infected cells (p0.01). ADMA was further investigated to identify the molecular mechanisms to explain its link to FoxO1. We found that unrestrained FoxO1 activity leads to increase of ADMA via downregulation of its degrading enzyme, dimethylaminohydrolase (DDAH) 1. In human subjects (n = 89) the FoxO1/DDAH1/ADMA pathway marks unstable atherosclerosis.Our results point to ADMA as a biomarker to track deregulated FoxO1 activity in vivo.
Published: 2015

189. Effect of ezetimibe on cholesterol absorption and lipoprotein composition in diabetes and metabolic syndrome

Author: Massimo Federici
Subjects: Drug, medicine.medical_specialty, medicine.drug_class, Lipoproteins, media_common.quotation_subject, Diabetes, Ezetimibe, Insulin resistance, Lipoprotein metabolism, Metabolic syndrome, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Animals, Humans, Cholesterol absorption inhibitor, Intestinal Mucosa, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Dyslipidemias, Cholesterol absorption, media_common, business.industry, Anticholesteremic Agents, General Medicine, medicine.disease, Intestines, Cholesterol, Treatment Outcome, Endocrinology, Diabetes Mellitus, Type 2, Intestinal Absorption, Liver, Azetidines, lipids (amino acids, peptides, and proteins), Cardiology and Cardiovascular Medicine, business, Lipoprotein, medicine.drug
Abstract: Ezetimibe exerts multiple favorable effects on the lipoprotein profile and reduces some inflammatory markers. Decreasing cholesterol synthesis with statin treatment can cause a compensatory increase in cholesterol absorption that reduces the efficacy of statin therapy, whereas addition of a cholesterol absorption inhibitor can improve outcomes. Recent evidence suggests a beneficial effect on atherosclerosis. In patients with diabetes, the effect of insulin resistance on low-density lipoprotein metabolism combined with the effect of hyperglycemia on cholesterol absorption may further diminish the favorable effects of statins. Further analysis is needed also to determine whether the stronger effects of ezetimibe seen in patients with diabetes are a consequence of an interaction of the drug with specific mechanisms.
Published: 2015

190. Liver protein profiles in insulin receptor-knockout mice reveal novel molecules involved in the diabetes pathophysiology

Author: Francesca Ferrelli, Alfonso Bellia, Nicola Di Daniele, Andrea Urbani, Luca Bova, Massimo Federici, Andrea Coppola, Roberto Arriga, Paolo Sbraccia, David Della-Morte, Davide Lauro, Donatella Pastore, Sara Caratelli, Simona D'Aguanno, Manfredi Tesauro, Augusto Orlandi, Barbara Capuani, Sergio Bernardini, Giulia Donadel, Francesca Pacifici, Michele De Canio, Giuseppe Sconocchia, and Anna Neri
Subjects: medicine.medical_specialty, Settore MED/09 - Medicina Interna, Proteome, Physiology, Knockout, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Inbred C57BL, Settore MED/13 - Endocrinologia, Mice, Liver disease, Insulin resistance, proteomics, Non-alcoholic Fatty Liver Disease, Physiology (medical), Internal medicine, Diabetes mellitus, insulin resistance, Diabetes Mellitus, medicine, Insulin, Animals, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Glycogen synthase, huntigtin, Settore MED/04 - Patologia Generale, Inflammation, Mice, Knockout, biology, Animal, Settore BIO/12, high-mobility group-B1, Disease Models, Animal, Liver, Metabolome, Mice, Inbred C57BL, Proteins, Proteomics, Receptor, Insulin, medicine.disease, Insulin receptor, Endocrinology, Biochemistry, Disease Models, Lipogenesis, biology.protein, Blood sugar regulation, Receptor
Abstract: Liver has a principal role in glucose regulation and lipids homeostasis. It is under a complex control by substrates such as hormones, nutrients, and neuronal impulses. Insulin promotes glycogen synthesis, lipogenesis, and lipoprotein synthesis and inhibits gluconeogenesis, glycogenolysis, and VLDL secretion by modifying the expression and enzymatic activity of specific molecules. To understand the pathophysiological mechanisms leading to metabolic liver disease, we analyzed liver protein patterns expressed in a mouse model of diabetes by proteomic approaches. We used insulin receptor-knockout (IR−/−) and heterozygous (IR+/−) mice as a murine model of liver metabolic dysfunction associated with diabetic ketoacidosis and insulin resistance. We evaluated liver fatty acid levels by microscopic examination and protein expression profiles by orthogonal experimental strategies using protein 2-DE MALDI-TOF/TOF and peptic nLC-MS/MS shotgun profiling. Identified proteins were then loaded into Ingenuity Pathways Analysis to find possible molecular networks. Twenty-eight proteins identified by 2-DE analysis and 24 identified by nLC-MS/MS shotgun were differentially expressed among the three genotypes. Bioinformatic analysis revealed a central role of high-mobility group box 1/2 and huntigtin never reported before in association with metabolic and related liver disease. A different modulation of these proteins in both blood and hepatic tissue further suggests their role in these processes. These results provide new insight into pathophysiology of insulin resistance and hepatic steatosis and could be useful in identifying novel biomarkers to predict risk for diabetes and its complications.
Published: 2015
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191. A genetic marker of hyperuricemia predicts cardiovascular events in a meta-analysis of three cohort studies in high risk patients

