Manioc : Portail | resultats 1 - 20 pour la recherche: Institut National de la Transfusion Sanguine [Paris] (INTS)

Éditeur(s) : HAL CCSD
Résumé : International audience
Coming from Crimea, the Black Death spread to Western Europe and North Africa during the 1340s. From 1346 to 1352, the plague killed an estimated 25-40% of Europeans of all age-groups [1] , i.e., 30 to 60% of Europe population. One of the earliest and most widely accepted explanations was that God was punishing humanity for their sins. One remedy for the curse was to do penitence. Thus in 1348 there rapidly arose a mass movement of flagellation [2]. In fact flagellation could not really help against such threat. The Black Death or Bubonic plague is caused by Yersinia pestis, a Eubacteria discovered in 1894 by Alexandre Yersin. It is transmitted by the bite of the flea Xenopsylla cheopsis. This flea lives by feeding the blood of many species besides man but its most preferred relationship is with the black rat (Rattus rattus). Fossilized remains of the plague flea have been found in large numbers in Amarna, Egypt [3, 4] about 1350 BC, and thus could be directly linked to the events described in the Book of Samuel [5, 6]. During the epidemic of Bubonic plague in London in 1665-1666, the known treatments were made use of, e.g. the so-famous Theriac or Venice Treacle which is used from the time of ancient Rome as a remedy against poison [7]. Since then, more specialized and novel treatments have been developed. However, since the characterization of Yersinia pestis, numerous drugs have been developed against it, e.g. gentamicin or doxycycline [8]. These researches had been carried out using more elaborated biochemical, biophysical and biological approaches.
Infectious disorders drug targets

Droits : info:eu-repo/semantics/OpenAccess
inserm-00395256
http://www.hal.inserm.fr/inserm-00395256
http://www.hal.inserm.fr/inserm-00395256/document
http://www.hal.inserm.fr/inserm-00395256/file/editorial.pdf
http://www.hal.inserm.fr/inserm-00395256/file/inserm-00395256_edited.pdf

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Aggregation of mononuclear and red blood cells through an {alpha}4{beta}1-Lu/basal cell adhesion molecule interaction in sickle cell disease. ; Aggregation of mononuclear and red blood cells through an {alpha}4{beta}1-Lu/basal cell adhesion molecule interaction in sickle cell disease. : Mononuclear and sickle red blood cell interactions
Auteur(s) : Chaar, Vicky Picot, Julien Renaud, Olivier Bartolucci, Pablo Nzouakou, Ruben Bachir, Dora Galactéros, Frédéric Colin, Yves
Auteurs secondaires : 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) Imagopole (CITECH) ; Institut Pasteur [Paris] Unité des maladies génétiques du globule rouge ; Assistance publique - Hôpitaux de Paris (AP-HP) - Hôpital Henri Mondor - Centre de référence des syndromes drépanocytaires majeurs - Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12) The investigation was supported by the Institut National de la Transfusion Sanguine (INTS), the Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Diderot Paris 7, a grant from the Agence Nationale de la Recherche (ANR, SCADHESION 2007), two grants from Région Ile-de-France (SESAME 2007 no. F-08-1104/R and IMAGOPOLE Project 2007) and a fellowship "maladies rares" from the Société Française de Médecine Interne (SNFMI) and Actélion.

Éditeur(s) : HAL CCSD Ferrata Storti Foundation
Résumé : International audience
BACKGROUND: Abnormal interactions between red blood cells, leukocytes and endothelial cells play a critical role in the occurrence of the painful vaso-occlusive crises associated with sickle cell disease. We investigated the interaction between circulating leukocytes and red blood cells which could lead to aggregate formation, enhancing the incidence of vaso-occlusive crises. DESIGN AND METHODS: Blood samples from patients with sickle cell disease (n=25) and healthy subjects (n=5) were analyzed by imaging and classical flow cytometry after density gradient separation. The identity of the cells in the peripheral blood mononuclear cell layer was determined using antibodies directed specifically against white (anti-CD45) or red (anti-glycophorin A) blood cells. RESULTS: Aggregates between red blood cells and peripheral blood mononuclear cells were visualized in whole blood from patients with sickle cell disease. The aggregation rate was 10-fold higher in these patients than in control subjects. Both mature red blood cells and reticulocytes were involved in these aggregates through their interaction with mononuclear cells, mainly with monocytes. The size of the aggregates was variable, with one mononuclear cell binding to one, two or several red blood cells. Erythroid Lu/basal cell adhesion molecule and α(4)β(1) integrin were involved in aggregate formation. The aggregation rate was lower in patients treated with hydroxycarbamide than in untreated patients. CONCLUSIONS: Our study gives visual evidence of the existence of circulating red blood cell-peripheral blood mononuclear cell aggregates in patients with sickle cell disease and shows that these aggregates are decreased during hydroxycarbamide treatment. Our results strongly suggest that erythroid Lu/basal cell adhesion molecule proteins are implicated in these aggregates through their interaction with α(4)β(1) integrin on peripheral blood mononuclear cells.
ISSN: 0390-6078

inserm-00821120
http://www.hal.inserm.fr/inserm-00821120
http://www.hal.inserm.fr/inserm-00821120/document
http://www.hal.inserm.fr/inserm-00821120/file/1841.full.pdf
DOI : 10.3324/haematol.2010.026294

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Association of adenylyl cyclase 6 rs3730070 polymorphism and hemolytic level in patients with sickle cell anemia
Auteur(s) : Cita, Kizzy-Clara Ferdinand, Séverine Connes, Philippe Brudey, Laura Tressieres, Benoît Etienne-Julan, Maryse Lemonne, Nathalie Tarer, Vanessa
Auteurs secondaires : Observatoire Régional de la Santé de la Guadeloupe ; Observatoire Régional de la Santé de la Guadeloupe Dynamique des Structures et Interactions des Macromolécules Biologiques- Pôle de La Réunion (DSIMB Réunion) ; Dynamique des Structures et Interactions des Macromolécules Biologiques (DSIMB) ; Institut National de la Transfusion Sanguine [Paris] (INTS) - Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Institut National de la Transfusion Sanguine [Paris] (INTS) - Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Université de la Réunion (UR) 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 Unité Transversale de la Drépanocytose ; CHU Pointe-à-Pitre/Abymes Service d'Orthopédie et de Traumatologie ; Université des Antilles et de la Guyane (UAG) - CHU Pointe-à-Pitre/Abymes Insern, UMR 763, Hôpital Robert Debré ; Université Paris Diderot - Paris 7 (UPD7) 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)

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