Author: "Russo, Roberta" / Topic: humans - Searchworks@Jio Institute Digital Library Search Results

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1. The use of next-generation sequencing in the diagnosis of rare inherited anaemias: A Joint BSH/EHA Good Practice Paper

Author: Roy, Noémi B. A., Da Costa, Lydie, Russo, Roberta, Bianchi, Paola, Mañú-Pereira, Maria del Mar, Fermo, Elisa, Andolfo, Immacolata, Clark, Barnaby, Proven, Melanie, Sanchez-Fernandez, Mayka, Van Wijk, Richard, Van der Zwaag, Bert, Layton, Mark, Rees, David, Iolascon, Achille, British Society for Haematology/ European Hematology Association, Institut Català de la Salut, [Roy NBA] Department of Haematology, Oxford University Hospitals, NHS Foundation Trust, Oxford, UK. NIHR BRC Blood Theme, Oxford, UK. [Da Costa L] Hôpital Universitaire Robert Debré, Paris, France. [Russo R] Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli Federico II, Naples, Italy. CEINGE Biotecnologie Avanzate, Naples, Italy. [Bianchi P, Fermo E] UOS Fisiopatologia delle Anemie, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico Milano, Milan, Italy. [Mañú-Pereira MDM] Grup de Recerca Translacional en Trastorns d'Anèmia Rara, Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain, Vall d'Hebron Barcelona Hospital Campus, Roy, Noémi B A, Da Costa, Lydie, Russo, Roberta, Bianchi, Paola, Del Mar Mañú-Pereira, Maria, Fermo, Elisa, Andolfo, Immacolata, Clark, Barnaby, Proven, Melanie, Sanchez, Mayka, van Wijk, Richard, van der Zwaag, Bert, Layton, Mark, Rees, David, and Iolascon, Achille
Subjects: Pathological Conditions, Signs and Symptoms::Pathologic Processes::Disease Attributes::Rare Diseases [DISEASES], Buenas prácticas, Otros calificadores::/diagnóstico [Otros calificadores], High-Throughput Nucleotide Sequencing, Anemia, Malalties rares - Diagnòstic, Hematology, Patient care, Atenció al pacient, afecciones patológicas, signos y síntomas::procesos patológicos::atributos de la enfermedad::enfermedades raras [ENFERMEDADES], Investigative Techniques::Genetic Techniques::Sequence Analysis::High-Throughput Nucleotide Sequencing [ANALYTICAL, DIAGNOSTIC AND THERAPEUTIC TECHNIQUES, AND EQUIPMENT], Mutation, Bones pràctiques, Anèmia - Diagnòstic, Atención al paciente, Other subheadings::/diagnosis [Other subheadings], Humans, Good practices, técnicas de investigación::técnicas genéticas::análisis de secuencias::secuenciación de nucleótidos de alto rendimiento [TÉCNICAS Y EQUIPOS ANALÍTICOS, DIAGNÓSTICOS Y TERAPÉUTICOS], Hemic and Lymphatic Diseases::Hematologic Diseases::Anemia [DISEASES], enfermedades hematológicas y linfáticas::enfermedades hematológicas::anemia [ENFERMEDADES], Seqüència de nucleòtids
Abstract: The British Society for Haematology (BSH) produces Good Practice Papers to recommend good practice in areas where there is a limited evidence base but for which a degree of consensus or uniformity is likely to be beneficial to patient care. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) nomenclature was used to evaluate levels of evidence and to assess the strength of recommendations. The GRADE criteria can be found at http://www.gradeworkinggroup.org. This Good Practice Paper was produced as a collaboration with the European Hematology Association (EHA) compiled according to the (BSH) process at http://scanmail.trustwave.com/?c=8248&d=68DV3b1jbPPsVn-8nm3kGS2D_-Hms9YWMWrrk5K8Eg&u=http%3a%2f%2fb-s-h%2eorg.uk. This guideline group included UK-based medical experts representing the BSH and members of the Red Cell and Iron Scientific Working Group (SWG) of EHA. Literature review details: MEDLINE, EMBASE and PubMED were searched systematically for publications in English from 2000 to 2019 using the following key words. ‘NGS’ and ‘next-generation sequencing’ or ‘high throughput sequencing’ AND ‘haemolytic anaemia’ or ‘DBA or ‘Diamond Blackfan anaemia’ or ‘CDA’ or ‘congenital dyserythropoietic anaemia’ or ‘sideroblastic anaemia’ or ‘HS' or ‘hereditary spherocytosis’ or ‘red cell membrane disorders’ or ‘red cell enzyme disorders’ or ‘PK deficiency’ or ‘PKD’. References from relevant publications were also searched. Conference abstracts were included if deemed to be of particular relevance. Review of the manuscript: Review of the manuscript was performed by the BSH Guidelines Committee General Haematology Task Force, the BSH Guidelines Committee and the General Haematology sounding board of the BSH. It was also on the members section of the BSH website for comment. It has also been reviewed by members of the EHA Red Cell and Iron SWG and the EHA Guidelines Executive Committee. info:eu-repo/semantics/publishedVersion
Published: 2022

2. Recommendations regarding splenectomy in hereditary hemolytic anemias

Author: Iolascon, Achille, Andolfo, Immacolata, Barcellini, Wilma, Corcione, Francesco, Garçon, Loïc, De Franceschi, Lucia, Pignata, Claudio, Graziadei, Giovanna, Pospisilova, Dagmar, Rees, David C., Montalembert, Mariane, Rivella, Stefano, Gambale, Antonella, Russo, Roberta, Ribeiro, Leticia, Vives-Corrons, Jules, Martinez, Patricia Aguilar, Kattamis, Antonis, Gulbis, Beatrice, Cappellini, Maria Domenica, Roberts, Irene, Tamary, Hannah, Cells, Working Study Group, EHA, Iron, Chair of Medical Genetics, Department of Molecular Medicine and Medical Biotechnologies, University Federico II, Naples, and CEINGE-Advanced Biotechnologies, Naples, Italy, Internal Medicine, Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Dept. of Pediatrics, Palacky University Olomouc, Department of Paediatric Haematology, Kings College Hospital, Service de pédiatrie générale, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Descartes - Paris 5 (UPD5)-Centre de Référence de la Drépanocytose-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), First Department of Paediatrics, Athens University, Thalassaemia Unit, 'Aghia Sofia' Children's Hospital, Pediatric Hematology Unit (Pediatric Hematology Unit), Schneider Children's Medical Center of Israel, Palacky University, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Descartes - Paris 5 (UPD5)-CHU Necker - Enfants Malades [AP-HP]-Centre de Référence de la Drépanocytose, Iolascon, Achille, Andolfo, Immacolata, Barcellini, Wilma, Corcione, Francesco, Garçon, Loïc, DE FRANCESCHI, Lucia, Pignata, Claudio, Graziadei, Giovanna, Pospisilova, Dagmar, Rees, David C, de Montalembert, Mariane, Rivella, Stefano, Gambale, Antonella, Russo, Roberta, Ribeiro, Leticia, Vives Corrons, Jule, Aguilar Martinez, Patricia, Kattamis, Antoni, Gulbis, Beatrice, Cappellini, MARIA DOMENICA, Roberts, Irene, and Tamary, Hannah
Subjects: medicine.medical_specialty, Pediatrics, Anemia, [SDV]Life Sciences [q-bio], medicine.medical_treatment, Thalassemia, Red Cells, Splenectomy, Guidelines as Topic, Disease, Antithrombotic Therapy, Anemia, Hemolytic, Congenital, Hereditary Hemolytic Anemia, Hereditary spherocytosis, Guideline Article, 03 medical and health sciences, Therapeutic approach, 0302 clinical medicine, Red Cell Membrane Disorder, Internal medicine, medicine, Humans, Infectious Disorder, Hematology, business.industry, Thrombosis, medicine.disease, 3. Good health, Surgery, Red Cell Enzyme Abnormalitie, 030220 oncology & carcinogenesis, business, Hématologie, 030215 immunology
Abstract: Hereditary hemolytic anemias are a group of disorders with a variety of causes, including red cell membrane defects, red blood cell enzyme disorders, congenital dyserythropoietic anemias, thalassemia syndromes and hemoglobinopathies. As damaged red blood cells passing through the red pulp of the spleen are removed by splenic macrophages, splenectomy is one possible therapeutic approach to the management of severely affected patients. However, except for hereditary spherocytosis for which the effectiveness of splenectomy has been well documented, the efficacy of splenectomy in other anemias within this group has yet to be determined and there are concerns regarding short- and long-term infectious and thrombotic complications. In light of the priorities identified by the European Hematology Association Roadmap we generated specific recommendations for each disorder, except thalassemia syndromes for which there are other, recent guidelines. Our recommendations are intended to enable clinicians to achieve better informed decisions on disease management by splenectomy, on the type of splenectomy and the possible consequences. As no randomized clinical trials, case control or cohort studies regarding splenectomy in these disorders were found in the literature, recommendations for each disease were based on expert opinion and were subsequently critically revised and modified by the Splenectomy in Rare Anemias Study Group, which includes hematologists caring for both adults and children., SCOPUS: ar.j, info:eu-repo/semantics/published
Published: 2017
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3. The European Hematology Association Roadmap for European Hematology Research: a consensus document

Author: Engert, Andreas, Balduini, Carlo, Brand, Anneke, Coiffier, Bertrand, Cordonnier, Catherine, Doehner, Hartmut, de Wit, Thom Duyvene, Eichinger, Sabine, Fibbe, Willem, Green, Tony, de Haas, Fleur, Iolascon, Achille, Jaffredo, Thierry, Rodeghiero, Francesco, Salles, Gilles, Schuringa, Jan Jacob, Andre, Marc, Andre-Schmutz, Isabelle, Bacigalupo, Andrea, Bochud, Pierre-Yves, den Boer, Monique, Bonini, Chiara, Camaschella, Clara, Cant, Andrew, Cappellini, Maria Domenica, Cazzola, Mario, Lo Celso, Cristina, Dimopoulos, Meletios, Douay, Luc, Dzierzak, Elaine, Einsele, Hermann, Ferreri, Andres, De Franceschi, Lucia, Gaulard, Philippe, Gottgens, Berthold, Greinacher, Andreas, Gresele, Paolo, Gribben, John, de Haan, Gerald, Hansen, John-Bjarne, Hochhaus, Andreas, Kadir, Rezan, Kaveri, Srini, Kouskoff, Valerie, Kuehne, Thomas, Kyrle, Paul, Ljungman, Per, Maschmeyer, Georg, Mendez-Ferrer, Simon, Milsom, Michael, Mummery, Christine, Ossenkoppele, Gert, Pecci, Alessandro, Peyvandi, Flora, Philipsen, Sjaak, Reitsma, Pieter, Maria Ribera, Jose, Risitano, Antonio, Rivella, Stefano, Ruf, Wolfram, Schroeder, Timm, Scully, Marie, Socie, Gerard, Staal, Frank, Stanworth, Simon, Stauder, Reinhard, Stilgenbauer, Stephan, Tamary, Hannah, Theilgaard-Monch, Kim, Thein, Swee Lay, Tilly, Herve, Trneny, Marek, Vainchenker, William, Vannucchi, Alessandro Maria, Viscoli, Claudio, Vrielink, Hans, Zaaijer, Hans, Zanella, Alberto, Zolla, Lello, Zwaginga, Jaap Jan, Martinez, Patricia Aguilar, van den Akker, Emile, Allard, Shubha, Anagnou, Nicholas, Andolfo, Immacolata, Andrau, Jean-Christophe, Angelucci, Emanuele, Anstee, David, Aurer, Igor, Avet-Loiseau, Herve, Aydinok, Yesim, Bakchoul, Tamam, Balduini, Alessandra, Barcellini, Wilma, Baruch, Dominique, Baruchel, Andre, Bayry, Jagadeesh, Bento, Celeste, van den Berg, Anke, Bernardi, Rosa, Bianchi, Paola, Bigas, Anna, Biondi, Andrea, Bohonek, Milos, Bonnet, Dominique, Borchmann, Peter, Borregaard, Niels, Braekkan, Sigrid, van den Brink, Marcel, Brodin, Ellen, Bullinger, Lars, Buske, Christian, Butzeck, Barbara, Cammenga, Jorg, Campo, Elias, Carbone, Antonino, Cervantes, Francisco, Cesaro, Simone, Charbord, Pierre, Claas, Frans, Cohen, Hannah, Conard, Jacqueline, Coppo, Paul, Vives Corrons, Joan-Lluis, da Costa, Lydie, Davi, Frederic, Delwel, Ruud, Dianzani, Irma, Domanovic, Dragoslav, Donnelly, Peter, Drnovsek, Tadeja Dovc, Dreyling, Martin, Du, Ming-Qing, Dufour, Carlo, Durand, Charles, Efremov, Dimitar, Eleftheriou, Androulla, Elion, Jacques, Emonts, Marieke, Engelhardt, Monika, Ezine, Sophie, Falkenburg, Fred, Favier, Remi, Federico, Massimo, Fenaux, Pierre, Fitzgibbon, Jude, Flygare, Johan, Foa, Robin, Forrester, Lesley, Galacteros, Frederic, Garagiola, Isabella, Gardiner, Chris, Garraud, Olivier, van Geet, Christel, Geiger, Hartmut, Geissler, Jan, Germing, Ulrich, Ghevaert, Cedric, Girelli, Domenico, Godeau, Bertrand, Goekbuget, Nicola, Goldschmidt, Hartmut, Goodeve, Anne, Graf, Thomas, Graziadei, Giovanna, Griesshammer, Martin, Gruel, Yves, Guilhot, Francois, von Gunten, Stephan, Gyssens, Inge, Halter, Jorg, Harrison, Claire, Harteveld, Cornelis, Hellstrom-Lindberg, Eva, Hermine, Olivier, Higgs, Douglas, Hillmen, Peter, Hirsch, Hans, Hoskin, Peter, Huls, Gerwin, Inati, Adlette, Johnson, Peter, Kattamis, Antonis, Kiefel, Volker, Kleanthous, Marina, Klump, Hannes, Krause, Daniela, Hovinga, Johanna Kremer, Lacaud, Georges, Lacroix-Desmazes, Sebastien, Landman-Parker, Judith, LeGouill, Steven, Lenz, Georg, von Lilienfeld-Toal, Marie, von Lindern, Marieke, Lopez-Guillermo, Armando, Lopriore, Enrico, Lozano, Miguel, MacIntyre, Elizabeth, Makris, Michael, Mannhalter, Christine, Martens, Joost, Mathas, Stephan, Matzdorff, Axel, Medvinsky, Alexander, Menendez, Pablo, Migliaccio, Anna Rita, Miharada, Kenichi, Mikulska, Malgorzata, Minard, Veronique, Montalban, Carlos, de Montalembert, Mariane, Montserrat, Emili, Morange, Pierre-Emmanuel, Mountford, Joanne, Muckenthaler, Martina, Mueller-Tidow, Carsten, Mumford, Andrew, Nadel, Bertrand, Navarro, Jose-Tomas, el Nemer, Wassim, Noizat-Pirenne, France, O'Mahony, Brian, Oldenburg, Johannes, Olsson, Martin, Oostendorp, Robert, Palumbo, Antonio, Passamonti, Francesco, Patient, Roger, de Latour, Regis Peffault, Pflumio, Francoise, Pierelli, Luca, Piga, Antonio, Pollard, Debra, Raaijmakers, Marc, Radford, John, Rambach, Ralf, Rao, A. Koneti, Raslova, Hana, Rebulla, Paolo, Rees, David, Ribrag, Vincent, Rijneveld, Anita, Rinalducci, Sara, Robak, Tadeusz, Roberts, Irene, Rodrigues, Charlene, Rosendaal, Frits, Rosenwald, Andreas, Rule, Simon, Russo, Roberta, Saglio, Guiseppe, Sanchez, Mayka, Scharf, Ruediger E., Schlenke, Peter, Semple, John, Sierra, Jorge, So-Osman, Cynthia, Manuel Soria, Jose, Stamatopoulos, Kostas, Stegmayr, Bernd, Stunnenberg, Henk, Swinkels, Dorine, Taborda Barata, Joao Pedro, Taghon, Tom, Taher, Ali, Terpos, Evangelos, Thachil, Jecko, Tissot, Jean Daniel, Touw, Ivo, Toye, Ash, Trappe, Ralf, Traverse-Glehen, Alexandra, Unal, Sule, Vaulont, Sophie, Viprakasit, Vip, Vitolo, Umberto, van Wijk, Richard, Wojtowicz, Agnieszka, Zeerleder, Sacha, Zieger, Barbara, Centre de Recherche des Cordeliers (CRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-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 - UFR de Médecine Pierre et Marie Curie (UPMC), Université Pierre et Marie Curie - Paris 6 (UPMC), Université Sorbonne Paris Cité (USPC), Institut National de la Santé et de la Recherche Médicale (INSERM), University Hospital of Cologne [Cologne], 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), Service d’Hématologie [Centre Hospitalier Lyon Sud - HCL], Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Hospices Civils de Lyon (HCL)-Hospices Civils de Lyon (HCL), Hospices Civils de Lyon (HCL), Department of Internal Medicine I, Medizinische Universität Wien = Medical University of Vienna, Service d'Hématologie [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Ege Üniversitesi, Engert, Andrea, Balduini, Carlo, Brand, Anneke, Coiffier, Bertrand, Cordonnier, Catherine, Döhner, Hartmut, De Wit, Thom Duyvené, Eichinger, Sabine, Fibbe, Willem, Green, Tony, De Haas, Fleur, Iolascon, Achille, Jaffredo, Thierry, Rodeghiero, Francesco, Sall Es, Gille, Schuringa, Jan Jacob, André, Marc, Andre Schmutz, Isabelle, Bacigalupo, Andrea, Bochud, Pierre Yve, Den Boer, Monique, Bonini, Chiara, Camaschella, Clara, Cant, Andrew, Cappellini, Maria Domenica, Cazzola, Mario, Celso, Cristina Lo, Dimopoulos, Meletio, Douay, Luc, Dzierzak, Elaine, Einsele, Hermann, Ferreri, André, De Franceschi, Lucia, Gaulard, Philippe, Gottgens, Berthold, Greinacher, Andrea, Gresele, Paolo, Gribben, John, De Haan, Gerald, Hansen, John Bjarne, Hochhaus, Andrea, Kadir, Rezan, Kaveri, Srini, Kouskoff, Valerie, Kühne, Thoma, Kyrle, Paul, Ljungman, Per, Maschmeyer, Georg, Méndez Ferrer, Simón, Milsom, Michael, Mummery, Christine, Ossenkoppele, Gert, Pecci, Alessandro, Peyvandi, Flora, Philipsen, Sjaak, Reitsma, Pieter, Ribera, José Maria, Risitano, ANTONIO MARIA, Rivella, Stefano, Ruf, Wolfram, Schroeder, Timm, Scully, Marie, Socie, Gerard, Staal, Frank, Stanworth, Simon, Stauder, Reinhard, Stilgenbauer, Stephan, Tamary, Hannah, Theilgaard Mönch, Kim, Thein, Swee Lay, Tilly, Hervé, Trneny, Marek, Vainchenker, William, Vannucchi, Alessandro Maria, Viscoli, Claudio, Vrielink, Han, Zaaijer, Han, Zanella, Alberto, Zolla, Lello, Zwaginga, Jaap Jan, Martinez, Patricia Aguilar, Van Den Akker, Emile, Allard, Shubha, Anagnou, Nichola, Andolfo, Immacolata, Andrau, Jean Christophe, Angelucci, Emanuele, Anstee, David, Aurer, Igor, Avet Loiseau, Hervé, Aydinok, Yesim, Bakchoul, Tamam, Balduini, Alessandra, Barcellini, Wilma, Baruch, Dominique, Baruchel, André, Bayry, Jagadeesh, Bento, Celeste, Van Den Berg, Anke, Bernardi, Rosa, Bianchi, Paola, Bigas, Anna, Biondi, Andrea, Bohonek, Milo, Bonnet, Dominique, Borchmann, Peter, Borregaard, Niel, Brækkan, Sigrid, Van Den Brink, Marcel, Brodin, Ellen, Bullinger, Lar, Buske, Christian, Butzeck, Barbara, Cammenga, Jörg, Campo, Elia, Carbone, Antonino, Cervantes, Francisco, Cesaro, Simone, Charbord, Pierre, Claas, Fran, Cohen, Hannah, Conard, Jacqueline, Coppo, Paul, Vives Corron, Joan Llui, Da Costa, Lydie, Davi, Frederic, Delwel, Ruud, Dianzani, Irma, Domanović, Dragoslav, Donnelly, Peter, Drnovšek, Tadeja Dovč, Dreyling, Martin, Du, Ming Qing, Dufour, Carlo, Durand, Charle, Efremov, Dimitar, Eleftheriou, Androulla, Elion, Jacque, Emonts, Marieke, Engelhardt, Monika, Ezine, Sophie, Falkenburg, Fred, Favier, Remi, Federico, Massimo, Fenaux, Pierre, Fitzgibbon, Jude, Flygare, Johan, Foà, Robin, Forrester, Lesley, Galacteros, Frederic, Garagiola, Isabella, Gardiner, Chri, Garraud, Olivier, Van Geet, Christel, Geiger, Hartmut, Geissler, Jan, Germing, Ulrich, Ghevaert, Cedric, Girelli, Domenico, Godeau, Bertrand, Gökbuget, Nicola, Goldschmidt, Hartmut, Goodeve, Anne, Graf, Thoma, Graziadei, Giovanna, Griesshammer, Martin, Gruel, Yve, Guilhot, Francoi, Von Gunten, Stephan, Gyssens, Inge, Halter, Jörg, Harrison, Claire, Harteveld, Corneli, Hellström Lindberg, Eva, Hermine, Olivier, Higgs, Dougla, Hillmen, Peter, Hirsch, Han, Hoskin, Peter, Huls, Gerwin, Inati, Adlette, Johnson, Peter, Kattamis, Antoni, Kiefel, Volker, Kleanthous, Marina, Klump, Hanne, Krause, Daniela, Hovinga, Johanna Kremer, Lacaud, George, Lacroix Desmazes, Sébastien, Landman Parker, Judith, Legouill, Steven, Lenz, Georg, Von Lilienfeld Toal, Marie, Von Lindern, Marieke, Lopez Guillermo, Armando, Lopriore, Enrico, Lozano, Miguel, Macintyre, Elizabeth, Makris, Michael, Mannhalter, Christine, Martens, Joost, Mathas, Stephan, Matzdorff, Axel, Medvinsky, Alexander, Menendez, Pablo, Migliaccio, Anna Rita, Miharada, Kenichi, Mikulska, Malgorzata, Minard, Véronique, Montalbán, Carlo, De Montalembert, Mariane, Montserrat, Emili, Morange, Pierre Emmanuel, Mountford, Joanne, Muckenthaler, Martina, Müller Tidow, Carsten, Mumford, Andrew, Nadel, Bertrand, Navarro, Jose Toma, El Nemer, Wassim, Noizat Pirenne, France, O’Mahony, Brian, Oldenburg, Johanne, Olsson, Martin, Oostendorp, Robert, Palumbo, Antonio, Passamonti, Francesco, Patient, Roger, De Latour, Regis Peffault, Pflumio, Francoise, Pierelli, Luca, Piga, Antonio, Pollard, Debra, Raaijmakers, Marc, Radford, John, Rambach, Ralf, Koneti Rao, A., Raslova, Hana, Rebulla, Paolo, Rees, David, Ribrag, Vincent, Rijneveld, Anita, Rinalducci, Sara, Robak, Tadeusz, Roberts, Irene, Rodrigues, Charlene, Rosendaal, Frit, Rosenwald, Andrea, Rule, Simon, Russo, Roberta, Saglio, Guiseppe, Sanchez, Mayka, Scharf, Rüdiger E., Schlenke, Peter, Semple, John, Sierra, Jorge, So Osman, Cynthia, Soria, José Manuel, Stamatopoulos, Kosta, Stegmayr, Bernd, Stunnenberg, Henk, Swinkels, Dorine, Barata, João Pedro Taborda, Taghon, Tom, Taher, Ali, Terpos, Evangelo, Thachil, Jecko, Tissot, Jean Daniel, Touw, Ivo, Toye, Ash, Trappe, Ralf, Traverse Glehen, Alexandra, Unal, Sule, Vaulont, Sophie, Viprakasit, Vip, Vitolo, Umberto, Van Wijk, Richard, Wójtowicz, Agnieszka, Zeerleder, Sacha, Zieger, Barbara, Hematology, Service d'hématologie clinique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), University of York [York, UK], 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), Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), 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), Pediatrics, Cell biology, Erasmus MC other, Pulmonary Medicine, Medical Oncology, Other departments, AII - Amsterdam institute for Infection and Immunity, Medical Microbiology and Infection Prevention, ACS - Amsterdam Cardiovascular Sciences, Clinical Haematology, Engert, A, Balduini, C, Brand, A, Coiffier, B, Cordonnier, C, Döhner, H, De, Wit, Td, Eichinger, S, Fibbe, W, Green, T, de Haas, F, Iolascon, A, Jaffredo, T, Rodeghiero, F, Salles, G, Schuringa, Jj, and the other authors of the EHA Roadmap for European Hematology, Research, Cancer Research UK, Biotechnology and Biological Sciences Research Council (BBSRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), De Wit, T, De Haas, F, Sall Es, G, Schuringa, J, André, M, Andre Schmutz, I, Bacigalupo, A, Bochud, P, Den Boer, M, Bonini, C, Camaschella, C, Cant, A, Cappellini, M, Cazzola, M, Celso, C, Dimopoulos, M, Douay, L, Dzierzak, E, Einsele, H, Ferreri, A, De Franceschi, L, Gaulard, P, Gottgens, B, Greinacher, A, Gresele, P, Gribben, J, De Haan, G, Hansen, J, Hochhaus, A, Kadir, R, Kaveri, S, Kouskoff, V, Kühne, T, Kyrle, P, Ljungman, P, Maschmeyer, G, Méndez Ferrer, S, Milsom, M, Mummery, C, Ossenkoppele, G, Pecci, A, Peyvandi, F, Philipsen, S, Reitsma, P, Ribera, J, Risitano, A, Rivella, S, Ruf, W, Schroeder, T, Scully, M, Socie, G, Staal, F, Stanworth, S, Stauder, R, Stilgenbauer, S, Tamary, H, Theilgaard Mönch, K, Thein, S, Tilly, H, Trneny, M, Vainchenker, W, Vannucchi, A, Viscoli, C, Vrielink, H, Zaaijer, H, Zanella, A, Zolla, L, Zwaginga, J, Martinez, P, Van Den Akker, E, Allard, S, Anagnou, N, Andolfo, I, Andrau, J, Angelucci, E, Anstee, D, Aurer, I, Avet Loiseau, H, Aydinok, Y, Bakchoul, T, Balduini, A, Barcellini, W, Baruch, D, Baruchel, A, Bayry, J, Bento, C, Van Den Berg, A, Bernardi, R, Bianchi, P, Bigas, A, Biondi, A, Bohonek, M, Bonnet, D, Borchmann, P, Borregaard, N, Brækkan, S, Van Den Brink, M, Brodin, E, Bullinger, L, Buske, C, Butzeck, B, Cammenga, J, Campo, E, Carbone, A, Cervantes, F, Cesaro, S, Charbord, P, Claas, F, Cohen, H, Conard, J, Coppo, P, Vives Corron, J, Da Costa, L, Davi, F, Delwel, R, Dianzani, I, Domanović, D, Donnelly, P, Drnovšek, T, Dreyling, M, Du, M, Dufour, C, Durand, C, Efremov, D, Eleftheriou, A, Elion, J, Emonts, M, Engelhardt, M, Ezine, S, Falkenburg, F, Favier, R, Federico, M, Fenaux, P, Fitzgibbon, J, Flygare, J, Foà, R, Forrester, L, Galacteros, F, Garagiola, I, Gardiner, C, Garraud, O, Van Geet, C, Geiger, H, Geissler, J, Germing, U, Ghevaert, C, Girelli, D, Godeau, B, Gökbuget, N, Goldschmidt, H, Goodeve, A, Graf, T, Graziadei, G, Griesshammer, M, Gruel, Y, Guilhot, F, Von Gunten, S, Gyssens, I, Halter, J, Harrison, C, Harteveld, C, Hellström Lindberg, E, Hermine, O, Higgs, D, Hillmen, P, Hirsch, H, Hoskin, P, Huls, G, Inati, A, Johnson, P, Kattamis, A, Kiefel, V, Kleanthous, M, Klump, H, Krause, D, Hovinga, J, Lacaud, G, Lacroix Desmazes, S, Landman Parker, J, Legouill, S, Lenz, G, Von Lilienfeld Toal, M, Von Lindern, M, Lopez Guillermo, A, Lopriore, E, Lozano, M, Macintyre, E, Makris, M, Mannhalter, C, Martens, J, Mathas, S, Matzdorff, A, Medvinsky, A, Menendez, P, Migliaccio, A, Miharada, K, Mikulska, M, Minard, V, Montalbán, C, De Montalembert, M, Montserrat, E, Morange, P, Mountford, J, Muckenthaler, M, Müller Tidow, C, Mumford, A, Nadel, B, Navarro, J, El Nemer, W, Noizat Pirenne, F, O’Mahony, B, Oldenburg, J, Olsson, M, Oostendorp, R, Palumbo, A, Passamonti, F, Patient, R, De Latour, R, Pflumio, F, Pierelli, L, Piga, A, Pollard, D, Raaijmakers, M, Radford, J, Rambach, R, Koneti Rao, A, Raslova, H, Rebulla, P, Rees, D, Ribrag, V, Rijneveld, A, Rinalducci, S, Robak, T, Roberts, I, Rodrigues, C, Rosendaal, F, Rosenwald, A, Rule, S, Russo, R, Saglio, G, Sanchez, M, Scharf, R, Schlenke, P, Semple, J, Sierra, J, So Osman, C, Soria, J, Stamatopoulos, K, Stegmayr, B, Stunnenberg, H, Swinkels, D, Barata, J, Taghon, T, Taher, A, Terpos, E, Thachil, J, Tissot, J, Touw, I, Toye, A, Trappe, R, Traverse Glehen, A, Unal, S, Vaulont, S, Viprakasit, V, Vitolo, U, Van Wijk, R, Wójtowicz, A, Zeerleder, S, Zieger, B, Andreas Engert, Carlo Balduini, Anneke Brand, Bertrand Coiffier, Catherine Cordonnier, Hartmut Döhner, Thom Duyvené de Wit, Sabine Eichinger, Willem Fibbe, Tony Green, Fleur de Haas, Achille Iolascon, Thierry Jaffredo, Francesco Rodeghiero, Gilles Salles, Jan Jacob Schuringa, the other authors of the EHA Roadmap for European Hematology Research, Anna Rita Migliaccio, EHA Roadmap for European Hematology, Research, Engert, A., Balduini, C., Brand, A., Coiffier, B., Cordonnier, C., Döhner, H., de Wit TD., Eichinger, S., Fibbe, W., Green, T., de Haas, F., Iolascon, A., Jaffredo, T., Rodeghiero, F., Salles, G., Schuringa, JJ., André, M., Andre-Schmutz, I., Bacigalupo, A., Bochud, PY., Boer, Md., Bonini, C., Camaschella, C., Cant, A., Cappellini, MD., Cazzola, M., Celso, CL., Dimopoulos, M., Douay, L., Dzierzak, E., Einsele, H., Ferreri, A., De Franceschi, L., Gaulard, P., Gottgens, B., Greinacher, A., Gresele, P., Gribben, J., de Haan, G., Hansen, JB., Hochhaus, A., Kadir, R., Kaveri, S., Kouskoff, V., Kühne, T., Kyrle, P., Ljungman, P., Maschmeyer, G., Méndez-Ferrer£££Simón£££ S., Milsom, M., Mummery, C., Ossenkoppele, G., Pecci, A., Peyvandi, F., Philipsen, S., Reitsma, P., Ribera, JM., Risitano, A., Rivella, S., Ruf, W., Schroeder, T., Scully, M., Socie, G., Staal, F., Stanworth, S., Stauder, R., Stilgenbauer, S., Tamary, H., Theilgaard-Mönch, K., Thein, SL., Tilly, H., Trneny, M., Vainchenker, W., Vannucchi, AM., Viscoli, C., Vrielink, H., Zaaijer, H., Zanella, A., Zolla, L., Zwaginga, JJ., Martinez, PA., van den Akker, E., Allard, S., Anagnou, N., Andolfo, I., Andrau, JC., Angelucci, E., Anstee, D., Aurer, I., Avet-Loiseau, H., Aydinok, Y., Bakchoul, T., Balduini, A., Barcellini, W., Baruch, D., Baruchel, A., Bayry, J., Bento, C., van den Berg, A., Bernardi, R., Bianchi, P., Bigas, A., Biondi, A., Bohonek, M., Bonnet, D., Borchmann, P., Borregaard, N., Brækkan, S., van den Brink, M., Brodin, E., Bullinger, L., Buske, C., Butzeck, B., Cammenga, J., Campo, E., Carbone, A., Cervantes, F., Cesaro, S., Charbord, P., Claas, F., Cohen, H., Conard, J., Coppo, P., Corrons, JL., Costa, Ld., Davi, F., Delwel, R., Dianzani, I., Domanović, D., Donnelly, P., Drnov?ek£££Tadeja Dovč£££ TD., Dreyling, M., Du, MQ., Dufour, C., Durand, C., Efremov, D., Eleftheriou, A., Elion, J., Emonts, M., Engelhardt, M., Ezine, S., Falkenburg, F., Favier, R., Federico, M., Fenaux, P., Fitzgibbon, J., Flygare, J., Foà, R., Forrester, L., Galacteros, F., Garagiola, I., Gardiner, C., Garraud, O., van Geet, C., Geiger, H., Geissler, J., Germing, U., Ghevaert, C., Girelli, D., Godeau, B., Gökbuget, N., Goldschmidt, H., Goodeve, A., Graf, T., Graziadei, G., Griesshammer, M., Gruel, Y., Guilhot, F., von Gunten, S., Gyssens, I., Halter, J., Harrison, C., Harteveld, C., Hellström-Lindberg, E., Hermine, O., Higgs, D., Hillmen, P., Hirsch, H., Hoskin, P., Huls, G., Inati, A., Johnson, P., Kattamis, A., Kiefel, V., Kleanthous, M., Klump, H., Krause, D., Hovinga, JK., Lacaud, G., Lacroix-Desmazes, S., Landman-Parker, J., LeGouill, S., Lenz, G., von Lilienfeld-Toal, M., von Lindern, M., Lopez-Guillermo, A., Lopriore, E., Lozano, M., MacIntyre, E., Makris, M., Mannhalter, C., Martens, J., Mathas, S., Matzdorff, A., Medvinsky, A., Menendez, P., Migliaccio, AR., Miharada, K., Mikulska, M., Minard, V., Montalbán, C., de Montalembert, M., Montserrat, E., Morange, PE., Mountford, J., Muckenthaler, M., Müller-Tidow, C., Mumford, A., Nadel, B., Navarro, JT., Nemer, We., Noizat-Pirenne, F., O'Mahony, B., Oldenburg, J., Olsson, M., Oostendorp, R., Palumbo, A., Passamonti, F., Patient, R., Peffault, R., Pflumio, F., Pierelli, L., Piga, A., Pollard, D., Raaijmakers, M., Radford, J., Rambach, R., Rao, AK., Raslova, H., Rebulla, P., Rees, D., Ribrag, V., Rijneveld, A., Rinalducci, S., Robak, T., Roberts, I., Rodrigues, C., Rosendaal, F., Rosenwald, A., Rule, S., Russo, R., Saglio, G., Sanchez, M., Scharf, RE., Schlenke, P., Semple, J., Sierra, J., So-Osman, C., Soria, JM., Stamatopoulos, K., Stegmayr, B., Stunnenberg, H., Swinkels, D., Barata£££João Pedro Taborda£££ JP., Taghon, T., Taher, A., Terpos, E., Thachil, J., Tissot, JD., Touw, I., Toye, A., Trappe, R., Traverse-Glehen, A., Unal, S., Vaulont, S., Viprakasit, V., Vitolo, U., van Wijk, R., Wójtowicz, A., Zeerleder, S., Zieger, B., Stem Cell Aging Leukemia and Lymphoma (SALL), and Çocuk Sağlığı ve Hastalıkları
Subjects: 0301 basic medicine, Cancer Research, diagnosis, Health Services for the Aged, ACUTE PROMYELOCYTIC LEUKEMIA, Medizin, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, EHA Roadmap for European Hematology Research, Antineoplastic Agent, 0302 clinical medicine, European Hematology Association Roadmap, Germany, PERIPHERAL T-CELL, Medicine and Health Sciences, Hematopoiesi, genetics, Molecular Targeted Therapy, [SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology, ComputingMilieux_MISCELLANEOUS, Hematology, Genome, Hematopoietic Stem Cell Transplantation, Anemia, Awareness, Supply & distribution, Combined Modality Therapy, 3. Good health, Europe, THROMBOPOIETIN-RECEPTOR AGONISTS, Blood Disorder, Italy, Austria, haematology, Medicine, France, Immunotherapy, Infection, [SDV.IMM.ALL] Life Sciences [q-bio]/Immunology/Allergology, Human, medicine.medical_specialty, Thrombopoietin Receptor Agonists, Consensus, Patients, Immunology, Antineoplastic Agents, Blood Coagulation, Gene Expression Profiling, Genetic Therapy, Genome, Human, Hematologic Diseases, Hematopoiesis, Humans, Consensu, [SDV.CAN]Life Sciences [q-bio]/Cancer, ACUTE MYELOID-LEUKEMIA, 1102 Cardiovascular Medicine And Haematology, Genetic therapy, methods, 03 medical and health sciences, blood, Internal medicine, medicine, Hematologi, THROMBOTIC THROMBOCYTOPENIC PURPURA, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, ACUTE LYMPHOBLASTIC-LEUKEMIA, therapy, business.industry, CHRONIC LYMPHOCYTIC-LEUKEMIA, supply & distribution, STEM-CELL TRANSPLANTATION, economics, Hematologic Disease, Opinion Article, Transplantation, 030104 developmental biology, Family medicine, therapeutic use, drug effects, RANDOMIZED-CONTROLLED-TRIAL, HEMOLYTIC-UREMIC SYNDROME, pathology, business, chemical synthesis, 030215 immunology, Stem Cell Transplantation, transplantation
Abstract: WOS: 000379156300012, PubMed ID: 26819058, The European Hematology Association (EHA) Roadmap for European Hematology Research highlights major achievements in diagnosis and treatment of blood disorders and identifies the greatest unmet clinical and scientific needs in those areas to enable better funded, more focused European hematology research. Initiated by the EHA, around 300 experts contributed to the consensus document, which will help European policy makers, research funders, research organizations, researchers, and patient groups make better informed decisions on hematology research. It also aims to raise public awareness of the burden of blood disorders on European society, which purely in economic terms is estimated at (sic)23 billion per year, a level of cost that is not matched in current European hematology research funding. In recent decades, hematology research has improved our fundamental understanding of the biology of blood disorders, and has improved diagnostics and treatments, sometimes in revolutionary ways. This progress highlights the potential of focused basic research programs such as this EHA Roadmap. The EHA Roadmap identifies nine 'sections' in hematology: normal hematopoiesis, malignant lymphoid and myeloid diseases, anemias and related diseases, platelet disorders, blood coagulation and hemostatic disorders, transfusion medicine, infections in hematology, and hematopoietic stem cell transplantation. These sections span 60 smaller groups of diseases or disorders. The EHA Roadmap identifies priorities and needs across the field of hematology, including those to develop targeted therapies based on genomic profiling and chemical biology, to eradicate minimal residual malignant disease, and to develop cellular immunotherapies, combination treatments, gene therapies, hematopoietic stem cell treatments, and treatments that are better tolerated by elderly patients., Biotechnology and Biological Sciences Research CouncilBiotechnology and Biological Sciences Research Council (BBSRC) [BB/L023776/1, BB/I00050X/1, BB/K021168/1]; Cancer Research UKCancer Research UK [11831]; Medical Research CouncilMedical Research Council UK (MRC) [G1000801a]; Novo Nordisk FondenNovo Nordisk [NNF12OC1015986]; British Heart FoundationBritish Heart Foundation [FS/09/039/27788]; Cancer Research UKCancer Research UK [12765]; Medical Research CouncilMedical Research Council UK (MRC) [MR/L022982/1, MC_UU_12009/8, MC_U137981013, MC_PC_12009]
Published: 2016
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4. Frequency of Left Ventricular Hypertrophy in Non-Valvular Atrial Fibrillation

