M. Laforet
University of Strasbourg
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Featured researches published by M. Laforet.
Transfusion | 2011
Jean-Pierre Cazenave; Hervé Isola; Chantal Waller; Isabelle Mendel; Daniel Kientz; M. Laforet; Jean‐Pierre Raidot; Gérard Kandel; Marie-Louise Wiesel; Laurence Corash
BACKGROUND: The Etablissement Français du Sang Alsace (EFS Alsace) successively implemented universal use of platelet additive solutions (PASs) and pathogen inactivation (PI) for platelet components (PCs). To assess the impact of these changes, EFS Alsace evaluated PC use, red blood cell (RBC) component use, and transfusion‐related adverse events after implementation of these new technologies.
Human Immunology | 1993
M. Laforet; Arlette Urlacher; Annie Falkenrodt; Bruno Lioure; Anne Parissiadis; Marie Marthe Tongio
In the present work, we describe a new DR14 allele. Sequencing of its second DRB1 exon showed it to be DRB1*1404 from codon numbers 9 to 56 and 61 to 86, and DRB1*11 from codons 57 to 60 inclusive.
Vox Sanguinis | 2004
J.‐P. Cazenave; B. Aleil; M.‐L. Wiesel; M. Laforet; H. Isola
Recent studies by van Rhenen et al. found that platelets treated with amotosalen hydrochloride and ultraviolet A (UVA) illumination (INTERCEPT Blood System; Baxter Healthcare, Deerfield, IL, USA) are therapeutically equivalent to conventional (untreated) platelets currently in use [1]. Such treatment inactivates a broad spectrum of transfusiontransmitted viruses, bacteria and parasites, as well as residual donor leucocytes. Prior to the implementation of this process for all platelet units, the EFS-Alsace blood centre in Strasbourg, France, undertook a series of validation studies. The objective of our study was to provide in vitro data on the quality of buffy-coat platelet concentrates (PCs) that were treated with amotosalen and UVA. Treated PCs were studied for a period of 8 days. In accordance with standard site procedures, PCs (n = 35) were prepared from pools of six BC units suspended in InterSol platelet additive solution (65%) and plasma (35%) prior to treatment with amotosalen and UVA. Treated PCs were stored at 22 ± 2 °C. PC parameters (mean ± standard deviation) were measured, in vitro, both before treatment on day 1 and after treatment on days 2, 5, 7 and 8 of storage, as reported in Table 1. The platelet yield before treatment was 4·5 ± 0·5 × 1011. As expected, following processing, significant differences were recorded in pH, lactate, lactate dehydrogenase (LDH), platelet factor 4 (PF4), soluble p-selectin, soluble platelet glycoprotein V (GpV), mean platelet volume, O2 partial pressure (pO2) and interleukin-8 (IL-8). Non-significant differences were observed in platelet swirling, CO2 partial pressure (pCO2) and tumour necrosis factor-α (TNF-α). On day 8, significant differences were observed in pH, lactate, LDH, PF4, soluble p-selectin, soluble GpV, mean platelet volume, pCO2 and TNF-α. Non-significant differences were observed in pO2 and IL-8. Platelet swirling was maintained for 8 days. The in vitro parameters showed normal metabolism and ageing of platelets for up to 8 days after treatment with amotosalen and UVA. From this, we conclude that such treatment is fully compatible with blood centre processing laboratory protocols, and can be used routinely in clinical practice to
Vox Sanguinis | 2006
H. Isola; D. Kientz; B. Aleil; P. Laeuffer; J. Weil; M.‐L. Wiesel; M. Laforet; Lily Lin; Veronique Mayaudon; J.‐P. Cazenave
Pathogen inactivation using the INTERCEPT Blood System™ requires platelet resuspension in InterSol™ and reduced plasma. Platelets in plasma collected on the Haemonetics MCS+® were processed on the INTERCEPT Preparation Set™ for plasma volume reduction and addition of InterSol. The use of the Preparation Set resulted in a mean platelet loss of 5·6 ± 3·4%. Subsequent photochemical treatment (PCT) with amotosalen and ultraviolet A light, and 7 days of storage, resulted in acceptable changes for platelet swirling, lactate, lactate dehydrogenase (LDH), platelet factor‐4 (PF4), p‐selectin, glycoprotein V (GpV), pO2, pCO2, tumour necrosis factor‐α (TNF‐α) and interleukin‐8 (IL‐8). All platelet units processed with the Preparation Set and PCT met European requirements for leucoreduction and pH values.