Author: Daniela Leonardis, Rosa M. Parlongo, Carmine Zoccali, Giovanni Tripepi, Belinda Spoto, Sabrina Prudente, M.C. Sanguedolce, Francesca Mallamaci, Stefano Rizza, Massimo Federici, Alessandra Testa, and Vincenzo Trischitta
Subjects: Genetic Markers, Male, Cardiovascular risk, Epidemiology, Polymorphism, Uric acid, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Endocrinology, Diabetes and Metabolism, Glucose Transport Proteins, Facilitative, Medicine (miscellaneous), Comorbidity, Hyperuricemia, Risk Assessment, Cohort Studies, Coronary artery disease, Predictive Value of Tests, Cause of Death, Internal medicine, Mendelian randomization, medicine, Humans, Myocardial infarction, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Aged, Cause of death, Polymorphism, Genetic, Nutrition and Dietetics, business.industry, Incidence, Cardiovascular Diseases, Female, Middle Aged, Survival Analysis, Cardiology and Cardiovascular Medicine, medicine.disease, Endocrinology, Intima-media thickness, Gene polymorphism, business, Cohort study
Abstract: Introduction The strongest genetic marker of uric acid levels, the rs734553 SNP in the GLUT9 urate transporter gene, predicts progression to kidney failure in CKD patients and associates with systolic BP and carotid intima media thickness in family-based studies. Methods Since genes are transmitted randomly (Mendelian randomization) we used this gene polymorphism as an unconfounded research instrument to further explore the link between uric acid and cardiovascular disease (cardiovascular death, and non-fatal myocardial infarction and stroke) in a meta-analysis of three cohort studies formed by high risk patients (MAURO: 755 CKD patients; GHS: 353 type 2 diabetics and coronary artery disease and the TVAS: 119 patients with myocardial infarction). Results In separate analyses of the three cohorts, the incidence rate of CV events was higher in patients with the rs734553 risk (T) allele (TT/GT) than in those without (GG patients) and the HR in TT/GT patients in the three cohorts (range 1.72–2.14) coherently signaled an excessive cardiovascular risk with no heterogeneity (I2 = 0.01). The meta-analytical estimate (total number of patients, n = 1227; total CV events, n = 222) of the HR for the combined end-point in TT/GT patients was twice higher (pooled HR: 2.04, 95% CI: 1.11–3.75, P = 0.02) than in GG homozygotes. Conclusions The T allele of the rs734553 polymorphism in the GLUT9 gene predicts a doubling in the risk for incident cardiovascular events in patients at high cardiovascular risk. Findings in this study are compatible with the hypothesis of a causal role of hyperuricemia in cardiovascular disease in high risk conditions.
Published: 2015