Author: Proietti M, Marra AM, Tassone EJ, De Vuono S, Corrao S, Gobbi P, Perticone F, Corazza GR, Basili S, Lip GY, Violi F, Raparelli V, ARAPACIS Study Investigators, GIS Group, Alessandri Cesare, Serviddio Gaetano, Fascetti Stefano, Serra Pietro, Palange Paolo, Greco Eleonora, Bruno Graziella, Averna Maurizio, Giammanco Antonina, Sposito Pietro, De Cristofaro Raimondo, De Gennaro Leonardo, Loria Paola, Pellegrini Elisa, Cominacini Luciano, Mozzini Chiara, Sprovieri Mario, Spagnuolo Vitaliano, Cerqua Giannantonio, Cerasola Giovanni, Mulé Giuseppe, Barbagallo Mario, Lo Sciuto Salvatore, Monteverde Alfredo, Saitta Antonino, Lo Gullo Alberto, Malatino Lorenzo, Cilia Chiara, Licata Giuseppe, Tuttolomondo Antonino, Conigliaro Roberta, Pinto Antonio, Di Raimondo Domenico, Signorelli Santo, Anzaldi Massimiliano, De Palma Daniela, Galderisi Maurizio, Cudemo Giuseppe, Galletti Ferruccio, Fazio Valeria, De Luca Nicola, Meccariello Alfonso, Caputo Dario, De Donato Maria Teresa, Iannuzi Arcangelo, Bresciani Alessandro, Giunta Riccardo, Cimini Claudia, Durante Mangoni Emanuele, Agrusta Federica, Iorio Federica, Adinolfi Luigi E, Sellitto Ausilia, Restivo Luciano, Bellis Paolo, Tirelli Paolo, Sacerdoti David, Pesce Paola, Vanni Dino, Iuliano Luigi, Ciacciarelli Marco, Pacelli Antonio, Palazzuoli Alberto, Cacciafesta Mauro, Gueli Nicola, Capeci William, Tarquinio Nicola, Pellegrini Francesco, Vincentelli Giovanni Maria, Ravallese Ferdinando, Santini Claudio, Letizia Claudio, Petramala Luigi, Zinnamosca Laura, Cilli Mirella, Savoriti Claudio, Falaschi Paolo, Martocchia Antonio, Stefanelli Manuela, Marigliano Vincenzo, Lo Iacono Cristina, Brusco Simona, Bertazzoni Giuliano, Attalla El Halabieh Elias, Paradiso Michele, Lizzi Eugenio Maria, Timmi Stefano, Battisti Paola, Cerci Sabina, Ciavolella Massimo, Di Veroli Claudio, Malci Francesco, De Ciocchis Anita, Abate Damiano, Castellino Pietro, Curto Irene, Vecchio Claudia, Mannarino Elmo, Pasqualini Leonella, Fattori Chiara, Pende Aldo, Denegri Andrea, Artom Nathan, Ricchio Roberto, Fimognari Filippo Luca, Alletto Maurizio, Messina Simona, Sesti Giorgio, Arturi Franco, Grembiale Alessandro, Perticone Francesco, Maio Raffaele, Scarpino Paola Elisa, Carullo Giuseppe, Sciacqua Angela, Frugiuele Pierluigi, Battaglia Giuseppe, Vidili Gianpaolo, Atzori Sebastiana, Delitala Giuseppe, Davì Giovanni, Angelucci Ermanno, Sestili Simona, Traisci Giancarlo, De Feudis Lucrezia, Di Michele Dario, Fava Alessandra, Balsano Clara, De Ciantis Pierpaolo, Desideri Giovambattista, Camerota Antonio, Migliacci Rino, Porciello Giovanni, Mezzetti Matteo, Gresele Paolo, Vedovati Cristina, Fierro Tiziana, Puccetti Luca, Scarpini Francesca, Bertolotti Marco, Mussi Chiara, Boddi Maria, Savino Andrea, Contri Silvia, Saller Alois, Fabris Fabrizio, Pesavento Raffaele, Filippi Lucia, Vedovetto Valentina, Puato Massimo, Treleani Martina, De Luca Elisabetta, De Zaiacomo Francesca, Giantin Valter, Semplicini Andrea, Minuz Pietro, Calabria Stefano, Romano Simone, Fantin Francesco, Manica Angela, Stockner Ingrid, Pattis Peter, Gutmann Bernhard, Catena Cristiana, Colussi GianLuca, Annoni Giorgio, Bruni Adriana Antonella, Castagna Alberto, Spinelli Diana, Corazza Gino Roberto, Miceli Emanuela, Padula, Schinco Giuseppina, Spreafico Sibilla, Secchi Beatrice, Vanoli Massimo, Casella Gianluca, Serra Maria Grazia, Longo Stefania, Antonaci Salvatore, Belfiore Anna, Ricci Lara, Ventrella Francesco, Iamele Luigi, Bianco Cesare, Santovito Donato, Cipollone Francesco, Nicolai Salvatore, Salvati Filippo, Rini Giovan Battista, Scozzari Francesca, Muiesan Maria Lorenza, Salvetti Massimo, Bazza Abramo, Picardi Antonio, De Vincentis Antonio, Cosio Paolo, Terzolo Massimo, Madaffari Bruno, Parasporo Bruno, Fenoglio Luigi, Bracco Christian, Melchio Remo, Gentili Tamira, Salvi Aldo, Nitti Cinzia, Falsetti L, Gabrielli Armando, Paglione Ivano, Capucci Alessandro, Brambatti Michela, Sparagna Armando, Tirotta Daniela, Andreozzi Paola, Ettorre Evaristo, Viscogliosi Giovanni, Rossi Fanelli Fillippo, Delfino Massimo, Glorioso Nicola, Melis Giada, Marras Gianfranca, Matta Michela, Sacco Andrea, Stellitano Elio, Scordo Anna, Russo Franco, Caruso Assunta Antonietta, Porreca Ettore, Santilli Francesca, Tana Marco, Ferri Claudio, Grassi Davide, Cheli Paola, Portincasa Piero, Muscianisi Giuseppe, Giordani Sara, Stanghellini Vincenzo, Sabbà Carlo, Suppressa Patrizia, Mancuso Gerardo, Bartone Mosè, Calipari Daniela, Arcidiacono Giuseppe, Bellanuova Ignazio, Ferraro Maria, Scalzo Antonio, Marigliano Giampietro, Cozzolino Domenico, Lampitella Antonio, Acri Vera, Galasso Domenico, Mazzei Francesca, Galasso Salvatore, Buratti Alberto, Porta Massimo, Brizzi Maria Felice, Fattorini Annalisa, Sampietro Francesca, D’Angelo Armando, Pala Marco, Fabbian Fabio, Manfredini Roberto, Moroni Carlo, Valente Lucia, Lopreiato Francesco, Parente Fernando, Moia Marco, Braham Simon, Rossi Marco, Pesce Margherita, Gentile Adelina, Catozzo Vania, Di Napoli Mariarosaria, Baciarello Giacinto, Rancan Elena, Ageno Walter, Guasti Luigina, Ciccaglioni Antonio, Negri Silvia, Polselli Marco, Abbate Rosanna, Marcucci Rossella, Cangemi Roberto, Pignataro Francesca Serena, Marco Proietti, Pastori Daniele, Ferro Domenico, Loffredo Lorenzo, Perri Ludovica, Catasca Elisa, Raparelli Valeria, Napoleone Laura, Talerico Giovanni, Calvieri Camilla, Vicario Tommasa, Russo Roberta, Saliola Mirella, Del Ben Maria, Angelico Francesco, Bucci Tommaso, Baratta Francesco, DATA AND SAFETY MONITORING BOARD (DSMB): Vestri Anna Rita, Farcomeni Alessio, Di Tanna Gianluca, STUDY COORDINATORS: Basili Stefania, Davi’ Giovanni, STEERING COMMITTEE OF ARAPACIS STUDY: Violi Francesco, Lip Gregory YH, Hiatt William R, Vestri Anna Rita, Mannucci Pier Mannuccio, Proietti Marco, Bazzini Cristina, Bianchi Paola Ilaria, Boari Benedetta, Buonauro Agostino, Buttà Carmelo, Buzzetti Elena, Carleo Pietro, Carrabba Maria Domenica, Castorani Luigi, Cecchetto Lara, Colombo Barbara Maria, De Giorgi Alfredo, De Vuono Stefano, Del Corso Lisette, Di Giosia Paolo, Falsetti Lorenzo, Forgione Alessandra, Hijazi Daniel, Lorusso Giusi, Marra Alberto Maria, Masala Maristella, Montebianco Abenavoli Ludovico, Murgia Giuseppe, Naccarato Paola, Pattoneri Paolo, Perego Francesca, Pinto Daniela, Pinna Miriam Pretti Vincenzo, Pucci Giacomo, Salinaro Francesco, Sirico Domenico, Tassone Eliezer Joseph, Torres Daniele, Vazzana Natale, Vecchio Claudia Rita, Vitale Francesco, Proietti M, Marra AM, Tassone EJ, De Vuono S, Corrao S, Gobbi P, Perticone F, Corazza GR, Basili S, Lip GY, Violi F, Raparelli V, ARAPACIS Study Investigators, GIS Group, Alessandri Cesare, Serviddio Gaetano, Fascetti Stefano, Serra Pietro, Palange Paolo, Greco Eleonora, Bruno Graziella, Averna Maurizio, Giammanco Antonina, Sposito Pietro, De Cristofaro Raimondo, De Gennaro Leonardo, Loria Paola, Pellegrini Elisa, Cominacini Luciano, Mozzini Chiara, Sprovieri Mario, Spagnuolo Vitaliano, Cerqua Giannantonio, Cerasola Giovanni, Mulé Giuseppe, Barbagallo Mario, Lo Sciuto Salvatore, Monteverde Alfredo, Saitta Antonino, Lo Gullo Alberto, Malatino Lorenzo, Cilia Chiara, Licata Giuseppe, Tuttolomondo Antonino, Conigliaro Roberta, Pinto Antonio, Di Raimondo Domenico, Signorelli Santo, Anzaldi Massimiliano, De Palma Daniela, Galderisi Maurizio, Cudemo Giuseppe, Galletti Ferruccio, Fazio Valeria, De Luca Nicola, Meccariello Alfonso, Caputo Dario, De Donato Maria Teresa, Iannuzi Arcangelo, Bresciani Alessandro, Giunta Riccardo, Cimini Claudia, Durante Mangoni Emanuele, Agrusta Federica, Iorio Federica, Adinolfi Luigi E, Sellitto Ausilia, Restivo Luciano, Bellis Paolo, Tirelli Paolo, Sacerdoti David, Pesce Paola, Vanni Dino, Iuliano Luigi, Ciacciarelli Marco, Pacelli Antonio, Palazzuoli Alberto, Cacciafesta Mauro, Gueli Nicola, Capeci William, Tarquinio Nicola, Pellegrini Francesco, Vincentelli Giovanni Maria, Ravallese Ferdinando, Santini Claudio, Letizia Claudio, Petramala Luigi, Zinnamosca Laura, Cilli Mirella, Savoriti Claudio, Falaschi Paolo, Martocchia Antonio, Stefanelli Manuela, Marigliano Vincenzo, Lo Iacono Cristina, Brusco Simona, Bertazzoni Giuliano, Attalla El Halabieh Elias, Paradiso Michele, Lizzi Eugenio Maria, Timmi Stefano, Battisti Paola, Cerci Sabina, Ciavolella Massimo, Di Veroli Claudio, Malci Francesco, De Ciocchis Anita, Abate Damiano, Castellino Pietro, Curto Irene, Vecchio Claudia, Mannarino Elmo, Pasqualini Leonella, Fattori Chiara, Pende Aldo, Denegri Andrea, Artom Nathan, Ricchio Roberto, Fimognari Filippo Luca, Alletto Maurizio, Messina Simona, Sesti Giorgio, Arturi Franco, Grembiale Alessandro, Perticone Francesco, Maio Raffaele, Scarpino Paola Elisa, Carullo Giuseppe, Sciacqua Angela, Frugiuele Pierluigi, Spagnuolo Vitaliano, Battaglia Giuseppe, Vidili Gianpaolo, Atzori Sebastiana, Delitala Giuseppe, Davì Giovanni, Angelucci Ermanno, Sestili Simona, Traisci Giancarlo, De Feudis Lucrezia, Di Michele Dario, Fava Alessandra, Balsano Clara, De Ciantis Pierpaolo, Desideri Giovambattista, Camerota Antonio, Migliacci Rino, Porciello Giovanni, Mezzetti Matteo, Gresele Paolo, Vedovati Cristina, Fierro Tiziana, Puccetti Luca, Scarpini Francesca, Bertolotti Marco, Mussi Chiara, Boddi Maria, Savino Andrea, Contri Silvia, Saller Alois, Fabris Fabrizio, Pesavento Raffaele, Filippi Lucia, Vedovetto Valentina, Puato Massimo, Fabris Fabrizio, Treleani Martina, De Luca Elisabetta, De Zaiacomo Francesca, Giantin Valter, Semplicini Andrea, Minuz Pietro, Calabria Stefano, Romano Simone, Fantin Francesco, Manica Angela, Stockner Ingrid, Pattis Peter, Gutmann Bernhard, Catena Cristiana, Colussi GianLuca, Annoni Giorgio, Bruni Adriana Antonella, Castagna Alberto, Spinelli Diana, Corazza Gino Roberto, Miceli Emanuela, Padula, Schinco Giuseppina, Spreafico Sibilla, Secchi Beatrice, Vanoli Massimo, Casella Gianluca, Serra Maria Grazia, Longo Stefania, Antonaci Salvatore, Belfiore Anna, Ricci Lara, Ventrella Francesco, Iamele Luigi, Bianco Cesare, Santovito Donato, Cipollone Francesco, Nicolai Salvatore, Salvati Filippo, Rini Giovan Battista, Scozzari Francesca, Muiesan Maria Lorenza, Salvetti Massimo, Bazza Abramo, Picardi Antonio, De Vincentis Antonio, Cosio Paolo, Terzolo Massimo, Madaffari Bruno, Parasporo Bruno, Fenoglio Luigi, Bracco Christian, Melchio Remo, Gentili Tamira, Salvi Aldo, Nitti Cinzia, Falsetti L, Gabrielli Armando, Paglione Ivano, Capucci Alessandro, Brambatti Michela, Sparagna Armando, Tirotta Daniela, Andreozzi Paola, Ettorre Evaristo, Viscogliosi Giovanni, Rossi Fanelli Fillippo, Delfino Massimo, Glorioso Nicola, Melis Giada, Marras Gianfranca, Matta Michela, Sacco Andrea, Stellitano Elio, Scordo Anna, Russo Franco, Caruso Assunta Antonietta, Porreca Ettore, Santilli Francesca, Tana Marco, Ferri Claudio, Grassi Davide, Cheli Paola, Portincasa Piero, Muscianisi Giuseppe, Giordani Sara, Stanghellini Vincenzo, Sabbà Carlo, Suppressa Patrizia, Mancuso Gerardo, Bartone Mosè, Calipari Daniela, Arcidiacono Giuseppe, Bellanuova Ignazio, Ferraro Maria, Scalzo Antonio, Marigliano Giampietro, Cozzolino Domenico, Lampitella Antonio, Acri Vera, Galasso Domenico, Mazzei Francesca, Galasso Salvatore, Buratti Alberto, Porta Massimo, Brizzi Maria Felice, Fattorini Annalisa, Sampietro Francesca, D’Angelo Armando, Pala Marco, Fabbian Fabio, Manfredini Roberto, Moroni Carlo, Valente Lucia, Lopreiato Francesco, Parente Fernando, Moia Marco, Braham Simon, Rossi Marco, Pesce Margherita, Gentile Adelina, Catozzo Vania, Di Napoli Mariarosaria, Baciarello Giacinto, Rancan Elena, Ageno Walter, Guasti Luigina, Ciccaglioni Antonio, Negri Silvia, Polselli Marco, Abbate Rosanna, Marcucci Rossella, Cangemi Roberto, Pignataro Francesca Serena, Marco Proietti, Pastori Daniele, Ferro Domenico, Loffredo Lorenzo, Perri Ludovica, Catasca Elisa, Raparelli Valeria, Napoleone Laura, Talerico Giovanni, Calvieri Camilla, Vicario Tommasa, Russo Roberta, Saliola Mirella, Del Ben Maria, Angelico Francesco, Bucci Tommaso, Baratta Francesco, DATA AND SAFETY MONITORING BOARD (DSMB): Vestri Anna Rita, Farcomeni Alessio, Di Tanna Gianluca, STUDY COORDINATORS: Basili Stefania, Davi’ Giovanni, STEERING COMMITTEE OF ARAPACIS STUDY: Violi Francesco, Perticone Francesco, Lip Gregory YH, Hiatt William R, Vestri Anna Rita, Corazza Gino Roberto, Mannucci Pier Mannuccio, Licata Giuseppe, Moroni Carlo, Proietti Marco, Anzaldi Massimiliano, Bazzini Cristina, Bianchi Paola Ilaria, Boari Benedetta, Bracco Christian, Buonauro Agostino, Buttà Carmelo, Buzzetti Elena, Calabria Stefano, Capeci William, Carleo Pietro, Carrabba Maria Domenica, Castorani Luigi, Cecchetto Lara, Cimini Claudia, Colombo Barbara Maria, De Giorgi Alfredo, De Vuono Stefano, Denegri Andrea, Del Corso Lisette, Di Giosia Paolo, Durante Mangoni Emanuele, Falsetti Lorenzo, Forgione Alessandra, Grassi Davide, Grembiale Alessandro, Hijazi Daniel, Iamele Luigi, Lorusso Giusi, Marra Alberto Maria, Masala Maristella, Montebianco Abenavoli Ludovico, Murgia Giuseppe, Naccarato Paola, Pattoneri Paolo, Perego Francesca, Pesce Paola, Petramala Luigi, Pinto Daniela, Pinna Miriam Pretti Vincenzo, Pucci Giacomo, Raparelli Valeria, Salinaro Francesco, Santilli Francesca, Scarpini Francesca, Sirico Domenico, Suppressa Patrizia, Tassone Eliezer Joseph, Torres Daniele, Vazzana Natale, Vecchio Claudia Rita, Vidili Gianpaolo, Vitale Francesco, Proietti, M., Marra, A., Tassone, E., De Vuono, S., Corrao, S., Gobbi, P., Perticone, F., Corazza, G., Basili, S., Lip, G., Violi, F., Raparelli, V., Marra, A. M., Tassone, E. J., Corazza, G. R., and Lip, G. Y. H.
Subjects: Registrie, Male, Cross-sectional study, Myocardial Infarction, Longitudinal Studie, Left ventricular hypertrophy, Cohort Studies, non-valvular atrial fibrillation, Atrial Fibrillation, 80 and over, Prevalence, echocardiography, Myocardial infarction, Longitudinal Studies, Prospective Studies, Registries, Prospective cohort study, Ultrasonography, Aged, 80 and over, education.field_of_study, Medicine (all), Atrial fibrillation, Diabetes Mellitu, Middle Aged, Left Ventricular, left ventricular hypertrophy, Italy, Hypertension, Cardiology, Age Distribution, Aged, Ankle Brachial Index, Cross-Sectional Studies, Diabetes Mellitus, Female, Humans, Hypertrophy, Left Ventricular, Logistic Models, Peripheral Arterial Disease, Cardiology and Cardiovascular Medicine, Human, medicine.medical_specialty, Logistic Model, Population, Concentric hypertrophy, Socio-culturale, non-valvular atrial fibrillation, left ventricular hypertrophy, echocardiography, cardiovascular diseases, Internal medicine, medicine, cardiovascular diseases, education, Cross-Sectional Studie, business.industry, Odds ratio, Hypertrophy, medicine.disease, Prospective Studie, Cohort Studie, business
Abstract: Left ventricular hypertrophy (LVH) is significantly related to adverse clinical outcomes in patients at high risk of cardiovascular events. In patients with atrial fibrillation (AF), data on LVH, that is, prevalence and determinants, are inconsistent mainly because of different definitions and heterogeneity of study populations. We determined echocardiographic-based LVH prevalence and clinical factors independently associated with its development in a prospective cohort of patients with non-valvular (NV) AF. From the "Atrial Fibrillation Registry for Ankle-brachial Index Prevalence Assessment: Collaborative Italian Study" (ARAPACIS) population, 1,184 patients with NVAF (mean age 72 ± 11 years; 56% men) with complete data to define LVH were selected. ARAPACIS is a multicenter, observational, prospective, longitudinal on-going study designed to estimate prevalence of peripheral artery disease in patients with NVAF. We found a high prevalence of LVH (52%) in patients with NVAF. Compared to those without LVH, patients with AF with LVH were older and had a higher prevalence of hypertension, diabetes, and previous myocardial infarction (MI). A higher prevalence of ankle-brachial index ≤0.90 was seen in patients with LVH (22 vs 17%, p = 0.0392). Patients with LVH were at significantly higher thromboembolic risk, with CHA2DS2-VASc ≥2 seen in 93% of LVH and in 73% of patients without LVH (p
Published: 2015
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5. Retrospective cohort study of 205 cases with congenital dyserythropoietic anemia type II: definition of clinical and molecular spectrum and identification of new diagnostic scores

Author: RUSSO, ROBERTA, IOLASCON, ACHILLE, Antonella Gambale, Concetta Langella, Immacolata Andolfo, Sule Unal, Russo, Roberta, Antonella, Gambale, Concetta, Langella, Andolfo, Immacolata, Sule, Unal, and Iolascon, Achille
Subjects: Adult, Male, Genotype, Vesicular Transport Proteins, Founder Effect, Phenotype, Mutation, Prevalence, Humans, Female, Registries, Alleles, Anemia, Dyserythropoietic, Congenital, Retrospective Studies
Abstract: Congenital Dyserythropoietic Anemia II (CDA II) is a rare hyporegenerative anemia of variable degree, whose causative gene is SEC23B. More than 60 causative mutations in 142 independent pedigrees have been described so far. However, the prevalence of the CDA II is probably underestimated, since its clinical spectrum was not yet well-defined and thus it is often misdiagnosed with more frequent clinically-related anemias. This study represents the first meta-analysis on clinical and molecular spectrum of CDA II from the largest cohort of cases ever described. We characterized 41 new cases and 18 mutations not yet associated to CDA II, thus expanding the global series to 205 cases (172 unrelated) and the total number of causative variants to 84. The 68.3% of patients are included in our International Registry of CDA II (Napoli, Italy). A genotype-phenotype correlation in three genotypic groups of patients was assessed. To quantify the degree of severity in each patient, a method based on ranking score was performed. We introduced a clinical index to easily discriminate patients with a well-compensated hemolytic anemia from those with ineffective erythropoiesis. Finally, the worldwide geographical distribution of SEC23B alleles highlighted the presence of multiple founder effects in different areas of the world.
Published: 2014

6. Prevalence of peripheral artery disease by abnormal ankle-brachial index in atrial fibrillation: implications for risk and therapy

Author: Violi, Francesco, Daví, Giovanni, Hiatt, William, Lip, Gregory Y. H., Corazza, Gino R., Perticone, Francesco, Proietti, Marco, Pignatelli, Pasquale, Vestri, Anna R., Basili, Stefania, Desideri, ARAPACIS Study Investigators Alessandri Cesare (Dipartimento di Scienze e Biotecnologie Medico-Chirurgiche, G., Sapienza-Università di Roma), Serviddio Gaetano (Department of Medical and Surgical Sciences, University of Foggia), Fascetti Stefano (UOC Medicina Generale, USL 12 Viareggio, Toscana), Serra, Pietro, Palange Paolo(UOC Medicina Interna, I, Dipartimento di Sanità Pubblica, e Malattie Infettive, Greco, Eleonora, Bruno Graziella (Medicina, 3, Department of Medical Sciences, Città della Salute e della Scienza, A. O., University of Turin), Averna, Maurizio, Giammanco Antonina (Dipartimento Biomedico di Medicina Interna, e Specialistica (DIBIMIS), Università di Palermo), Sposito Pietro (Azienda Ospedaliera Ospedali Riuniti Papardo Piemonte, Messina), De Cristofaro Raimondo, De Gennaro Leonardo(Istituto di Medicina Interna, e Geriatria, Centro Emostasi, e Trombosi, Gemelli, Policlinico A., Roma), Loria, Paola, Pellegrini Elisa(Medicina Interna ad Indirizzo Metabolico, – NOCSAE Baggiovara, Department of Internal Medicine, Endocrinology, Metabolism and Geriatrics, Università degli Studi di Modena, e Reggio Emilia), Cominacini, Luciano, Mozzini Chiara (Dipartimento di Medicina, Sezione di Medicina Interna, D, Università di Verona), Sprovieri, Mario, Spagnuolo Vitaliano (UOC Medicina d'Urgenza, e PS, Stabilimento Ospedaliero dell'Annunziata, Cosenza), Cerqua Giannantonio (UOC Medicina Interna per l'Urgenza, S Giovanni Addolorata, Ao, Cerasola Giovanni, Mulé Giuseppe (Università degli Studi di Palermo), Barbagallo, Mario, Lo Sciuto Salvatore, Monteverde Alfredo(UOC di Geriatria, e Lungodegenza, Azienda Ospedaliera Universitaria Policlinico, Aoup, Palermo), Saitta, Antonino, Lo Gullo Alberto (UOC Medicina Interna, Università di Messina), Malatino, Lorenzo, Cilia Chiara (Clinica Medica, Ospedale, Cannizzaro, Università degli Studi di Catania), Licata, Giuseppe, Tuttolomondo, Antonino, Conigliaro Roberta (UOC Medicina Interna, e Cardioangiologia, Dipartimento Biomedico di Medicina Interna, e Specialistica, Università degli Studi di Palermo), Pinto, Antonio, Di Raimondo Domenico (UOC Medicina Vascolare, Dipartimento Biomedico di Medicina Interna e Specialistica, (Di. Bi. M. I. S. )., Signorelli, Santo, Anzaldi Massimiliano (Dipartimento di Medicina Interna, e Patologia, Università degli studi di Catania), De Palma Daniela, Galderisi, Maurizio, Cudemo Giuseppe (Dipartimento di Medicina Clinica, e Sperimentale, AUP Federico II di Napoli), Galletti, Ferruccio, Fazio Valeria(Dipartimento di Medicina Clinica, e Chirurgia, Università di Napoli Federico II), De Luca Nicola, Meccariello Alfonso (Centro Ipertensione, AUO Federico II, Napoli), Caputo, Dario, De Donato Maria Teresa (UO Medicina Interna, Azienda Ospedaliera Universitaria San Giovanni di Dio, e Ruggi D'Aragona, Salerno), Iannuzi, Arcangelo, Bresciani Alessandro (Divisione di Medicina Interna, Cardarelli, Osp. A., Giunta, Riccardo, Cimini Claudia (V Divisione Medicina Interna ed Immunoallergologia, Policlinico, Sun, Utili, Riccardo, Durante Mangoni Emanuele, Agrusta Federica (Medicina Infettivologica, e dei Trapianti, Monaldi, Ao, Sun, Napoli), Adinolfi Luigi, E., Sellitto, Cristiana, Restivo Luciano (Medicina Interna, Seconda Università di Napoli, Ospedale di Marcianise), Bellis, Paolo, Tirelli Paolo (UOC Medicina Interna e di Urgenza, e Pronto Soccorso, del Loreto Nuovo, P. O. S. M., Loreto, Mare), Sacerdoti, David, Pesce Paola (Clinica Medica, 5, Dipartimento di Medicina DIMED, Università degli Studi di Padova), Vanni Dino (UO Medicina Interna Arezzo, Ospedale San Donato, Azienda USL, 8 Arezzo), Iuliano, Luigi, Ciacciarelli, Marco, Pacelli Antonio (Department of Medico-Surgical Sciences and Biotechnology, Vascular Biology, Mass Spectrometry Lab, Sapienza-University of Rome), Palazzuoli Alberto (Sezione Cardiologia, Dipartimento di Medicina Interna, e Malattie Metaboliche, Università di Siena, Ospedale Le Scotte), Cacciafesta, Mauro, Gueli Nicola (UOC di Medicina Geriatrica, e Riabilitazione, Sapienza- Università di Roma, Capeci, William, Tarquinio, Nicola, Pellegrini Francesco (UO Medicina 'SS Benvenuto, e Rocco', Dipartimento di Medicina Interna, Asur, Marche, Area Vasta, n. 2., ex ZT 7), Vincentelli Giovanni Maria (UOS Breve Osservazione, Calibita 'Fatebenefratelli' Isola Tiberina, Ospedale S. 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Osp. Univ., Genova), Ricchio, Roberto, Fimognari Filippo Luca (UOC Geriatria, Azienda Ospedaliera di Cosenza, Alletto, Maurizio, Messina Simona (Unità Operativa di Medicina, Elia, Ospedale S., Caltanissetta), Sesti, Giorgio, Arturi, Franco, Grembiale Alessandro (Università degli Studi, UOC Medicina Interna, Policlinico Universitario 'Mater Domini'), Scarpino Paola Elisa, Carullo Giuseppe (Cattedra di Medicina Interna, UO Malattie Cardiovascolari, Campus Universitario di Germaneto, Università Magna Graecia di Catanzaro), Frugiuele, Pierluigi, Spagnuolo Vitaliano (UOC Medicina Interna, e Reumatologia, Stabilimento Ospedaliero Annunziata, Azienda Ospedaliera Cosenza), Battaglia Giuseppe (UO Lungodegenza, Serra San Bruno, S. O., ASP Vibo Valentia), Vidili, Gianpaolo, Atzori, Sebastiana, Delitala Giuseppe (Clinica Medica, Dipartimento di Medicina Clinica, e Sperimentale, Aou, Sassari), Davì, Giovanni, Angelucci, Ermanno, Sestili Simona (UOC di Clinica Medica, PO Clinicizzato di Chieti), Traisci, Giancarlo, De Feudis Lucrezia (UOC Medicina Interna, 2, PO di Pescara), Di Michele Dario, Fava Alessandra (UOC Medicina Interna, Asl, Teramo), Balsano, Clara, De Ciantis Pierpaolo (Dipartimento di Medicina Interna, e Sanità Pubblica, Università, dell'Aquila), Desideri, Giovambattista, Camerota Antonio (UOC Geriatria, e Lungodegenza Geriatrica, Dipartimento Medico ORM, Avezzano), Po, Migliacci, Rino, Medicina Interna, Porciello Giovanni (S. C., Ospedale della Valdichiana, Cortona, Usl, 8 Arezzo), Mezzetti Matteo (UOC Medicina Interna Ospedale del Casentino-Direttore Dr. Emilio Santoro, AUSL8 Arezzo), Gresele, Paolo, Vedovati, Cristina, Fierro Tiziana (Dipartimento di Medicina Interna, Sezione di Medicina Interna, e Cardiovascolare, Università di Perugia), Puccetti, Luca, Scarpini Francesca (Centro Aterosclerosi, Trombosi, e Coagulopatie, Università degli Studi di Siena, Azienda Ospedaliero-Universitaria Senese), Bertolotti, Marco, Mussi Chiara (UO Geriatria, Università degli Studi di Modena e Reggio Emilia), Dipartimento Integrato di Medicina Endocrinologia Metabolismo e Geriatria., Boddi, Maria, Savino, Andrea, Contri Silvia (Dipartimento di Area Critica Medico- Chirurgica, Università degli Studi di Firenze), Saller, Alois, Fabris Fabrizio (Clinica Medica1, Medicina Interna CLOPD, Departement of Medicine DIMED, University of Padova, Italy), Pesavento, Raffaele, Filippi, Lucia, Vedovetto Valentina (Dipartimento di Scienze Cardiologiche, Toraciche, e Vascolari, Clinica Medica, 2, Azienda Ospedaliera-Università di Padova), Puato Massimo (Clinica Medica IV, Dipartimento di Medicina, Azienda Ospedaliera Universitaria Padova, Padova), Fabris, Fabrizio, Treleani Martina (UOA Medicina, Policlinico, Universitario, Maselli, Monica, Corradin Maria Luisa, Giantin Valter (Clinica Geriatrica, Università di Padova), Semplicini Andrea (Medicina Interna, 1, Giovanni e Paolo, Ospedale SS., Venezia), Minuz, Pietro, Calabria, Stefano, Romano Simone (Sezione di Medicina Interna, C, Università di Verona, Aoui, Verona), Fantin, Francesco, Manica Angela (Dipartimento di Medicina, Sezione di Geriatria, Stockner, Ingrid, Pattis, Peter, Wiedermann), Gutmann Bernhard (Divisione di Medicina Interna-Direttore Prof. J., Ospedale centrale di Bolzano), Catena, Cristiana, Colussi GianLuca (Hypertension Unit and Division of Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy), Annoni, Giorgio, Bruni Adriana Antonella, Castagna Alberto (Clinica Geriatrica, Università degli Studi di Milano- Bicocca, Dipartimento di Scienze della Salute, AO San Gerardo, Monza), Spinelli Diana (Medicina Interna 1a, Dipartimento di Scienze Cliniche, e di Comunità, Fondazione, Irccs, Università di Milano), Corazza Gino Roberto, Miceli, Emanuela, Padula Donatella (Clinica Medica, I, Reparto, 11, IRCCS Policlinico San Matteo di Pavia, Pavia), Schinco, Giuseppina, Spreafico Sibilla (UOC Geriatria, Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico), Secchi Beatrice (UOC Medicina Interna, Ospedale, Bassini, Milano), Vanoli, Massimo, Casella Gianluca (SC Medicina Interna, Azienda Ospedaliera della Provincia di Lecco, Ospedale di Merate, Lecco), Serra Maria Grazia (UOC Medicina, Panico', Azienda Ospedaliera 'Cardinale G., Lecce), Longo, Stefania, Antonaci Salvatore (UOC Medicina Interna, Azienda Ospedaliera Policlinico, Bari), Belfiore, Anna, Giuseppe Palasciano, Frualdo Mariella (Clinica Medica 'A. Murri'-Direttore Prof., Ventrella, Francesco, Iamele Luigi (Struttura Complessa di Medicina Interna, Cerignola, Asl, Foggia), Bianco Cesare (UOC Medicina Interna, Tropea), Santovito, Donato, Mezzetti, Andrea, Cipollone Francesco (Centro di Eccellenza Europeo, e di Riferimento Regionale per l'Aterosclerosi, l'Ipertensione Arteriosa, e le Dislipidemie, Università, Chieti), Nicolai, Salvatore, Salvati Filippo (UO Medicina Interna, Ospedale di Ortona, ASL 02 Abruzzo), Rini Giovan Battista, Scozzari Francesca (UOC Medicina Interna ed Ipertensione, Dipartimento Biomedico di Medicina Interna e Specialistica (Di. Bi. M. I., S), Giaccone' di Palermo), Policlinico 'P., Muiesan Maria Lorenza, Salvetti, Massimo, Bazza Abramo (Dipartimento di Scienze Cliniche, e Sperimentali, Università di Brescia, 2° Medicina Generale Spedali Civili, Brescia), Picardi, Antonio, De Vincentis Antonio (UOC Medicina Clinica, Policlinico Universitario Campus Bio-Medico, Cosio, Paolo, Terzolo Massimo (Medicina Interna, 1, Dipartimento di Scienze Cliniche, e Biologiche, AOU San Luigi Gonzaga, Università di Torino), Madaffari, Bruno, Parasporo Bruno (UO Medicina Interna, Azienda Ospedaliera Bianchi Melacrino Morelli, Reggio, Calabria), Fenoglio, Luigi, Bracco, Christian, Melchio Remo (SC Medicina Interna, Croce e Carle, AO S., Cuneo), Gentili, Tamira, Salvi Aldo (Medicina Generale, - Settore Subintensivo, Azienda, Ospedaliero-Universitaria, Ancona), Nitti, Cinzia, Falsetti Lorenzo (Medicina Generale, - Settore Ordinario, Gabrielli, Armando, Paglione Ivano (Clinica Medica, Capucci, Alessandro, Brambatti, Michela, Sparagna Armando (Clinica di Cardiologia, Ospedale, Torrette, Tirotta Daniela (UO Medicina Generale IV, Ospedale, Cervesi, Cattolica), Andreozzi, Paola, Ettorre, Evaristo, Cipriani Elisa (Area Geriatria, DAI Medicina Interna, Sapienza-Università di Roma, Rossi Fanelli Fillippo, Delfino Massimo (UOC Medicina Interna, H, Immunologia, Clinica, Nutrizione, Clinica, Endocrinologia, Glorioso, Nicola, Melis, Giada, Marras, Gianfranca, Matta Michela (Ambulatorio Ipertensione Arteriosa, e Patologie Correlate, Aou, Sassari, Sassari), Sacco Andrea (UOC Medicina Interna, PO Madonna delle Grazie, Matera), Stellitano, Elio, Scordo Anna (UO Medicina, PO 'Tiberio Evoli', Melito Porto Salvo), Russo, Franco, Caruso Assunta Antonietta (UOC Medicina Generale di Rogliano, AO di Cosenza), Porreca, Ettore, Santilli, Francesca, Tana Marco (UO Medicina Interna, e Geriatria, Ospedale Clinicizzato Colle Dell'Ara, D'Annunzio, Università G., Chieti-Pescara), Ferri, Claudio, Grassi, Davide, Di Giosia Paolo (Divisione di Medicina Interna Universitaria, - Ospedale San Salvatore, Dipartimento, Mesva, Università, Dell'Aquila, L'Aquila), Portincasa Piero (Clinica Medica 'Murri', Dipartimento di Scienze Mediche, e Oncologia Umana, Università degli Studi di Bari), Muscianisi Giuseppe (ASP Reggio Calabria, Saline Joniche), Giordani, Sara, Stanghellini Vincenzo (Dipartimento di Scienze Mediche, e Chirurgiche, Università degli Studi di Bologna), Sabbà, Carlo, Suppressa Patrizia (UOC Geriatria e Centro di assistenza, e ricerca sovraziendale per le malattie rare, Mancuso, Giuseppe, Bartone, Mosè, Calipari Daniela (UOC Medicina Interna, Presidio, Ospedaliero, ASP di Catanzaro), Arcidiacono, Giuseppe, Bellanuova Ignazio (UOC Cardiologia, e UTIC, Catania), Ferraro, Maria, Scalzo, Antonio, Marigliano Giampietro (ASP Cosenza), Cozzolino, Domenico, Lampitella, Antonio, Acri Vera (Dipartimento di Internistica Clinica, e Sperimentale, Galasso, Domenico, Mazzei, Francesca, Galasso Salvatore (RSA Madonna di Porto Gimigliano, Catanzaro), Buratti Alberto (Azienda Ospedaliera della Provincia di Pavia, UO Medicina Interna, Ospedale, Civile, Casorate, Primo, Porta, Massimo, Brizzi Maria Felice (SC Medicina Interna 1U, Azienda, Ospedaliera, Torino), Fattorini, Annalisa, Sampietro, Francesca, D’Angelo Armando (Coagulation Service and Thrombosis Research Unit, IRCCS Ospedale San Raffaele, Pala, Marco, Fabbian, Fabio, Manfredini Roberto (UOC Clinica Medica, Anna, Azienda Ospedaliera-Universitaria S., Ferrara), Moroni, Carlo, Valente, Lucia, Lopreiato Francesco (Laboratorio di Ecocardiografia-Cardiologia Preventiva, DAI Cuore, e Grossi Vasi, Parente Fernando (UOC Medicina Interna, Granata Massimo (Immunologia Clinica, A, Moia, Marco, Braham Simon (Fondazione IRCCS Ca'Granda, Ospedale Maggiore Policlinico, Rossi, Marco, Pesce Margherita (Dipartimento di Medicina Clinica, e Sperimentale, Università di Pisa), Gentile, Adelina, Catozzo Vania (UO Medicina, Ldp, Loreto, Ferranti, Edoardo, Soldini, Maurizio, Di Napoli Mariarosaria, Baciarello Giacinto (UOC Cardiologia Preventiva, e Riabilitativa, Rancan, Elena, Ageno, Walter, Guasti Luigina (Dipartimento di Medicina Clinica, e Sperimentale, Università, Dell'Insubria, Varese), Ciccaglioni, Antonio, Negri, Silvia, Polselli Marco (Centro Elettro-Stimolazione Cardiaca, Prisco Domenico (SOD Patologia Medica, Aou, Careggi, Firenze), Pignataro Francesca Serena, Pastori, Daniele, Ferro, Domenico, Loffredo, Lorenzo, Cangemi, Roberto, Perri, Ludovica, Polimeni, Licia, Catasca, Elisa, Raparelli, Valeria, Napoleone, Laura, Schillizzi, Marianna, Vicario, Tommasa, Russo, Roberta, Gentile Maria Cristina, Saliola, Mirella, Del Ben Maria, Angelico Francesco (I Clinica Medica, Sapienza-Università di, Roma)., Violi F, Daví G, Hiatt W, Lip GY, Corazza GR, Perticone F, Proietti M, Pignatelli P, Vestri AR, Basili S, ARAPACIS Study Investigators: […, Alessandri C, Serviddio G, Fascetti S, Serra P, Palange P, Greco E, Bruno G, Averna M, Giammanco A, Sposito P, De Cristofaro R, De Gennaro L, Loria P, Pellegrini E, Cominacini L, Mozzini C, Spovieri M, Spagnuolo V, Cerqua G, Cerasola G, Mulé G, Barbagallo M, Lo Sciuto S, Monteverde A, Saitta A, Lo Gullo A, Malatino L, Cilia C, Licata G, Tuttolomondo A, Conigliaro R, Pinto A, Di Raimondo D, Signorelli S, Anzaldi M, De Palma D, Galderisi M, Cudemo G, Galletti F, Fazio V, De Luca N, Meccariello A, Caputo D, De Donato MT, Iannuzi A, Bresciani A, Giunta R, Cimini C, Utili R, Durante M, Emanuele AF, Adinolfi LE, Cristiana S, Restivo L, Bellis P, Tirelli P, Sacerdoti D, Pesce P, Vanni D, Iuliano L, Palazzuoli A, Cacciafesta M, Gueli N, Capeci W, Tarquino N, Pellegrini F, Vincentelli GM, Ravallese F, Santini C, Letizia C, Petramala L, Zinnamosca L, Cilli M, Savoriti C, Falaschi P, Martocchia A, Stefanelli M, Marigliano V, Lo Iacono C, Brusco S, Bertazzoni G, El Halabieh Elias A, Paradiso M, Lizzi EM, Stefano T, Paola B, Cerci S, Ciavolella M, Di Veroli C, Malci F, De Ciocchis A, Abate D, Castellino P, Curto I, Vecchio C, Mannarino E, Pasqualini L, Fattori C, Pende A, Denegri A, Nathan A, Ricchio R, Fimognari FL, Alletto M, Messina S, Sesti G, Arturi F, Gembiale A, Scarpino PE, Carullo G, Pierluigi F, Battaglia G, Vadili G, Atzori S, Delitala G, Davì G, Angelucci E, Simona S, Giancarlo T, De Feudis L, Di Michele D, Fava A, Balsano C, De Ciantis P, Giovambattista D, Camerota A, Migliacci R, Porciello G, Mezzetti M, Gresele P, Vedovati C, Fierro T, Puccetti L, Scarpini F, Bertolotti M, Mussi C, Boddi M, Savino A, Contri S, Saller A, Fabris F, Pesavento R, Filippi L, Vedovetto V, Puato M, Treleani M, Maselli M, Corradin ML, Giantin V, Semplicini A, Minuz P, Calabria S, Romano S, Fantin F, Manica A, Stockner I, Pattis P, Guttman B, Catena C, Colussi GL, Annoni G, Bruni AA, Castagna A, Miceli E, Padula D, Schinco G, Spreafico S, Secchi B, Vanoli M, Casella G, Serra MG, Longo S, Antonaci S, Belfiore A, Frualdo M, Francesco V, Iamele L, Bianco C, Santovito D, Mezzetti A, Cipollone F, Nicolai S, Salvati F, Battista RG, Scozzari F, Muiesan ML, Salvetti M, Bazza A, Picardi A, De Vincentis A, Cosio P, Terzolo M, Fenoglio L, Bracco C, Melchio R, Gentili T, Salvi A, Nitti C, Falsetti L, Gabrielli A, Paglione I, Capucci A, Brambatti M, Sparagna A, Tirotta D, Andreozzi P, Ettorrre E, Cipriani E, Fanelli Fillippo R, Delfino M, Glorioso N, Melis G, Marras G, Matta M, Sacco A, Stellitano E, Scordo A, Russo F, Caruso Assunta A, Porreca E, Santilli F, Tana M, Ferri C, Grassi D, Di Giosia P, Portincasa P, Muscianisi G, Giordani S, Stanghellini V, Sabbà C, Supressa P, Mancuso G, Bartone M, Calipari D, Arcidiacono G, Bellanuova I, Ferraro M, Scalzo A, Marigliano G, Cozzolina D, Lampitella A, Acri V, Galasso D, Mazzei F, Galasso S, Buratti A, Porto M, Brizzi MF, Fattorini A, Sampietro F, D'Angelo A, Pala M, Fabbian F, Manfredini R, Moroni C, Valente L, Lopreiato F, Parente F, Granata M, Moia M, Braham S, Rossi M, Pesce M, Gentile A, Catozzzo V, Ferranti E, Soldini M, Di Napoli M, Baciarello G, Rancan E, Ageno W, Guasti L, Ciccaglioni A, Negri S, Polselli M, Prisco D, Pignataro FS, Pastori D, Ferro D, Loffredo L, Cangemi R, Perri L, Polimeni L, Catasca E, Raparelli V, Napoleone L, Schillizzi M, Vicario T, Russo R, Gentile MC, Saliola M, Del Ben M, Angelico F, Farcomeni A, Di Tanna G, Davi' G, Traisci G, Montebianco Abenavoli L, Grembiale A, Di Minno G, Durante ME, Pattoneri P, Boari B, Fabio G, Perego F, Bianchi Paola I, Angeli A, Colombo BM, Giannelli G, Vidili G, Torres D, Hijazl D, Gatta A, Mannucci Mannuccio P, Licata G., and …]
Subjects: Adult, Male, Risk, therapy, atrial fibrillation, cardiovascular disease, peripheral vascular disease, Aged, Atrial Fibrillation, Female, Humans, Internal Medicine, Italy, Middle Aged, Peripheral Arterial Disease, Prevalence, Registries, Societies, Medical, Ankle Brachial Index, ATRIAL FIBRILLATION, Cardiology and Cardiovascular Medicine, Medical, RISK FACTORS, cardiovascular diseases, Societies
Abstract: To the Editor: Nonvalvular atrial fibrillation (NVAF) is the most common sustained arrhythmia encountered in clinical practice and is associated with a 5-fold increased risk for stroke (1). Moreover, patients with NVAF often suffer from atherosclerotic complications such as acute myocardial infarction (AMI) (2). Peripheral artery disease (PAD) is an established marker of systemic atherosclerosis but its prevalence in NVAF is still unclear. We reasoned that inclusion of ankle-brachial index (ABI), which is an established tool for diagnosis of PAD (3), in the CHA2DS2-VASc (4) score would better define the prevalence of vascular disease. To address this issue, the Italian Society of Internal Medicine (SIMI) established an Italian registry documenting ABI in NVAF patients. The Atrial Fibrillation Registry for the ARAPACIS (Ankle-brachial Index Prevalence Assessment: Collaborative Italian Study) study is an independent research project involving all Regional Councils of SIMI. The first objective of the study was to estimate the prevalence of ABI ≤0.90 in NVAF patients. Consecutive patients with NVAF referred to internal medicine wards were eligible for the enrollment. Enrollment started in October 2010 and continued until October 30, 2012. Patients were enrolled if they were 18 years or older and had a diagnosis of NVAF, recording during the qualifying admission/consultation or in the preceding 12 months, and if it was possible to obtain the ABI measurement. Exclusion criteria included the following: acquired or congenital valvular AF, active cancer, disease with life expectancy 0.90 (93% vs. 82%; p < 0.0001). Logistic regression analysis demonstrated that ABI ≤0.90 was significantly associated with a smoking habit (odds ratio [OR]: 1.99; 95% confidence interval [CI]: 1.48 to 2.66; p < 0.0001), diabetes (OR: 1.93; 95% CI: 1.51 to 2.46; p < 0.0001), age class 65 to 74 years (OR: 2.05; 95% CI: 1.40 to 3.07; p < 0.0001), age class ≥75 years (OR: 3.12; 95% CI: 2.16 to 4.61; p < 0.0001), and history of previous transient ischemic attack/stroke (OR: 1.64; 95% CI: 1.20 to 2.24; p = 0.002). Vascular disease, as assessed by the history elements of CHA2DS2VASc score, was recorded in 17.3% of patients; inclusion of ABI ≤0.90 in the definition of vascular disease yielded a total prevalence of 33%. A higher prevalence of vascular disease was detected if ABI ≤0.90 was included in the CHA2DS2VASc score (Fig. 1). CHA2DS2VASc including ABI ≤0.90 was more associated with previous stroke (43%; OR: 1.85; 95% CI: 1.41 to 2.44; p < 0.0001) compared to CHA2DS2VASc with ABI 0.91 to 1.39 (23%; OR: 1.52; 95% CI: 1.10 to 2.11; p = 0.0117). To the best of our knowledge, there is no large-scale study that specifically examined the prevalence of ABI ≤0.90 in NVAF. In our population, 21% had ABI ≤0.90 indicating that NVAF is often associated with systemic atherosclerosis. The CHADS2 has been recently refined with the CHA2DS2-VASc score, which includes vascular disease as documented by a history of AMI, symptomatic PAD, or detection of atherosclerotic plaque in the aortic arch (4). Comparison of vascular prevalence as assessed by CHA2DS2-VASc score and/or ABI ≤0.90 is of interest to define the potentially positive impact of measuring ABI in the management of NVAF patients. Inclusion of ABI ≤0.90 in the definition of vascular disease greatly increased the prevalence of vascular disease, which increased from 17.3% (based on history alone) to 33% (based on ABI) in the entire population. If ABI ≤0.90 was encompassed in the definition of vascular disease of CHA2DS2-VASc score the prevalence of vascular disease increased in every risk class. Inclusion of ABI ≤0.90 in the CHA2DS2-VASc score allowed us to better define the risk profile of NVAF patients with an up-grading of the risk score in each CHA2DS2-VASc score category. This may have important therapeutic implications if the new score could be tested prospectively, as a higher number of NVAF patients would potentially be candidates for an anticoagulant treatment by measuring ABI. A prospective study is, therefore, necessary to validate the risk score of this new definition of vascular disease. In conclusion, this study provides the first evidence that one-fifth of NVAF patients had an ABI ≤0.90, indicating that it may represent a simple and cheap method to better define the prevalence of vascular disease in NVAF.
Published: 2013