Archive | 2008
Jean-Pierre Cazenave; Chantal Waller; Isabelle Mendel; Daniel Kientz; Gérard Kandel; Jean‐Pierre Raidot; Marie-Louise Wiesel; M. Laforet; Hervé Isola
Blood transfusion is a critical supportive therapy for health care. The demand for platelet components (PCs), either derived from apheresis or from whole blood buffy coats, has continually increased as health care technology and life expectancy have increased. The public and the medical community expect that PCs for transfusion will be safe and available when needed. Pharmaceutical standards for medications to be administered intravenously to patients require sterility and absence of pyrogens. However, sterilization or inactivation of pathogens remains a major challenge for blood components. A number of physical methods (heat, light, and filtration) and chemical techniques (solvent-detergent) have been applied with success to therapeutic plasma and purified plasma proteins. However, pathogen inactivation treatment of the labile cellular blood components (platelets and red blood cells) has been much more difficult to achieve without significant loss of cell viability and cell function. The safety of labile blood products, including PCs, has previously been ensured by medical and biological donor selection measures. While these measures have improved the safety of blood transfusion, they are reactive and have not eliminated the risk of transfusion-transmitted infection. In addition to the residual risk of recognized viral, bacterial and parasitic contamination of PCs, there is the recurring risk associated with emerging pathogens as demonstrated by several recent epidemics and a continuing pattern of emergence and reemergence of transfusion-transmitted pathogens [1]. Pathogen inactivation of PCs has been implemented into routine practice and offers the potential to protect against the residual risk of known pathogens and the risk of emerging pathogens for which diagnostic tests are not available. Recently, this technology has demonstrated its utility during an epidemic of an emerging pathogen, and represents a paradigm shift in the approach to blood transfusion safety.
Vox Sanguinis | 2018
Catherine Ravanat; Arnaud Dupuis; N. Marpaux; Christian Naegelen; Guillaume Mourey; H. Isola; M. Laforet; Pascal Morel; Christian Gachet
Small batch‐pooled (mini‐pool) whole blood (WB)‐derived plasma could be an alternative cost‐effective source of therapeutic plasma (TP), but carries an increased risk of transfusion‐transmitted infection due to exposure of the recipient to several donors. This risk can be mitigated by inactivation of pathogens susceptible to the amotosalen‐UVA (AUVA)‐treatment. We evaluated the conservation of coagulation factors in AUVA‐plasma prepared from WB stored overnight under routine operating conditions, to determine its therapeutic efficacy. Thrombin generation (TG) by the AUVA‐plasma was used to provide an integrated measure of the hemostatic capacity.
Blood | 2003
Dirk Jan van Rhenen; Stephane Marblie; M. Laforet; Kathryn B. Davis; Maureen G. Conlan; Bruno Lioure; Hans Gulliksson; Jean-Pierre Cazenave; Peyton S. Metzel; Derwood Pamphilon; Laurence Corash; Jocelyne Flament; Per Ljungman; Harald Klüter; Hans Vermeij; Veronique Mayaudon; Lily Lin; Mies Kappers-Klunne; Don Buchholz; Georgine E. de Greef
Tissue Antigens | 1999
M. Laforet; N. Froelich; A. Parissiadis; A. Schell; B. Pfeiffer; J.‐P. Cazenave; Marie Marthe Tongio
Transfusion and Apheresis Science | 2001
Daniel Kientz; M. Laforet; Hervé Isola; Jean-Pierre Cazenave
Tissue Antigens | 1994
M. Laforet; Arlette Urlacher; M. M. Tongio