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<datestamp>2017-12-21</datestamp>
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<title lang=en>Impact of eNOS polymorphisms on red blood cell aggregation in sickle cell disease</title>
<creator>Ferdinand, Séverine</creator>
<creator>Connes, Philippe</creator>
<creator>Brudey, Laura</creator>
<creator>Cita, Kizzy-Clara</creator>
<creator>Tressières, Benoit</creator>
<creator>Lemonne, Nathalie</creator>
<creator>Hardy-Dessources, Marie-Dominique</creator>
<creator>Lamarre, Yann</creator>
<creator>Waltz, Xaxier</creator>
<creator>Etienne-Julan, Maryse</creator>
<creator>Romana, Marc</creator>
<contributor>Observatoire Régional de la Santé de la Guadeloupe ; Observatoire Régional de la Santé de la Guadeloupe</contributor>
<contributor>Université des Antilles et de la Guyane (UAG)</contributor>
<contributor>Centre d'Investigation Clinique Antilles-Guyane (CIC - Antilles Guyane) ; Université des Antilles et de la Guyane (UAG) - Institut National de la Santé et de la Recherche Médicale (INSERM) - CHU de Pointe-à-Pitre - Centre Hospitalier de Cayenne Andrée Rosemon - CHU de Fort de France</contributor>
<contributor>CHU de Pointe-à-Pitre ; CHU de Pointe-à-Pitre</contributor>
<contributor>Protéines de la membrane érythrocytaire et homologues non-érythroides ; Université des Antilles et de la Guyane (UAG) - Institut National de la Transfusion Sanguine [Paris] (INTS) - Université Paris Diderot - Paris 7 (UPD7) - Université de la Réunion (UR) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Region Guadeloupe</contributor>
<description>International audience</description>
<source>ISSN: 1079-9796</source>
<source>EISSN: 1096-0961</source>
<source>Blood Cells, Molecules and Diseases</source>
<publisher>Elsevier</publisher>
<identifier>hal-01263890</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-01263890</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-01263890/document</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-01263890/file/Ferdinand%20et%20al.%20eNOS%20and%20RBC%20rheology%20in%20SCD_BCMD.pdf</identifier>
<source>https://hal.archives-ouvertes.fr/hal-01263890</source>
<source>Blood Cells, Molecules and Diseases, Elsevier, 2015, 55 (2), pp.151-3</source>
<identifier>PUBMED : 26142331</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/26142331</relation>
<language>en</language>
<subject>[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Hemorheological abnormalities have been well characterized in sickle cell disease (SCD) and seem to modulate the clinical severity [1]. For instance, increased blood viscosity raises the risk for frequent vaso-occlusive crisis (VOC) and increased red blood cell (RBC) aggregates robustness (i.e., RBC disaggregation threshold) enhances the risks for acute chest syndrome (ACS) [2]. Moreover, patients with the most rigid RBCs are characterized by high hemolytic rate, which increases the risks to develop leg ulcers or glomerulopathy [3]. However, except few studies supporting an effect of alpha-thalassemia and oxidative stress [1] on RBC rheological properties of SCD patients, very few experiments focused on the genetic and cellular factors modulating blood rheology in this disease.</description>
<date>2015-07-31</date>
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