7. Congenital dyserythropoietic anaemias: new acquisitions

Author: Iolascon, Achille, Russo, Roberta, Esposito, Maria Rosaria, Piscopo, Carmelo, Asci, Roberta, De Falco, Luigia, and Di Noce, Francesca
Subjects: Reviews, Humans, Anemia, Dyserythropoietic, Congenital, Blood Cell Count, Hematopoiesis
Published: 2011

8. A first update on mapping the human genetic architecture of COVID-19

Author: COVID-19 Host Genetics Initiative, Pathak, GA, Karjalainen, J, Stevens, C, Neale, BM, Daly, M, Ganna, A, Andrews, SJ, Kanai, M, Cordioli, M, Polimanti, R, Harerimana, N, Pirinen, M, Liao, RG, Chwialkowska, K, Trankiem, A, Balaconis, MK, Nguyen, H, Solomonson, M, Veerapen, K, Wolford, B, Roberts, G, Park, D, Ball, CA, Coignet, M, McCurdy, S, Knight, S, Partha, R, Rhead, B, Zhang, M, Berkowitz, N, Gaddis, M, Noto, K, Ruiz, L, Pavlovic, M, Hong, EL, Rand, K, Girshick, A, Guturu, H, Baltzell, AH, Niemi, MEK, Rahmouni, S, Guntz, J, Beguin, Y, Pigazzini, S, Nkambule, L, Georges, M, Moutschen, M, Misset, B, Darcis, G, Guiot, J, Azarzar, S, Gofflot, S, Claassen, S, Malaise, O, Huynen, P, Meuris, C, Thys, M, Jacques, J, Leonard, P, Frippiat, F, Giot, J-B, Sauvage, A-S, Frenckell, CV, Belhaj, Y, Lambermont, B, Nakanishi, T, Morrison, DR, Mooser, V, Richards, JB, Butler-Laporte, G, Forgetta, V, Li, R, Ghosh, B, Laurent, L, Belisle, A, Henry, D, Abdullah, T, Adeleye, O, Mamlouk, N, Kimchi, N, Afrasiabi, Z, Rezk, N, Vulesevic, B, Bouab, M, Guzman, C, Petitjean, L, Tselios, C, Xue, X, Afilalo, J, Afilalo, M, Oliveira, M, Brenner, B, Brassard, N, Durand, M, Schurr, E, Lepage, P, Ragoussis, J, Auld, D, Chassé, M, Kaufmann, DE, Lathrop, GM, Adra, D, Hayward, C, Glessner, JT, Shaw, DM, Campbell, A, Morris, M, Hakonarson, H, Porteous, DJ, Below, J, Richmond, A, Chang, X, Polikowski, H, Lauren, PE, Chen, H-H, Wanying, Z, Fawns-Ritchie, C, North, K, McCormick, JB, Glessner, JR, Gignoux, CR, Wicks, SJ, Crooks, K, Barnes, KC, Daya, M, Shortt, J, Rafaels, N, Chavan, S, Timmers, PRHJ, Wilson, JF, Tenesa, A, Kerr, SM, D’Mellow, K, Shahin, D, El-Sherbiny, YM, von Hohenstaufen, KA, Sobh, A, Eltoukhy, MM, Nkambul, L, Elhadidy, TA, Abd Elghafar, MS, El-Jawhari, JJ, Mohamed, AAS, Elnagdy, MH, Samir, A, Abdel-Aziz, M, Khafaga, WT, El-Lawaty, WM, Torky, MS, El-shanshory, MR, Yassen, AM, Hegazy, MAF, Okasha, K, Eid, MA, Moahmed, HS, Medina-Gomez, C, Ikram, MA, Uitterlinden, AG, Mägi, R, Milani, L, Metspalu, A, Laisk, T, Läll, K, Lepamets, M, Esko, T, Reimann, E, Naaber, P, Laane, E, Pesukova, J, Peterson, P, Kisand, K, Tabri, J, Allos, R, Hensen, K, Starkopf, J, Ringmets, I, Tamm, A, Kallaste, A, Alavere, H, Metsalu, K, Puusepp, M, Batini, C, Tobin, MD, Venn, LD, Lee, PH, Shrine, N, Williams, AT, Guyatt, AL, John, C, Packer, RJ, Ali, A, Free, RC, Wang, X, Wain, LV, Hollox, EJ, Bee, CE, Adams, EL, Palotie, A, Ripatti, S, Ruotsalainen, S, Kristiansson, K, Koskelainen, S, Perola, M, Donner, K, Kivinen, K, Kaunisto, M, Rivolta, C, Bochud, P-Y, Bibert, S, Boillat, N, Nussle, SG, Albrich, W, Quinodoz, M, Kamdar, D, Suh, N, Neofytos, D, Erard, V, Voide, C, Friolet, R, Vollenweider, P, Pagani, JL, Oddo, M, zu Bentrup, FM, Conen, A, Clerc, O, Marchetti, O, Guillet, A, Guyat-Jacques, C, Foucras, S, Rime, M, Chassot, J, Jaquet, M, Viollet, RM, Lannepoudenx, Y, Portopena, L, Bochud, PY, Desgranges, F, Filippidis, P, Guéry, B, Haefliger, D, Kampouri, EE, Manuel, O, Munting, A, Papadimitriou-Olivgeris, M, Regina, J, Rochat-Stettler, L, Suttels, V, Tadini, E, Tschopp, J, Van Singer, M, Viala, B, Boillat-Blanco, N, Brahier, T, Hügli, O, Meuwly, JY, Pantet, O, Gonseth Nussle, S, Bochud, M, D’Acremont, V, Estoppey Younes, S, Albrich, WC, Cerny, A, O’Mahony, L, von Mering, C, Frischknecht, M, Kleger, G-R., Filipovic, M, Kahlert, CR, Wozniak, H, Negro, TR, Pugin, J, Bouras, K, Knapp, C, Egger, T, Perret, A, Montillier, P, di Bartolomeo, C, Barda, B, de Cid, R, Carreras, A, Moreno, V, Kogevinas, M, Galván-Femenía, I, Blay, N, Farré, X, Sumoy, L, Cortés, B, Mercader, JM, Guindo-Martinez, M, Torrents, D, Garcia-Aymerich, J, Castaño-Vinyals, G, Dobaño, C, Gori, M, Renieri, A, Mari, F, Mondelli, MU, Castelli, F, Vaghi, M, Rusconi, S, Montagnani, F, Bargagli, E, Franchi, F, Mazzei, MA, Cantarini, L, Tacconi, D, Feri, M, Scala, R, Spargi, G, Nencioni, C, Bandini, M, Caldarelli, GP, Canaccini, A, Ognibene, A, D’Arminio Monforte, A, Girardis, M, Antinori, A, Francisci, D, Schiaroli, E, Scotton, PG, Panese, S, Scaggiante, R, Monica, MD, Capasso, M, Fiorentino, G, Castori, M, Aucella, F, Biagio, AD, Masucci, L, Valente, S, Mandalà, M, Zucchi, P, Giannattasio, F, Coviello, DA, Mussini, C, Tavecchia, L, Crotti, L, Rizzi, M, Rovere, MTL, Sarzi-Braga, S, Bussotti, M, Ravaglia, S, Artuso, R, Perrella, A, Romani, D, Bergomi, P, Catena, E, Vincenti, A, Ferri, C, Grassi, D, Pessina, G, Tumbarello, M, Pietro, MD, Sabrina, R, Luchi, S, Furini, S, Dei, S, Benetti, E, Picchiotti, N, Sanarico, M, Ceri, S, Pinoli, P, Raimondi, F, Biscarini, F, Stella, A, Zguro, K, Capitani, K, Tanfoni, M, Fallerini, C, Daga, S, Baldassarri, M, Fava, F, Frullanti, E, Valentino, F, Doddato, G, Giliberti, A, Tita, R, Amitrano, S, Bruttini, M, Croci, S, Meloni, I, Mencarelli, MA, Rizzo, CL, Pinto, AM, Beligni, G, Tommasi, A, Sarno, LD, Palmieri, M, Carriero, ML, Alaverdian, D, Busani, S, Bruno, R, Vecchia, M, Belli, MA, Mantovani, S, Ludovisi, S, Quiros-Roldan, E, Antoni, MD, Zanella, I, Siano, M, Emiliozzi, A, Fabbiani, M, Rossetti, B, Bergantini, L, D’Alessandro, M, Cameli, P, Bennett, D, Anedda, F, Marcantonio, S, Scolletta, S, Guerrini, S, Conticini, E, Frediani, B, Spertilli, C, Donati, A, Guidelli, L, Corridi, M, Croci, L, Piacentini, P, Desanctis, E, Cappelli, S, Verzuri, A, Anemoli, V, Pancrazzi, A, Lorubbio, M, Miraglia, FG, Venturelli, S, Cossarizza, A, Vergori, A, Gabrieli, A, Riva, A, Paciosi, F, Andretta, F, Gatti, F, Parisi, SG, Baratti, S, Piscopo, C, Russo, R, Andolfo, I, Iolascon, A, Carella, M, Merla, G, Squeo, GM, Raggi, P, Marciano, C, Perna, R, Bassetti, M, Sanguinetti, M, Giorli, A, Salerni, L, Parravicini, P, Menatti, E, Trotta, T, Coiro, G, Lena, F, Martinelli, E, Mancarella, S, Gabbi, C, Maggiolo, F, Ripamonti, D, Bachetti, T, Suardi, C, Parati, G, Bottà, G, Domenico, PD, Rancan, I, Bianchi, F, Colombo, R, Barbieri, C, Acquilini, D, Andreucci, E, Segala, FV, Tiseo, G, Falcone, M, Lista, M, Poscente, M, Vivo, OD, Petrocelli, P, Guarnaccia, A, 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Susanna, Meloni, Ilaria, Mencarelli, Maria Antonietta, Rizzo, Caterina Lo, Pinto, Anna Maria, Beligni, Giada, Tommasi, Andrea, Sarno, Laura Di, Palmieri, Maria, Carriero, Miriam Lucia, Alaverdian, Diana, Busani, Stefano, Bruno, Raffaele, Vecchia, Marco, Belli, Mary Ann, Mantovani, Stefania, Ludovisi, Serena, Quiros-Roldan, Eugenia, Antoni, Melania Degli, Zanella, Isabella, Siano, Matteo, Emiliozzi, Arianna, Fabbiani, Massimiliano, Rossetti, Barbara, Bergantini, Laura, D’Alessandro, Miriana, Cameli, Paolo, Bennett, David, Anedda, Federico, Marcantonio, Simona, Scolletta, Sabino, Guerrini, Susanna, Conticini, Edoardo, Frediani, Bruno, Spertilli, Chiara, Donati, Alice, Guidelli, Luca, Corridi, Marta, Croci, Leonardo, Piacentini, Paolo, Desanctis, Elena, Cappelli, Silvia, Verzuri, Agnese, Anemoli, Valentina, Pancrazzi, Alessandro, Lorubbio, Maria, Miraglia, Federica Gaia, Venturelli, Sophie, Cossarizza, Andrea, Vergori, Alessandra, Gabrieli, Arianna, Riva, Agostino, Paciosi, Francesco, Andretta, Francesca, Gatti, Francesca, Parisi, Saverio Giuseppe, Baratti, Stefano, Piscopo, Carmelo, Russo, Roberta, Andolfo, Immacolata, Iolascon, Achille, Carella, Massimo, Merla, Giuseppe, Squeo, Gabriella Maria, Raggi, Pamela, Marciano, Carmen, Perna, Rita, Bassetti, Matteo, Sanguinetti, Maurizio, Giorli, Alessia, Salerni, Lorenzo, Parravicini, Pierpaolo, Menatti, Elisabetta, Trotta, Tullio, Coiro, Gabriella, Lena, Fabio, Martinelli, Enrico, Mancarella, Sandro, Gabbi, Chiara, Maggiolo, Franco, Ripamonti, Diego, Bachetti, Tiziana, Suardi, Claudia, Parati, Gianfranco, Bottà, Giordano, Domenico, Paolo Di, Rancan, Ilaria, Bianchi, Francesco, Colombo, Riccardo, Barbieri, Chiara, Acquilini, Donatella, Andreucci, Elena, Segala, Francesco Vladimiro, Tiseo, Giusy, Falcone, Marco, Lista, Mirjam, Poscente, Monica, Vivo, Oreste De, Petrocelli, Paola, Guarnaccia, Alessandra, Baroni, Silvia, van Heel, David A., Hunt, Karen A., Trembath, Richard C., Huang, Qin Qin, Martin, Hilary C., Mason, Dan, 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Vorasuk, Pongpanich, Monnat, Phokaew, Chureerat, Chetruengchai, Wanna, Putchareon, Opa, Torvorapanit, Pattama, Puthanakit, Thanyawee, Suchartlikitwong, Pintip, Nilaratanakul, Voraphoj, Sodsai, Pimpayao, Brumpton, Ben M., Hveem, Kristian, Willer, Cristen, Zhou, Wei, Rogne, Tormod, Solligard, Erik, Åsvold, Bjørn Olav, Franke, Lude, Boezen, Marike, Deelen, Patrick, Claringbould, Annique, Lopera, Esteban, Warmerdam, Robert, Vonk, Judith. M., van Blokland, Irene, Lanting, Pauline, Ori, Anil P. S., Feng, Yen-Chen Anne, Mercader, Josep, Weiss, Scott T., Karlson, Elizabeth W., Smoller, Jordan W., Murphy, Shawn N., Meigs, James B., Woolley, Ann E., Green, Robert C., Perez, Emma F., Zöllner, Sebastian, Wang, Jiongming, Beck, Andrew, Sloofman, Laura G., Ascolillo, Steven, Sebra, Robert P., Collins, Brett L., Levy, Te, Buxbaum, Joseph D., Sealfon, Stuart C., Jordan, Daniel M., Thompson, Ryan C., Gettler, Kyle, Chaudhary, Kumardeep, Belbin, Gillian M., Preuss, Michael, Hoggart, Clive, Choi, Sam, Underwood, Slayton J., Salib, Irene, Britvan, Bari, Keller, Katherine, Tang, Lara, Peruggia, Michael, Hiester, Liam L., Niblo, Kristi, Aksentijevich, Alexandra, Labkowsky, Alexander, Karp, Avromie, Zlatopolsky, Menachem, Zyndorf, Marissa, Charney, Alexander W., Beckmann, Noam D., Schadt, Eric E., Abul-Husn, Noura S., Cho, Judy H., Itan, Yuval, Kenny, Eimear E., Loos, Ruth J. F., Nadkarni, Girish N., Do, Ron, O’Reilly, Paul, Huckins, Laura M., Ferreira, Manuel A. R., Abecasis, Goncalo R., Leader, Joseph B., Cantor, Michael N., Justice, Anne E., Carey, Dave J., Chittoor, Geetha, Josyula, Navya Shilpa, Kosmicki, Jack A., Horowitz, Julie E., Baras, Ari, Gass, Matthew C., Yadav, Ashish, Mirshahi, Tooraj, Hottenga, Jouke Jan, Bartels, Meike, de geus, Eco E. J. C., Nivard, Michel M. G., Verma, Anurag, Ritchie, Marylyn D., Rader, Daniel, Li, Binglan, Verma, Shefali S., Lucas, Anastasia, Bradford, Yuki, Abedalthagafi, Malak, Alaamery, Manal, Alshareef, Abdulraheem, Sawaji, Mona, Massadeh, Salam, AlMalik, Abdulaziz, Alqahtani, Saleh, Baraka, Dona, Harthi, Fawz Al, Alsolm, Ebtehal, Safieh, Leen Abu, Alowayn, Albandary M., Alqubaishi, Fatimah, Mutairi, Amal Al, Mangul, Serghei, Almutairi, Mansour, Aljawini, Nora, Albesher, Nour, Arabi, Yaseen M., Mahmoud, Ebrahim S., Khattab, Amin K., Halawani, Roaa T., Alahmadey, Ziab Z., Albakri, Jehad K., Felemban, Walaa A., Suliman, Bandar A., Hasanato, Rana, Al-Awdah, Laila, Alghamdi, Jahad, AlZahrani, Deema, AlJohani, Sameera, Al-Afghani, Hani, AlDhawi, Nouf, AlBardis, Hadeel, Alkwai, Sarah, Alswailm, Moneera, Almalki, Faisal, Albeladi, Maha, Almohammed, Iman, Barhoush, Eman, Albader, Anoud, Alotaibi, Sara, Alghamdi, Bader, Jung, Junghyun, fawzy, Mohammad S., Alrashed, May, Zeberg, Hugo, Nkambul, Lindo, Frithiof, Robert, Hultström, Michael, Lipcsey, Miklo, Tardif, Nicola, Rooyackers, Olav, Grip, Jonathan, Maricic, Tomislav, Helgeland, Øyvind, Magnus, Per, Trogstad, Lill-Iren S., Lee, Yunsung, Harris, Jennifer R., Mangino, Massimo, Spector, Tim D., Emma, Duncan, Moutsianas, Louka, Caulfield, Mark J., Scott, Richard H., Kousathanas, Athanasio, Pasko, Dorota, Walker, Susan, Stuckey, Alex, Odhams, Christopher A., Rhodes, Daniel, Fowler, Tom, Rendon, Augusto, Chan, Georgia, Arumugam, Prabhu, Karczewski, Konrad J., Martin, Alicia R., Wilson, Daniel J., Spencer, Chris C. A., Crook, Derrick W., Wyllie, David H., O’Connell, Anne Marie, Atkinson, Elizabeth G., Tsuo, Kristin, Baya, Nikola, Turley, Patrick, Gupta, Rahul, Walters, Raymond K., Palmer, Duncan S., Sarma, Gopal, Cheng, Nathan, Lu, Wenhan, Churchhouse, Claire, Goldstein, Jacqueline I., King, Daniel, Seed, Cotton, Daly, Mark J., Finucane, Hilary, Bryant, Sam, Satterstrom, F. Kyle, Band, Gavin, Earle, Sarah G., Lin, Shang-Kuan, Arning, Nicola, Koelling, Nil, Armstrong, Jacob, Rudkin, Justine K., Callier, Shawneequa, Cusick, Caroline, Soranzo, Nicole, Zhao, Jing Hua, Danesh, John, Angelantonio, Emanuele Di, Butterworth, Adam S., Sun, Yan V., Huffman, Jennifer E., Cho, Kelly, O’Donnell, Christopher J., Tsao, Phil, Gaziano, J. Michael, Peloso, Gina, Ho, Yuk-Lam, Smieszek, Sandra P., Polymeropoulos, Christo, Polymeropoulos, Vasilio, Polymeropoulos, Mihael H., Przychodzen, Bartlomiej P., Fernandez-Cadenas, Israel, Planas, Anna M., Perez-Tur, Jordi, Llucià-Carol, Laia, Cullell, Natalia, Muiño, Elena, Cárcel-Márquez, Jara, DeDiego, Marta L., Iglesias, Lara Lloret, Soriano, Alex, Rico, Veronica, Agüero, Daiana, Bedini, Josep L., Lozano, Francisco, Domingo, Carlo, Robles, Veronica, Ruiz-Jaén, Francisca, Márquez, Leonardo, Gomez, Juan, Coto, Eliecer, Albaiceta, Guillermo M., García-Clemente, Marta, Dalmau, David, Arranz, Maria J., Dietl, Beatriz, Serra-Llovich, Alex, Soler, Pere, Colobrán, Roger, Martín-Nalda, Andrea, Martínez, Alba Parra, Bernardo, David, Rojo, Silvia, Fiz-López, Aida, Arribas, Elisa, de la Cal-Sabater, Paloma, Segura, Tomá, González-Villa, Esther, Serrano-Heras, Gemma, Martí-Fàbregas, Joan, Jiménez-Xarrié, Elena, de Felipe Mimbrera, Alicia, Masjuan, Jaime, García-Madrona, Sebastian, Domínguez-Mayoral, Anna, Villalonga, Joan Montaner, Menéndez-Valladares, Paloma, Chasman, Daniel I., Sesso, Howard D., Manson, JoAnn E., Buring, Julie E., Ridker, Paul M., Franco, Giulianini, Davis, Lea, Lee, Sulggi, Priest, Jame, Sankaran, Vijay G., van Heel, David, Biesecker, Le, Kerchberger, V. Eric, Baillie, J. Kenneth, APH - Personalized Medicine, APH - Health Behaviors & Chronic Diseases, Biological Psychology, APH - Mental Health, AMS - Sports, AMS - Ageing & Vitality, APH - Methodology, Mccurdy, Shannon, Mccormick, Joseph B., Macarthur, Daniel, Maclaughlin, Bev, Lefaive, Jonathon, Almalik, Abdulaziz, Alzahrani, Deema, Aljohani, Sameera, Aldhawi, Nouf, Albardis, Hadeel, Fawzy, Mohammad S., Dediego, Marta L., Stem Cell Aging Leukemia and Lymphoma (SALL), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Life Course Epidemiology (LCE), Groningen Research Institute for Asthma and COPD (GRIAC), University of Zurich, COVID-19 Host Genetics Initiative, Barcelona Supercomputing Center, COVID-19 Genetics Initiative, including authors, Institute for Molecular Medicine Finland, and Data Science Genetic Epidemiology Lab
Subjects: Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC], Quantitative Trait Loci, MUC5B PROMOTER POLYMORPHISM, Genome-wide association studies, COVID-19 (Malaltia), UFSP13-7 Evolution in Action: From Genomes to Ecosystems, COVID-19 (Disease), Settore BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICA, SDG 3 - Good Health and Well-being, Humans, genetics, Genetic variation, Genomes, Medicinsk genetik, 1000 Multidisciplinary, Multidisciplinary, Chromosome Mapping, COVID-19, Human Genetics, 10124 Institute of Molecular Life Sciences, covid-19, 3121 General medicine, internal medicine and other clinical medicine, 570 Life sciences, biology, Medical Genetics
Abstract: Matters arising from: Mapping the human genetic architecture of COVID-19 Original Article published on 08 July 2021 https://www.nature.com/articles/s41586-021-03767-x The COVID-19 pandemic continues to pose a major public health threat, especially in countries with low vaccination rates. To better understand the biological underpinnings of SARS-CoV-2 infection and COVID-19 severity, we formed the COVID-19 Host Genetics Initiative1. Here we present a genome-wide association study meta-analysis of up to 125,584 cases and over 2.5 million control individuals across 60 studies from 25 countries, adding 11 genome-wide significant loci compared with those previously identified2. Genes at new loci, including SFTPD, MUC5B and ACE2, reveal compelling insights regarding disease susceptibility and severity. Here we present meta-analyses bringing together 60 studies from 25 countries (Fig. 1 and Supplementary Table 1) for three COVID-19-related phenotypes: (1) individuals critically ill with COVID-19 on the basis of requiring respiratory support in hospital or who died as a consequence of the disease (9,376 cases, of which 3,197 are new in this data release, and 1,776,645 control individuals); (2) individuals with moderate or severe COVID-19 defined as those hospitalized due to symptoms associated with the infection (25,027 cases, 11,386 new and 2,836,272 control individuals); and (3) all cases with reported SARS-CoV-2 infection regardless of symptoms (125,584 cases, 76,022 new and 2,575,347 control individuals). Most studies have reported results before the roll out of the COVID-19 vaccination campaign. An overview of the study design is provided in Supplementary Fig. 1. We found a total of 23 genome-wide significant loci (P
Published: 2022
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9. Rheumatoid arthritis and osteogenesis imperfecta: is there a genetic causal association?