192. Iron status in obesity: An independent association with metabolic parameters and effect of weight loss

Author: Valeria Guglielmi, Alfonso Bellia, R.T. Ciotto, Massimo Federici, Monica D’Adamo, Davide Lauro, and Paolo Sbraccia
Subjects: Adult, Male, medicine.medical_specialty, Settore MED/09 - Medicina Interna, Endocrinology, Diabetes and Metabolism, Iron, Medicine (miscellaneous), Overweight, Transaminase, Body Mass Index, Settore MED/13 - Endocrinologia, Insulin resistance, Weight loss, Internal medicine, Nonalcoholic fatty liver disease, Weight Loss, medicine, Humans, Aspartate Aminotransferases, Obesity, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Adiposity, Aged, Caloric Restriction, Retrospective Studies, Ferritin, Nutrition and Dietetics, biology, business.industry, Iron status, Alanine Transaminase, Middle Aged, medicine.disease, Lipids, Endocrinology, Treatment Outcome, Ferritins, biology.protein, Female, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Body mass index, Biomarkers
Abstract: Growing evidence has shown that ferritin concentrations are associated with obesity and insulin resistance, and with nonalcoholic fatty liver disease. However, it is unclear whether ferritin is simply an inflammatory marker, or it may directly contribute to the pathogenesis of obesity-related metabolic alterations. The aim of our study was to investigate the independent associations of ferritin levels with metabolic parameters in overweight/obese subjects before and after hypocaloric diet-induced weight changes.A sample study of 48 premenopausal, 39 postmenopausal women and 50 men was retrospectively analyzed. Clinical, bioimpedentiometry and biochemical data from baseline evaluations and after 3, 6 and 12 months of hypocaloric diet were collected. In the whole sample study, the baseline values of ferritin concentrations were positively correlated with body mass index (BMI) (r = 0.21, p 0.05) and mass body fat (MBF) (r = 0.26, p 0.05), whereas the serum iron level was negatively correlated with MBF (r = -0.29, p 0.05). In premenopausal women, BMI-adjusted ferritin concentrations were negatively associated with high-density lipoprotein-cholesterol and positively related with triglycerides and aspartate aminotransferase. Moreover, the quantitative ferritin reduction at 12 months was positively associated with the relative reduction of BMI (r = 0.34, p 0.05). Finally, the association between changes of alanine aminotransferase and ferritin levels at 12 months from baseline turned out to be independent of respective BMI changes (β = 0.31, p 0.05).In obesity, ferritin, putatively entailing increased iron storage, is independently associated with lipid derangements and transaminase levels, and the association with the latter persists after weight changes.
Published: 2015

193. Relationship between plasma free fatty acids and uncoupling protein-3 gene expression in skeletal muscle of obese subjects:in vitroevidence of a causal link

Author: Massimo Federici, Monica D’Adamo, Guido Tamburrano, A. Buongiorno, Davide Lauro, Nicola Di Daniele, Gianfranco Silecchia, Maria Sole Basso, Paolo Sbraccia, Frida Leonetti, and Renato Lauro
Subjects: medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Leptin, Insulin, medicine.medical_treatment, Skeletal muscle, Biology, Glucose clamp technique, Endocrinology, medicine.anatomical_structure, Internal medicine, Gene expression, medicine, Uncoupling protein, Myocyte, UCP3
Abstract: OBJECTIVE To investigate whether skeletal muscle uncoupling protein-2 (UCP2) and uncoupling protein-3 (UCP3) gene expression is altered in massive obesity and whether it correlates with in vivo insulin sensitivity and with metabolic and hormonal status. DESIGN Quantification of UCP2 and UCP3 gene expression in skeletal muscle of obese and lean subjects displaying different degrees of insulin sensitivity. PATIENTS Fourteen obese and 10 age- and sex-matched healthy control subjects with a mean body mass index (BMI) of 43.6 +/- 1.4 and 22.8 +/- 1.8 (+/- SEM), respectively. MEASUREMENTS Insulin sensitivity by glucose clamp, body composition by bio-impedance, fasting plasma glucose, insulin, leptin and free fatty acids (FFA). Skeletal muscle UCP2 and UCP3 mRNA levels by quantitative reverse transcription polymerase chain reaction (RT-PCR). RESULTS No significant differences in UCP2 or UCP3 mRNA levels were found between obese and control subjects. No significant correlation was observed, in both groups, between UCP2 or UCP3 mRNA levels and both anthropometrical and metabolic parameters. In contrast, a highly significant correlation was observed between skeletal muscle UCP3, but not UCP2, mRNA levels and plasma FFA in the obese, but not in the lean, group. Furthermore, exposure of human myocytes to FFA for 24 h strongly induced both UCP3 and peroxisome proliferator-activated receptor-gamma (PPARgamma) but not UCP2 gene expression. CONCLUSIONS FFA levels correlate strongly with skeletal muscle UCP3 mRNA levels in obese, but not in lean, subjects; in addition, in human myocytes, high FFA concentrations promote UCP3 expression. Our studies therefore provide evidence that supports a role for increased plasma FFA concentrations in the regulation of human skeletal muscle UCP3 gene expression.
Published: 2002
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194. TO045MIRNA EXPRESSION IN URINARY SAMPLES OF PATIENTS WITH TYPE 2 DIABETES AS BIOMARKER FOR RENAL FIBROSIS IN DIABETIC NEPHROPATHY