Author: Ilaria Mormile, Roberta Russo, Immacolata Andolfo, Amato de Paulis, Francesca Wanda Rossi, Domenico Rendina, Mormile, Ilaria, Russo, Roberta, Andolfo, Immacolata, de Paulis, Amato, Rossi, Francesca Wanda, and Rendina, Domenico
Subjects: Arthritis, Rheumatoid, Endocrinology, Diabetes and Metabolism, Humans, Osteogenesis Imperfecta
Published: 2022

10. The Serum Metabolome of Moderate and Severe COVID-19 Patients Reflects Possible Liver Alterations Involving Carbon and Nitrogen Metabolism

Author: Anna Annunziata, Francesco Maria Fusco, Alessandro Di Minno, Margherita Ruoppolo, Giuseppe Castaldo, Chiara Dell’Isola, Roberta Russo, Armando Cevenini, Immacolata Andolfo, Mario Capasso, Giuseppe Fiorentino, Roberta Fedele, Gabriella Fabbrocini, Cecilia Calabrese, Marianna Caterino, Michele Costanzo, Ivan Gentile, Monica Gelzo, Roberto Parrella, Maurizio D’Abbraccio, Caterino, Marianna, Costanzo, Michele, Fedele, Roberta, Cevenini, Armando, Gelzo, Monica, DI MINNO, Alessandro, Andolfo, Immacolata, Capasso, Mario, Russo, Roberta, Annunziata, Anna, Calabrese, Cecilia, Fiorentino, Giuseppe, D’Abbraccio, Maurizio, Dell’Isola, Chiara, Maria Fusco, Francesco, Parrella, Roberto, Fabbrocini, Gabriella, Gentile, Ivan, Castaldo, Giuseppe, Ruoppolo, Margherita, Caterino, M., Costanzo, M., Fedele, R., Cevenini, A., Gelzo, M., Di Minno, A., Andolfo, I., Capasso, M., Russo, R., Annunziata, A., Calabrese, C., Fiorentino, G., D'Abbraccio, M., Dell'Isola, C., Fusco, F. M., Parrella, R., Fabbrocini, G., Gentile, I., Castaldo, G., and Ruoppolo, M.
Subjects: coronavirus, Physiology, Disease, medicine.disease_cause, Severity of Illness Index, Medicine, Biology (General), Amino Acids, Spectroscopy, Coronavirus, mass spectrometry, Discriminant Analysis, General Medicine, metabolomics, Pathophysiology, Computer Science Applications, Amino Acid, Chemistry, Liver, Metabolome, Cytokines, Discriminant Analysi, Metabolic Networks and Pathways, Human, QH301-705.5, Nitrogen, Coronaviru, Context (language use), Metabolomic, serum cytokines, Catalysis, Article, Inorganic Chemistry, Metabolomics, Severity of illness, Humans, Physical and Theoretical Chemistry, Least-Squares Analysis, Serum cy-tokine, Cytokine, Molecular Biology, QD1-999, Least-Squares Analysi, business.industry, SARS-CoV-2, Organic Chemistry, lactic acid, Metabolic Networks and Pathway, COVID-19, Biomarker, Metabolism, Carbon, business, Biomarkers
Abstract: COVID-19 is a global threat that has spread since the end of 2019, causing severe clinical sequelae and deaths, in the context of a world pandemic. The infection of the highly pathogenetic and infectious SARS-CoV-2 coronavirus has been proven to exert systemic effects impacting the metabolism. Yet, the metabolic pathways involved in the pathophysiology and progression of COVID-19 are still unclear. Here, we present the results of a mass spectrometry-based targeted metabolomic analysis on a cohort of 52 hospitalized COVID-19 patients, classified according to disease severity as mild, moderate, and severe. Our analysis defines a clear signature of COVID-19 that includes increased serum levels of lactic acid in all the forms of the disease. Pathway analysis revealed dysregulation of energy production and amino acid metabolism. Globally, the variations found in the serum metabolome of COVID-19 patients may reflect a more complex systemic perturbation induced by SARS-CoV-2, possibly affecting carbon and nitrogen liver metabolism.
Published: 2021

11. Mapping the human genetic architecture of COVID-19

Author: Niemi, MEK, Karjalainen, J, Liao, RG, Neale, BM, Daly, M, Ganna, A, Pathak, GA, Andrews, SJ, Kanai, M, Veerapen, K, Fernandez-Cadenas, I, Schulte, EC, Striano, P, Marttila, M, Minica, C, Marouli, E, Karim, MA, Wendt, FR, Savage, J, Sloofman, L, Butler-Laporte, G, Kim, H-N, Kanoni, S, Okada, Y, Byun, J, Han, Y, Uddin, MJ, Smith, GD, Willer, CJ, Buxbaum, JD, Mehtonen, J, Finucane, H, Cordioli, M, Martin, AR, Zhou, W, Pasaniuc, B, Julienne, H, Aschard, H, Shi, H, Yengo, L, Polimanti, R, Ghoussaini, M, Schwartzentruber, J, Dunham, I, Chwialkowska, K, Francescatto, M, Trankiem, A, Balaconis, MK, Davis, L, Lee, S, Priest, J, Renieri, A, Sankaran, VG, van Heel, D, Deelen, P, Richards, JB, Nakanishi, T, Biesecker, L, Kerchberger, VE, Kenneth, J, Mari, F, Bernasconi, A, Ceri, S, Canakoglu, A, Wolford, B, Faucon, A, Dutta, AK, Schurmann, C, Harry, E, Birney, E, Nguyen, H, Nasir, J, Kaunisto, M, Solomonson, M, Dueker, N, Vadgama, N, Limou, S, Rahmouni, S, Mbarek, H, Darwish, D, Uddin, MM, Albertos, R, Perez-Tur, J, Li, R, Folkersen, L, Moltke, I, Koelling, N, Teumer, A, Kousathanas, A, Utrilla, A, Verdugo, RA, Zarate, R, Medina-Gomez, C, Gomez-Cabrero, D, Carnero-Montoro, E, Cadilla, CL, Moreno-Estrada, A, Garmendia, A, Moya, L, Sedaghati-Khayat, B, Boua, PR, Fave, M-J, Francioli, L, Lemacon, A, Migeotte, I, Patel, S, Varnai, R, Szentpeteri, JL, Sipeky, C, Colombo, F, von Hohenstaufen, K, Lio, P, Vallerga, C, Wang, Q, Tanigawa, Y, Im, H, Han, C, Song, H, Lim, J, Lee, Y, Kim, S, Im, S, Atanasovska, B, Ahmad, HF, Boer, C, Jansen, P, Franke, L, Kaja, E, Pasko, D, Kennis-Szilagyi, I, Kornilov, SA, Prijatelj, V, Prokic, I, Sivanadhan, I, Perumal, S, Esmaeeli, S, Pearson, NM, Auton, A, Shelton, JF, Shastri, AJ, Filshtein-Sonmez, T, Coker, D, Symons, A, Esparza-Gordillo, J, Aslibekyan, S, O'Connell, J, Ye, C, Weldon, CH, Perera, M, O'Leary, K, Tuck, M, O'Brien, T, Meltzer, D, O'Donnell, P, Nutescu, E, Yang, G, Alarcon, C, Herrmann, S, Mazurek, S, Banagan, J, Hamidi, Z, Barbour, A, Raffat, N, Moreno, D, Friedman, P, Ferwerda, B, van de Beek, D, Brouwer, MC, Vlaar, APJ, Wiersinga, WJ, Posthuma, D, Tissink, E, Zwinderman, AHK, Uffelmann, E, van Agtmael, M, Algera, AG, van Baarle, F, Bax, D, Beudel, M, Bogaard, HJ, Bomers, M, Bonta, PI, Bos, L, Botta, M, de Brabander, J, de Bree, G, de Bruin, S, Bugiani, M, Bulle, E, Chouchane, O, Cloherty, A, Dongelmans, D, Elbers, P, Fleuren, L, Geerlings, S, Geerts, B, Geijtenbeek, T, Girbes, A, Goorhuis, B, Grobusch, MP, Hafkamp, F, Hagens, L, Hamann, J, Harris, V, Hemke, R, Hermans, SM, Heunks, L, Hollmann, M, Horn, J, Hovius, JW, de Jong, MD, Koning, R, van Mourik, N, Nellen, J, Nossent, EJ, Paulus, F, Peters, E, van der Poll, T, Preckel, B, Prins, JM, Raasveld, J, Reijnders, T, Schinkel, M, Schultz, MJ, Schuurman, A, Sigaloff, K, Smit, M, Stijnis, CS, Stilma, W, Teunissen, C, Thoral, P, Tsonas, A, van der Valk, M, Veelo, D, de Vries, H, van Vugt, M, Wouters, D, Minnaar, RP, Kromhout, A, van Uffelen, KWJ, Wolterman, RA, Roberts, G, Park, D, Ball, CA, Coignet, M, McCurdy, S, Knight, S, Partha, R, Rhead, B, Zhang, M, Berkowitz, N, Gaddis, M, Noto, K, Ruiz, L, Pavlovic, M, Hong, EL, Rand, K, Girshick, A, Guturu, H, Baltzell, AH, Guntz, J, Beguin, Y, Pigazzini, S, Nkambule, L, Bouysran, Y, Busson, A, Peyrassol, X, Wilkin, F, Pichon, B, Smits, G, Vandernoot, I, Goffard, J-C, Georges, M, Moutschen, M, Misset, B, Darcis, G, Guiot, J, Jadot, L, Azarzar, S, Dellot, P, Gofflot, S, Claassen, S, Bertrand, A, Parzibut, G, Clarinval, M, Moermans, C, Malaise, O, El Kandoussi, K, Thonon, R, Huynen, P, Mesdagh, A, Melo, S, Jacques, N, Di Valentin, E, Giroule, F, Collignon, A, Radermecker, C, Lebrun, M, Peree, H, Latour, S, Barada, O, Sanchez, J, Josse, C, Boujemla, B, Meunier, M, Mariavelle, E, Anania, S, Gazon, H, Juszczak, D, Fadeur, M, Camby, S, Meuris, C, Thys, M, Jacques, J, Henket, M, Leonard, P, Frippiat, F, Giot, J-B, Sauvage, A-S, Von Frenckell, C, Mni, M, Wery, M, Staderoli, A, Belhaj, Y, Lambermont, B, Morrison, DR, Mooser, V, Forgetta, V, Ghosh, B, Laurent, L, Belisle, A, Henry, D, Abdullah, T, Adeleye, O, Mamlouk, N, Kimchi, N, Afrasiabi, Z, Rezk, N, Vulesevic, B, Bouab, M, Guzman, C, Petitjean, L, Tselios, C, Xue, X, Afilalo, J, Afilalo, M, Oliveira, M, Brenner, B, Brassard, N, Durand, M, Schurr, E, Lepage, P, Ragoussis, J, Auld, D, Chasse, M, Kaufmann, DE, Lathrop, GM, Adra, D, Davis, LK, Cox, NJ, Below, JE, Sealock, JM, Faucon, AB, Shuey, MM, Polikowsky, HG, Petty, LE, Shaw, DM, Chen, H-H, Zhu, W, Ludwig, KU, Schroeder, J, Maj, C, Rolker, S, Noethen, MM, Fazaal, J, Keitel, V, Jensen, B-EO, Feldt, T, Kurth, I, Marx, N, Dreher, M, Pink, I, Cornberg, M, Illig, T, Lehmann, C, Schommers, P, Augustin, M, Rybniker, J, Knopp, L, Eggermann, T, Volland, S, Altmueller, J, Berger, MM, Brenner, T, Hinney, A, Witzke, O, Bals, R, Herr, C, Ludwig, N, Walter, J, Fuchsberger, C, Pattaro, C, De Grandi, A, Pramstaller, P, Emmert, D, Melotti, R, Foco, L, Mascalzoni, D, Gogele, M, Domingues, F, Hicks, A, Gignoux, CR, Wicks, SJ, Crooks, K, Barnes, KC, Daya, M, Shortt, J, Rafaels, N, Chavan, S, Goldstein, DB, Kiryluk, K, Sengupta, S, Chung, W, Reilly, MP, Khan, A, Wang, C, Povysil, G, Bhardwaj, N, Gharavi, AG, Ionita-Laza, I, Shang, N, O'Byrne, SM, Nandakumar, R, Menon, A, So, YS, Hod, E, Pendrick, D, Park, S-K, Kim, H-L, Kang, CK, Lee, H-J, Song, K-H, Yoon, KJ, Paik, N-J, Seok, W, Yoon, H, Joo, E-J, Chang, Y, Ryu, S, Park, WB, Park, JS, Park, KU, Ham, SY, Jung, J, Kim, ES, Kim, HB, Ellinghaus, D, Degenhardt, F, Caceres, M, Juzenas, S, Lenz, TL, Albillos, A, Julia, A, Heidecker, B, Garcia, F, Kurth, F, Tran, F, Hanses, F, Zoller, H, Holter, JC, Fernandez, J, Sander, LE, Rosenstiel, P, Koehler, P, de Cid, R, Asselta, R, Schreiber, S, Hehr, U, Prati, D, Baselli, G, Valenti, L, Bujanda, L, Banales, JM, Duga, S, D'Amato, M, Romero-Gomez, M, Buti, M, Invernizzi, P, Franke, A, Hov, JR, Karlsen, TH, Folseraas, T, Maya-Miles, D, Teles, A, Azuure, C, Wacker, EM, Uellendahl-Werth, F, Elabd, H, Arora, J, Lerga-Jaso, J, Wienbrandt, L, Ruehlemann, MC, Wendorff, M, Vadla, MS, Lenning, OB, Oezer, O, Myhre, R, Raychaudhuri, S, Tanck, A, Gassner, C, Hemmrich-Stanisak, G, Kaessens, J, Basso, MEF, Schulzky, M, Wittig, M, Braun, N, Wesse, T, Albrecht, W, Yi, X, Ortiz, AB, Garrido Chercoles, A, Ruiz, A, Mantovani, A, Holten, AR, Mayer, A, Cherubini, A, Protti, A, Aghemo, A, Gerussi, A, Ramirez, A, Braun, A, Barreira, A, Lleo, A, Kildal, AB, Glueck, A, Carreras Nolla, A, Latiano, A, Dyrhol-Riise, AM, Muscatello, A, Voza, A, Rando-Segura, A, Solier, A, Karina, B, Cortes, B, Mateos, B, Nafria-Jimenez, B, Schaefer, B, Bellinghausen, C, Ferrando, C, Quereda, C, Skurk, C, Thibeault, C, Spinner, CD, Lange, C, Hu, C, Cappadona, C, Bianco, C, Sancho, C, Hoff, DAL, Galimberti, D, Jimenez, D, Pestana, D, Toapanta, D, Azzolini, E, Scarpini, E, Helbig, ET, Urrechaga, E, Paraboschi, EM, Pontali, E, Reverter, E, Navas, E, Arana, E, Garcia Sanchez, F, Ceriotti, F, Malvestiti, F, Mesonero, F, Pezzoli, G, Lamorte, G, Neb, H, My, I, Hernandez, I, de Rojas, I, Galvan-Femenia, I, Heyckendorf, J, Badia, JR, Schneider, J, Goikoetxea, J, Kraft, J, Mueller, KE, Gaede, KI, Garcia-Etxebarria, K, Tonby, K, Heggelund, L, Izquierdo-Sanchez, L, Sumoy, L, Lippert, LJ, Terranova, L, Garbarino, L, Tellez, L, Roade, L, Ostadreza, M, Intxausti, M, Kogevinas, M, Gutierrez-Stampa, MA, Vehreschild, MJGT, Marquie, M, Castoldi, M, Cecconi, M, Boada, M, Seilmaier, MJ, Mazzocco, M, Rodriguez-Gandia, M, Imaz Ayo, N, Blay, N, Martinez, N, Cornely, OA, Palmieri, O, Tentorio, P, Rodrigues, PM, Espana, PP, Hoffmann, P, Bacher, P, Suwalski, P, de Pablo, R, Nieto, R, Badalamenti, S, Ciesek, S, Bombace, S, Wilfling, S, Brunak, S, Heilmann-Heimbach, S, Ripke, S, Bahmer, T, Landmesser, U, Protzer, U, Rimoldi, V, Skogen, V, Andrade, V, Moreno, V, Poller, W, Farre, X, Wang, X, Khodamoradi, Y, Karadeniz, Z, de Salazar, A, Palom, A, Garcia-Fernandez, A-E, Blanco-Grau, A, Zanella, A, 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Brent, Nakanishi, Tomoko, Biesecker, Le, Kerchberger, V. Eric, Baillie, J. 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J., Wiersinga, W. Joost, Posthuma, Danielle, Tissink, Elleke, Koos Zwinderman, A. H., Uffelmann, Emil, van Agtmael, Michiel, Algera, Anne Geke, van Baarle, Frank, Bax, Diane, Beudel, Martijn, Jan Bogaard, Harm, Bomers, Marije, Bonta, Peter I., Bos, Lieuwe, Botta, Michela, de Brabander, Justin, de Bree, Godelieve, de Bruin, Sanne, Bugiani, Marianna, Bulle, Esther, Chouchane, Osoul, Cloherty, Alex, Dongelmans, Dave, Elbers, Paul, Fleuren, Luca, Geerlings, Suzanne, Geerts, Bart, Geijtenbeek, Theo, Girbes, Armand, Goorhuis, Bram, Grobusch, Martin P., Hafkamp, Florianne, Hagens, Laura, Hamann, Jorg, Harris, Vanessa, Hemke, Robert, Hermans, Sabine M., Heunks, Leo, Hollmann, Marku, Horn, Janneke, Hovius, Joppe W., de Jong, Menno D., Koning, Rutger, van Mourik, Niel, Nellen, Jeannine, Nossent, Esther J., Paulus, Frederique, Peters, Edgar, van der Poll, Tom, Preckel, Bennedikt, Prins, Jan M., Raasveld, Jorinde, Reijnders, Tom, Schinkel, Michiel, Schultz, Marcus J., Schuurman, Alex, Sigaloff, Kim, Smit, Marry, Stijnis, Cornelis S., Stilma, Willemke, Teunissen, Charlotte, Thoral, Patrick, Tsonas, Anissa, van der Valk, Marc, Veelo, Denise, de Vries, Heder, van Vugt, Michèle, Wouters, Dorien, Minnaar, René P., Kromhout, Adrie, van Uffelen, Kees W. 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Mark, Adra, Darin, Davis, Lea K., Cox, Nancy J., Below, Jennifer E., Sealock, Julia M., Faucon, Annika B., Shuey, Megan M., Polikowsky, Hannah G., Petty, Lauren E., Shaw, Douglas M., Chen, Hung-Hsin, Zhu, Wanying, Ludwig, Kerstin U., Schröder, Julia, Maj, Carlo, Rolker, Selina, Nöthen, Markus M., Fazaal, Julia, Keitel, Verena, Jensen, Björn-Erik Ole, Feldt, Torsten, Kurth, Ingo, Marx, Nikolau, Dreher, Michael, Pink, Isabell, Cornberg, Marku, Illig, Thoma, Lehmann, Clara, Schommers, Philipp, Augustin, Max, Rybniker, Jan, Knopp, Lisa, Eggermann, Thoma, Volland, Sonja, Altmüller, Janine, Berger, Marc M., Brenner, Thorsten, Hinney, Anke, Witzke, Oliver, Bals, Robert, Herr, Christian, Ludwig, Nicole, Walter, Jörn, Fuchsberger, Christian, Pattaro, Cristian, De Grandi, Alessandro, Pramstaller, Peter, Emmert, David, Melotti, Roberto, Foco, Luisa, Mascalzoni, Deborah, Gögele, Martin, Domingues, Francisco, Hicks, Andrew, Gignoux, Christopher R., Wicks, Stephen J., Crooks, Kristy, Barnes, Kathleen C., Daya, Michelle, Shortt, Jonathan, Rafaels, Nichola, Chavan, Sameer, Goldstein, David B., Kiryluk, Krzysztof, Sengupta, Soumitra, Chung, Wendy, Reilly, Muredach P., Khan, Atla, Wang, Chen, Povysil, Gundula, Bhardwaj, Nitin, Gharavi, Ali G., Ionita-Laza, Iuliana, Shang, Ning, O’Byrne, Sheila M., Nandakumar, Renu, Menon, Amritha, So, Yat S., Hod, Eldad, Pendrick, Danielle, Park, Soo-Kyung, Kim, Hyung-Lae, Kang, Chang Kyung, Lee, Hyo-Jung, Song, Kyoung-Ho, Jae Yoon, Kyung, Paik, Nam-Jong, Seok, Woojin, Yoon, Heejun, Joo, Eun-Jeong, Chang, Yoosoo, Ryu, Seungho, Park, Wan Beom, Su Park, Jeong, Un Park, Kyoung, Ham, Sin Young, Jung, Jongtak, Kim, Eu Suk, Kim, Hong Bin, Ellinghaus, David, Degenhardt, Frauke, Cáceres, Mario, Juzenas, Simona, Lenz, Tobias L., Albillos, Agustín, Julià, Antonio, Heidecker, Bettina, Garcia, Federico, Kurth, Florian, Tran, Florian, Hanses, Frank, Zoller, Heinz, Holter, Jan C., Fernández, Javier, Sander, Leif Erik, Rosenstiel, Philip, Koehler, Philipp, de Cid, Rafael, Asselta, Rosanna, Schreiber, Stefan, Hehr, Ute, Prati, Daniele, Baselli, Guido, Valenti, Luca, Bujanda, Lui, Banales, Jesus M., Duga, Stefano, D’Amato, Mauro, Romero-Gómez, Manuel, Buti, Maria, Invernizzi, Pietro, Franke, Andre, Hov, Johannes R., Karlsen, Tom H., Folseraas, Trine, Maya-Miles, Dougla, Teles, Ana, Azuure, Clinton, Wacker, Eike Matthia, Uellendahl-Werth, Florian, Elabd, Hesham, Arora, Jatin, Lerga-Jaso, Jon, Wienbrandt, Lar, Rühlemann, Malte Christoph, Wendorff, Mareike, Vadla, May Sissel, Lenning, Ole Bernt, Özer, Onur, Myhre, Ronny, Raychaudhuri, Soumya, Tanck, Anja, Gassner, Christoph, Hemmrich-Stanisak, Georg, Kässens, Jan, Figuera Basso, Maria E., Schulzky, Martin, Wittig, Michael, Braun, Nicole, Wesse, Tanja, Albrecht, Wolfgang, Yi, Xiaoli, Ortiz, Aaron Blandino, Chercoles, Adolfo Garrido, Ruiz, Agustín, Mantovani, Alberto, Holten, Aleksander Rygh, Mayer, Alena, Cherubini, Alessandro, Protti, Alessandro, Aghemo, Alessio, Gerussi, Alessio, Ramirez, Alfredo, Braun, Alice, Barreira, Ana, Lleo, Ana, Kildal, Anders Benjamin, Glück, Andrea, Nolla, Anna Carrera, Latiano, Anna, Dyrhol-Riise, Anne Ma, Muscatello, Antonio, Voza, Antonio, Rando-Segura, Ariadna, Solier, Aurora, Karina, Banasik, Cortes, Beatriz, Mateos, Beatriz, Nafria-Jimenez, Beatriz, Schaefer, Benedikt, Bellinghausen, Carla, Ferrando, Carlo, Quereda, Carmen, Skurk, Carsten, Thibeault, Charlotte, Spinner, Christoph D., Lange, Christoph, Hu, Cinzia, Cappadona, Claudio, Bianco, Cristiana, Sancho, Cristina, Lihaug Hoff, Dag Arne, Galimberti, Daniela, Jiménez, David, Pestaña, David, Toapanta, David, Azzolini, Elena, Scarpini, Elio, Helbig, Elisa T., Urrechaga, Eloisa, Paraboschi, Elvezia Maria, Pontali, Emanuele, Reverter, Enric, Navas, Enrique, Arana, Eunate, Sánchez, Félix García, Ceriotti, Ferruccio, Malvestiti, Francesco, Mesonero, Francisco, Pezzoli, Gianni, Lamorte, Giuseppe, Neb, Holger, My, Ilaria, Hernández, Isabel, de Rojas, Itziar, Galván-Femenia, Iván, Heyckendorf, Jan, Badia, Joan Ramon, Schneider, Jochen, Goikoetxea, Josune, Kraft, Julia, Müller, Karl Erik, Gaede, Karoline I., Garcia-Etxebarria, Koldo, Tonby, Kristian, Heggelund, Lar, Izquierdo-Sanchez, Laura, Sumoy, Lauro, Lippert, Lena J., Terranova, Leonardo, Garbarino, Lucia, Téllez, Lui, Roade, Luisa, Ostadreza, Mahnoosh, Intxausti, Maider, Kogevinas, Manoli, Gutiérrez-Stampa, María A., Vehreschild, Maria J. G. T., Marquié, Marta, Castoldi, Massimo, Cecconi, Maurizio, Boada, Mercè, Seilmaier, Michael J., Mazzocco, Michela, Rodríguez-Gandía, Miguel, Ayo, Natale Imaz, Blay, Natalia, Martínez, Nilda, Cornely, Oliver A., Palmieri, Orazio, Tentorio, Paolo, Rodrigues, Pedro M., España, Pedro P., Hoffmann, Per, Bacher, Petra, Suwalski, Phillip, de Pablo, Raúl, Nieto, Rosa, Badalamenti, Salvatore, Ciesek, Sandra, Bombace, Sara, Wilfling, Sibylle, Brunak, Søren, Heilmann-Heimbach, Stefanie, Ripke, Stephan, Bahmer, Thoma, Landmesser, Ulf, Protzer, Ulrike, Rimoldi, Valeria, Skogen, Vegard, Andrade, Victor, Moreno, Victor, Poller, Wolfgang, Farre, Xavier, Wang, Xiaomin, Khodamoradi, Yascha, Karadeniz, Zehra, de Salazar, Adolfo, Palom, Adriana, Garcia-Fernandez, Alba-Estela, Blanco-Grau, Albert, Zanella, Alberto, Bandera, Alessandra, Nebel, Almut, Biondi, Andrea, Caballero-Garralda, Andrea, Gori, Andrea, Lind, Andrea, Fracanzani, Anna Ludovica, Peschuck, Anna, Pesenti, Antonio, de la Horra, Carmen, Milani, Chiara, Paccapelo, Cinzia, Angelini, Claudio, Cea, Cristina, Muñiz-Diaz, Eduardo, Sandoval, Elena, Calderón, Enrique J., Solligård, Erik, Aziz, Fátima, Martinelli-Boneschi, Filippo, Peyvandi, Flora, Blasi, Francesco, Medrano, Francisco J., Rodriguez-Frias, Francisco, Müller, Fredrik, Grasselli, Giacomo, Costantino, Giorgio, Cardamone, Giulia, Foti, Giuseppe, Matullo, Giuseppe, Kurihara, Hayato, Afset, Jan Egil, Damås, Jan Kristian, Ampuero, Javier, Martín, Javier, Erdmann, Jeanette, Bergan, Jona, Goerg, Siegfried, Ferrusquía-Acosta, Jose, Quero, Jose Hernández, Delgado, Juan, Guerrero, Juan M., Risnes, Kari, Bettini, Laura Rachele, Moreira, Leticia, Gustad, Lise Tuset, Santoro, Luigi, Scudeller, Luigia, Riveiro-Barciela, Mar, Schaefer, Marco, Carrabba, Maria, Valsecchi, Maria G., Hernandez-Tejero, María, Acosta-Herrera, Marialbert, D’Angiò, Mariella, Baldini, Marina, Cazzaniga, Marina, Ciccarelli, Michele, Bocciolone, Monica, Miozzo, Monica, Chueca, Natalia, Montano, Nicola, Faverio, Paola, Preatoni, Paoletta, Bonfanti, Paolo, Omodei, Paolo, Castro, Pedro, Ferrer, Ricard, Gualtierotti, Roberta, Gallego-Durán, Rocío, Morilla, Rubén, Haider, Sammra, Marsal, Sara, Aneli, Serena, Pelusi, Serena, Bosari, Silvano, Aliberti, Stefano, Dudman, Susanne, Zheng, Tenghao, Pumarola, Toma, Cejudo, Trinidad Gonzalez, Monzani, Valter, Friaza, Vicente, Peter, Wolfgang, Dopazo, Ximo, May, Sandra, Grimsrud, Marit M., Gudbjartsson, Daniel F., Stefansson, Kari, Sulem, Patrick, Sveinbjornsson, Gardar, Melsted, Pall, Norddahl, Gudmundur, Swerford Moore, Kristjan Helgi, Thorsteinsdottir, Unnur, Holm, Hilma, Alarcón-Riquelme, Marta E., Bernardo, David, Martínez-Bueno, Manuel, Rello, Silvia Rojo, Magi, Reedik, Milani, Lili, Metspalu, Andre, Laisk, Triin, Läll, Kristi, Lepamets, Maarja, Esko, Tõnu, Reimann, Ene, Naaber, Paul, Laane, Edward, Pesukova, Jaana, Peterson, Pärt, Kisand, Kai, Tabri, Jekaterina, Allos, Raili, Hensen, Kati, Starkopf, Joel, Ringmets, Inge, Tamm, Anu, Kallaste, Anne, Alavere, Helene, Metsalu, Kristjan, Puusepp, Mairo, Kristiansson, Kati, Koskelainen, Sami, Perola, Marku, Donner, Kati, Kivinen, Katja, Palotie, Aarno, Rivolta, Carlo, Bochud, Pierre-Yve, Bibert, Stéphanie, Boillat, Noémie, Nussle, Semira Gonseth, Albrich, Werner, Quinodoz, Mathieu, Kamdar, Dhryata, Suh, Noémie, Neofytos, Dionysio, Erard, Véronique, Voide, Cathy, Bochud, P. 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Mandalà, Marco, Zucchi, Patrizia, Giannattasio, Ferdinando, Coviello, Domenico A., Mussini, Cristina, Bosio, Giancarlo, Tavecchia, Luisa, Crotti, Lia, Rizzi, Marco, La Rovere, Maria Teresa, Sarzi-Braga, Simona, Bussotti, Maurizio, Ravaglia, Sabrina, Artuso, Rosangela, Perrella, Antonio, Romani, Davide, Bergomi, Paola, Catena, Emanuele, Vincenti, Antonella, Ferri, Claudio, Grassi, Davide, Pessina, Gloria, Tumbarello, Mario, Di Pietro, Massimo, Sabrina, Ravaglia, Luchi, Sauro, Barbieri, Chiara, Acquilini, Donatella, Andreucci, Elena, Paciosi, Francesco, Segala, Francesco Vladimiro, Tiseo, Giusy, Falcone, Marco, Lista, Mirjam, Poscente, Monica, De Vivo, Oreste, Petrocelli, Paola, Guarnaccia, Alessandra, Baroni, Silvia, Perticaroli, Valentina, Furini, Simone, Dei, Simona, Benetti, Elisa, Picchiotti, Nicola, Sanarico, Maurizio, Ceri, Stefano, Pinoli, Pietro, Raimondi, Francesco, Biscarini, Filippo, Stella, Alessandra, Bergomi, Mattia, Zguro, Kristina, Capitani, Katia, Tanfoni, Marco, 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Piacentini, Paolo, Desanctis, Elena, Cappelli, Silvia, Verzuri, Agnese, Anemoli, Valentina, Pancrazi, Alessandro, Lorubbio, Maria, Merlini, Esther, Miraglia, Federica Gaia, Venturelli, Sophie, Cossarizza, Andrea, Vergori, Alessandra, Gabrieli, Arianna, Riva, Agostino, Andretta, Francesca, Gatti, Francesca, Parisi, Saverio Giuseppe, Baratti, Stefano, Piscopo, Carmelo, Russo, Roberta, Andolfo, Immacolata, Iolascon, Achille, Carella, Massimo, Merla, Giuseppe, Squeo, Gabriella Maria, Raggi, Pamela, Marciano, Carmen, Perna, Rita, Bassetti, Matteo, Sanguinetti, Maurizio, Giorli, Alessia, Salerni, Lorenzo, Parravicini, Pierpaolo, Menatti, Elisabetta, Trotta, Tullio, Coiro, Gabriella, Lena, Fabio, Martinelli, Enrico, Mancarella, Sandro, Gabbi, Chiara, Maggiolo, Franco, Ripamonti, Diego, Bachetti, Tiziana, Suardi, Claudia, Parati, Gianfranco, Bottà, Giordano, Di Domenico, Paolo, Rancan, Ilaria, Bianchi, Francesco, Colombo, Riccardo, van Heel, David A., Hunt, Karen A., Trembath, Richard C., Huang, Qin Qin, Martin, Hilary C., Mason, Dan, Trivedi, Bhavi, Wright, John, Finer, Sarah, Griffiths, Christopher J., Akhtar, Shaheen, Anwar, Mohammad, Arciero, Elena, Ashraf, Samina, Breen, Gerome, Chung, Raymond, Curtis, Charles J., Chowdhury, Maharun, Colligan, Grainne, Deloukas, Pano, Durham, Ceri, Griffiths, Chri, Hurles, Matt, Hussain, Shapna, Islam, Kamrul, Khan, Ahsan, Khan, Amara, Lavery, Cath, Lee, Sang Hyuck, Lerner, Robin, Macarthur, Daniel, Maclaughlin, Bev, Martin, Hilary, Miah, Shefa, Newman, Bill, Safa, Nishat, Tahmasebi, Farah, Smith, Albert V., Boughton, Andrew P., Li, Kevin W., Lefaive, Jonathon, Annis, Aubrey, Jannes, Cinthia E., Krieger, Jose E., Pereira, Alexandre C., Velho, Mariliza, Marques, Emanuelle, Lima, Isabella Ramo, Tada, Mauricio Teruo, Valino, Karina, Mccarthy, Mark, Rosenberger, Carrie, Lee, Jong Eun, Chang, Diana, Hammer, Christian, Hunkapiller, Julie, Mahajan, Anubha, Pendergrass, Sarah, Sucheston-Campbell, Lara, Yaspan, Brian, Lee, Hyun Soo, Shin, Eunsoon, Jang, Hye Yoon, Kim, Sunmie, Kym, Sungmin, Kim, Yeon-Sook, Jeong, Hyeongseok, Kwon, Ki Tae, Kim, Shin-Woo, Kim, Jin Yong, Jang, Young Rock, Kim, Hyun ah, Lee, Ji Yeon, Lee, Jeong Eun, Lee, Shinwon, Choe, Kang-Won, Kang, Yu Min, Jee, Sun Ha, Jung, Keum Ji, Parikh, Victoria, Ashley, Euan, Wheeler, Matthew, Rivas, Manuel, Bustamante, Carlo, Pinksy, Benjamin, Febbo, Phillip, Farh, Kyle, Schroth, Gary P., Desouza, Franci, Dalton, Karen, Christle, Jeff, Deboever, Christopher, Szalma, Sándor, Rubinacci, Simone, Delaneau, Olivier, Gorzynski, John, de Jong, Hannah, Sutton, Shirley, Youlton, Nathan, Joshi, Ruchi, Jimenez-Morales, David, Hughes, Christopher, Amar, David, Ioannidis, Alex, Hershman, Steve, Kirillova, Anna, Seo, Kinya, Huang, Yong, Shoura, Massa, Hammond, Nathan, Watson, Nathaniel, Raja, Archana, Huang, Chunhong, Sahoo, Malaya, Wang, Hannah, Zhen, Jimmy, Rakitko, Alexander, Ilinsky, Valery, Yermakovich, Danat, Popov, Iaroslav, Chernitsov, Alexander, Kovalenko, Elena, Krasnenko, Anna, Plotnikov, Nikolay, Stetsenko, Ivan, Kim, Anna, Cirulli, Elizabeth T., Schiabor Barrett, Kelly M., Bolze, Alexandre, White, Simon, Washington, Nicole L., Lu, James T., Riffle, Stephen, Tanudjaja, Francisco, Wang, Xueqing, Ramirez, Jimmy M., Leonetti, Nicole, Sandoval, Efren, Neveux, Iva, Dabe, Shaun, Grzymski, Joseph J., Esteban Miñano, Juan Ignacio, Aguirre, Luis A., López-Collazo, Eduardo, de la Mata Pazos, Manuel, Cerrato, Luciano, Lozano-Rodríguez, Roberto, Avendaño-Ortiz, José, Arcos, Verónica Terrón, Montalbán-Hernández, Karla Marina, Quiroga, Jaime Valentín, Pascual-Iglesias, Alejandro, Maroun-Eid, Charbel, Martín-Quirós, Alejandro, Namkoong, Ho, Imoto, Seiya, Katayama, Kazuhiko, Fukunaga, Koichi, Kitagawa, Yuko, Sato, Toshiro, Hasegawa, Naoki, Kumanogoh, Atsushi, Kimura, Akinori, Ai, Masumi, Tokunaga, Katsushi, Kanai, Takanori, Miyano, Satoru, Ogawa, Seishi, Edahiro, Ryuya, Sonehara, Kyuto, Shirai, Yuya, Ishii, Makoto, Kabata, Hiroki, Masaki, Katsunori, Kamata, Hirofumi, Ikemura, Shinnosuke, Chubachi, Shotaro, Okamori, Satoshi, Terai, Hideki, Tanaka, Hiromu, Morita, Atsuho, Lee, Ho, Asakura, Takanori, Sasaki, Junichi, Morisaki, Hiroshi, Uwamino, Yoshifumi, Nanki, Kosaku, Mikami, Yohei, Tomono, Kazunori, Kato, Kazuto, Matsuda, Fumihiko, Takahashi, Meiko, Hizawa, Nobuyuki, Takeda, Yoshito, Hirata, Haruhiko, Shiroyama, Takayuki, Miyawaki, Satoru, Suzuki, Ken, Maeda, Yuichi, Nii, Takuro, Noda, Yoshimi, Niitsu, Takayuki, Adachi, Yuichi, Enomoto, Takatoshi, Amiya, Saori, Hara, Reina, Takahashi, Kunihiko, Anzai, Tatsuhiko, Hasegawa, Takanori, Ito, Satoshi, Koike, Ryuji, Endo, Akifumi, Uchimura, Yuji, Miyazaki, Yasunari, Honda, Takayuki, Tateishi, Tomoya, Tohda, Shuji, Ichimura, Naoya, Sonobe, Kazunari, Sassa, Chihiro, Nakajima, Jun, Nannya, Yasuhito, Omae, Yosuke, Takahashi, Kazuhisa, Harada, Norihiro, Hiki, Makoto, Takagi, Haruhi, Nakamura, Ai, Tagaya, Etsuko, Kawana, Masatoshi, Arimura, Ken, Ishiguro, Takashi, Takayanagi, Noboru, Isono, Taisuke, Takaku, Yotaro, Takano, Kenji, Anan, Ryusuke, Nakajima, Yukiko, Nakano, Yasushi, Nishio, Kazumi, Ueda, Soichiro, Hayashi, Reina, Tateno, Hiroki, Hase, Isano, Yoshida, Shuichi, Suzuki, Shoji, Mitamura, Keiko, Saito, Fumitake, Ueda, Tetsuya, Azuma, Masanori, Nagasaki, Tadao, Yasui, Yoshinori, Hasegawa, Yoshinori, Mutoh, Yoshikazu, Yoshiyama, Takashi, Shoko, Tomohisa, Kojima, Mitsuaki, Adachi, Tomohiro, Ishikawa, Motonao, Takahashi, Kenichiro, Watanabe, Kazuyoshi, Manabe, Tadashi, Ito, Fumimaro, Fukui, Takahiro, Funatsu, Yohei, Koh, Hidefumi, Hirai, Yoshihiro, Kawashima, Hidetoshi, Narita, Atsuya, Niwa, Kazuki, Sekikawa, Yoshiyuki, Saito, Fukuki, Yoshiya, Kazuhisa, Yoshihara, Tomoyuki, Suzuki, Yusuke, Nakayama, Sohei, Masuzawa, Keita, Nishi, Koichi, Nishitsuji, Masaru, Tani, Maiko, Inoue, Takashi, Hirano, Toshiyuki, Kobayashi, Keigo, Miyazawa, Naoki, Kimura, Yasuhiro, Sado, Reiko, Ogura, Takashi, Kitamura, Hideya, Murohashi, Kota, Nakachi, Ichiro, Baba, Rie, Arai, Daisuke, Fuke, Satoshi, Saito, Hiroshi, Kuwahara, Naota, Fujiwara, Akiko, Okada, Takenori, Baba, Tomoya, Noda, Junya, Mashimo, Shuko, Yagi, Kazuma, Shiomi, Tetsuya, Hashiguchi, Mizuha, Odani, Toshio, Mochimaru, Takao, Oyamada, Yoshitaka, Mori, Nobuaki, Izumi, Namiki, Nagata, Kaoru, Taki, Reiko, Murakami, Koji, Yamada, Mitsuhiro, Sugiura, Hisatoshi, Hayashi, Kentaro, Shimizu, Tetsuo, Gon, Yasuhiro, Fujitani, Shigeki, Tsuchida, Tomoya, Yoshida, Toru, Kagaya, Takashi, Kita, Toshiyuki, Sakagami, Satoru, Kimizuka, Yoshifumi, Kawana, Akihiko, Nakamura, Yoshihiko, Ishikura, Hiroyasu, Takata, Tohru, Kikuchi, Takahide, Taniyama, Daisuke, Nakamura, Morio, Kodama, Nobuhiro, Kaneyama, Yasunari, Maeda, Shunsuke, Nagasaki, Yoji, Okamoto, Masaki, Ishihara, Sayoko, Ito, Akihiro, Chihara, Yusuke, Takeuchi, Mayumi, Onoi, Keisuke, Hashimoto, Naozumi, Wakahara, Keiko, Ando, Akira, Masuda, Makoto, Wakabayashi, Aya, Watanabe, Hiroki, Sageshima, Hisako, Nakada, Taka-Aki, Abe, Ryuzo, Shimada, Tadanaga, Kawamura, Kodai, Ichikado, Kazuya, Nishiyama, Kenta, Yamasaki, Masaki, Hashimoto, Satoru, Kusaka, Yu, Ohba, Takehiko, Isogai, Susumu, Takada, Minoru, Kanda, Hidenori, Komase, Yuko, Sano, Fumiaki, Asano, Koichiro, Oguma, Tsuyoshi, Harada, Masahiro, Takahashi, Takeshi, Shibusawa, Takayuki, Abe, Shinji, Kono, Yuta, Togashi, Yuki, Izumo, Takehiro, Inomata, Minoru, Awano, Nobuyasu, Ogawa, Shinichi, Ogata, Tomouki, Ishihara, Shoichiro, Kanehiro, Arihiko, Ozaki, Shinji, Fuchimoto, Yasuko, Kitagawa, Yuichiro, Yoshida, Shozo, Ogura, Shinji, Nishiyama, Kei, Yoshida, Kousuke, Beppu, Satoru, Fukuyama, Satoru, Eriguchi, Yoshihiro, Yonekawa, Akiko, Inoue, Yoshiaki, Yamagata, Kunihiro, Chiba, Shigeru, Narumoto, Osamu, Nagai, Hideaki, Ooshima, Nobuharu, Motegi, Mitsuru, Sagara, Hironori, Tanaka, Akihiko, Ohta, Shin, Shibata, Yoko, Tanino, Yoshinori, Sato, Yuki, Yamada, Yuichiro, Hashino, Takuya, Shinoki, Masato, Iwagoe, Hajime, Imamura, Tomonori, Umeda, Akira, Shimada, Hisato, Endo, Mayu, Hayashi, Shinichi, Takahashi, Mai, Nakano, Shigefumi, Yatomi, Masakiyo, Maeno, Toshitaka, Ishii, Tomoo, Utsugi, Mitsuyoshi, Ono, Akihiro, Kanaoka, Kensuke, Ihara, Shoichi, Komuta, Kiyoshi, Boezen, Marike, Claringbould, Annique, Lopera, Esteban, Warmerdam, Robert, Vonk, Judith. M., van Blokland, Irene, Lanting, Pauline, Ori, Anil P. S., Obeidat, Ma’En, Hernández Cordero, Ana I., Sin, Don D., Bossé, Yohan, Joubert, Philippe, Hao, Ke, Nickle, David, Timens, Wim, van den Berge, Maarten, Feng, Yen-Chen Anne, Mercader, Josep, Weiss, Scott T., Karlson, Elizabeth W., Smoller, Jordan W., Murphy, Shawn N., Meigs, James B., Woolley, Ann E., Green, Robert C., Perez, Emma F., Zöllner, Sebastian, Wang, Jiongming, Beck, Andrew, Sloofman, Laura G., Ascolillo, Steven, Sebra, Robert P., Collins, Brett L., Levy, Te, Sealfon, Stuart C., Jordan, Daniel M., Thompson, Ryan C., Gettler, Kyle, Chaudhary, Kumardeep, Belbin, Gillian M., Preuss, Michael, Hoggart, Clive, Choi, Sam, Underwood, Slayton J., Salib, Irene, Britvan, Bari, Keller, Katherine, Tang, Lara, Peruggia, Michael, Hiester, Liam L., Niblo, Kristi, Aksentijevich, Alexandra, Labkowsky, Alexander, Karp, Avromie, Zlatopolsky, Menachem, Zyndorf, Marissa, Charney, Alexander W., Beckmann, Noam D., Schadt, Eric E., Abul-Husn, Noura S., Cho, Judy H., Itan, Yuval, Kenny, Eimear E., Loos, Ruth J. F., Nadkarni, Girish N., Do, Ron, O’Reilly, Paul, Huckins, Laura M., Ferreira, Manuel A. R., Abecasis, Goncalo R., Leader, Joseph B., Cantor, Michael N., Justice, Anne E., Carey, Dave J., Chittoor, Geetha, Josyula, Navya Shilpa, Kosmicki, Jack A., Horowitz, Julie E., Baras, Ari, Gass, Matthew C., Yadav, Ashish, Mirshahi, Tooraj, Jan Hottenga, Jouke, Bartels, Meike, de Geus, Eco J. C., Nivard, Michel G., Verma, Anurag, Ritchie, Marylyn D., Rader, Daniel, Li, Binglan, Verma, Shefali S., Lucas, Anastasia, Bradford, Yuki, Zara, Federico, Salpietro, Vincenzo, Scala, Marcello, Iacomino, Michele, Scudieri, Paolo, Bocciardi, Renata, Minetti, Carlo, Riva, Antonella, Vari, Maria Stella, Rahier, Jean-Françoi, Giorgio, Elisa, Carli, Diana, Louis, Edouad, Bulik, Cynthia M., Landén, Mikael, Brusco, Alfredo, Ferrero, Giovanni Battista, Madia, Francesca, Fundín, Bengt, Ismail, Said I., Saad, Chadi, Al-Sarraj, Yaser, Badji, Radja Messai, Al-Muftah, Wadha, Al Thani, Asma, Afifi, Nahla, Klovins, Jani, Rovite, Vita, Rescenko, Raimond, Peculis, Raiti, Ustinova, Monta, Zeberg, Hugo, Frithiof, Robert, Hultström, Michael, Lipcsey, Miklo, Johnson, Ruth, Geschwind, Daniel H., Freimer, Nelson, Butte, Manish J., Ding, Yi, Chiu, Alec, Chang, Timothy S., Boutros, Paul, Moutsianas, Louka, Caulfield, Mark J., Scott, Richard H., Walker, Susan, Stuckey, Alex, Odhams, Christopher A., Rhodes, Daniel, Fowler, Tom, Rendon, Augusto, Chan, Georgia, Arumugam, Prabhu, Karczewski, Konrad J., Wilson, Daniel J., Spencer, Chris A., Crook, Derrick W., Wyllie, David H., O’Connell, Anne Marie, Atkinson, Elizabeth G., Tsuo, Kristin, Baya, Nikola, Turley, Patrick, Gupta, Rahul, Walters, Raymond K., Palmer, Duncan S., Sarma, Gopal, Cheng, Nathan, Lu, Wenhan, Churchhouse, Claire, Goldstein, Jacqueline I., King, Daniel, Seed, Cotton, Daly, Mark J., Bryant, Sam, Satterstrom, F. Kyle, Band, Gavin, Earle, Sarah G., Lin, Shang-Kuan, Arning, Nicola, Armstrong, Jacob, Rudkin, Justine K., Callier, Shawneequa, Cusick, Caroline, Soranzo, Nicole, Zhao, Jing Hua, Danesh, John, Di Angelantonio, Emanuele, Butterworth, Adam S., Sun, Yan V., Huffman, Jennifer E., Cho, Kelly, O’Donnell, Christopher J., Tsao, Phil, Gaziano, J. Michael, Peloso, Gina, Ho, Yuk-Lam, Mian, Michael, Scaggiante, Federica, Chang, Xiao, Glessner, Joseph R., Hakonarson, Hakon, Mcguigan, Peter J., Prockter Moore, Luke Stephen, Vizcaychipi, Marcela Paola, Hall, Kathryn, Campbell, Andy, Nichol, Ailstair, Ward, Geraldine, Page, Valerie Joan, Semple, Malcolm G., Adeniji, Kayode, Agranoff, Daniel, Agwuh, Ken, Ail, Dhiraj, Aldera, Erin L., Alegria, Ana, Angus, Brian, Ashish, Abdul, Atkinson, Dougal, Bari, Shahedal, Barlow, Gavin, Barnass, Stella, Barrett, Nichola, Bassford, Christopher, Basude, Sneha, Baxter, David, Beadsworth, Michael, Bernatoniene, Jolanta, Berridge, John, Best, Nicola, Bothma, Pieter, Chadwick, David, Brittain-Long, Robin, Bulteel, Naomi, Burden, Tom, Burtenshaw, Andrew, Caruth, Vikki, Chambler, Duncan, Chee, Nigel, Child, Jenny, Chukkambotla, Srikanth, Clark, Tom, Collini, Paul, Cosgrove, Catherine, Cupitt, Jason, Cutino-Moguel, Maria-Teresa, Dark, Paul, Dawson, Chri, Dervisevic, Samir, Donnison, Phil, Douthwaite, Sam, Drummond, Andrew, Durand, Ingrid, Dushianthan, Ahilanadan, Dyer, Tristan, Evans, Cariad, Eziefula, Chi, Fegan, Christopher, Finn, Adam, Fullerton, Duncan, Garg, Sanjeev, Garg, Atul, Gkrania-Klotsas, Effrossyni, Godden, Jo, Goldsmith, Arthur, Graham, Clive, Hardy, Elaine, Hartshorn, Stuart, Harvey, Daniel, Havalda, Peter, Hawcutt, Daniel B., Hobrok, Maria, Hodgson, Luke, Hormis, Anil, Jacobs, Michael, Jain, Susan, Jennings, Paul, Kaliappan, Agilan, Kasipandian, Vidya, Kegg, Stephen, Kelsey, Michael, Kendall, Jason, Kerrison, Caroline, Kerslake, Ian, Koch, Oliver, Koduri, Gouri, Koshy, George, Laha, Shondipon, Laird, Steven, Larkin, Susan, Leiner, Tama, Lillie, Patrick, Limb, Jame, Linnett, Vanessa, Little, Jeff, Lyttle, Mark, Macmahon, Michael, Macnaughton, Emily, Mankregod, Ravish, Masson, Huw, Matovu, Elijah, Mccullough, Katherine, Mcewen, Ruth, Meda, Manjula, Mills, Gary H., Minton, Jane, Ward, Karl, Mirfenderesky, Mariyam, Mohandas, Kavya, Mok, Quen, Moon, Jame, Moore, Elinoor, Morgan, Patrick, Morris, Craig, Mortimore, Katherine, Moses, Samuel, Mpenge, Mbiye, Mulla, Rohinton, Murphy, Michael, Nagel, Megan, Nagarajan, Thapa, Nelson, Mark, O’Shea, Matthew K., Otahal, Igor, Ostermann, Marlie, Pais, Mark, Panchatsharam, Selva, Papakonstantinou, Danai, Paraiso, Hassan, Patel, Brij, Pattison, Natalie, Pepperell, Justin, Peters, Mark, Phull, Mandeep, Pintus, Stefania, Pooni, Jagtur Singh, Post, Frank, Price, David, Prout, Rachel, Rae, Nikola, Reschreiter, Henrik, Reynolds, Tim, Richardson, Neil, Roberts, Mark, Roberts, Devender, Rose, Alistair, Rousseau, Guy, Ryan, Brendan, Saluja, Taranprit, Shah, Aarti, Shanmuga, Prad, Sharma, Anil, Shawcross, Anna, Sizer, Jeremy, Shankar-Hari, Manu, Smith, Richard, Snelson, Catherine, Spittle, Nick, Staines, Nikki, Stambach, Tom, Stewart, Richard, Subudhi, Pradeep, Szakmany, Tama, Tatham, Kate, Thomas, Jo, Thompson, Chri, Thompson, Robert, Tridente, Ascanio, Tupper-Carey, Darell, Twagira, Mary, Ustianowski, Andrew, Vallotton, Nick, Vincent-Smith, Lisa, Visuvanathan, Shico, Vuylsteke, Alan, Waddy, Sam, Wake, Rachel, Walden, Andrew, Welters, Ingeborg, Whitehouse, Tony, Whittaker, Paul, Whittington, Ashley, Papineni, Padmasayee, Wijesinghe, Meme, Williams, Martin, Wilson, Lawrence, Cole, Sarah, Winchester, Stephen, Wiselka, Martin, Wolverson, Adam, Wooton, Daniel G., Workman, Andrew, Yates, Bryan, Young, Peter, Beale, Rupert, Bretherick, Andrew D., Clohisey, Sara, Fourman, Max Head, Furniss, Jame, Gountouna, Elvina, Grimes, Graeme, Haley, Chri, Harrison, David, Hayward, Caroline, Keating, Sean, Klaric, Lucija, Klenerman, Paul, Law, Andy, Meynert, Alison M., Millar, Jonathan, Pairo-Castineira, Erola, Parkinson, Nichola, Ponting, Chris P., Porteous, David J., Rawlik, Konrad, Richmond, Anne, Rowan, Kathy, Russell, Clark D., Shen, Xia, Shih, Barbara, Tenesa, Albert, Vitart, Veronique, Wang, Bo, Wilson, James F., Wu, Yang, Yang, Jian, Yang, Zhijian, Zechner, Marie, Zhai, Ranran, Zheng, Chenqing, Norman, Lisa, Pius, Riinu, Drake, Thomas M., Fairfield, Cameron J., Knight, Stephen R., Mclean, Kenneth A., Murphy, Derek, Shaw, Catherine A., Dalton, Jo, Girvan, Michelle, Saviciute, Egle, Roberts, Stephanie, Harrison, Janet, Marsh, Laura, Connor, Marie, Halpin, Sophie, Jackson, Clare, Gamble, Carrol, Leeming, Gary, Law, Andrew, Wham, Murray, Hendry, Ro, Scott-Brown, Jame, Begg, Colin, Hinds, Charle, Wai Ho, Antonia Ying, Horby, Peter W., Knight, Julian, Ling, Lowell, Maslove, David, Mcauley, Danny, Montgomery, Hugh, Nichol, Alistair, Openshaw, Peter J. M., Summers, Charlotte, Walsh, Timothy, Armstrong, Lisa, Bates, Hayley, Dooks, Emma, Farquhar, Fiona, Hairsine, Brigid, Mcparland, C., Packham, Sophie, Alldis, Zoe, Astin-Chamberlain, Raine, Bibi, Fatima, Biddle, Jack, Blow, Sarah, Bolton, Matthew, Borra, Catherine, Bowles, Ruth, Burton, Maudrian, Choudhury, Yasmin, Collier, David, Cox, Amber, Easthope, Amy, Ebano, Patrizia, Fotiadis, Stavro, Gurasashvili, Jana, Halls, Rosslyn, Hartridge, Pippa, Kallon, Delordson, Kassam, Jamila, Lancoma-Malcolm, Ivone, Matharu, Maninderpal, May, Peter, Mitchelmore, Oliver, Newman, Tabitha, Patel, Mital, Pheby, Jane, Pinzuti, Irene, Prime, Zoe, Prysyazhna, Oleksandra, Shiel, Julian, Taylor, Melanie, Tierney, Carey, Wood, Suzanne, Zak, Anne, Zongo, Olivier, Forsey, Miranda, Nicholson, Anne, Riches, Joanne, Vertue, Mark, Wasson, Christopher, Finn, Stephanie, Green, Jackie, Collins, Erin, King, Bernadette, Grauslyte, Lina, Hussain, Musarat, Pogreban, Tatiana, Rosaroso, Lace, Salciute, Erika, Franke, George, Wong, Joanna, George, Aparna, Akeroyd, Louise, Bano, Shereen, Bromley, Matt, Gurr, Lucy, Lawton, Tom, Morgan, Jame, Sellick, Kirsten, Warren, Deborah, Wilkinson, Brian, Mcgowan, Janet, Ledgard, Camilla, Stacey, Amelia, Pye, Kate, Bellwood, Ruth, Bentley, Michael, Loosley, Ronda, Mcguinness, Heather, Tench, Helen, Wolf-Roberts, Rebecca, Gibson, Sian, Lyle, Amanda, Mcneela, Fiona, Radhakrishnan, Jayachandran, Hughes, Alistair, Ali, Asifa, Brady, Megan, Dale, Sam, Dance, Annalisa, Gledhill, Lisa, Greig, Jill, Hanson, Kathryn, Holdroyd, Kelly, Home, Marie, Kelly, Diane, Kitson, Ro, Matapure, Lear, Melia, Deborah, Mellor, Samantha, Nortcliffe, Tonicha, Pinnell, Jez, Robinson, Matthew, Shaw, Lisa, Shaw, Ryan, Thomis, Lesley, Wilson, Alison, Wood, Tracy, Bayo, Lee-Ann, Merwaha, Ekta, Ishaq, Tahira, Hanley, Sarah, Antcliffe, David, Banach, Dorota, Brett, Stephen, Coghlan, Phoebe, Fernandez, Ziortza, Gordon, Anthony, Rojo, Roceld, Arias, Sonia Sousa, Templeton, Maie, Jha, Rajeev, Krishnamurthy, Vinodh, Lim, Lai, Bi, Rehana, Scholefield, Barney, Ashton, Lydia, Williams, Alison, Cheyne, Claire, Saunderson, Anne, Allan, Angela, Anderson, Felicity, Kaye, Callum, Liew, Jade, Medhora, Jasmine, Scott, Teresa, Trumper, Erin, Botello, Adriana, Polgarova, Petra, Stroud, Katerina, Meaney, Eoghan, Jones, Megan, Ng, Anthony, Agrawal, Shruti, Pathan, Nazima, White, Deborah, Daubney, Esther, Elston, Kay, Parker, Robert, Reddy, Amie, Turner-Bone, Ian, Wilding, Laura, Harding, Peter, Jacob, Reni, Jones, Cathy, Denmade, Craig, Croft, Maria, White, Ian, Lim, Li, Griffin, Denise, Muchenje, Nycola, Mupudzi, Mcdonald, Partridge, Richard, Conyngham, Jo-Anna, Thomas, Rachel, Wright, Mary, Corral, Maria Alvarez, Bastion, Victoria, Clarke, Daphene, David, Beena, Kent, Harriet, Lorusso, Rachel, Lubimbi, Gamu, Murdoch, Sophie, Penacerrada, Melchizedek, Thomas, Alastair, Valentine, Jennifer, Vochin, Ana, Wulandari, Retno, Djeugam, Brice, Dawson, Joy, Garrioch, Sweyn, Tolson, Melanie, Aldridge, Jonathan, de Almeida Martins, Laura Gome, Carungcong, Jaime, Beavis, Sarah, Dale, Katie, Gascoyne, Rachel, Hawes, Joanne, Pritchard, Kelly, Stevenson, Lesley, Whileman, Amanda, Cowley, Anne, Highgate, Judith, Crawley, Rikki, Crew, Abigail, Cunningham, Mishell, Daniels, Allison, Harrison, Laura, Hope, Susan, Inweregbu, Ken, Jones, Sian, Lancaster, Nicola, Matthews, Jamie, Nicholson, Alice, Wray, Gemma, Benham, Leonie, Bradshaw, Zena, Brown, Joanna, Caswell, Melanie, Melling, Sarah, Preston, Stephen, Slawson, Nicola, Stoddard, Emma, Warden, Scott, Combes, Edward, Joefield, Teishel, Monnery, Sonja, Beech, Valerie, Trotman, Sallyanne, Hopkins, Bridget, Scriven, Jame, Thrasyvoulou, Laura, Willis, Heather, Anderson, Susan, Birch, Janine, Collins, Emma, Hammerton, Kate, O’Leary, Ryan, Abernathy, Caroline, Foster, Louise, Gratrix, Andrew, Martinson, Vicky, Parkinson, Priyai, Stones, Elizabeth, Carbral-Ortega, Llucia, Kapoor, Ritoo, Loader, David, Castle, Karen, Brandwood, Craig, Smith, Lara, Clark, Richard, Birchall, Katie, Kolakaluri, Laurel, Baines, Deborah, Sukumaran, Anila, Mapfunde, Isheunesu, Meredith, Megan, Morris, Lucy, Ryan, Lucy, Clark, Amy, Sampson, Julia, Peters, Cecilia, Dent, Martin, Langley, Margaret, Ashraf, Saima, Wei, Shuying, Andrew, Angela, Chablani, Manish, Kirkby, Amy, Netherton, Kimberley, Bates, Michelle, Dasgin, Jo, Gill, Jaspret, Nilsson, Annette, Apetri, Elena, Basikolo, Cathrine, Blackledge, Bethan, Catlow, Laura, Charles, Bethan, Doonan, Reece, Harris, Jade, Harvey, Alice, Horner, Daniel, Knowles, Karen, Lee, Stephanie, Lomas, Diane, Lyons, Chloe, Marsden, Tracy, Mclaughlan, Danielle, Mcmorrow, Liam, Pendlebury, Jessica, Perez, Jane, Poulaka, Maria, Proudfoot, Nicola, Slaughter, Melanie, Slevin, Kathryn, Thomas, Vicky, Walker, Danielle, Michael, Angiy, Collis, Matthew, Clark, Martyn, Coulding, Martina, Jude, Edward, Mccormick, Jacqueline, Mercer, Oliver, Potla, Darsh, Rehman, Hafiz, Savill, Heather, Turner, Victoria, Davey, Miriam, Golden, David, Seaman, Rebecca, Hunt, Jodie, Dearden, Joy, Dobson, Emma, Mulcahy, Michelle, Munt, Sheila, O’Connor, Grainne, Philbin, Jennifer, Rishton, Chloe, Tully, Redmond, Winnard, Sarah, Cagova, Lenka, Fofano, Adama, Garner, Lucie, Holcombe, Helen, Mepham, Sue, Mitchell, Alice Michael, Mwaura, Lucy, Praman, K., Vuylsteke, Alain, Zamikula, Julie, Bercades, Georgia, Brealey, David, Hass, Ingrid, Maccallum, Niall, Martir, Glady, Raith, Eamon, Reyes, Anna, Smyth, Deborah, Taylor, Abigail, Hughes, Rachel Anne, Thomas, Helen, Rees, Alun, Duskova, Michaela, Phipps, Janet, Brooks, Suzanne, Edwards, Michelle, Alexander, Peter, Allen, Schvearn, Bradley-Potts, Joanne, Brantwood, Craig, Egan, Jasmine, Felton, Timothy, Padden, Grace, Ward, Luke, Moss, Stuart, Glasgow, Susannah, Beesley, Kate, Board, Sarah, Kubisz-Pudelko, Agnieszka, Lewis, Alison, Perry, Je, Pippard, Lucy, Wood, Di, Buckley, Clare, Brown, Alison, Gregory, Jane, O’Connell, Susan, Smith, Tim, Belagodu, Zakaula, Fuller, Bridget, Gherman, Anca, Olufuwa, Olumide, Paramsothy, Remi, Stuart, Carmel, Oakley, Naomi, Kamundi, Charlotte, Tyl, David, Collins, Katy, Silva, Pedro, Taylor, June, King, Laura, Coates, Charlotte, Crowley, Maria, Wakefield, Phillipa, Beadle, Jane, Johnson, Laura, Sargeant, Janet, Anderson, Madeleine, Jardine, Catherine, Williams, Dewi, Parris, Victoria, Quaid, Sheena, Watson, Ekaterina, Melville, Julie, Naisbitt, Jay, Joseph, Rosane, Lazo, Maria, Walton, Olivia, Neal, Alan, Hill, Michaela, Kannan, Thogulava, Wild, Laura, Allan, Elizabeth, Darlington, Kate, Davies, Ffyon, Easton, Jack, Kumar, Sumit, Lean, Richard, Menzies, Daniel, Pugh, Richard, Qiu, Xinyi, Davies, Llino, Williams, Hannah, Scanlon, Jeremy, Davies, Gwyneth, Mackay, Callum, Lewis, Joannne, Rees, Stephanie, Coetzee, Samantha, Gales, Alistair, Raj, Meena, Sell, Craig, Langton, Helen, Watters, Malcolm, Novis, Catherine, Arbane, Gill, Bociek, Aneta, Campos, Sara, Grau, Neu, Jones, Tim Owen, Lim, Rosario, Marotti, Martina, Whitton, Christopher, Barron, Anthony, Collins, Ciara, Kaul, Sundeep, Passmore, Heather, Prendergast, Claire, Reed, Anna, Rogers, Paula, Shokkar, Rajvinder, Woodruff, Meriel, Middleton, Hayley, Polgar, Oliver, Nolan, Claire, Thwaites, Vicky, Mahay, Kanta, Sri-Chandana, Chunda, Scherewode, Joslan, Stephenson, Lorraine, Marsh, Sarah, Bancroft, Hollie, Bellamy, Mary, Carmody, Margaret, Daglish, Jacqueline, Moore, Faye, Rhodes, Joanne, Sangombe, Mirriam, Kadiri, Salma, Ayers, Amanda, Harrison, Wendy, North, Julie, Cavazza, Anna, Cockrell, Maeve, Corcoran, Eleanor, Depante, Maria, Finney, Clare, Jerome, Ellen, Mcphail, Mark, Nayak, Monalisa, Noble, Harriet, O’Reilly, Kevin, Pappa, Evita, Saha, Rohit, Saha, Sian, Smith, John, Knighton, Abigail, Gill, Mandy, Paul, Paul, Ratnam, Valli, Shelton, Sarah, Wynter, Inez, Baptista, David, Crowe, Rebecca, Fernandes, Rita, Herdman-Grant, Rosaleen, Joseph, Anna, Loveridge, Adam, Mckenley, India, Morino, Eriko, Naranjo, Andre, Simms, Richard, Sollesta, Kathryn, Swain, Andrew, Venkatesh, Harish, Khera, Jacyntha, Fox, Jonathan, Barber, Russell, Hewitt, Claire, Hilldrith, Annette, Jackson-Lawrence, Karen, Shepardson, Sarah, Wills, Maryanne, Butler, Susan, Tavares, Silvia, Cunningham, Amy, Hindale, Julia, Arif, Sarwat, George, Linsha, Twiss, Sophie, Wright, David, Holland, Maureen, Keenan, Natalie, Lyons, Marc, Wassall, Helen, Marsh, Chri, Mahenthran, Mervin, Carter, Emma, Kong, Thoma, Adanini, Oluronke, Bhatia, Nikhil, Msiska, Maine, Mew, Louise, Mwaura, Esther, Williams, Felicity, Wren, Lynn, Sutherland, Sara-Beth, Battle, Ceri, Brinkworth, Elaine, Harford, Rachel, Murphy, Carl, Newey, Luke, Rees, Tabitha, Williams, Marie, Arnold, Sophie, Hardy, John, Houlden, Henry, Moncur, Eleanor, Tariq, Ambreen, Tucci, Arianna, Convery, Karen, Fottrell-Gould, Deirdre, Hudig, Lisa, Keshet-Price, Jocelyn, Randell, Georgina, Stammers, Katie, Abdelrazik, Marwa, Bakthavatsalam, Dhanalakshmi, Elhassan, Munzir, Ganesan, Arunkumar, Haldeos, Anne, Moreno-Cuesta, Jeronimo, Purohit, Dharam, Vincent, Rachel, Xavier, Kugan, Rohit, Kumar, Alasdair, Frater, Saleem, Malik, David, Carter, Jenkins, Samuel, Lamond, Zoe, Wall, Alanna, Reynolds, Jessica, Campbell, Helen, Thompsom, Maria, Dodds, Steve, Duffy, Stacey, Butcher, Deborah, O’Sullivan, Susie, Butterworth-Cowin, Nicola, Deacon, Bethan, Hibbert, Meg, Pothecary, Carla, Tetla, Dariusz, Woodford, Christopher, Durga, Latha, Kennard-Holden, Gareth, de Gordoa, Laura Ortiz-Ruiz, Peasgood, Emily, Phillips, Claire, Skinner, Denise, Gaylard, Jane, Mullan, Dee, Newman, Julie, Davies, Ellie, Roche, Lisa, Sathe, Sonia, Brimfield, Lutece, Daly, Zoe, Pogson, David, Rose, Steve, Collins, Amy, Khaliq, Waqa, Gude, Estefania Treu, Allen, Louise, Beranova, Eva, Crisp, Nikki, Deery, Joanne, Hazelton, Tracy, Knight, Alicia, Price, Carly, Tilbey, Sorrell, Turki, Salah, Turney, Sharon, Giles, Julian, Booth, Simon, Bell, Gillian, English, Katy, Katary, Amro, Wilcox, Louise, Campbell, Rachael, Clarke, Noreen, Whiteside, Jonathan, Mascarenhas, Mairi, Donaldson, Avril, Matheson, Joanna, Barrett, Fiona, O’Hara, Marianne, O’Keefe, Laura, Bradley, Clare, Collier, Dawn, Walker, Rachel, Maynard, Victoria, Patel, Tahera, Smith, Matthew, Kazi, Aayesha, Hartley, Janice, Dykes, Joseph, Hijazi, Muhammad, Keith, Sarah, Khan, Meherunnisa, Ryan-Smith, Janet, Springle, Philippa, Thomas, Jacqueline, Truman, Nick, Saad, Samuel, Coleman, Dabheoc, Fine, Christopher, Matt, Roseanna, Gay, Bethan, Dalziel, Jack, Ali, Syamlan, Goodchild, Drew, Harling, Rhiannan, Bhatterjee, Ravi, Goddard, Wendy, Davison, Chloe, Duberly, Stephen, Hargreaves, Jeanette, Bolton, Rachel, Verlander, Mark, Williams, Alexandra, Blackman, Helen, Creagh-Brown, Ben, Donlon, Sinead, Michalak-Glinska, Natalia, Mtuwa, Sheila, Pristopan, Veronika, Salberg, Armorel, Smith, Eleanor, Stone, Sarah, Piercy, Charle, Verula, Jerik, Burda, Dorota, Montaser, Rugia, Harden, Lesley, Mayangao, Irving, Marriott, Cheryl, Bradley, Paul, Harris, Celia, Cooper, Joshua, Finch, Cheryl, Liderth, Sarah, Quinn, Alison, Waddington, Natalia, Fidler, Katy, Tagliavini, Emma, Donnelly, Kevin, Abel, Lynn, Brett, Michael, Digby, Brian, Gemmell, Lisa, Hornsby, Jame, Macgoey, Patrick, O’Neil, Pauline, Price, Richard, Rodden, Natalie, Rooney, Kevin, Sundaram, Radha, Thomson, Nicola, Flanagan, Rebecca, Hughes, Gareth, Latham, Scott, Mckenna, Emma, Anderson, Jennifer, Hull, Robert, Rhead, Kat, Branney, Debbie, Frankham, Jordan, Pitts, Sally, White, Nigel, Cristiano, Daniele, Dormand, Natalie, Farzad, Zohreh, Gummadi, Mahitha, Liyanage, Kamal, Patel, Brijesh V., Salmi, Sara, Sloane, Geraldine, Varghese, Mathew, Zborowski, Anelise C., Bean, Sarah, Burt, Karen, Spivey, Michael, Eastgate-Jackson, Christine, Filipe, Helder, Martin, Daniel, Maharajh, Amitaa, Garcia, Sara Mingo, De Neef, Mark, Lynch, Ceri, Howe, Gwenllian Sera, Singh, Jayaprakash, Turner, Keri, Ellis, Hannah, Stroud, Natalie, Cherian, Shiney, Cutler, Sean, Heron, Anne Emma, Roynon-Reed, Anna, Williams, Gemma, Richards, Owen, Cheema, Yusuf, Ahmad, Norfaizan, Barker, Joann, Bauchmuller, Kri, Bird, Sarah, Cawthron, Kay, Harrington, Kate, Jackson, Yvonne, Kibutu, Faith, Lenagh, Becky, Masuko, Shamiso, Raithatha, Ajay, Wiles, Matthew, Willson, Jayne, Newell, Helen, Lye, Alison, Nwafor, Lorenza, Jarman, Claire, Rowland-Jones, Sarah, Foote, David, Cole, Joby, Thompson, Roger, Watson, Jame, Hesseldon, Lisa, Macharia, Irene, Chetam, Luke, Smith, Jacqui, Ford, Amber, Anderson, Samantha, Birchall, Kathryn, Housley, Kay, Walker, Sara, Milner, Leanne, Hanratty, Helena, Trower, Helen, Phillips, Patrick, Oxspring, Simon, Donne, Ben, Bevan, Emily, Martin, Jane, Trodd, Dawn, Watson, Geoff, Brown, Caroline Wrey, Bunni, Lara, Jennings, Claire, Latif, Monica, Marshall, Rebecca, Subramanian, Gayathri, Bandla, Nageswar, Gellamucho, Minnie, Davies, Michelle, Thompson, Christopher, Trim, Fiona, Eapen, Beena, Ahmed, Cecilia, Baines, Balvinder, Clamp, Sarah, Colley, Julie, Haq, Risna, Hayes, Anne, Hulme, Jonathan, Hussain, Samia, Joseph, Sibet, Kumar, Rita, Maqsood, Zahira, Purewal, Manjit, Chandler, Ben, Elliott, Kerry, Mallinson, Janine, Turnbull, Alison, Dent, Kathy, Horsley, Elizabeth, Akhtar, Muhmmad Nauman, Pearson, Sandra, Potoczna, Dorota, Spencer, Sue, Blakemore, Hayley, Borislavova, Borislava, Faulkner, Beverley, Gendall, Emma, Goff, Elizabeth, Hayes, Kati, Thomas, Matt, Worner, Ruth, Smith, Kerry, Stephens, Deanna, Delgado, Carlos Castro, Dawson, Deborah, Ding, Lijun, Durrant, Georgia, Ezeobu, Obiageri, Farnell-Ward, Sarah, Harrison, Abiola, Kanu, Rebecca, Leaver, Susannah, Maccacari, Elena, Manna, Soumendu, Saluzzio, Romina Peperman, Queiroz, Joana, Samakomva, Tinashe, Sicat, Christine, Texeira, Joana, Da Gloria, Edna Fernande, Lisboa, Ana, Rawlins, John, Mathew, Jisha, Kinch, Ashley, Hurt, William Jame, Shah, Nirav, Clark, Victoria, Thanasi, Maria, Yun, Nikki, Patel, Kamal, Crickmore, Vikki, Debreceni, Gabor, Wilkins, Joy, Nicol, Liz, Burn, Iona, Hambrook, Geraldine, Manso, Katarina, Penn, Ruth, Shanmugasundaram, Pradeep, Tebbutt, Julie, Thornton, Danielle, Rostron, Anthony, Roy, Alistair, Woods, Lindsey, Cornell, Sarah, Wakinshaw, Fiona, Rogerson, Kimberley, Jarmain, Jordan, Anderson, Peter, Archer, Katie, Austin, Karen, Davis, Caroline, Durie, Alison, Kelsall, Olivia, Thrush, Jessica, Vigurs, Charlie, Wood, Hannah-Louise, Tranter, Helen, Harrison, Alison, Cowley, Nichola, Mcalindon, Michael, Digby, Stephen, Low, Emma, Morgan, Aled, Cother, Naiara, Rankin, Tobia, Clayton, Sarah, Mccurdy, Alex, Allibone, Suzanne, Mary-Genetu, Roman, Patel, Amit, Mac, Ainhi, Murphy, Anthony, Mahjoob, Parisa, Nazari, Roonak, Worsley, Lucy, Fagan, Andrew, Mohamed Ali, Inthakab Ali, Beaumont, Karen, Blunt, Mark, Coton, Zoe, Curgenven, Hollie, Elsaadany, Mohamed, Fernandes, Kay, Ally, Sameena Mohamed, Rangarajan, Harini, Sarathy, Varun, Selvanayagam, Sivarupan, Vedage, Dave, White, Matthew, Fernandez-Roman, Jaime, Hamilton, David O., Johnson, Emily, Johnston, Brian, Martinez, Maria Lopez, Mulla, Suleman, Shaw, David, Waite, Alicia A. C., Waugh, Victoria, Welters, Ingeborg D., Williams, Karen, Bemand, Thoma, Black, Ethel, Rosa, Arnold Dela, Howle, Ryan, Jhanji, Shaman, Baikady, Ravishankar Rao, Tatham, Kate Colette, Thomas, Benjamin, Halkes, Matthew, Mercer, Pauline, Thornton, Lorraine, West, Joe, Baird, Tracy, Ruddy, Jim, Reece-Anthony, Rosie, Birt, Mark, Cowton, Amanda, Kay, Andrea, Kent, Melanie, Potts, Kathryn, Wilkinson, Ami, Naylor, Suzanne, Brown, Ellen, Clark, Michele, Purvis, Sarah, Cole, Jade, Davies, Rhy, Duffin, Donna, Hill, Helen, Player, Ben, Thomas, Emma, Williams, Angharad, Beith, Claire Marie, Black, Karen, Clements, Suzanne, Morrison, Alan, Strachan, Dominic, Taylor, Margaret, Clarkson, Michelle, D’Sylva, Stuart, Norman, Kathryn, Coventry, Tina, Fowler, Susan, Mcgregor, Amanda, Brady, Ailbhe, Chan, Rebekah, Mcivor, Shane, Prady, Helena, Whittle, Helen, Mathew, Bijoy, Clapham, Melanie, Harper, Rosemary, Poultney, Una, Rice, Polly, Mutch, Rachel, Baird, Yolanda, Butler, Aaron, Chadbourn, Indra, Folkes, Linda, Fox, Heather, Gardner, Amy, Gomez, Raquel, Hobden, Gillian, King, Kirsten, Margarson, Michael, Martindale, Tim, Meadows, Emma, Raynard, Dana, Thirlwall, Yvette, Helm, David, Margalef, Jordi, Greer, Sandra, Shuker, Karen, Smuts, Sara, Duffield, Joseph, Smith, Oliver, Mallon, Lewi, Claire, Watkin, Birkinshaw, Isobel, Carter, Joseph, Howard, Kate, Ingham, Joanne, Joy, Rosie, Pearson, Harriet, Roche, Samantha, Scott, Zoe, Knights, Ellen, Price, Alicia, Thomas, Alice, Thorpe, Chri, Abraheem, Azmerelda, Bamford, Peter, Cawley, Kathryn, Dunmore, Charlie, Faulkner, Maria, Girach, Rumanah, Jeffrey, Helen, Jones, Rhianna, London, Emily, Nagra, Imrun, Nasir, Farah, Sainsbury, Hannah, Smedley, Clare, Khade, Reena, Sundar, Ashok, Tsinaslanidis, George, Behan, Teresa, Burnett, Caroline, Hatton, Jonathan, Heeney, Elaine, Mitra, Atideb, Newton, Maria, Pollard, Rachel, Stead, Rachael, Birch, Jenny, Bough, Laura, Goodsell, Josie, Tutton, Rebecca, Williams, Patricia, Williams, Sarah, Winter-Goodwin, Barbara, Auld, Fiona, Donnachie, Joanne, Edmond, Ian, Prentice, Lynn, Runciman, Nikole, Salutous, Dario, Symon, Lesley, Todd, Anne, Turner, Patricia, Short, Abigail, Sweeney, Laura, Murdoch, Euan, Senaratne, Dhaneesha, Burns, Karen, Higham, Andrew, Anderson, Taya, Hawcutt, Dan, O’Malley, Laura, Rad, Laura, Rogers, Naomi, Saunderson, Paula, Allison, Kathryn Sian, Afolabi, Deborah, Whitbread, Jennifer, Jones, Dawn, Dore, Rachael, Lankester, Liana, Nikitas, Nikita, Wells, Colin, Stowe, Bethan, Spencer, Kayleigh, Cathcart, Susanne, Duffy, Katharine, Puxty, Alex, Puxty, Kathryn, Turner, Lynne, Ireland, Jane, Semple, Gary, Barry, Peter, Hilltout, Paula, Evitts, Jayne, Tyler, Amanda, Waldron, Joanne, Irvine, Val, Shelley, Benjamin, Akinkugbe, Olugbenga, Bamford, Alasdair, Beech, Emily, Belfield, Holly, Bell, Michael, Davies, Charlene, Jones, Gareth A. L., Mchugh, Tara, Meghari, Hamza, O’Neill, Lauran, Peters, Mark J., Ray, Samiran, Tomas, Ana Luisa, Gorman, Claire, Gupta, Abhinav, Timlick, Elizabeth, Brady, Rebecca, Bonner, Stephen, Hugill, Keith, Jones, Jessica, Liggett, Steven, Bashyal, Archana, Davidson, Neil, Hutton, Paula, Mckechnie, Stuart, Wilson, Jean, Flint, Neil, Rekha, Patel, Hales, Dawn, Cruz, Carina, Gopal, Shameer, Harris, Nichola, Lake, Victoria, Metherell, Stella, Radford, Elizabeth, Clement, Ian, Patel, Bijal, Gulati, A., Hays, Carole, Webster, K., Hudson, Anne, Webster, Andrea, Stephenson, Elaine, Mccormack, Louise, Slater, Victoria, Nixon, Rachel, Hanson, Helen, Fearby, Maggie, Kelly, Sinead, Bridgett, Victoria, Robinson, Philip, Almaden-Boyle, Christine, Austin, Pauline, Cabrelli, Louise, Cole, Stephen, Casey, Matt, Chapman, Susan, Whyte, Clare, Brayne, Adam, Fisher, Emma, Hunt, Jane, Jackson, Peter, Kaye, Duncan, Love, Nichola, Parkin, Juliet, Tuckey, Victoria, van Koutrik, Lynne, Carter, Sasha, Andrew, Benedict, Findlay, Louise, Adams, Katie, Bruce, Michelle, Connolly, Karen, Duncan, Tracy, T. -Michael, Helen, Lindergard, Gabriella, Hey, Samuel, Fox, Claire, Alfonso, Jordan, Durrans, Laura Jayne, Guerin, Jacinta, Hruska, Martin, Eltayeb, Ayaa, Lamb, Thoma, Hodgkiss, Tracey, Cooper, Lisa, Rothwell, Joanne, Dennis, Catherine, Mcgregor, Alastair, Srikaran, Sinduya, Sukha, Anisha, Davies, Kim, O’Brien, Linda, Omar, Zohra, Perkins, Emma, Lewis, Tracy, Sutherland, Isobel, Brooke, Hollie, Buckley, Sarah, Suarez, Jose Cebrian, Charlesworth, Ruth, Hansson, Karen, Norris, John, Poole, Alice, Rose, Alastair, Sandhu, Rajdeep, Sloan, Brendan, Smithson, Elizabeth, Thirumaran, Muthu, Wagstaff, Veronica, Metcalfe, Alexandra, Camsooksai, Julie, Humphrey, Charlotte, Jenkins, Sarah, Wadams, Beverley, Death, Yasmin, Adams, Colene, Agasou, Anita, Arden, Tracie, Bowes, Amy, Boyle, Pauline, Beekes, Mandy, Button, Heather, Capps, Nigel, Carnahan, Mandy, Carter, Anne, Childs, Danielle, Donaldson, Denise, Hard, Kelly, Hurford, Fran, Hussain, Yasmin, Javaid, Ayesha, Jones, Jame, Jose, Sanal, Leigh, Michael, Martin, Terry, Millward, Helen, Motherwell, Nichola, Rikunenko, Rachel, Stickley, Jo, Summers, Julie, Ting, Louise, Tivenan, Helen, Tonks, Louise, Wilcox, Rebecca, Bokhari, Maria, Lucas, Rachael, Mccormick, Wendy, Ritzema, Jenny, Sanderson, Amanda, Wild, Helen, Baxter, Nicola, Henderson, Steven, Kennedy-Hay, Sophie, Mcparland, Christopher, Rooney, Laura, Sim, Malcolm, Mccreath, Gordan, Brunton, Mark, Caterson, Je, Coles, Holly, Frise, Matthew, Rai, Sabi Gurung, Keating, Liza, Tilney, Emma, Bartley, Shauna, Bhuie, Parminder, Downes, Charlotte, Holding, Kathleen, Riches, Katie, Hilton, Mary, Hayman, Mel, Subramanian, Deepak, Daniel, Priya, Zitter, Letizia, Benyon, Sarah, Marriott, Suzie, Park, Linda, Keenan, Samantha, Gordon, Elizabeth, Quinn, Helen, Baines, Kizzy, Andrew, Gillian, Barclay, Lucy, Callaghan, Marie, Clark, Sarah, Hope, Dave, Marshall, Lucy, Mcculloch, Corrienne, Briton, Kate, Singleton, Jo, Birch, Sophie, Simpson, Kerry, Craig, Jayne, Demetriou, Carrie, Eckbad, Charlotte, Hierons, Sarah, Howie, Lucy, Mitchard, Sarah, Ramos, Lidia, Serrano-Ruiz, Alfredo, White, Katie, Kelly, Fiona, Amin, Vishal, Anastasescu, Elena, Anumakonda, Vikram, Karthik, Komala, Kausar, Rizwana, Reid, Karen, Smith, Jacqueline, Imeson-Wood, Janet, Bellini, Arianna, Bryant, Jade, Mayer, Anton, Pickard, Amy, Roe, Nichola, Sowter, Jason, Howlett, Alex, Criste, Kristine, Cusack, Rebecca, Golder, Kim, Golding, Hannah, Jones, Oliver, Leggett, Samantha, Male, Michelle, Marani, Martyna, Prager, Kirsty, Williams, Toran, Roberts, Belinda, Salmon, Karen, Gondo, Prisca, Hadebe, B., Kayani, Abdul, Masunda, Bridgett, Ahmed, Ashar, Morris, Anna, Jakkula, Sriniva, Long, Kate, Whiteley, Simon, Wilby, Elizabeth, Ogg, Bethan, Moultrie, Sam, Odam, M., Bewley, Jeremy, Garland, Zoe, Grimmer, Lisa, Gumbrill, Bethany, Johnson, Rebekah, Sweet, Katie, Webster, Denise, Efford, Georgia, Bennett, Sara, Goodwin, Emma, Jackson, Matthew, Kent, Alissa, Tibke, Clare, Woodyatt, Wiesia, Zaki, Ahmed, Daniel, Amelia, Finn, Joanne, Saha, Rajnish, Bremmer, Pamela, Allan, J., Geary, T., Houston, Gordon, Meikle, A., O’Brien, P., Bell, Dina, Boyle, Rosalind, Douglas, Katie, Glass, Lynn, Lee, Emma, Lennon, Liz, Rattray, Austin, Charnock, Rob, Mcfarland, Denise, Cosgrove, Denise, Attwood, Ben, Parsons, Penny, Carmody, Siobhain, Oblak, Metod, Popescu, Monica, Thankachen, Mini, Baruah, Rosie, Morris, Sheila, Ferguson, Susie, Shepherd, Amy, Altabaibeh, Abdelhakim, Alvaro, Ana, Gilbert, Kayleigh, Ma, Louise, Mostoles, Loreta, Parmar, Chetan, Simpson, Kathryn, Jetha, Champa, Booker, Lauren, Pratley, Anezka, Cosier, Tracey, Millen, Gemma, Schumacher, Natasha, Weston, Heather, Rand, Jame, Alex, Beatrice, Bach, Benjamin, Barclay, Wendy S., Bogaert, Debby, Chand, Meera, Cooke, Graham S., Docherty, Annemarie B., Dunning, Jake, da Silva Filipe, Ana, Fletcher, Tom, Green, Christoper A., Harrison, Ewen M., Hiscox, Julian A., Ijaz, Samreen, Khoo, Saye, Lim, Wei Shen, Mentzer, Alexander J., Merson, Laura, Noursadeghi, Mahdad, Moore, Shona C., Palmarini, Massimo, Paxton, William A., Pollakis, Georgio, Price, Nichola, Rambaut, Andrew, Robertson, David L., Sancho-Shimizu, Vanessa, Scott, Janet T., de Silva, Thushan, Sigfrid, Louise, Solomon, Tom, Sriskandan, Shiranee, Stuart, David, Tedder, Richard S., Thomson, Emma C., Roger Thompson, A. A., Thwaites, Ryan S., Turtle, Lance C. W., Gupta, Rishi K., Palmieri, Carlo, Swann, Olivia V., Zambon, Maria, Dumas, Marc-Emmanuel, Griffin, Julian L., Takats, Zoltan, Chechi, Kanta, Andrikopoulos, Petro, Osagie, Anthonia, Olanipekun, Michael, Liggi, Sonia, Lewis, Matthew R., Correia, Gonçalo dos Santo, Sands, Caroline J., Takis, Panteleimon, Maslen, Lynn, Greenhalf, William, Shaw, Victoria, Mcdonald, Sarah E., Keating, Seán, Ahmed, Katie A., Armstrong, Jane A., Ashworth, Milton, Asiimwe, Innocent G., Bakshi, Siddharth, Barlow, Samantha L., Booth, Laura, Brennan, Benjamin, Bullock, Katie, Catterall, Benjamin W. A., Clark, Jordan J., Clarke, Emily A., Cooper, Louise, Cox, Helen, Davis, Christopher, Dincarslan, Oslem, Dunn, Chri, Dyer, Philip, Elliott, Angela, Evans, Anthony, Finch, Lorna, Fisher, Lewis W. S., Foster, Terry, Garcia-Dorival, Isabel, Gunning, Philip, Hartley, Catherine, Jensen, Rebecca L., Jones, Christopher B., Jones, Trevor R., Khandaker, Shadia, King, Katharine, Kiy, Robyn T., Koukorava, Chrysa, Lake, Annette, Lant, Suzannah, Latawiec, Diane, Lavelle-Langham, Lara, Lefteri, Daniella, Lett, Lauren, Livoti, Lucia A., Mancini, Maria, Mcdonald, Sarah, Mcevoy, Laurence, Mclauchlan, John, Metelmann, Soeren, Miah, Nahida S., Middleton, Joanna, Mitchell, Joyce, Murphy, Ellen G., Penrice-Randal, Rebekah, Pilgrim, Jack, Prince, Tessa, Reynolds, Will, Ridley, P. Matthew, Sales, Debby, Shaw, Victoria E., Shears, Rebecca K., Small, Benjamin, Subramaniam, Krishanthi S., Szemiel, Agnieska, Taggart, Aislynn, Tanianis-Hughes, Jolanta, Thomas, Jordan, Trochu, Erwan, van Tonder, Libby, Wilcock, Eve, Zhang, J. Eunice, Flaherty, Lisa, Maziere, Nicole, Cass, Emily, Carracedo, Alejandra Doce, Carlucci, Nicola, Holmes, Anthony, Massey, Hannah, Murphy, Lee, Wrobel, Nicola, Mccafferty, Sarah, Morrice, Kirstie, Maclean, Alan, Armstrong, Ruth, Boz, Ceilia, Brown, Adam, Coutts, Audrey, Cullum, Louise, Day, Nicky, Donnelly, Lorna, Duncan, Esther, Fawkes, Angie, Finernan, Paul, Gilchrist, Tammy, Golightly, Ailsa, Hafezi, Katarzyna, Law, Dawn, Law, Rachel, Law, Sarah, Macgillivray, Louise, Mal, Hanning, Mcmaster, Ellie, Meikle, Jen, Oosthuyzen, Wilna, Paterson, Trevor, Stenhouse, Andrew, Swets, Maaike, Szoor-McElhinney, Helen, Taneski, Filip, Wackett, Tony, Ward, Mairi, Weaver, Jane, Coyle, Judy, Gallagher, Bernadette, Lidstone-Scott, Rebecca, Hamilton, Debbie, Schon, Katherine, Furlong, Anita, Biggs, Heather, Griffiths, Fiona, Andrews, Eleanor, Brickell, Kathy, Smyth, Michelle, Murphy, Lorna, Carson, Gail, Hardwick, Hayley, Donohue, Chloe, Pérez-Tur, Jordi [0000-0002-9111-1712], Martín, Javier [0000-0002-2202-0622], Institute for Molecular Medicine Finland [Helsinki] (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki-University of Helsinki, Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], Massachusetts General Hospital [Boston], A list of authors and their affiliations appears in the Supplementary Information, Helsingin yliopisto = Helsingfors universitet = University of Helsinki-Helsingin yliopisto = Helsingfors universitet = University of Helsinki, ANR-20-CO11-0001,AABIFNCOV,Bases génétiques et immunologiques des auto-anticorps contre les interférons de type I prédisposant aux formes sévères de COVID-19.(2020), ANR-20-COVI-0003,GENCOVID,Identification des défauts monogéniques de l'immunité responsables des formes sévères de COVID-19 chez les patients précédemment en bonne santé(2020), ANR-21-COVR-0039,GenMIS-C,Recherche des Déficits immunitaires innées monogéniques prédisposant au syndrome inflammatoire multisystémique chez l'enfant.(2021), UCL - SSS/IREC/GAEN - Pôle d'Hépato-gastro-entérologie, UCL - (MGD) Service de gastro-entérologie, Niemi, M, Karjalainen, J, Liao, R, Neale, B, Daly, M, Ganna, A, Pathak, G, Andrews, S, Kanai, M, Veerapen, K, Fernandez-Cadenas, I, Schulte, E, Striano, P, Marttila, M, Minica, C, Marouli, E, Karim, M, Wendt, F, Savage, J, Sloofman, L, Butler-Laporte, G, Kim, H, Kanoni, S, Okada, Y, Byun, J, Han, Y, Uddin, M, Smith, G, Willer, C, Buxbaum, J, Mehtonen, J, Finucane, H, Cordioli, M, Martin, A, Zhou, W, Pasaniuc, B, Julienne, H, Aschard, H, Shi, H, Yengo, L, Polimanti, R, Ghoussaini, M, Schwartzentruber, J, Dunham, I, Chwialkowska, K, Francescatto, M, Trankiem, A, Balaconis, M, Davis, L, Lee, S, Priest, J, Renieri, A, Sankaran, V, van Heel, D, Deelen, P, Richards, J, Nakanishi, T, Biesecker, L, Kerchberger, V, Baillie, J, Mari, F, Bernasconi, A, Baillie, S, Canakoglu, A, 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A., de Almeida Martins, L. G., Mclaughlan, D., Mcmorrow, L., Mccormick, J., Mitchell, A. M., Maccallum, N., Hughes, R. A., Jones, T. O., Mcphail, M., Mckenley, I., Sutherland, S. -B., de Gordoa, L. O. -R., Gude, E. T., Macgoey, P., Mckenna, E., Patel, B. V., Zborowski, A. C., Garcia, S. M., Howe, G. S., Heron, A. E., Mills, G. H., Brown, C. W., Akhtar, M. N., Delgado, C. C., Saluzzio, R. P., Da Gloria, E. F., Hurt, W. J., Wood, H. -L., Mcalindon, M., Mccurdy, A., Ali, I. A. M., Ally, S. M., Hamilton, D. O., Lopez Martinez, M., Waite, A. A. C., Welters, I. D., Rosa, A. D., Baikady, R. R., Tatham, K. C., Beith, C. M., Mcgregor, A., Mcivor, S., Allison, K. S., Jones, G. A. L., Mchugh, T., Peters, M. J., Tomas, A. L., Mckechnie, S., Mccormack, L., Michael, H. T., Durrans, L. J., Suarez, J. C., Death, Y., Mccormick, W., Mccreath, G., Rai, S. G., Mcculloch, C., Mcfarland, D., Barclay, W. S., Cooke, G. S., Docherty, A. B., Green, C. A., Harrison, E. M., Hiscox, J. A., Lim, W. S., Mentzer, A. J., Paxton, W. A., Robertson, D. L., Scott, J. T., Tedder, R. S., Thomson, E. C., Thwaites, R. S., Gupta, R. K., Swann, O. V., Dumas, M. -E., Griffin, J. L., Lewis, M. R., dos Santos Correia, G., Sands, C. J., Mcdonald, S. E., Ahmed, K. A., Armstrong, J. A., Asiimwe, I. G., Barlow, S. L., Catterall, B. W. A., Clark, J. J., Clarke, E. A., Fisher, L. W. S., Jensen, R. L., Jones, C. B., Jones, T. R., Kiy, R. T., Livoti, L. A., Mcdonald, S., Mcevoy, L., Mclauchlan, J., Miah, N. S., Moore, S. C., Murphy, E. G., Matthew Ridley, P., Shaw, V. E., Shears, R. K., Subramaniam, K. S., Eunice Zhang, J., Carracedo, A. D., Mccafferty, S., Turtle, L. C. W., Data Science Genetic Epidemiology Lab, Institute for Molecular Medicine Finland, HUS Helsinki and Uusimaa Hospital District, University of Helsinki, Research Programs Unit, Doctoral Programme in Population Health, Centre of Excellence in Complex Disease Genetics, Aarno Palotie / Principal Investigator, Genomics of Neurological and Neuropsychiatric Disorders, and University of Zurich
Subjects: Male, 45/43, Autoimmunity, Autoimmunity/genetics, Body Mass Index, COVID-19/genetics, COVID-19/virology, Critical Illness, Female, Genetic Loci/genetics, Genetic Predisposition to Disease, Genome-Wide Association Study, Geographic Mapping, Hospitalization, Host-Pathogen Interactions/genetics, Humans, Inflammation/complications, Information Dissemination, Multifactorial Inheritance, Racial Groups/genetics, SARS-CoV-2/pathogenicity, Smoking, environmental risk factors, Q1, 631/208, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Genetics, Genome-wide association studies, SARS-CoV-2, Viral infection, GWAS, Aetiology, Lung, QC, 0303 health sciences, HERITABILITY, 3. Good health, covid-19, Science & Technology - Other Topics, Identification (biology), Infection, Human, 631/208/205/2138, Settore BIO/11 - Biologia Molecolare, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Clinical Research, Biodefense, Genetics, GENOME-WIDE ASSOCIATION, Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk genetikk: 714 [VDP], METAANALYSIS, 1000 Multidisciplinary, [SDV.GEN]Life Sciences [q-bio]/Genetics, Science & Technology, Prevention, Racial Groups, Pneumonia, genetic architecture, Human genetics, Genetic Loci, genetic factors, 570 Life sciences, biology, 030217 neurology & neurosurgery, Medizin, Infektionsmedicin, Genome-wide association studies, Settore BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICA, Pandemic, 2.1 Biological and endogenous factors, pandemi, Multidisciplinary, article, Public Health, Global Health, Social Medicine and Epidemiology, Racial Group, 10124 Institute of Molecular Life Sciences, Host-Pathogen Interaction, Multidisciplinary Sciences, Infectious Diseases, Host-Pathogen Interactions, Critical Illne, COVID-19, GWAS, genetic factors, environmental risk factors, therapy, Infectious Medicine, Coronavirus disease 2019 (COVID-19), SUSCEPTIBILITY LOCI, General Science & Technology, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Computational biology, Biology, Vaccine Related, 692/699/255/2514, Environmental risk, Mendelian randomization, COVID-19 Host Genetics Initiative, QH426, 631/326/596/4130, 030304 developmental biology, Inflammation, therapy, SARS-CoV-2, Human Genome, COVID-19, Genetic architecture, Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi, Emerging Infectious Diseases, Good Health and Well Being, Viral infection, 3111 Biomedicine
Abstract: Niemi, Mari E. K. et al. 39 páginas, figuras y tablas. Contiene material suplementario., The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3-7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease.
Published: 2021
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12. Advances in understanding the pathogenesis of red cell membrane disorders