Author: Matteo Accetturo, Massimo Federici, Giuseppe Grandaliano, Francesco Pesce, Simona Simone, Annarita Oranger, Giovanni Pertosa, Francesca Conserva, Antonella Di Franco, Salvatore De Cosmo, Mariagrazia Barozzino, Chiara Divella, Rossella Menghini, Paola Pontrelli, Vincenzo Trischitta, Massimo Papale, Giuseppe Castellano, and Loreto Gesualdo
Subjects: Transplantation, medicine.medical_specialty, business.industry, Urinary system, Type 2 diabetes, medicine.disease, Gastroenterology, Diabetic nephropathy, Nephrology, Internal medicine, Renal fibrosis, Medicine, Biomarker (medicine), business
Published: 2017
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195. Nonalcoholic fatty liver disease and age are strong indicators for atherosclerosis in morbid obesity

Author: Rosa Ortiz, Gerard Blasco, Gemma Xifra, Massimo Federici, Josep Daunis-i-Estadella, José Manuel Fernández-Real, Josep Puig, Emili Loshuertos, Wifredo Ricart, Salvador Pedraza, Jaume Codina, and Víctor Cuba
Subjects: Adult, Male, Risk, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Biopsy, Carotid Intima-Media Thickness, Sensitivity and Specificity, Body Mass Index, Morbid obesity, Endocrinology, Non-alcoholic Fatty Liver Disease, Internal medicine, Positive predicative value, Nonalcoholic fatty liver disease, Prevalence, Medicine, Humans, Obesity, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, 2. Zero hunger, medicine.diagnostic_test, Anthropometry, business.industry, Age Factors, Middle Aged, medicine.disease, Atherosclerosis, 3. Good health, Obesity, Morbid, Fatty Liver, Liver, Multivariate Analysis, Female, Steatosis, business, Body mass index
Abstract: SummaryObjective Whether nonalcoholic fatty liver disease (NAFLD) can predict atherosclerosis in obese patients remains unclear. The aim of our study was to investigate the usefulness of NAFLD and other cardiometabolic parameters in predicting subclinical atherosclerosis in obese patients. Design, Patients and Measurements We studied 314 consecutive obese subjects (223 women; mean age, 45·04 ± 9·34 years; body mass index 44·3 ± 5 kg/m2) and 47 healthy lean individuals. Hepatic steatosis and atherosclerosis [carotid intima-media thickness (cIMT) >0·8 mm and/or presence of plaques] were evaluated ultrasonographically. Liver biopsies were obtained in 51 patients. Results In obese patients, mean c-IMT was greater in those with NAFLD (P
Published: 2014

196. Abstract 13423: Pharmacologic Inhibition of the NLRP3 Inflammasome Improves Left Ventricular Dysfunction after Severe Ischemic and Non-Ischemic Injury

Author: Benjamin W. Van Tassell, Stefano Toldo, Carlo Marchetti, Antonio Abbate, Jeremy E. Chojnacki, Andrea Nordio, Chiara Sonnino, Eleonora Mezzaroma, Shijun Zhang, Salvatore Carbone, and Massimo Federici
Subjects: medicine.medical_specialty, business.industry, Ischemia, Infarction, Inflammasome, Anterior Descending Coronary Artery, medicine.disease, Physiology (medical), Internal medicine, Heart failure, Anesthesia, medicine, Cardiology, Myocardial infarction, Cardiology and Cardiovascular Medicine, business, Ligation, Reperfusion injury, medicine.drug
Abstract: Introduction: The formation of the NLRP3 inflammasome during injury to the heart amplifies the inflammatory response and mediates further damage. An inhibitor of the NLRP3 inflammasome was shown to reduce ischemia/reperfusion injury in the mouse. Hypothesis: We hypothesize that the NLRP3 inflammasome inhibitor would limit left ventricular (LV) dysfunction following severe ischemic (non-reperfused myocardial infarction [MI]) and non-ischemic (doxorubicin-induced) injury to heart. Methods: Adult male CD-1 male mice underwent permanent ligation of the left anterior descending coronary artery to induce a large non-reperfused MI (ischemic model) or injection of doxorubicin 10mg/kg to induce LV systolic dysfunction (non-ischemic model). The NLRP3 inflammasome inhibitor (16673-34-0, 100 mg/kg) or vehicle (N=6-8 per each group) were administered intraperitoneally daily for 7 days. Transthoracic echocardiography was performed to measure LV end-diastolic diameter (EDD) and LV fractional shortening (FS). We used Masson’s Trichrome stain to measure infarct size (ischemic model) or interstitial fibrosis (non-ischemic model). Results: Permanent coronary ligation led to a large non-reperfused MI and a significant increase in LVEDD and a reduction in LVFS (ischemic model). When compared with vehicle, treatment with the NLRP3 inflammasome inhibitor significantly limited LV enlargement (4.53±0.14 vs vehicle 4.95±0.04mm, P=0.006) and limited systolic dysfunction after AMI (Figure). A significant increase in interstitial fibrosis and reduction in LVFS was seen after doxorubicin treatment (non-ischemic model), and treatment with the inhibitor significantly reduced interstitial fibrosis (0.73%±0.14 vs vehicle 3.35%±0.83, P=0.001) and preserved LVFS (Figure). Conclusion: Inhibition of the NLRP3 inflammasome using a small molecule, 16673-34-0, reduces cardiac injury and limits LV systolic dysfunction following ischemic and non-ischemic injury.
Published: 2014
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197. Can renin inhibition by Aliskiren prove itself in atherosclerosis prevention?

Author: Massimo Federici and Ben Arpad Kappel
Subjects: Male, business.industry, Angiotensin II, Pharmacology, Aliskiren, Atherosclerosis, Renin, Amides, chemistry.chemical_compound, chemistry, Atherosclerosis prevention, Fumarates, Renin–angiotensin system, Medicine, Animals, Humans, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, business, Cardiology and Cardiovascular Medicine
Published: 2014

198. IL-21 is a major negative regulator of IRF4-dependent lipolysis affecting Tregs in adipose tissue and systemic insulin sensitivity

Author: Marchetti, Giovanni Monteleone, Teresa Mezza, Fernandez Real Jm, Casagrande, Andrea Giaccari, Gian Pio Sorice, José María Moreno-Navarrete, Michele Cavalera, Arianna Marino, Maria Mavilio, Massimo Federici, Rossella Menghini, Loredana Fiorentino, Renato Lauro, and Marta Fabrizi
Subjects: medicine.medical_specialty, Normal diet, Endocrinology, Diabetes and Metabolism, Adipose tissue macrophages, insulino-sensibilità, Adipose tissue, Inflammation, Biology, interleuchina 21, Insulin resistance, Internal medicine, Internal Medicine, medicine, Lipolysis, interleukin 21, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Settore BIO/12, Interleukin, Settore MED/13 - ENDOCRINOLOGIA, Stromal vascular fraction, medicine.disease, adipose tissue, insulin sensitivty, Endocrinology, tessuto adiposo, Immunology, medicine.symptom
Abstract: Obesity elicits immune cell infiltration of adipose tissue provoking chronic low-grade inflammation. Regulatory T cells (Tregs) are specifically reduced in adipose tissue of obese animals. Since interleukin (IL)-21 plays an important role in inducing and maintaining immune-mediated chronic inflammatory processes and negatively regulates Treg differentiation/activity, we hypothesized that it could play a role in obesity-induced insulin resistance. We found IL-21 and IL-21R mRNA expression upregulated in adipose tissue of high-fat diet (HFD) wild-type (WT) mice and in stromal vascular fraction from human obese subjects in parallel to macrophage and inflammatory markers. Interestingly, a larger infiltration of Treg cells was seen in the adipose tissue of IL-21 knockout (KO) mice compared with WT animals fed both normal diet and HFD. In a context of diet-induced obesity, IL-21 KO mice, compared with WT animals, exhibited lower body weight, improved insulin sensitivity, and decreased adipose and hepatic inflammation. This metabolic phenotype is accompanied by a higher induction of interferon regulatory factor 4 (IRF4), a transcriptional regulator of fasting lipolysis in adipose tissue. Our data suggest that IL-21 exerts negative regulation on IRF4 and Treg activity, developing and maintaining adipose tissue inflammation in the obesity state.
Published: 2014