Author: Achille Iolascon, Roberta Russo, Immacolata Andolfo, Iolascon, A., Andolfo, I., and Russo, Roberta
Subjects: Hereditary elliptocytosis, Erythrocytes, Abnormal, Spherocytosis, Hereditary, Biology, Anemia, Hemolytic, Congenital, Hereditary spherocytosis, genetic heterogeneity, 03 medical and health sciences, 0302 clinical medicine, variable expressivity, medicine, Humans, Alleles, hereditary stomatocytosi, Overhydrated hereditary stomatocytosis, Erythrocyte Membrane, hereditary spherocytosi, Elliptocytosis, Hereditary, Membrane Proteins, Hematology, medicine.disease, Southeast Asian ovalocytosis, Cell biology, Red blood cell, medicine.anatomical_structure, Hereditary stomatocytosis, 030220 oncology & carcinogenesis, Dehydrated hereditary stomatocytosis, next-generation sequencing, Hereditary pyropoikilocytosis, 030215 immunology
Abstract: Hereditary erythrocyte membrane disorders are caused by mutations in genes encoding various transmembrane or cytoskeletal proteins of red blood cells. The main consequences of these genetic alterations are decreased cell deformability and shortened erythrocyte survival. Red blood cell membrane defects encompass a heterogeneous group of haemolytic anaemias caused by either (i) altered membrane structural organisation (hereditary spherocytosis, hereditary elliptocytosis, hereditary pyropoikilocytosis and Southeast Asian ovalocytosis) or (ii) altered membrane transport function (overhydrated hereditary stomatocytosis, dehydrated hereditary stomatocytosis or xerocytosis, familial pseudohyperkalaemia and cryohydrocytosis). Herein we provide a comprehensive review of the recent literature on the molecular genetics of erythrocyte membrane defects and their reported clinical consequences. We also describe the effect of low-expression genetic variants on the high inter- and intra-familial phenotype variability of erythrocyte structural defects.
Published: 2019
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13. Germline mutations and new copy number variants among 40 pediatric cancer patients suspected for genetic predisposition

Author: Sabrina Giglio, Gianluca De Rosa, Valentina Contestabile, Antonella Gambale, Lucia De Martino, Barbara Pasini, Lucia Quaglietta, Roberta Russo, Rita Genesio, Immacolata Andolfo, Piero Pignataro, Achille Iolascon, Mario Capasso, Rosanna Parasole, Gambale, A., Russo, Roberta, Andolfo, I., Quaglietta, L., De Rosa, G., Contestabile, Valentina, De Martino, L., Genesio, R., Pignataro, P., Giglio, S., Capasso, M., Parasole, R., Pasini, B., and Iolascon, A.
Subjects: cancer predisposition syndrome, Male, 0301 basic medicine, Oncology, medicine.medical_specialty, Adolescent, DNA Copy Number Variations, genotype-phenotype relationship, 030105 genetics & heredity, Germline, genetic testing, 03 medical and health sciences, Germline mutation, Neoplasms, Internal medicine, cancer predisposition syndromes, Gene duplication, Genetics, medicine, Genetic predisposition, Humans, Genetic Predisposition to Disease, Copy-number variation, Child, Alleles, Genetic Association Studies, Germ-Line Mutation, Genetics (clinical), Genetic testing, medicine.diagnostic_test, business.industry, Age Factors, Infant, Astrocytoma, Genomics, medicine.disease, Pediatric cancer, 030104 developmental biology, Child, Preschool, Female, business
Abstract: Cancer predisposition syndromes (CPS) result from germline pathogenic variants, and they are increasingly recognized in the etiology of many pediatric cancers. Herein, we report the genetic/genomic analysis of 40 pediatric patients enrolled from 2016 to 2018. Our diagnostic workflow was successful in 50% of screened cases. Overall, the proportion of CPS in our case series is 10.9% (20/184) of enrolled patients. Interestingly, 12.5% of patients achieved a conclusive diagnosis through the analysis of chromosomal imbalance. Indeed, we observed germline microdeletions/duplications of regions encompassing cancer-related genes in 50% of patients undergoing array-CGH: EIF3H duplication in a patient with infantile desmoplastic astrocytoma and low-grade Glioma; SLFN11 deletion, SOX4 duplication, and PARK2 partial deletion in three neuroblastoma patients; a PTPRD partial deletion in a child diagnosed with glioblastoma multiforme. Finally, we identified two cases due to DICER1 germline mutations.
Published: 2019
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14. The BMP-SMAD pathway mediates the impaired hepatic iron metabolism associated with the ERFE-A260S variant

Author: Francesco Manna, Roberta Marra, Gianluca De Rosa, Achille Iolascon, Immacolata Andolfo, Barbara Eleni Rosato, Roberta Russo, Antonella Gambale, Andolfo, Immacolata, Rosato, BARBARA ELENI, Marra, Roberta, De Rosa, G., Manna, F., Gambale, A., Iolascon, A., and Russo, Roberta
Subjects: Ineffective erythropoiesis, Adult, Male, medicine.medical_specialty, Iron Overload, Congenital dyserythropoietic anemia type II, Adolescent, Anemia, Bone Morphogenetic Protein 6, Peptide Hormones, Smad Proteins, SMAD, Biology, medicine.disease_cause, Severity of Illness Index, Cell Line, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Hepcidins, Hepcidin, Internal medicine, medicine, Humans, Blood Transfusion, Erythropoiesis, Child, Genetic Association Studies, Anemia, Dyserythropoietic, Congenital, fungi, food and beverages, Hematology, Erythroferrone, medicine.disease, Recombinant Proteins, Endocrinology, Liver, 030220 oncology & carcinogenesis, Bone Morphogenetic Proteins, Hepatic stellate cell, biology.protein, Female, 030215 immunology, Signal Transduction
Abstract: The erythroferrone (ERFE) is the erythroid regulator of hepatic iron metabolism by suppressing the expression of hepcidin. Congenital dyserythropoietic anemia type II (CDAII) is an inherited hyporegenerative anemia due to biallelic mutations in the SEC23B gene. Patients with CDAII exhibit marked clinical variability, even among individuals sharing the same pathogenic variants. The ERFE expression in CDAII is increased and related to abnormal erythropoiesis. We identified a recurrent low-frequency variant, A260S, in the ERFE gene in 12.5% of CDAII patients with a severe phenotype. We demonstrated that the ERFE-A260S variant leads to increased levels of ERFE, with subsequently marked impairment of iron regulation pathways at the hepatic level. Functional characterization of ERFE-A260S in the hepatic cell system demonstrated its modifier role in iron overload by impairing the BMP/SMAD pathway. We herein described for the first time an ERFE polymorphism as a genetic modifier variant. This was with a mild effect on disease expression, under a multifactorial-like model, in a condition of iron-loading anemia due to ineffective erythropoiesis.
Published: 2019

15. Diagnosis and management of congenital dyserythropoietic anemias

Author: Antonella Gambale, Immacolata Andolfo, Achille Iolascon, Roberta Russo, Gambale, Antonella, Iolascon, Achille, Andolfo, Immacolata, and Russo, Roberta
Subjects: Ineffective erythropoiesis, Pathology, medicine.medical_specialty, Iron Overload, Lineage (genetic), Anemia, differential diagnosi, medicine.disease_cause, Diagnosis, Differential, 03 medical and health sciences, 0302 clinical medicine, Bone Marrow, Molecular genetics, molecular genetic, medicine, follow up, Animals, Humans, Reticulocytopenia, patient management, Anemia, Dyserythropoietic, Congenital, business.industry, Disease Management, Hematology, medicine.disease, Inherited anemia, Patient management, ineffective erythropoiesi, 030220 oncology & carcinogenesis, Bone Marrow failure syndromes, Immunology, Differential diagnosis, business, 030215 immunology
Abstract: Congenital dyserythropoietic anemias (CDAs) are inherited disorders hallmarked by chronic hyporegenerative anemia, relative reticulocytopenia, hemolytic component and iron overload. They represent a subtype of the inherited bone marrow failure syndromes, characterized by impaired differentiation and proliferation of the erythroid lineage. Three classical types were defined by marrow morphology, even if the most recent classification recognized six different genetic types. The pathomechanisms of CDAs are different, but all seem to involve the regulation of DNA replication and cell division. CDAs are often misdiagnosed, since either morphological abnormalities or clinical features can be commonly identified in other clinically-related anemias. However, differential diagnosis is essential for guiding both follow up and management of the patients.
Published: 2016
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16. Label-Free Optical Marker for Red-Blood-Cell Phenotyping of Inherited Anemias

Author: Antonella Gambale, Alessia Bramanti, Vittorio Bianco, Martina Mugnano, Roberta Russo, Achille Iolascon, Pietro Ferraro, Francesco Merola, Lisa Miccio, Pasquale Memmolo, Immacolata Andolfo, Mugnano, Martina, Memmolo, Pasquale, Miccio, Lisa, Merola, Francesco, Bianco, Vittorio, Bramanti, Alessia, Gambale, Antonella, Russo, Roberta, Andolfo, Immacolata, Iolascon, Achille, and Ferraro, Pietro
Subjects: 0301 basic medicine, Pathology, medicine.medical_specialty, Erythrocytes, quantitative phase imaging, Anemia, Thalassemia, Disease, 01 natural sciences, Analytical Chemistry, 010309 optics, 03 medical and health sciences, 0103 physical sciences, medicine, label-free microscopy, Humans, Biomarkers, Phenotype, Optical Imaging, Label free, Chemistry, medicine.disease, Red blood cell, 030104 developmental biology, medicine.anatomical_structure, Blood disease, Differential diagnosis, anemia diagnosis
Abstract: The gold-standard methods for anemia diagnosis are complete blood counts and peripheral-smear observations. However, these do not allow for a complete differential diagnosis as that requires biochemical assays, which are label-dependent techniques. On the other hand, recent studies focus on label-free quantitative phase imaging (QPI) of blood samples to investigate blood diseases by using video-based morphological methods. However, when sick cells are very similar to healthy ones in terms of morphometric features, identification of a blood disease becomes challenging even with QPI. Here, we introduce a label-free optical marker (LOM) to detect red-blood-cell (RBC) phenotypes, demonstrating that a single set of all-optical parameters can clearly identify a signature directly related to an erythrocyte disease through modeling each RBC as a biological lens. We tested this novel biophotonic analysis by proving that several inherited anemias, such as iron-deficiency anemia, thalassemia, hereditary spherocytosis, and congenital dyserythropoietic anemia, can be identified and sorted, thus opening a novel route for blood diagnosis on a completely different concept based on LOMs.
Published: 2018
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17. Multi-gene panel testing improves diagnosis and management of patients with hereditary anemias

Author: Roberta Marra, Antonella Gambale, Roberta Russo, Sule Unal, Piero Pignataro, Gian Luca Forni, Barbara Eleni Rosato, Paola Caforio, Francesco Manna, Kottayam Radhakrishnan, Valeria Pinto, Achille Iolascon, Giovanna Tomaiuolo, Immacolata Andolfo, Russo, Roberta, Andolfo, Immacolata, Manna, Francesco, Gambale, Antonella, Marra, Roberta, Rosato, Barbara Eleni, Caforio, Paola, Pinto, Valeria, Pignataro, Piero, Radhakrishnan, Kottayam, Unal, Sule, Tomaiuolo, Giovanna, Forni, Gian Luca, and Iolascon, Achille
Subjects: Proband, Adult, Male, Pediatrics, medicine.medical_specialty, Adolescent, Anemia, medicine.disease_cause, Anemia, Hemolytic, Congenital, Hereditary spherocytosis, 03 medical and health sciences, Epilepsy, Young Adult, 0302 clinical medicine, hemic and lymphatic diseases, medicine, Humans, Genetic Testing, Diagnostic Errors, Child, Genetic Association Studies, Anemia, Dyserythropoietic, Congenital, Mutation, business.industry, Disease Management, Genetic Variation, High-Throughput Nucleotide Sequencing, Infant, Hematology, medicine.disease, 030220 oncology & carcinogenesis, Child, Preschool, Cohort, Female, business, Congenital dyserythropoietic anemia, Stomatocytosis, 030215 immunology
Abstract: Mutations in more than 70 genes cause hereditary anemias (HA), a highly heterogeneous group of rare/low frequency disorders in which we included: hyporegenerative anemias, as congenital dyserythropoietic anemia (CDA) and Diamond-Blackfan anemia; hemolytic anemias due to erythrocyte membrane defects, as hereditary spherocytosis and stomatocytosis; hemolytic anemias due to enzymatic defects. The study describes the diagnostic workflow for HA, based on the development of two consecutive versions of a targeted-NGS panel, including 34 and 71 genes, respectively. Seventy-four probands from 62 unrelated families were investigated. Our study includes the most comprehensive gene set for these anemias and the largest cohort of patients described so far. We obtained an overall diagnostic yield of 64.9%. Despite 54.2% of cases showed conclusive diagnosis fitting well to the clinical suspicion, the multi-gene analysis modified the original clinical diagnosis in 45.8% of patients (nonmatched phenotype-genotype). Of note, 81.8% of nonmatched patients were clinically suspected to suffer from CDA. Particularly, 45.5% of the probands originally classified as CDA exhibited a conclusive diagnosis of chronic anemia due to enzymatic defects, mainly due to mutations in PKLR gene. Interestingly, we also identified a syndromic CDA patient with mild anemia and epilepsy, showing a homozygous mutation in CAD gene, recently associated to early infantile epileptic encephalopathy-50 and CDA-like anemia. Finally, we described a patient showing marked iron overload due to the coinheritance of PIEZO1 and SEC23B mutations, demonstrating that the multi-gene approach is valuable not only for achieving a correct and definitive diagnosis, but also for guiding treatment.
Published: 2018

18. Epicardial adipose tissue: new parameter for cardiovascular risk assessment in high risk populations

Author: Domenico Russo, Roberta Russo, Biagio Di Iorio, Luca Di Lullo, Russo, Roberta, Di Iorio, Biagio, Di Lullo, Luca, and Russo, Domenico
Subjects: Nephrology, medicine.medical_specialty, Epicardial adipose tissue · Cardiovascular risk · Coronary artery disease · Chronic kidney disease · Coronary artery calcification, Population, Inflammation, 030204 cardiovascular system & hematology, Bioinformatics, Risk Assessment, Severity of Illness Index, Coronary artery disease, Pathogenesis, 03 medical and health sciences, Paracrine signalling, 0302 clinical medicine, Adipokines, Predictive Value of Tests, Risk Factors, Internal medicine, medicine, Animals, Humans, 030212 general & internal medicine, education, Adiposity, Kidney, education.field_of_study, business.industry, digestive, oral, and skin physiology, medicine.disease, Prognosis, Coronary arteries, medicine.anatomical_structure, Adipose Tissue, Cardiovascular Diseases, medicine.symptom, business, Pericardium, Signal Transduction
Abstract: Epicardial adipose tissue (EAT) is localized between the myocardial surface and visceral layer of the pericardium. It is a metabolically active organ that secretes several cytokines which modulate cardiovascular morphology and function. EAT may interact locally with coronary arteries through paracrine secretion mechanisms. Cytokines from peri-adventitial EAT may pass through the coronary wall by diffusion from the outside to the inside, interacting with cells. An additional potential mechanism by which EAT interacts locally with coronary arteries may be the vasocrine secretion.EAT may play a significant role as a modulator of cardiac functions. In physiologic conditions, EAT has biochemical cardio-protective properties, secreting anti-atherosclerosis substances; in metabolic disease states, EAT secretes bioactive molecules that may play an important role in the pathogenesis of coronary artery disease and cardiac arrhythmias by promoting atherosclerosis. EAT has been evaluated both in the general population and in metabolic disease states that are characterized by inflammation, such as cardiovascular diseases and chronic kidney disease.This review focuses on the current state of knowledge on EAT as a reliable new parameter for cardiovascular risk stratification in high risk populations.
Published: 2018

19. Simultaneous abdominal wall defect repair and Tenckhoff catheter placement in candidates for peritoneal dialysis

Author: Domenico Russo, Giuseppina Sannino, Maurizio Sodo, Tania Strazzullo, Giovanni Merola, Gennaro Argentino, Roberta Russo, Umberto Bracale, Sodo, Maurizio, Bracale, Umberto, Argentino, Gennaro, Merola, Giovanni, Russo, Roberta, Sannino, Giuseppina, Strazzullo, Tania, and Russo, Domenico
Subjects: Adult, Male, Nephrology, medicine.medical_specialty, Time Factors, Incisional hernia, medicine.medical_treatment, Peritoneal dialysis, Hernia, Inguinal, 030230 surgery, Kidney, Polypropylenes, 03 medical and health sciences, Catheters, Indwelling, 0302 clinical medicine, Internal medicine, medicine, Humans, Incisional Hernia, Contraindication, Herniorrhaphy, Aged, Aged, 80 and over, Peritoneal catheter, Catheter insertion, business.industry, Abdominal wall defect, Inguinal hernia, Equipment Design, Middle Aged, Surgical Mesh, medicine.disease, Surgery, Treatment Outcome, Surgical mesh, Italy, 030220 oncology & carcinogenesis, Female, Kidney Diseases, Original Article, Radiology, business, Hernia, Umbilical, Glomerular Filtration Rate
Abstract: Introduction The presence of pre-existing abdominal wall defect (AWD) could represent a potential contraindication for peritoneal dialysis (PD) treatment. We report the results of our 6-year experience involving simultaneous repair of pre-existing AWD and catheter insertion for PD. Methods Patients with estimated glomerular filtration rate (e-GFR) 7–10 ml/min attending a single nephrology clinic between January 2008 and December 2014 were evaluated. Simultaneous AWD repair and catheter placement was performed. For inguinal (IH) or umbilical hernia (UH), a prolene mesh repair technique was adopted. Except for one case of total anaesthesia, the surgical procedure was performed under either spinal or local anaesthesia. Ceftazidime alone or in association with quinolones was administered 1 h before surgery in a single dose. Patients were discharged 2 days after surgery, and returned to the clinic twice during the 1st week for peritoneum washing (first volume of peritoneal dialysis solution: 300 ml). From week 3, volume (2000 ml) and dwells were personalized according to the patient’s clinical condition; options were: incremental PD, standard PD, or continuous cycling PD. Surgical follow-up was planned at 1, 6, and 12 months. Results Peritoneal catheters were inserted in 170 patients. IH, UH and incisional hernia were found in 18, 2 and 1 patients, respectively. IH was bilateral in 4 patients; concomitant IH and UH occurred in 1 patient. There were no deaths, nor intra-operative complications apart from scrotal haematoma in 1 patient. Over a mean follow-up of 551 days (range 342–1274) no hernia recurrence was registered and the peritoneal catheter continued functioning without problems. Conclusions Simultaneous AWD repair and peritoneal catheter placement seems a reliable and safe surgical procedure that allows patients with AWD to benefit from PD treatment.
Published: 2015
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20. Next generation research and therapy in red blood cell diseases

Author: Immacolata Andolfo, Roberta Russo, Achille Iolascon, Russo, Roberta, Andolfo, Immacolata, and Iolascon, Achille
Subjects: 0301 basic medicine, medicine.medical_specialty, Biomedical Research, Erythrocytes, business.industry, Hematology, 03 medical and health sciences, Red blood cell, Glucosephosphate Dehydrogenase Deficiency, Editorial, 030104 developmental biology, medicine.anatomical_structure, Immunology, medicine, Animals, Humans, Medical genetics, Myocyte, Technology innovation, business
Abstract: Pathogenetic studies on red blood cell (RBC) diseases have always represented a powerful model for the study of medical genetics and for technology innovation in both diagnostics and research. This has mainly been due to the availability of these cells compared to others, such as neurons, myocytes
Published: 2016
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21. Neuronal hemoglobin affects dopaminergic cells' response to stress

Author: Paolo Ascenzi, Stefano Espinoza, Mauro Giacca, Margherita Francescatto, Roberta Russo, Daniela Cesselli, Lorena Zentilin, Francesca Persichetti, Marta Codrich, Giampiero Leanza, Stefano Gustincich, Silvia Zucchelli, Maria Bertuzzi, Antonio Paolo Beltrami, Codrich, M, Bertuzzi, M, Russo, R, Francescatto, M, Espinoza, S, Zentilin, L, Giacca, M, Cesselli, D, Beltrami, Ap, Ascenzi, Paolo, Zucchelli, S, Persichetti, F, Leanza, G, Gustincich, S., Marta, Codrich, Bertuzzi, Maria, Russo, Roberta, Francescatto, Margherita, Espinoza, Stefano, Zentilin, Lorena, Giacca, Mauro, Cesselli, Daniela, Beltrami, Antonio Paolo, Zucchelli, Silvia, Persichetti, Francesca, Leanza, Giampiero, and Stefano, Gustincich
Subjects: 0301 basic medicine, MULTIPLE SYSTEM ATROPHY, 1-Methyl-4-phenylpyridinium, Cancer Research, Mouse, ALPHA-SYNUCLEIN, Dopamine, Gene Expression, Epigenesis, Genetic, PARKINSONS-DISEASE, GENE-EXPRESSION, SH-SY5Y CELLS, COMPLEX-I, MICE, AUTOPHAGY, BRAINS, TRANSCRIPTION, Hemoglobins, chemistry.chemical_compound, 0302 clinical medicine, Settore BIO/13 - Biologia Applicata, Viral Vector, Parkinson's Disease, MPTP, Dopaminergic, Brain, Parkinson Disease, Cell biology, Substantia Nigra, Biochemistry, Original Article, Hemoglobin, Stress, Autophagy, Motor Learning, medicine.drug, Stre, Immunology, Substantia nigra, Biology, 03 medical and health sciences, Cellular and Molecular Neuroscience, Neurochemical, Rotenone, Dopaminergic Cell, medicine, Animals, Humans, Parkinson Disease, Secondary, Cell Biology, Dopaminergic Neurons, 030104 developmental biology, chemistry, 030217 neurology & neurosurgery, Homeostasis
Abstract: Hemoglobin (Hb) is the major protein in erythrocytes and carries oxygen (O2) throughout the body. Recently, Hb has been found synthesized in atypical sites, including the brain. Hb is highly expressed in A9 dopaminergic (DA) neurons of the substantia nigra (SN), whose selective degeneration leads to Parkinson’s disease (PD). Here we show that Hb confers DA cells’ susceptibility to 1-methyl-4-phenylpyridinium (MPP+) and rotenone, neurochemical cellular models of PD. The toxic property of Hb does not depend on O2 binding and is associated with insoluble aggregate formation in the nucleolus. Neurochemical stress induces epigenetic modifications, nucleolar alterations and autophagy inhibition that depend on Hb expression. When adeno-associated viruses carrying α- and β-chains of Hb are stereotaxically injected into mouse SN, Hb forms aggregates and causes motor learning impairment. These results position Hb as a potential player in DA cells’ homeostasis and dysfunction in PD.
Published: 2017

22. Kinome expression profiling of human neuroblastoma tumors identifies potential drug targets for ultra highrisk patients

Author: Maddalena Raia, Giampietro Viola, Lucia Pezone, Marianna Avitabile, Matthias Fischer, Fiorina Casale, Flora Cimmino, Roberta Russo, Jan Koster, Concetta Langella, Mario Capasso, Achille Iolascon, Francesco Manna, CCA - Cancer biology and immunology, Oncogenomics, Cancer Center Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, Russo, Roberta, Cimmino, Flora, Pezone, Lucia, Manna, Francesco, Avitabile, Marianna, Langella, Concetta, Koster, Jan, Casale, Fiorina, Raia, Maddalena, Viola, Giampietro, Fischer, Matthia, Iolascon, Achille, and Capasso, Mario
Subjects: 0301 basic medicine, Oncology, Enzymologic, Cancer Research, Antineoplastic Agents, Cell Cycle, Cell Line, Tumor, Cell Survival, Enzyme Inhibitors, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, HSP90 Heat-Shock Proteins, Histone Deacetylase Inhibitors, Humans, Macrolides, Molecular Targeted Therapy, Neuroblastoma, Phosphotransferases, Bioinformatics, Antineoplastic Agent, chemistry.chemical_compound, 0302 clinical medicine, Histone Deacetylase Inhibitor, Enzyme Inhibitor, Medicine, Kinome, Tumor, Standard treatment, Phosphotransferase, General Medicine, Cell cycle, Radicicol, 030220 oncology & carcinogenesis, Macrolide, Human, medicine.medical_specialty, Cell Line, 03 medical and health sciences, Internal medicine, Survival rate, Neoplastic, business.industry, Gene signature, medicine.disease, Gene expression profiling, HSP90 Heat-Shock Protein, 030104 developmental biology, chemistry, Gene Expression Regulation, business
Abstract: Neuroblastoma (NBL) accounts for >7% of malignancies in patients younger than 15 years. Low- and intermediate-risk patients exhibit excellent or good prognosis after treatment, whereas for high-risk (HR) patients, the estimated 5-year survival rates is still
Published: 2017

23. Multiple clinical forms of dehydrated hereditary stomatocytosis arise from mutations in PIEZO1

Author: Maria D'Armiento, Lucia De Franceschi, Seth L. Alper, Boris E. Shmukler, Stanley L. Schrier, David H. Vandorpe, Annalisa Vetro, Maria Rosaria Esposito, Bertil Glader, Achille Iolascon, Orsetta Zuffardi, Jean Delaunay, Donatella Montanaro, Carla Auriemma, Gordon W. Stewart, Immacolata Andolfo, Ivan Limongelli, Roberta Russo, Carlo Brugnara, Luigia De Falco, Rupa Narayan, Fara Vallefuoco, Andolfo, I, Alper, Sl, De Franceschi, L, Auriemma, C, Russo, Roberta, De Falco, L, Vallefuoco, F, Esposito, Mr, Vandorpe, Dh, Shmukler, Be, Narayan, R, Montanaro, D, D'Armiento, Maria, Vetro, A, Limongelli, I, Zuffardi, O, Glader, Be, Schrier, Sl, Brugnara, C, Stewart, Gw, Delaunay, J, and Iolascon, Achille
Subjects: Adult, Hemolytic anemia, Hydrops Fetalis, Molecular Sequence Data, Immunology, Mice, Transgenic, Anemia, Hemolytic, Congenital, Transfection, medicine.disease_cause, Models, Biological, Biochemistry, Ion Channels, Mice, Xenopus laevis, MISSENSE MUTATION, medicine, Animals, Humans, Missense mutation, HEMOLYTIC ANEMIA, Amino Acid Sequence, Genetics, Mutation, Sequence Homology, Amino Acid, business.industry, PIEZO1, Gene Expression Regulation, Developmental, Cell Biology, Hematology, Embryo, Mammalian, medicine.disease, Molecular biology, Pedigree, medicine.anatomical_structure, stomatocytosis, Dehydrated hereditary stomatocytosis, Female, Bone marrow, business, Cation transport, Stomatocytosis
Abstract: Autosomal dominant dehydrated hereditary stomatocytosis (DHSt) usually presents as a compensated hemolytic anemia with macrocytosis and abnormally shaped red blood cells (RBCs). DHSt is part of a pleiotropic syndrome that may also exhibit pseudohyperkalemia and perinatal edema. We identified PIEZO1 as the disease gene for pleiotropic DHSt in a large kindred by exome sequencing analysis within the previously mapped 16q23-q24 interval. In 26 affected individuals among 7 multigenerational DHSt families with the pleiotropic syndrome, 11 heterozygous PIEZO1 missense mutations cosegregated with disease. PIEZO1 is expressed in the plasma membranes of RBCs and its messenger RNA, and protein levels increase during in vitro erythroid differentiation of CD34(+) cells. PIEZO1 is also expressed in liver and bone marrow during human and mouse development. We suggest for the first time a correlation between a PIEZO1 mutation and perinatal edema. DHSt patient red cells with the R2456H mutation exhibit increased ion-channel activity. Functional studies of PIEZO1 mutant R2488Q expressed in Xenopus oocytes demonstrated changes in ion-channel activity consistent with the altered cation content of DHSt patient red cells. Our findings provide direct evidence that R2456H and R2488Q mutations in PIEZO1 alter mechanosensitive channel regulation, leading to increased cation transport in erythroid cells.
Published: 2013
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24. Hypomorphic mutations of SEC23B gene account for mild phenotypes of congenital dyserythropoietic anemia type II

Author: Elizabeth Yang, Concetta Langella, Francesco Vitiello, Roberta Russo, Achille Iolascon, Fara Vallefuoco, Antonella Gambale, Torben Ek, Maria Rosaria Esposito, Russo, Roberta, Langella, C, Esposito, Mr, Gambale, A, Vitiello, F, Vallefuoco, F, Ek, T, Yang, E, and Iolascon, Achille
Subjects: Adult, Male, CDA II, Congenital dyserythropoietic anemia type II, Genotype, Nonsense mutation, Vesicular Transport Proteins, Biology, Compound heterozygosity, medicine.disease_cause, Article, Exon, medicine, Humans, Amino Acid Sequence, Child, Molecular Biology, Gene, Anemia, Dyserythropoietic, Congenital, Genetics, Mutation, Polymorphism, Genetic, Base Sequence, Genotype–phenotype correlation, Hypomorphic mutations, Cell Biology, Hematology, Exons, medicine.disease, Phenotype, Introns, Pedigree, Molecular Medicine, Female, RNA Splice Sites, SEC23B
Abstract: Congenital dyserythropoietic anemia type II, a recessive disorder of erythroid differentiation, is due to mutations in SEC23B, a component of the core trafficking machinery COPII. In no case homozygosity or compound heterozygosity for nonsense mutation(s) was found. This study represents the first description of molecular mechanisms underlying SEC23B hypomorphic genotypes by the analysis of five novel mutations. Our findings suggest that reduction of SEC23B gene expression is not associated with CDA II severe clinical presentation; conversely, the combination of a hypomorphic allele with one functionally altered results in more severe phenotypes. We propose a mechanism of compensation SEC23A-mediated which justifies these observations.
Published: 2013

25. New insights on hereditary erythrocyte membrane defects

Author: Achille Iolascon, Immacolata Andolfo, Antonella Gambale, Roberta Russo, Andolfo, Immacolata, Russo, Roberta, Gambale, Antonella, and Iolascon, Achille
Subjects: Cell Membrane Permeability, Membrane permeability, Hydrops Fetalis, Spherocytosis, Review Article, Spherocytosis, Hereditary, Biology, Anemia, Hemolytic, Congenital, 03 medical and health sciences, 0302 clinical medicine, medicine, Missense mutation, Humans, Spectrin, Familial pseudohyperkalemia, Ion channel, Genetics, Erythrocyte Membrane, Hematology, medicine.disease, Red blood cell, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Dehydrated hereditary stomatocytosis, Hyperkalemia, 030215 immunology
Abstract: After the first proposed model of the red blood cell membrane skeleton 36 years ago, several additional proteins have been discovered during the intervening years, and their relationship with the pathogenesis of the related disorders have been somewhat defined. The knowledge of erythrocyte membrane structure is important because it represents the model for spectrin-based membrane skeletons in all cells and because defects in its structure underlie multiple hemolytic anemias. This review summarizes the main features of erythrocyte membrane disorders, dividing them into structural and altered permeability defects, focusing particularly on the most recent advances. New proteins involved in alterations of the red blood cell membrane permeability were recently described. The mechanoreceptor PIEZO1 is the largest ion channel identified to date, the fundamental regulator of erythrocyte volume homeostasis. Missense, gain-of-function mutations in the PIEZO1 gene have been identified in several families as causative of dehydrated hereditary stomatocytosis or xerocytosis. Similarly, the KCNN4 gene, codifying the so called Gardos channel, has been recently identified as a second causative gene of hereditary xerocytosis. Finally, ABCB6 missense mutations were identified in different pedigrees of familial pseudohyperkalemia. New genomic technologies have improved the quality and reduced the time of diagnosis of these diseases. Moreover, they are essential for the identification of the new causative genes. However, many questions remain to solve, and are currently objects of intensive studies.
Published: 2016

26. Protease inhibitors-based therapy induces acquired spherocytic-like anaemia and ineffective erythropoiesis in chronic hepatitis C virus patients

Author: Sara Piovesan, Roberta Russo, Pierluigi Toniutto, Achille Iolascon, Lucia De Franceschi, Francesco Michelangelo Turrini, Francesca Lupo, D. Ieluzzi, Alessandro Matte, Angela Siciliano, Alfredo Alberti, Elena Raffetti, Francesco Donato, Denis Dissegna, Valeria Zuliani, Giovanna Fattovich, Lupo, Francesca, Russo, Roberta, Iolascon, Achille, Ieluzzi, Donatella, Siciliano, Angela, Toniutto, Pierluigi, Matté, Alessandro, Piovesan, Sara, Raffetti, Elena, Turrini, Francesco, Dissegna, Deni, Donato, Francesco, Alberti, Alfredo, Zuliani, Valeria, Fattovich, Giovanna, and De Franceschi, Lucia
Subjects: 0301 basic medicine, Ineffective erythropoiesis, chronic hepatitis C, first-generation protease inhibitors, microparticles, spherocytic-like anaemia, Adult, Aged, Antiviral Agents, Drug Monitoring, Drug Therapy, Combination, Erythrocyte Indices, Erythrocyte Membrane, Erythropoiesis, Female, Humans, Interferon-alpha, Male, Middle Aged, Polymorphism, Single Nucleotide, Proline, Protease Inhibitors, Pyrophosphatases, Ribavirin, Treatment Outcome, Anemia, Hepatitis C, Chronic, Oligopeptides, Hepatology, medicine.disease_cause, Telaprevir, first-generation protease inhibitor, chemistry.chemical_compound, 0302 clinical medicine, hemic and lymphatic diseases, Chronic, Single Nucleotide, Hepatitis C, microparticle, Combination, ITPA, medicine.drug, Biology, 03 medical and health sciences, Drug Therapy, Boceprevir, medicine, Polymorphism, Red Cell, medicine.disease, 030104 developmental biology, chemistry, Immunology, 030215 immunology
Abstract: Background & Aims The addition of protease inhibitors, boceprevir (BOC) or telaprevir (TRV), to peg-interferon and ribavirin (PR) increases the incidence of anaemia in patients with chronic hepatitis C virus (HCV) infection. Although genetic variants in inosine triphosphatase (ITPA) gene have been linked to the haemolytic anaemia induced by PR, the mechanism sustaining severe anaemia during triple therapy is still unknown. This study aims to elucidate the molecular mechanisms underlying anaemia in chronic HCV patients with combined therapy. Methods We studied 59 patients with chronic HCV genotype-1: 29 treated with TRV/PR and 30 with BOC/PR. We evaluated biochemical and haematological parameters, red cell index at baseline, 4, 12, 16 and 24 weeks of treatment; in a subgroup, we performed functional studies: osmotic fragility, red cell membrane protein separation, mass spectrometry analysis, quantification of erythroid microparticles release. IL28B and ITPA polymorphisms were also evaluated. Results We found early acute normochromic normocytic haemolytic anaemia (4–8 weeks) followed by a late macrocytic hypo-regenerative anaemia with inappropriate low reticulocyte count (12–24 weeks). Studies on red cells revealed: (i) presence of spherocytes; (ii) increased osmotic fragility; (iii) abnormalities in red cell membrane protein composition; (iv) reduced membrane-cytoskeleton stability; (v) increased release of erythroid microparticles. ITPA polymorphisms impacted only the early phase of anaemia. Conclusions The bimodal pattern of anaemia in chronic HCV patients on triple therapy might be because of acquired spherocytic-like anaemia in the early phase, followed by hyporegenerative anaemia, most likely related to the combined effects of PR and TRV or BOC on erythropoiesis.
Published: 2016

27. A Dyserythropoietic Anemia Associated with Homozygous Hb Plasencia [α125(H8)Leu→Arg (α2)] (HBA2:c.377T>G), A Variant with an Unstable α Chain

Author: Hermann Heimpel, Odile Fenneteau, Jean Delaunay, Achille Iolascon, Loïc Garçon, Madeleine Fénéant-Thibault, Roberta Russo, Maria Rosaria Esposito, Serge Pissard, Garçon, L, Iolascon, Achille, Pissard, S, Esposito, Mr, Russo, Roberta, Fenneteau, O, Fénéant Thibault, M, Heimpel, H, and Delaunay, J.
Subjects: Adult, Anemia, Hemoglobins, Abnormal, Thalassemia, DNA Mutational Analysis, Clinical Biochemistry, Mutation, Missense, Biology, alpha-Globins, hemic and lymphatic diseases, medicine, Humans, Missense mutation, Genetics (clinical), Anemia, Dyserythropoietic, Congenital, Base Sequence, Microcytosis, Biochemistry (medical), Erythroid Hyperplasia, Hematology, medicine.disease, anemia, Molecular biology, CDA, Immunology, Female, Hemoglobin, Congenital dyserythropoietic anemia, dyserythropoiesi, Dyserythropoietic anemia
Abstract: A female patient of Portuguese origin, who was born to consanguineous parents, presented with moderate anemia, mild jaundice and splenomegaly. Bone marrow aspiration showed an erythroid hyperplasia and binucleate erythroblasts, evoking a congenital dyserythropoietic anemia, type II (CDA II). Although microcytosis cast some doubt on the diagnosis, investigation was pursued along this line. The CDA II was finally ruled out as underglycosylation of band 3, remnants of endoplasmic reticulum cisternae and mutations in the SEC23B gene were all missing. On the other hand, analysis of the α-globin genes showed a base substitution at codon 125 (CTG→CGG) of the α2-globin gene, ascertaining a homozygosity for Hb Plasencia (HBA2:c.377T>G). This variant has an unstable α chain. In the absence of a thorough work-up, dyserythropoietic anemia associated with hemoglobin (Hb) variants having a moderately unstable α chain, may be mistaken for CDA II.
Published: 2010
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28. Mutational spectrum in congenital dyserythropoietic anemia type II: Identification of 19 novel variants in SEC23B gene

Author: Maria Rosaria Esposito, Roberta Asci, Gian Luca Forni, Vedat Uygun, Roberta Russo, Jean Delaunay, Silverio Perrotta, Achille Iolascon, Antonella Gambale, Ugo Ramenghi, Russo, Roberta, Esposito, Mr, Asci, R, Gambale, A, Perrotta, S, Ramenghi, U, Forni, Gl, Uygun, V, Delaunay, J, Iolascon, Achille, Russo, R, Perrotta, Silverio, and Iolascon, A.
Subjects: Male, Anemia, Dyserythropoietic anemia, Genotype, Congenital dyserythropoietic anemia type II, DNA Mutational Analysis, Nonsense mutation, Vesicular Transport Proteins, Biology, Compound heterozygosity, medicine.disease_cause, History, 21st Century, Exon, Gene Frequency, Bone Marrow, medicine, Missense mutation, Humans, Family, Erythropoiesis, Registries, Anemia, Dyserythropoietic, Congenital, Genetics, Mutation, Computational Biology, Genetic Variation, Hematology, History, 20th Century, medicine.disease, anemia, dyserythropoiesis, CDA, Female, Allelic heterogeneity, Sequence Alignment, eryhtropoiesi, Research Article
Abstract: SEC23B gene encodes an essential component of the coat protein complex II (COPII)-coated vesicles. Mutations in this gene cause the vast majority the congenital dyserythropoietic anemia Type II (CDA II), a rare disorder resulting from impaired erythropoiesis. Here, we investigated 28 CDA II patients from 21 unrelated families enrolled in the CDA II International Registry. Overall, we found 19 novel variants [c.2270 A>C p.H757P; c.2149−2 A>G; c.1109+1 G>A; c.387(delG) p.L129LfsX26; c.1858 A>G p.M620V; c.1832 G>C p.R611P; c.1735 T>A p.Y579N; c.1254 T>G p.I418M; c.1015 C>T p.R339X; c.1603 C>T p.R535X; c.1654 C>T p.L552F; c.1307 C>T p.S436L; c.279+3 A>G; c. 2150(delC) p.A717VfsX7; c.1733 T>C p.L578P; c.1109+5 G>A; c.221+31 A>G; c.367 C>T p.R123X; c.1857_1859delCAT; p.I619del] in the homozygous or the compound heterozygous state. Homozygosity or compound heterozygosity for two nonsense mutations was never found. In four cases the sequencing analysis has failed to find two mutations. To discuss the putative functional consequences of missense mutations, computational analysis and sequence alignment were performed. Our data underscore the high allelic heterogeneity of CDA II, as the most of SEC23B variations are inherited as private mutations. In this mutation update, we also provided a tool to improve and facilitate the molecular diagnosis of CDA II by defining the frequency of mutations in each exon. Am. J. Hematol., 2010. © 2010 Wiley-Liss, Inc.
Published: 2010

29. Molecular analysis of 42 patients with congenital dyserythropoietic anemia type II: new mutations in the SEC23B gene and a search for a genotype-phenotype relationship

Author: Silverio Perrotta, Jean Delaunay, Roberta Russo, Achille Iolascon, Roberta Asci, Madeleine Fénéant-Thibault, Loïc Garçon, Carmelo Piscopo, Maria Rosaria Esposito, Iolascon, Achille, Russo, Roberta, Esposito, Mr, Asci, R, Piscopo, C, Perrotta, S, Fénéant Thibault, M, Garçon, L, Delaunay, J., Iolascon, A, Russo, R, Perrotta, Silverio, and FÉNÉANT THIBAULT, M
Subjects: Adult, Genetic Markers, Male, Adolescent, Genotype, Congenital dyserythropoietic anemia type II, Nonsense mutation, Mutation, Missense, Vesicular Transport Proteins, Editorials and Perspectives, Biology, Compound heterozygosity, medicine.disease_cause, Cohort Studies, Young Adult, Gene Frequency, medicine, Humans, Missense mutation, Child, Allele frequency, Anemia, Dyserythropoietic, Congenital, Genetics, Mutation, Infant, Newborn, Infant, Hematology, Middle Aged, medicine.disease, Phenotype, Codon, Nonsense, Child, Preschool, red cell, Female, Original Article, Congenital dyserythropoietic anemia
Abstract: BACKGROUND: The most frequent form of congenital dyserythropoietic anemia is the type II form. Recently it was shown that the vast majority of patients with congenital dyserythropoietic anemia type II carry mutations in the SEC23B gene. Here we established the molecular basis of 42 cases of congenital dyserythropoietic anemia type II and attempted to define a genotype-phenotype relationship. DESIGN AND METHODS: SEC23B gene sequencing analysis was performed to assess the diversity and incidence of each mutation in 42 patients with congenital dyserythropoietic anemia type II (25 described exclusively in this work), from the Italian and the French Registries, and the relationship of these mutations with the clinical presentation. To this purpose, we divided the patients into two groups: (i) patients with two missense mutations and (ii) patients with one nonsense and one missense mutation. RESULTS: We found 22 mutations of uneven frequency, including seven novel mutations. Compound heterozygosity for a missense and a nonsense mutation tended to produce a more severe clinical presentation, a lower reticulocyte count, a higher serum ferritin level, and, in some cases, more pronounced transfusion needs, than homozygosity or compound heterozygosity for two missense mutations. Homozygosity or compound heterozygosity for two nonsense mutations was never found. CONCLUSIONS: This study allowed us to determine the most frequent mutations in patients with congenital dyserythropoietic anemia type II. Correlations between the mutations and various biological parameters suggested that the association of one missense mutation and one nonsense mutation was significantly more deleterious that the association of two missense mutations. However, there was an overlap between the two categories.
Published: 2009
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30. A predicted functional single-nucleotide polymorphism of bone morphogenetic protein-4 gene affects mRNA expression and shows a significant association with cutaneous melanoma in Southern Italian population

Author: Mario Capasso, Fabrizio Ayala, Roberta Asci, Rosa Anna Avvisati, Achille Iolascon, Roberta Russo, Capasso, Mario, Ayala, F., Russo, Roberta, Avvisati, R. A., Asci, R., and Iolascon, Achille
Subjects: Adult, Male, Cancer Research, medicine.medical_specialty, Skin Neoplasms, Genetic Linkage, Gene Expression, Single-nucleotide polymorphism, Bone Morphogenetic Protein 4, Biology, Polymorphism, Single Nucleotide, Molecular genetics, Genetic variation, Genotype, Gene expression, medicine, Humans, SNP, Genetic Predisposition to Disease, RNA, Messenger, Allele, Melanoma, Gene, Genetics, Computational Biology, General Medicine, Middle Aged, Genetics, Population, Italy, Oncology, Case-Control Studies, Female, Forecasting
Abstract: Purpose An altered expression of bone morphogenetic protein 4 (BMP4) has been found in malignant melanoma cells. We performed an association study to investigate the eVect of putative functional single nucleotide polymorphisms (SNPs) of BMP4 on development of cutaneous melanoma (CM). Methods We selected the predicted functional SNPs 6007 C/T (rs17563) and i3445 T/G (rs4898820) by the combination of three computational tools (FASTSNP, F-SNP and SNP Function Portal) plus another tool (SNP@promoter) skilled in identifying SNPs in transcription regulatory regions. Both SNPs were genotyped in a case–control study of 215 individuals with CM and 342 controls. We also evaluated the BMP4 hypothetical mRNA secondary structure by GeneBee program, the BMP4 mRNA levels and protein concentrations according to the genotype of two selected SNPs in transformed B-cells of 80 controls and in plasma samples of 38 controls, respectively. Results The BMP4 T-allele was associated with CM (OR: 1.39, 95% CI: 1.09–1.78, P = 0.007). The T-allele was predicted to change mRNA structure and the BMP4 mRNA levels were signiWcantly higher in T-allele carriers compared with C-allele carriers (P = 0.01), even the BMP4 protein plasma levels were higher among T-allele carries, but without reaching the statistical signiWcance. No signiWcant association was found between the SNP i3445 T/G alleles and either the risk of CM, or the mRNA levels of BMP4. Conclusions This study evidences the relevance of using bioinformatics tools in searching for cancer-associated gene polymorphisms and suggests that the predicted functional SNP 6007 C/T aVects BMP4 gene expression and the risk to development of CM.
Published: 2009
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31. Red cells in post-genomic era: impact of personalized medicine in the treatment of anemias

Author: Roberta Russo, Immacolata Andolfo, Achille Iolascon, Iolascon, Achille, Andolfo, Immacolata, and Russo, Roberta
Subjects: Erythrocytes, Decision Making, Genomics, Bioinformatics, Models, Biological, Drug treatment, Medicine, Humans, Genetic variability, Precision Medicine, Adverse effect, Genetics, business.industry, Pharmacogenetic, Medicine (all), Editorials, Genetic Variation, Anemia, Hematology, Erythrocyte, Pharmacogenetics, Pharmacogenomics, Genomic, Personalized medicine, business, Human
Abstract: Over many years of research on pharmacogenetics and pharmacogenomics, we are now aware that the genetic variability among individuals is able to explain the remarkable diversity of either the therapeutic or the adverse effects observed during drug treatment. The term pharmacogenomics refers to the
Published: 2015

32. Imaging of the peritoneum evaluated by 99mTc-icodextrin scintigraphy in peritoneal dialysis patients: preliminary data

Author: Bruno Memoli, Andrea Memoli, Gennaro Argentino, Luigi Celentano, Roberta Russo, Tommasina Strazzullo, Immacolata Daniela Maresca, Maurizio Sodo, Argentino, Gennaro, Russo, Roberta, Maresca, IMMACOLATA DANIELA, Strazzullo, Tommasina, Memoli, Andrea, Sodo, Maurizio, Celentano, Luigi, and Memoli, Bruno
Subjects: Male, medicine.medical_treatment, Organotechnetium Compounds, Hernia, Inguinal, Tissue Adhesions, Scintigraphy, Icodextrin, Dialysis Solution, Dialysis Solutions, Tissue Distribution, Glucans, Peritoneal Cavity, medicine.diagnostic_test, Hematology, General Medicine, Middle Aged, Thorax, Glucan, medicine.anatomical_structure, Tissue Adhesion, Nephrology, Extravasation of Diagnostic and Therapeutic Material, Female, Radiology, Peritoneum, Peritoneal Dialysis, Human, Adult, medicine.medical_specialty, Peritoneal dialysis, Peritoneal Dialysi, Peritoneal cavity, medicine, Retroperitoneal space, Animals, Humans, Retroperitoneal Space, Organotechnetium Compound, Aged, Tomography, Emission-Computed, Single-Photon, business.industry, Animal, 99mTc-icodextrin, Rats, Radiography, Glucose, Rat, Kidney Failure, Chronic, Radiopharmaceuticals, business, Nuclear medicine, Extravasation of Diagnostic and Therapeutic Materials
Abstract: Aim: In this study, we proposed a peritoneal scintigraphy with a different marker, the 99mTechnetium-Icodextrin, to evaluate the distribution of the dialysate within the peritoneal cavity in peritoneal dialysis (PD) patients. Methods: 99mTc-Icodextrin scintigraphy was performed in 16 PD patients. 0.5 ml of 7.5% Icodextrin solution was labeled with 74 megabecquerel (MBq) of 99mTc and then added to 2,000 ml of dialysate solution (2.5% dextrose). The peritoneum scintigraphy was performed by a SPECT gamma camera with the peritoneal cavity filled and after the complete drainage of the radio compound-dialysate mixture. The images were reviewed for evidence of peritoneal leaks, hernias, loculated fluid collections, and peritoneal membrane adhesions. Results: Abnormal findings were detected by 99mTc-Icodextrin scintigraphy in 4 (25%) out of 16 patients and included retroperitoneal (n = 1), diaphragmatic (n = 1) and inguinal (n = 1) leakages and peritoneal membrane adhesions (n = 1). Conclusions: Peritoneum scintigraphy with 99mTc-Icodextrin is a useful method to detect some complications occurring during peritoneal dialysis; it offers excellent imaging to assess these complications.
Published: 2014

33. Evidence That p-Cresol and IL-6 Are Adsorbed by the HFR Cartridge: Towards a New Strategy to Decrease Systemic Inflammation in Dialyzed Patients?

Author: Bruno Memoli, Eleonora Riccio, Gennaro Argentino, Roberta Russo, Mauro Cataldi, Maristella Minco, Lucia Grumetto, Bruna Guida, Stefania Brancaccio, Loredana Postiglione, Andrea Memoli, Riccio, Eleonora, Cataldi, Mauro, Minco, Maristella, Argentino, Gennaro, Russo, Roberta, Brancaccio, Stefania, Memoli, Andrea, Grumetto, Lucia, Postiglione, Loredana, Guida, Bruna, and Memoli, Bruno
Subjects: Male, medicine.medical_treatment, lcsh:Medicine, Systemic inflammation, Toxicology, Vascular Medicine, Cresols, Blood plasma, Chronic Kidney Disease, Toxin Binding, Medicine and Health Sciences, p-Cresol, lcsh:Science, Multidisciplinary, biology, Dialysi, Middle Aged, Nephrology, Female, Hemodialysis, medicine.symptom, Research Article, Biotechnology, medicine.medical_specialty, Serum albumin, Cardiology, Inflammation, Hemodiafiltration, Peripheral blood mononuclear cell, End stage renal disease, Hfr cell, Internal medicine, parasitic diseases, Medical Dialysis, medicine, Humans, Serum Albumin, Aged, IL-6, business.industry, Interleukin-6, lcsh:R, Biology and Life Sciences, Atherosclerosis, Hemodialysis Solutions, Surgery, Endocrinology, biology.protein, Kidney Failure, Chronic, lcsh:Q, Medical Devices and Equipment, Adsorption, Clinical Medicine, business
Abstract: Introduction Hemodialysis (HD) and hemodiafiltration clear only with a low efficiency the plasma from interleukin-6 and p-cresol, two protein-bound uremic toxins associated with high cardiovascular risk in end stage renal disease. HFR Supra is a double-chamber hemodiafiltration system in which the ultrafiltrate returns to the patient after its regeneration through a resin cartridge that binds hydrophobic and protein-bound solutes. In the present study, we evaluated whether the HFR cartridge can also bind total p-cresol and IL-6 and remove them from the ultrafiltrate. Methods We compared the levels of IL-6 and p-cresol in ultrafiltrate samples collected at the inlet (UFin) and at the outlet (UFout) of the cartridge at the start or at the end of a 240 min HFR session in 12 inflamed chronic HD patients. The pro-inflammatory activity of the ultrafiltrate samples was also determined by evaluating the changes that they induced in IL-6 mRNA expression and protein release in peripheral blood mononuclear cells from 12 healthy volunteers. IL-6 and p-cresol circulating levels were also assessed in peripheral plasma blood samples collected before and after HFR and, for comparison, a control HD. Results p-Cresol and IL-6 were lower in UFout than in UFin both at the start and at the end of the HFR session, suggesting that they were retained by the cartridge. IL-6 mRNA expression and release were lower in PBMC incubated with UFout collected at the end than with UFin collected at the start of HFR, suggesting that passage through the cartridge reduced UF pro-inflammatory activity. Plasma total p-cresol decreased by about 53% after HFR, and 37% after HD. IL-6 circulating values were unmodified by either these dialysis procedures. Conclusions This study shows that the HFR-Supra cartridge retains total p-cresol and IL-6 in the ultrafiltrate and lowers plasma total p cresol but not IL-6 levels. Trial Registration ClinicalTrials.gov NCT01865773
Published: 2014

34. Successful hematopoietic stem cell transplantation in a patient with congenital dyserythropoietic anemia type II

Author: Mualla Cetin, Concetta Langella, Baris Kuskonmaz, Roberta Russo, Duygu Uçkan Çetinkaya, Fatma Gumruk, Achille Iolascon, Tülin Revide Şayli, Sule Unal, Betul Tavil, Acil Tıp, Sule, Unal, Russo, Roberta, Fatma, Gumruk, Baris, Kuskonmaz, Mualla, Cetin, Tulin, Sayli, Betul, Tavil, Concetta, Langella, Iolascon, Achille, and Duygu Uckan, Cetinkaya
Subjects: Ineffective erythropoiesis, Genetic Markers, Pediatrics, medicine.medical_specialty, Heterozygote, Congenital dyserythropoietic anemia type II, medicine.medical_treatment, Vesicular Transport Proteins, Hematopoietic stem cell transplantation, medicine.disease_cause, Compound heterozygosity, immune system diseases, medicine, Humans, Sibling, Anemia, Dyserythropoietic, Congenital, Transplantation, business.industry, Siblings, Hematopoietic Stem Cell Transplantation, medicine.disease, With congenital dyserythropoietic anemia, surgical procedures, operative, Curative treatment, Child, Preschool, Pediatrics, Perinatology and Child Health, Immunology, Mutation, Female, business, Rare disease
Abstract: CDA are a group of inherited, rare diseases that are characterized by dyserythropoiesis and ineffective erythropoiesis associated with transfusion dependency in approximately 10% of cases. For these latter patients, the only curative treatment is HSCT. There are very limited data on HSCT experience in this rare disease. Herein, we report a five-yr six-month-old girl with compound heterozygous mutations in SEC23B gene, who was diagnosed to have CDA type II and underwent successful HSCT from her matched sibling donor.
Published: 2014

35. Replication of GWAS-identified neuroblastoma risk loci strengthens the role of BARD1 and affirms the cumulative effect of genetic variations on disease susceptibility

Author: John M. Maris, Mario Capasso, Marilena De Mariano, Sharon J. Diskin, Francesca Totaro, Hakon Hakonarson, Flora Cimmino, Luca Longo, Marcella Devoto, Roberta Russo, Achille Iolascon, Gian Paolo Tonini, Capasso, Mario, Diskin, Sj, Totaro, F, Longo, L, Mariano, Md, Russo, Roberta, Cimmino, F, Hakonarson, H, Tonini, Gp, Devoto, M, Maris, Jm, and Iolascon, Achille
Subjects: Male, Risk, Cancer Research, Linkage disequilibrium, Adolescent, Genotype, Ubiquitin-Protein Ligases, Original Manuscript, Single-nucleotide polymorphism, Genome-wide association study, Biology, Polymorphism, Single Nucleotide, Linkage Disequilibrium, Neuroblastoma, Gene Frequency, Cell Line, Tumor, Genetic variation, Humans, SNP, Genetic Predisposition to Disease, Allele, Child, Allele frequency, Genetics, Tumor Suppressor Proteins, Infant, General Medicine, Genetic Loci, Case-Control Studies, Child, Preschool, Female, Transcriptome, Genome-Wide Association Study
Abstract: Several neuroblastoma (NB) susceptibility loci have been identified within LINC00340, BARD1, LMO1, DUSP12, HSD17B12, DDX4, IL31RA, HACE1 and LIN28B by genome-wide association (GWA) studies including European American individuals. To validate and comprehensively evaluate the impact of the identified NB variants on disease risk and phenotype, we analyzed 16 single nucleotide polymorphisms (SNPs) in an Italian population (370 cases and 809 controls). We assessed their regulatory activity on gene expression in lymphoblastoid (LCLs) and NB cell lines. We evaluated the cumulative effect of the independent loci on NB risk and high-risk phenotype development in Italian and European American (1627 cases and 2575 controls) populations. All NB susceptibility genes replicated in the Italian dataset except for DDX4 and IL31RA, and the most significant SNP was rs6435862 in BARD1 (P = 8.4 × 10(-15)). BARD1 showed an additional and independent SNP association (rs7585356). This variant influenced BARD1 mRNA expression in LCLs and NB cell lines. No evidence of epistasis among the NB-associated variants was detected, whereas a cumulative effect of risk variants on NB risk (European Americans: P (trend) = 6.9 × 10(-30), Italians: P (trend) = 8.55 × 10(13)) and development of high-risk phenotype (European Americans: P (trend) = 6.9 × 10(-13), Italians: P (trend) = 2.2 × 10(-1)) was observed in a dose-dependent manner. These results provide further evidence that the risk loci identified in GWA studies contribute to NB susceptibility in distinct populations and strengthen the role of BARD1 as major genetic contributor to NB risk. This study shows that even in the absence of interaction the combination of several low-penetrance alleles has potential to distinguish subgroups of patients at different risks of developing NB.
Published: 2013

36. Integration of Pharmacogenetics and Pharmacogenomics in Drug Development: Implications for Regulatory and Medical Decision Making in Pediatric Diseases

Author: Judith A Wessels, Evelyne Jacqz-Aigrain, Ineke Jonker, Ron H.N. van Schaik, Chiara Piana, Achille Iolascon, Roberta Russo, Sabine Fürst-Recktenwald, Linda Surh, Oscar Della Pasqua, Piana, C, Surh, L, Furst Recktenwald, S, Iolascon, Achille, Jacqz Aigrain, Em, Jonker, I, Russo, Roberta, van Schaik, Rh, Wessels, J, and Della Pasqua, O. E.
Subjects: Adult, Genetic Markers, medicine.medical_specialty, pediatric drug development, regulatory/scientific affairs, Pharmacology, Risk Assessment, 030226 pharmacology & pharmacy, law.invention, 03 medical and health sciences, Patient safety, 0302 clinical medicine, Risk Factors, law, Drug Discovery, medicine, Humans, Drug Dosage Calculations, Pharmacology (medical), Dosing, Precision Medicine, Child, Intensive care medicine, Drug Approval, Drug Labeling, Clinical pharmacology, business.industry, Patient Selection, Age Factors, Precision medicine, 3. Good health, Drug development, medical practice, Pharmacogenetics, Pharmacogenomics, Practice Guidelines as Topic, Good clinical practice, Patient Safety, clinical pharmacology, business, 030217 neurology & neurosurgery
Abstract: This article aims to provide an overview of the current situation regarding pharmacogenetic and pharmacogenomic (PG) studies in pediatrics, with a special focus on the role of PG data in the regulatory decision-making process. Despite the gap in pharmacogenetic research due to the lack of translational studies in adults and children, several technologies exist in drug development and biomarkers validation, which could supply valuable information concerning labeling and dosing recommendations. If performed under strict good clinical practice quality criteria, such findings could be included in the submission package of new chemical entities and used as additional information for prescribers, supporting further evaluation and understanding of the efficacy and safety profile of new medicines. Even though regulatory authorities may be aware of the potential role of PG in medical practice and guidances are available about the integration of PG in drug development, most data obtained from PG studies are not used by prescribers. The challenge is to better understand whether PG markers can be used to assess potential differences in drug response during the clinical program, so PG data can be integrated into the regulatory decision-making process, enabling the introduction of labeling information that promotes optimal dosing in the pediatric population.
Published: 2012