199. Loss of TIMP3 exacerbates atherosclerosis in ApoE null mice

Author: Claudia Rossi, Viviana Casagrande, Giuseppe Pugliese, Robert Stöhr, Andrea Urbani, Stefano Menini, Marina Cardellini, Michele Cavalera, Maria Mavilio, Massimo Federici, and Rossella Menghini
Subjects: Apolipoprotein E, Male, medicine.medical_specialty, Proteases, Stromal cell, TIMP3, Knockout, Inflammation, Biology, Mice, Apolipoproteins E, Atherosclerosis, Metabolomics, Metabolism, Internal medicine, medicine.artery, medicine, Animals, Settore MED/49 - Scienze Tecniche Dietetiche Applicate, Receptor, Plaque, Atherosclerotic, Mice, Knockout, Tissue Inhibitor of Metalloproteinase-3, Aorta, Settore BIO/12, Macrophages, Tissue inhibitor of metalloproteinase, medicine.disease, Plaque, Atherosclerotic, 3. Good health, Endocrinology, Immunology, medicine.symptom, Cardiology and Cardiovascular Medicine, Infiltration (medical)
Abstract: Background Tissue inhibitor of metalloproteinase 3 (TIMP3) is a stromal protein that inhibits the activity of various proteases and receptors. We have previously shown TIMP3 to be downregulated in metabolic and inflammatory disorders, such as type 2 diabetes mellitus. We have now generated an ApoE −/− Timp3 −/− mouse model in which, through the use of genetics, metabolomics and in-vivo phenotypical analysis we investigated the role of TIMP3 in the development of atherosclerosis. Methods and results En face aorta analysis and aortic root examination showed that ApoE −/− Timp3 −/− mice show increased atherosclerosis with increased infiltration of macrophages into the plaque. Serum concentration of MCP-1 were elevated in the serum of ApoE −/− Timp3 −/− mice coupled with an expansion of the inflammatory (M1) Gr1+ macrophages, both in the circulation and within the aortic tissue. Targeted analysis of metabolites revealed a trend to reduced short chain acylcarnitines. Conclusions Our study shows that lack of TIMP3 increases inflammation and polarizes macrophages towards a more inflammatory phenotype resulting in increased atherosclerosis.
Published: 2014

200. AN INHIBITOR OF THE NLRP3 INFLAMMASOME 16673-34-0 REDUCES INFARCT SIZE IN A MOUSE MODEL OF MYOCARDIAL ISCHEMIA REPERFUSION INJURY

Author: Massimo Federici, Antonio Abbate, Jeremy E. Chojnacki, Stefano Toldo, Carlo Marchetti, Shijun Zhang, Benjamin W. Van Tassell, Eleonora Mezzaroma, and Norbert F. Voelkel
Subjects: medicine.medical_specialty, Myocardial ischemia, business.industry, Internal medicine, medicine, Cardiology, Inflammasome, business, Infarct size, medicine.disease, Cardiology and Cardiovascular Medicine, Reperfusion injury, medicine.drug
Published: 2014
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