37. A novel GLA mutation in a Fabry family with glucose-6-phosphate dehydrogenase deficiency

Author: Antonio Pisani, Bianca Visciano, Roberta Russo, Giusi R. Mozzillo, Caterina Porto, Ilaria De Maggio, Gianfranco Pontarelli, Guglielmo R.D. Villani, Bruno Cianciaruso, Paola Di Natale, Pisani, Antonio, B., Visciano, Russo, Roberta, G. R., Mozzillo, C., Porto, I., De Maggio, R., Russo, Pontarelli, Gianfranco, Villani, GUGLIELMO ROSARIO DOMENI, Cianciaruso, Bruno, and DI NATALE, Paola
Subjects: Male, Adolescent, DNA Mutational Analysis, Dehydrogenase, Glucosephosphate Dehydrogenase, medicine.disease_cause, Young Adult, Exon, hemic and lymphatic diseases, G6PD deficiency, parasitic diseases, medicine, Humans, Enzyme Replacement Therapy, Genetic Predisposition to Disease, Gene, Sequence Deletion, Mutation, Fabry disease, business.industry, nutritional and metabolic diseases, Favism, Exons, Enzyme replacement therapy, Middle Aged, medicine.disease, mutations, Molecular biology, Pedigree, Isoenzymes, Glucosephosphate Dehydrogenase Deficiency, Phenotype, Nephrology, alpha-Galactosidase, Mutation testing, Female, business, Glucose-6-phosphate dehydrogenase deficiency
Abstract: Fabry disease is an X-linked lysosomal disease caused by mutations of the alpha-galactosidase A (GLA) gene at chromosome subband Xq22.1. To date, more than 600 genetic mutations have been identified to determine the nature and frequency of the molecular lesions causing the classical and milder variant phenotypes and for precise carrier detection. We report here a Fabry family (mother, son and daughter) where the alpha-galactosidase A defect was associated with a glucose-6-phosphate dehydrogenase (G6PD) deficiency. Mutation analysis revealed for the GLA gene the presence of a new mutation, i.e., a small deletion (c.452delA) on exon 3 and for the G6PD gene the presence of 2 mutations, p.V68M (G6PD Asahi, G6PD A+) and p.N126D (G6PD A+) on exon 3 and exon 4, respectively.
Published: 2012

38. Role of cardiac MRI in evaluating patients with Anderson-Fabry disease: assessing cardiac effects of long-term enzyme replacement therapy

Author: Giancarlo Messalli, Letizia Spinelli, Marco Salvatore, G. Avitabile, Delfina Iodice, Santo Dellegrottaglie, Filippo Cademartiri, Massimo Imbriaco, Antonio Pisani, R. Russo, Pisani, Antonio, Messalli, Giancarlo, Imbriaco, Massimo, Avitabile, Giuseppe, Russo, Roberta, Iodice, Delfina, Spinelli, Letizia, Dellegrottaglie, Santo, Cademartiri, F., and Salvatore, Marco
Subjects: Adult, Male, medicine.medical_specialty, Heart Diseases, Vectorcardiography, Magnetic Resonance Imaging, Cine, Disease, Muscle hypertrophy, Risk Factors, Internal medicine, otorhinolaryngologic diseases, medicine, Humans, Enzyme Replacement Therapy, Radiology, Nuclear Medicine and imaging, Neuroradiology, medicine.diagnostic_test, business.industry, Lipid metabolism, Magnetic resonance imaging, Interventional radiology, General Medicine, Enzyme replacement therapy, Isoenzymes, Anderson-Fabry Disease, alpha-Galactosidase, cardiovascular system, Cardiology, Fabry Disease, Female, business
Abstract: Anderson-Fabry disease is a multisystemic disorder of lipid metabolism secondary to X-chromosome alterations and is frequently associated with cardiac manifestations such as left ventricular (LV) hypertrophy, gradually leading to an alteration in cardiac performance. The purpose of this study was to monitor, using magnetic resonance imaging (MRI), any changes produced by enzyme replacement therapy with agalsidase beta at the cardiac level in patients with Anderson-Fabry disease.Sixteen (ten men, six women) patients with genetically confirmed Anderson-Fabry disease underwent cardiac MRI before starting enzyme replacement therapy (baseline study) and after 48 months of treatment with agalsidase beta at the dose of 1 mg/kg (follow-up study).After 48 months of treatment, a significant reduction in LV mass and wall thickness was observed: 187±59 g vs. 149±44 g, and 16±3 mm vs. 13±3 mm, respectively. A significant reduction in T2 relaxation time was noted at the level of the interventricular septum (81±3 ms vs. 67±7 ms), at the apical level (80±8 ms vs. 63±6 ms) and at the level of the lateral wall (82±8 ms vs. 63±10 ms) (p0.05). No significant variation was observed in ejection fraction between the two studies (65±3% vs. 64±2%; p0.05) (mean bias 1.0); however, an improvement was noted in the New York Heart Association (NYHA) class of the majority of patients (12/16) (p0.05).In patients with Anderson-Fabry disease undergoing enzyme replacement therapy with agalsidase beta, MRI documented a significant reduction in myocardial T2 relaxation time, a significant decrease in maximal myocardial thickness and in total LV mass. MRI did not reveal significant improvements in LV global systolic function; however, improvement in NYHA functional class was noted, consistent with improved diastolic function.
Published: 2012

39. Two founder mutations in the SEC23B gene account for the relatively high frequency of CDA II in the Italian population

Author: Maria Luisa Serra, Hannah Tamary, Antonella Gambale, Roberta Russo, Mario Capasso, Achille Iolascon, Lucio Luzzatto, Ilaria De Maggio, Annaelena Troiano, Jean Delaunay, Maria Rosaria Esposito, Russo, Roberta, Gambale, A, Esposito, Mr, Serra, Ml, Troiano, A, De Maggio, I, Capasso, Mario, Luzzatto, L, Delaunay, J, Tamary, H, and Iolascon, Achille
Subjects: Male, Lineage (genetic), Congenital dyserythropoietic anemia type II, DNA Mutational Analysis, Vesicular Transport Proteins, Biology, medicine.disease_cause, Polymorphism, Single Nucleotide, Evolution, Molecular, Gene Frequency, medicine, Prevalence, Humans, Registries, Allele frequency, Gene, Genetic Association Studies, Anemia, Dyserythropoietic, Congenital, Genetics, Mutation, Mediterranean Region, Haplotype, Hematology, medicine.disease, Italian population, Founder Effect, Europe, Amino Acid Substitution, Haplotypes, Italy, Female, Founder effect, Research Article
Abstract: Congenital Dyserythropoietic Anemia type II is an autosomal recessive disorder characterized by unique abnormalities in the differentiation of cells of the erythroid lineage. The vast majority of CDA II cases result from mutations in the SEC23B gene. To date, 53 different causative mutations have been reported in 86 unrelated cases (from the CDA II European Registry), 47 of them Italian. We have now identified SEC23B mutations in 23 additional patients, 17 Italians and 6 non-Italian Europeans. The relative allelic frequency of the mutations was then reassessed in a total of 64 Italian and 45 non-Italian unrelated patients. Two mutations, E109K and R14W, account for over one-half of the cases of CDA II in Italy. Whereas the relative frequency of E109K is similar in Italy and in the rest of Europe (and is also prevalent in Moroccan Jews), the relative frequency of R14W is significantly higher in Italy (26.3% vs. 10.7%). By haplotype analysis we demonstrated that both are founder mutations in the Italian population. By using the DMLE+ program our estimate for the age of the E109K mutation in Italian population is ≈2,200 years; whereas for the R14W mutation it is ≈3,000 years. We hypothesize that E109K may have originated in the Middle East and may have spread in the heyday of the Roman Empire. Instead, R14W may have originated in Southern Italy. The relatively high frequency of the R14W mutation may account for the known increased prevalence of CDA II in Italy. Am. J. Hematol. 86:727–732, 2011. © 2011 Wiley-Liss, Inc.
Published: 2011

40. Congenital dyserythropoietic anemias

Author: Jean Delaunay, Achille Iolascon, Roberta Russo, Iolascon, Achille, Russo, Roberta, Delaunay, J., Iolascon, A., Andolfo, I., and Russo, R.
Subjects: Ineffective erythropoiesis, Pathology, Hydrops Fetalis, Peptide Hormones, Vesicular Transport Proteins, medicine.disease_cause, Bioinformatics, Biochemistry, Mice, hemic and lymphatic diseases, Erythropoiesis, Zebrafish, Anemia, Dyserythropoietic, Congenital, Mice, Knockout, Hematology, biology, Hematopoietic Stem Cell Transplantation, High-Throughput Nucleotide Sequencing, Nuclear Proteins, Hereditary disorders, Erythroferrone, medicine.anatomical_structure, Phenotype, Molecular Diagnostic Techniques, Microtubule-Associated Proteins, Dyserythropoietic anemia, medicine.medical_specialty, Iron Overload, Genotype, Anemia, Immunology, Kruppel-Like Transcription Factors, Diagnosis, Differential, Genetic Heterogeneity, Hepcidins, Hepcidin, Internal medicine, Molecular genetics, medicine, Animals, Humans, Blood Transfusion, Glycoproteins, Cytopenia, Cell Biology, medicine.disease, Disease Models, Animal, biology.protein, Bone marrow, Differential diagnosis, Modifier Genes, Time to diagnosis
Abstract: PURPOSE OF REVIEW: Congenital dyserythropoietic anemias (CDAs) are rare hereditary disorders characterized by ineffective erythropoiesis and by distinct morphological abnormalities of erythroblasts in the bone marrow. Characteristic morphological aberrations were the cornerstone of diagnosis, but following the identification of several causative genes, the molecular approach could represent a rapid tool for the identification of these conditions. This review presents advances in diagnosis and classification of CDAs. RECENT FINDINGS: The classification of CDAs has long been based on morphological features. Now, the discovery of some of the responsible genes allows reconsideration of part of the classification. The first CDA partly accounted for genetically has been CDA 1, through the discovery in 2002 of the gene responsible, CDAN1, encoding codanin-1. Recently, the dramatic identification of the genes responsible for CDA II, SEC23B, and for a hitherto unnamed CDA, KLF1, took place. SEC23B encodes SEC23B which is a component of the coated vesicles transiting from the endoplasmic reticulum to the cis compartment of the Golgi apparatus. A unique mutation in KLF1, which encodes the erythroid transcription factor KLF1, causes major ultrastructural abnormalities, the persistence of embryonic and fetal hemoglobins, and the absence of some red cell membrane proteins. SUMMARY: Studies of genotype-phenotype relationship, as has already been done for CDA II, will allow a more accurate prognosis. Identification of the responsible genes has opened new vistas for research on CDAs.
Published: 2011

41. Pediatric pharmacogenetic and pharmacogenomic studies: the current state and future perspectives

Author: Mario Capasso, Roberta Russo, Achille Iolascon, Paolo Paolucci, Russo, Roberta, Capasso, Mario, Paolucci, P, and Iolascon, Achille
Subjects: Pharmacology, Drug Prescribing, Genetic Variation, Genome-wide association study, General Medicine, Biology, Bioinformatics, Pediatrics, Drug treatment, Pharmacogenetics, Pharmacogenomics, pharmacogenomic studies, Genetic variation, Humans, Pharmacology (medical), Pediatric pharmacogenetic, Genetic variability, Child, Pediatric pharmacogenetic, pharmacogenomic studies, Forecasting, Pediatric population
Abstract: Genetic differences among individuals can explain some of the variability observed during drug treatment. Many studies have correlated the different pharmacological response to genetic variability, but most of them have been conducted on adult populations. Much less attention has been given to the pediatric population. Pediatric patients constitute a vulnerable group with regard to rational drug prescribing since they present differences arising from the various stages of development. However, only a few steps have been made in developmental pharmacogenomics. This review attempts to describe the current methods for pharmacogenetic and pharmacogenomic studies, providing some of the most studied examples in pediatric patients. It also gives an overview on the implication and importance of microRNA polymorphisms, transcriptomics, metabonomics, and proteomics in pharmacogenetics and pharmacogenomics studies.
Published: 2011

42. MDM2 SNP309 and p53 Arg72Pro in cutaneous melanoma: association between SNP309 GG genotype and tumor Breslow thickness

Author: Paolo A. Ascierto, Antonella Gambale, Fabrizio Ayala, Roberta Russo, Nicola Mozzillo, Achille Iolascon, Mario Capasso, Rosa Anna Avvisati, Capasso, Mario, Ayala, Fabio, Avvisati, Ra, Russo, Roberta, Gambale, A, Mozzillo, N, Ascierto, Pa, and Iolascon, Achille
Subjects: Adult, Male, medicine.medical_specialty, Skin Neoplasms, Genotype, SNP, Single-nucleotide polymorphism, Biology, Gastroenterology, Polymorphism, Single Nucleotide, Breslow Thickness, MDM2, Internal medicine, Genetics, medicine, Humans, Melanoma, Genetics (clinical), Neoplasm Staging, Proto-Oncogene Proteins c-mdm2, Odds ratio, medicine.disease, Prognosis, Molecular biology, Minor allele frequency, Case-Control Studies, Cutaneous melanoma, Female, Age of onset, Tumor Suppressor Protein p53
Abstract: A functional single nucleotide polymorphism (SNP) 309 T/G within mouse double minute 2 (MDM2) gene has been linked to onset and outcome of disease in tumors. Two published studies have shown discordant results regarding the effect of this SNP on age at diagnosis of cutaneous melanoma (CM) in Caucasian female populations. Here, we examined the age at diagnosis and clinical associations of CM with SNP309 and the related polymorphism, p53 Arg72Pro, in an Italian population (249 CM patients and 291 cancer-free controls) composed of women and men. MDM2 intronic region of 294 bp was directly sequenced, whereas Arg72Pro SNP was analyzed by polymerase chain reaction-restriction fragment length polymorphism. No associations were found among the SNP309, Arg72Pro, risk of CM, age at diagnosis and presence of metastasis in total subjects and when stratified according to the gender. The SNP309 was significantly associated with tumor Breslow thickness. The P-value in the minor allele recessive mode was 0.02, and the odds ratio (OR) adjusted for gender and age was 3.11 (95% confidential interval (CI)=1.21–8.00). The SNP309 is not associated with the risk and age of onset of CM, and the presence of metastasis in an Italian population but the SNP309 GG may be a risk genotype for increasing in tumor Breslow thickness.
Published: 2010

43. Regulation of divalent metal transporter 1 (DMT1) non-IRE isoform by the microRNA Let-7d inerythroid cells

Author: Marisa Gorrese, Luigia De Falco, Roberta Asci, Achille Iolascon, Roberta Russo, Simona Colucci, Immacolata Andolfo, Massimo Zollo, Andolfo, I, De Falco, L, Asci, R, Russo, R, Colucci, S, Gorrese, M, Zollo, Massimo, Iolascon, Achille, and Russo, Roberta
Subjects: Gene isoform, Iron, Blotting, Western, Endosomes, Response Elements, Erythroid Cells, Cell Line, Tumor, Sequence Homology, Nucleic Acid, hemic and lymphatic diseases, microRNA, Humans, Protein Isoforms, Gene silencing, RNA, Messenger, 3' Untranslated Regions, Cation Transport Proteins, Regulation of gene expression, Base Sequence, biology, Reverse Transcriptase Polymerase Chain Reaction, fungi, digestive, oral, and skin physiology, Alternative splicing, Cell Differentiation, Hematology, DMT1, Flow Cytometry, Molecular biology, Gene Expression Regulation, Neoplastic, MicroRNAs, Cell culture, Mutagenesis, Site-Directed, biology.protein, Original Article, K562 Cells, K562 cells
Abstract: BACKGROUND: Divalent metal transporter 1 (DMT1) is a widely expressed metal-iron transporter gene encoding four variant mRNA transcripts, differing for alternative promoter at 5' (DMT1 1A and 1B) and alternative splicing at 3' UTR, differing by a specific sequence either containing or lacking an iron regulatory element (+IRE and -IRE, respectively). DMT1-IRE might be the major DMT1 isoform expressed in erythroid cells, although its regulation pathways are still unknown. DESIGN AND METHODS: The microRNA (miRNA) Let-7d (miR-Let-7d) was selected by the analysis of four miRNAs, predicted to target the DMT1-IRE gene in CD34(+) hematopoietic progenitor cells, in K562 and in HEL cells induced to erythroid differentiation. Using a luciferase reporter assay we demonstrated the inhibition of DMT1-IRE by miR-Let-7d in K562 and HEL cells. The function of miR-Let-7d in erythroid cells was evaluated by the flow cytometry analysis of erythroid differentiation markers, by benzidine staining and by iron flame atomic absorption for the evaluation of iron concentration in the endosomes from K562 cells over-expressing miR-Let-7d. RESULTS: We show that in erythroid cells, DMT1-IRE expression is under the regulation of miR-Let-7d. DMT1-IRE and miR-Let-7d are inversely correlated with CD34(+) cells, K562 and HEL cells during erythroid differentiation. Moreover, overexpression of miR-Let-7d decreases the expression of DMT1-IRE at the mRNA and protein levels in K562 and HEL cells. MiR-Let-7d impairs erythroid differentiation of K562 cells by accumulation of iron in the endosomes. CONCLUSIONS: Overall, these data suggest that miR-Let-7d participates in the finely tuned regulation of iron metabolism by targeting DMT1-IRE isoform in erythroid cells.
Published: 2010

44. Galectin-1 and Its Involvement in Hepatocellular Carcinoma Aggressiveness

Author: Mario Capasso, Massimo Roncalli, Achille Iolascon, Luigi Terracciano, Natalia Rosso, Roberta Russo, Vittorio Di Maso, Luigi Tornillo, Claudio Tiribelli, Daniela Spano, D., Spano, R., Russo, V. D., Maso, N., Rosso, L. M., Terracciano, M., Roncalli, L., Tornillo, M., Capasso, Tiribelli, Claudio, A., Iolascon, Spano, D, Russo, Roberta, Di Maso, V, Rosso, N, Terracciano, Lm, Roncalli, M, Tornillo, L, Capasso, Mario, Tiribelli, C, and Iolascon, Achille
Subjects: Male, Pathology, Galectin 1, genetics/metabolism, Aged, Carcinoma, Hepatocellular, genetics/metabolism/pathology, Cell Line, Tumor, Cell Movement, genetics, Female, Galectin 1, biosynthesis/genetics/metabolism, Gene Expression Profiling, Histocytochemistry, Humans, Intracellular Signaling Peptides and Proteins, genetics/metabolism, Liver Neoplasms, genetics/metabolism/pathology, Male, Middle Aged, Neoplasm Invasiveness, Oligonucleotide Array Sequence Analysis, Phosphorylation, Protein-Tyrosine Kinases, genetics/metabolism, Signal Transduction, Statistics, Nonparametric, Tissue Array Analysis, Metastasis, Pathogenesis, genetics/metabolism/pathology, Cell Movement, Phosphorylation, genetics/metabolism, Liver Neoplasm, Genetics (clinical), Oligonucleotide Array Sequence Analysis, Tumor, Histocytochemistry, Statistics, Liver Neoplasms, Intracellular Signaling Peptides and Proteins, hepatocellular carcinoma, Middle Aged, Protein-Tyrosine Kinases, genetics/metabolism/pathology, Male, Middle Aged, Neoplasm Invasiveness, Oligonucleotide Array Sequence Analysis, Phosphorylation, Protein-Tyrosine Kinase, Hepatocellular carcinoma, Galectin-1, Molecular Medicine, gene expression profile, Female, Research Article, Signal Transduction, medicine.medical_specialty, Stromal cell, Carcinoma, Hepatocellular, genetics/metabolism, Signal Transduction, Statistic, Biology, biosynthesis/genetics/metabolism, Statistics, Nonparametric, Cell Line, Cell Line, Tumor, Genetics, medicine, Carcinoma, Humans, Syk Kinase, galectin-1, Nonparametric, Neoplasm Invasiveness, Molecular Biology, Aged, Gene Expression Profiling, medicine.disease, Molecular medicine, digestive system diseases, Gene expression profiling, Tissue Array Analysis, biosynthesis/genetics/metabolism, Gene Expression Profiling, Histocytochemistry, Humans, Intracellular Signaling Peptides and Protein
Abstract: Hepatocellular carcinoma is one of the most common cancers worldwide. Despite several efforts to elucidate hepatocellular carcinoma molecular pathogenesis, it is still not fully understood. To acquire further insights into the molecular mechanisms of hepatocellular carcinoma, we performed a systematic functional genomic approach on human HuH-7 and JHH-6 cells. The subsequent analysis of the differentially expressed genes in human specimens revealed a molecular signature of 11 genes from which we selected the LGALS1 gene, which was overexpressed in hepatocellular carcinoma, The expression analysis in humans of Galectin-1 (Gal-1), the protein encoded by LGALS1, showed a Gal-1 preferential accumulation in the stromal tissue around hepatocellular carcinoma tumors. Moreover, a significant association between increased expression of Gal-1 in hepatocellular carcinoma and the presence of metastasis was observed. Interestingly, Gal-1 overexpression resulted in an increase of cell migration and invasion. In conclusion, this study provides a portfolio of targets useful for future investigations into molecular marker-discovery studies on a large number of patients and functional assays. In addition, our data provide evidence that Gal-1 plays a role in hepatocellular carcinoma cell migration and invasion, and we suggest that further studies should be conducted to fully establish the role of Gal-1 in hepatocellular carcinoma pathogenesis and evaluate Gal-1 as a potential molecular therapeutic target. (C) 2010 The Feinstein Institute for Medical Research, www.feinsteininstitute.org Online address: http://www.molmed.org doi: 10.2119/molmed.2009.00119
Published: 2010
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45. SOCS3 and IRS-1 gene expression differs between genotype 1 and genotype 2 hepatitis C virus-infected HepG2 cells

Author: M. Svelto, Mario Capasso, Vincenzo La Mura, Daniela Spano, Roberto Torella, Claudio Tiribelli, Roberta Russo, Eliana Persico, Marcello Persico, Immacolata Andolfo, Achille Iolascon, Persico, M., Russo, Roberta, Persico, E., Svelto, M., Spano, D., Andolfo, I., La Mura, V., Capasso, Mario, Tiribelli, C., Torella, R., and Iolascon, Achille
Subjects: hepatitis C virus, Genotype, Hepacivirus, Hepatitis C virus, Clinical Biochemistry, genetics/metabolism, suppressor of cytokine signaling 3 (SOCS3), Suppressor of Cytokine Signaling Proteins, Virus Replication, medicine.disease_cause, Virus, Flaviviridae, Gene Expression Regulation, Genotype, Hep G2 Cells, Hepacivirus, physiology, Hepatitis C, genetics/metabolism, Humans, Insulin Receptor Substrate Proteins, genetics/metabolism, Proto-Oncogene Proteins c-akt, metabolism, Suppressor of Cytokine Signaling Proteins, genetics/metabolism, Virus Replication, Gene expression, medicine, Humans, SOCS3, biology, Biochemistry (medical), insulin receptor substrate 1 (IRS-1), Hep G2 Cells, General Medicine, biology.organism_classification, Hepatitis C, Virology, Gene Expression Regulation, Suppressor of Cytokine Signaling 3 Protein, physiology, Insulin Receptor Substrate Proteins, metabolism, Proto-Oncogene Proteins c-akt, Viral load
Abstract: Background: The poor response to antiviral treatment of hepatitis C virus (HCV)-infected patients with genotype 1b has been associated with a higher prevalence of metabolic syndrome. However, the molecular link between these clinical entities is not clear. The goal of this study was to clarify the role of genotype 1b and 2 in the genetic expression of suppressor of cytokine signaling 3 (SOCS3) and insulin receptor substrate 1 (IRS-1). Methods: We infected human hepatocellular carcinoma cell line (HepG2) cells with human HCV genotype 1b or 2 and measured the gene and protein expression of SOCS3 at various times. We also evaluated impairment in the insulin pathway by analysis of IRS-1 and phospho-AKT. For the control, we used HepG2 cell cultures treated with non-infectious serum. We also demonstrated the occurrence of HCV infection by the detection of both positive and negative strands in the cells and culture medium. To test infection of the HepG2 cells, we performed quantitative real-time polymerase chain reaction (qRT-PCR) of viral load at different time points. We analyzed the viral genotype in the pellet and supernatant. Results: At each time point, we found positive and negative strands in the infected cells, while in the medium we found positive, but no negative strands. We also detected the presence of the correct genotype in the medium. Two weeks following infection when the viral load was higher, we tested genotype 1b and 2 infected cells. SOCS3 gene expression was significantly higher in genotype 1b-infected cells (median 2.56; mean 2.82±0.59) compared with genotype 2 (median 1.34; mean 1.46±0.31) (p=0.04) and control cells (median 1.09; mean 1.02±0.11, p=0.02). There was no difference between cells exposed to genotype 2 and control cells. Conversely, IRS-1 was significantly lower in genotype 1b-infected cells (median 15.97; mean 15.45±0.67) compared with genotype 2-infected cells (median 16.45; mean 16.44±0.01, p=0.04). Statistically significant differences were seen when comparing the pAKT/AKT ratio in genotype 1b-infected cells (0.19±0.034) and not genotype 1b-infected (genotype 2-infected and non-infected) cells (0.253±0.004, p=0.03). This inverse regulation is compatible with interactions between the molecular expression of SOCS3, IRS-1 and phospho-AKT mediated by the genotype 1b virus. Conclusions: Up-regulation of the SOCS3 gene might be one of the mechanisms governing non-response to therapy and expression of insulin resistance mediated via a direct mechanism at this level of genotype 1b HCV. Clin Chem Lab Med 2009;47:1217–25.
Published: 2009
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46. Mutations affecting the secretory COPII coat component SEC23B cause congenital dyserythropoietic anemia type II

Author: Karlheinz Holzmann, Markus Rojewski, Silverio Perrotta, Rainer Pepperkok, Hermann Heimpel, Barry H. Paw, Achille Iolascon, Katja Heinrich, Luigia De Falco, Wen Chen, Daniela Spano, Wyatt Horsley, Jean Delaunay, Roberta Russo, Maria Rosaria Esposito, Ulrich Pannicke, Karl-Peter Hopfner, Brigitte Joggerst, Jonas Denecke, Fatima Verissimo, Klaus Schwarz, Nikolaus S. Trede, Schwarz, K., Iolascon, A., Verissimo, F., Trede, N., Horsley, W., Chen, W., Paw, B., Hopfner, K., Holzmann, K., Russo, R., Esposito, M., Spano, D., DE FALCO, L., Heinrich, K., Joggerst, B., Rojewski, M., Perrotta, Silverio, Denecke, J., Pannicke, U., Delaunay, J., Pepperkok, R., Heimpel, H., Iolascon, Achille, Trede, N. S., Paw, B. H., Hopfner, K. P., Russo, Roberta, Esposito, M. R., De Falco, L., Rojewski, M. T., and Perrotta, S.
Subjects: Congenital dyserythropoietic anemia type II, Anemia, DNA Mutational Analysis, Vesicular Transport Proteins, CDAII, Biology, medicine.disease_cause, Cell Line, Erythroid Cells, hemic and lymphatic diseases, congenital dyserythropoietic anemia type II, Genetics, medicine, Animals, Humans, COPII, Zebrafish, Anemia, Dyserythropoietic, Congenital, Cell Nucleus, Mutation, diseritropoiesi, SEC23A, medicine.disease, anemia, Molecular biology, dyserythropoiesis, Phenotype, Jaw, globulo rosso, Immunology, COP-Coated Vesicles, Congenital dyserythropoietic anemia, SEC23B, Cytokinesis, Dyserythropoietic anemia
Abstract: Congenital dyserythropoietic anemias (CDAs) are phenotypically and genotypically heterogeneous diseases(1-4). CDA type II (CDAII) is the most frequent CDA. It is characterized by ineffective erythropoiesis and by the presence of bi- and multinucleated erythroblasts in bone marrow, with nuclei of equal size and DNA content, suggesting a cytokinesis disturbance(5). Other features of the peripheral red blood cells are protein and lipid dysglycosylation and endoplasmic reticulum double-membrane remnants(4,6). Development of other hematopoietic lineages is normal. Individuals with CDAII show progressive splenomegaly, gallstones and iron overload potentially with liver cirrhosis or cardiac failure. Here we show that the gene encoding the secretory COPII component SEC23B is mutated in CDAII. Short hairpin RNA (shRNA)-mediated suppression of SEC23B expression recapitulates the cytokinesis defect. Knockdown of zebrafish sec23b also leads to aberrant erythrocyte development. Our results provide in vivo evidence for SEC23B selectivity in erythroid differentiation and show that SEC23A and SEC23B, although highly related paralogous secretory COPII components, are nonredundant in erythrocyte maturation.
Published: 2009
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47. Pharmacogenomics and pharmacogenetics: individual genetic profile and pharmacological response

Author: Iolascon, A., Roberta Russo, Capasso, M., Iolascon, Achille, Russo, Roberta, and Capasso, Mario
Subjects: Pharmacogenetics, Humans
Published: 2009

48. Elevated expression and polymorphisms of SOCS3 influence patient response to antiviral therapy in chronic hepatitis C

Author: Achille Iolascon, Claudio Tiribelli, Roberta Russo, Eliana Persico, L.S. Crocè, Marcello Persico, Mario Capasso, Persico, M, Capasso, Mario, Russo, Roberta, Persico, E, Crocè, L, Tiribelli, C, Iolascon, Achille, Capasso, M, Russo, R, Croce', Saveria, Tiribelli, Claudio, and Iolascon, A.
Subjects: Male, LINKAGE DISEQUILIBRIUM, LYMPHOBLASTOID CELL-LINES, Suppressor of Cytokine Signaling Proteins, chemistry.chemical_compound, Pegylated interferon, Treatment Failure, LYMPHOBLASTOID CELL-LINES, PERIPHERAL-BLOOD CELLS, IFN-ALPHA, CYTOKINE SIGNALING-3, GENE-EXPRESSION, LINKAGE DISEQUILIBRIUM, SUSTAINED RESPONSE, VIRUS-INFECTION, PLUS RIBAVIRIN, MESSENGER-RNA, GENE-EXPRESSION, Cell Line, Transformed, Gastroenterology, Hepatitis C, Middle Aged, Prognosis, PLUS RIBAVIRIN, CYTOKINE SIGNALING-3, Treatment Outcome, Drug Therapy, Combination, Female, MESSENGER-RNA, PERIPHERAL-BLOOD CELLS, medicine.drug, Adult, Genetic Markers, Alpha interferon, Single-nucleotide polymorphism, VIRUS-INFECTION, Antiviral Agents, Polymorphism, Single Nucleotide, Virus, Ribavirin, medicine, Humans, RNA, Messenger, Interferon alfa, SUSTAINED RESPONSE, Aged, business.industry, Gene Expression Profiling, Haplotype, IFN-ALPHA, Interferon-alpha, Hepatitis C, Chronic, medicine.disease, Virology, chemistry, Haplotypes, Suppressor of Cytokine Signaling 3 Protein, Immunology, business, Biomarkers
Abstract: BACKGROUND:The response to antiviral therapy of chronic hepatitis C virus (HCV) infection is determined by virological, environmental and genetic factors.OBJECTIVE:The hypothesis was tested that the expression of specific genes and their haplotype frequencies can differentiate between non-responders (NRs) and sustained virological responders (SVRs) to antiviral treatment.METHODS:A methodological approach based on molecular marker discovery and validation was used to study the genes influencing the antiviral treatment in lymphoblastoid cell lines from 74 genotype 1b HCV patients (44 from Southern Italy and 30 from Northern Italy) treated with pegylated interferon (IFN) alpha and ribavirin. Furthermore, an association study was performed, testing three single nucleotide polymorphisms (SNPs) of suppressor of cytokine signalling 3 (SOCS3) in 162 NR and 184 SVR subjects (SOCS3 -8464 A/C (rs12952093), -4874 A/G (rs4969170) and 1383 A/G, (rs4969168)).RESULTS:SOCS3 basal expression levels were significantly increased in two independent sets of NR groups (p
Published: 2007

49. Comparative proteomic expression profile in all-trans retinoic acid differentiated neuroblastoma cell line

Author: Nicola Zambrano, Flora Cimmino, Achille Iolascon, Massimo Zollo, Roberta Russo, Daniela Spano, Mario Capasso, Cimmino, F, Spano, D, Capasso, Mario, Zambrano, Nicola, Russo, Roberta, Zollo, Massimo, and Iolascon, Achille
Subjects: Proteomics, Retinoic acid, Protein Array Analysis, Tretinoin, Biology, Biochemistry, chemistry.chemical_compound, Neuroblastoma, Cytosol, Peripheral Nervous System Neoplasms, Cell Line, Tumor, medicine, Humans, Electrophoresis, Gel, Two-Dimensional, Nuclear protein, all-trans-retinoic acid, Cell Nucleus, Cancer, Computational Biology, General Chemistry, TUMOR-SUPPRESSOR PROTEIN, DEAD BOX GENE, BONE-MARROW-TRANSPLANTATION, HIGH-RISK NEUROBLASTOMA, PROMYELOCYTIC LEUKEMIA, GEL-ELECTROPHORESIS, N-MYC, HEPATOCELLULAR-CARCINOMA, PROGNOSTIC-SIGNIFICANCE, HYPOTHETICAL PROTEINS, medicine.disease, Molecular biology, Prefoldin, Neoplasm Proteins, chemistry, Cell culture, LAN-5 human neuroblastoma cell line, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, 2D-DIGE, Chromatography, Liquid
Abstract: Neuroblastoma (NB) is an infant tumor which frequently differentiates into neurons. We used two-dimensional differential in-gel electrophoresis (2D-DIGE) to analyze the cytosolic and nuclear protein expression patterns of LAN-5 cells following neuronal differentiating agent all-trans-retinoic acid treatment. We identified several candidate proteins, from which G beta 2 and Prefoldin 3 may have a role on NB development. These results strength the use of proteomics to discover new putative protein targets in cancer.
Published: 2007
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50. Suppressor of cytokine signaling 3 (SOCS3) expression and hepatitis C virus-related chronic hepatitis: Insulin resistance and response to antiviral therapy

Author: Claudio Tiribelli, Roberta Russo, Daniela Spano, Marcello Persico, Eliana Persico, Francesco Moschella, Achille Iolascon, Flora Masutti, L.S. Crocè, Roberto Torella, M. Svelto, Mario Capasso, Vincenzo La Mura, Persico, M, Capasso, Mario, Persico, E, Svelto, Maria, Russo, Roberta, Spano, D, Crocè, L, La Mura, V, Moschella, F, Masutti, F, Torella, R, Tiribelli, C, Iolascon, Achille, M., Persico, M., Capasso, E., Persico, M., Svelto, R., Russo, D., Spano, Croce', Saveria, V. L., Mura, F., Moschella, Masutti, Flora, R., Torella, Tiribelli, Claudio, and A., Iolascon
Subjects: Male, Hepacivirus, Biopsy, genetics/metabolism, drug therapy/genetics/metabolism, Humans, Insulin Resistance, Suppressor of Cytokine Signaling Proteins, medicine.disease_cause, Suppressor of cytokine signaling 3, NECROSIS-FACTOR-ALPHA, PLUS RIBAVIRIN, GENE-EXPRESSION, STEATOSIS, GENOTYPE-1, INFECTION, CYTOKINE-SIGNALING-3, TIME, PCR, Polyethylene Glycols, Cohort Studies, chemistry.chemical_compound, Pegylated interferon, drug therapy/genetics/metabolism, Genotype, therapeutic use, Liver, genetics, genetics/physiology, Interferon-alpha, Chronic, genetics/physiology, Metabolic Syndrome, biology, Metabolic Syndrome X, digestive, oral, and skin physiology, Hepatitis C, Middle Aged, Recombinant Proteins, therapeutic use, Suppressor of Cytokine Signaling Protein, Treatment Outcome, Liver, Combination, Drug Therapy, Combination, Female, Adult, Aged, Antiviral Agents, therapeutic use, Biopsy, Cell Line, Cohort Studies, Drug Therapy, Combination, Female, Genotype, Hepacivirus, genetics, Hepatitis C, metabolism/pathology/virology, Male, Metabolic Syndrome X, genetics/metabolism, Middle Aged, Polyethylene Glycols, therapeutic use, Recombinant Proteins, Ribavirin, therapeutic use, Suppressor of Cytokine Signaling Proteins, genetics/metabolism, Treatment Outcome, medicine.drug, Adult, medicine.medical_specialty, Combination, Female, Genotype, Hepaciviru, Hepatitis C virus, Interferon alpha-2, association study, Antiviral Agents, Cell Line, Drug Therapy, Internal medicine, Ribavirin, medicine, genetics/metabolism, Middle Aged, Polyethylene Glycol, Humans, metabolism/pathology/virology, Aged, Hepatitis, Hepatology, Interferon-alpha, Hepatitis C, Chronic, biology.organism_classification, medicine.disease, chemistry, Adult, Aged, Antiviral Agent, Suppressor of Cytokine Signaling 3 Protein, therapeutic use, Immunology, response to antiviral therapy, Insulin Resistance
Abstract: The response to antiviral therapy is lower in hepatitis C virus (HCV) patients with genotype 1 than in those with genotype 2. Overexpression of the suppressor of cytokine signaling 3 (SOCS3) gene in liver tissue is associated with a poorer treatment outcome in patients with chronic hepatitis C viral genotype 1. Also, insulin resistance has been implicated in nonresponse to an anti-HCV treatment. To understand why HCV genotype 1 patients respond differently, we investigated SOCS3 gene expression, metabolic syndrome (MS), and the response to therapy in a cohort of patients with HCV-related hepatitis. A total of 198 patients (108 with genotype 1 and 90 with genotype 2) treated with pegylated interferon plus ribavirin were consecutively enrolled in the study. We measured SOCS3 expression in Epstein-Barr virus-transformed lymphoblastoid cell lines derived from peripheral lymphocytes of a subset of 130 patients. MS was more frequent in genotype 1 patients than in genotype 2 patients (P < 0.01). Nonresponders (P < 0.01), MS (P < 0.001), and genotype 1 (P < 0.001) were significantly related to SOCS3 overexpression. However, SOCS3 levels were higher in nonresponders also, regardless of the genotype (P < 0.01). In a univariate analysis, the genotype (P < 0.001), age (P < 0.001), SOCS3 (P < 0.001), and MS (P < 0.001) were significantly related to the response to therapy. However, in a multivariate analysis, SOCS3 was the only independent predictor of the response (odds ratio = 6.7; P < 0.005). CONCLUSION: We speculate that SOCS3 expression per se may influence the response to antiviral therapy and that the genotype 1b virus might induce its up-regulation. This may account for the different responses to therapy between genotype 1-infected and genotype 2-infected patients.
Published: 2007
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