Philippe Chadebech

ORCID: 0000-0003-0757-4309
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About
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Research Areas
  • Blood groups and transfusion
  • Hemoglobinopathies and Related Disorders
  • Erythrocyte Function and Pathophysiology
  • Microtubule and mitosis dynamics
  • Cancer-related Molecular Pathways
  • Blood transfusion and management
  • Hepatitis B Virus Studies
  • Neonatal Health and Biochemistry
  • Blood properties and coagulation
  • Platelet Disorders and Treatments
  • Iron Metabolism and Disorders
  • Cancer Treatment and Pharmacology
  • Immunodeficiency and Autoimmune Disorders
  • Erythropoietin and Anemia Treatment
  • Blood donation and transfusion practices
  • Cell death mechanisms and regulation
  • Diabetes and associated disorders
  • Hemoglobin structure and function
  • Genomic variations and chromosomal abnormalities
  • Polydiacetylene-based materials and applications
  • Complement system in diseases
  • Heparin-Induced Thrombocytopenia and Thrombosis
  • Heme Oxygenase-1 and Carbon Monoxide
  • Blood disorders and treatments
  • Cancer-related molecular mechanisms research

Inserm
2013-2023

Université Paris-Est Créteil
2014-2023

Établissement Français du Sang
2013-2023

Institut Mondor de Recherche Biomédicale
2013-2023

Université Paris Cité
2023

Laboratory of Excellence GR-Ex
2016-2022

Biologie Intégrée du Globule Rouge
2017

Centre National de la Recherche Scientifique
1997-2003

Hôpital Edouard Herriot
2003

Université Toulouse III - Paul Sabatier
1999-2000

Abstract Delayed hemolytic transfusion reaction (DHTR) is a life‐threatening complication of in sickle cell disease (SCD). The frequency DHTR underestimated because its symptoms mimic those vaso‐occlusive crisis and antibodies (Abs) are often not detectable. No predictive factors for identifying patients likely to develop have yet been defined. We conducted prospective single‐center observational study over 30 months adult patients. included 694 episodes (TEs) 311 patients, divided into...

10.1002/ajh.24908 article EN American Journal of Hematology 2017-09-19

Delayed hemolytic transfusion reaction (DHTR) is a life-threatening complication in sickle cell disease (SCD) characterized by recurrence of complications, recipient red blood (RBC) destruction, and frequently no detectable antibody. Phosphatidylserine (PS) exposure signs suicidal RBC death or eryptosis involved vasoocclusive crisis (VOC).Transfusion was monitored 48 SCD patients for up to 20 days. PS evaluated vivo on patient RBCs (PS-RBCs) at five time points vitro after incubation donor...

10.1111/j.1537-2995.2009.02199.x article EN Transfusion 2009-04-28

The complement system is an innate immune defense cascade that can cause tissue damage when inappropriately activated. Evidence for over activation has been reported in small cohorts of patients with sickle cell disease (SCD). However, the mechanism governing SCD not elucidated. Here, we observe plasma concentration sC5b-9, a reliable marker terminal activation, increased at steady state 61% untreated patients. We show greater vitro promoted by erythrocytes compared to normal ones, although...

10.1002/ajh.25742 article EN American Journal of Hematology 2020-01-28

Background Delayed haemolytic transfusion reaction ( DHTR ) is mainly caused by an immune response to transfused red blood cells RBC s). Immunized patients have a high risk of producing antibodies in further transfusion. Controlling the s therefore major goal sickle cell disease SCD ). Study design We report observational study eight alloimmunized with history severe who were treated rituximab before new prevent immunization and . Results Five showed good clinical outcome following preceded...

10.1111/vox.12217 article EN Vox Sanguinis 2014-12-18

Delayed hemolytic transfusion reaction (DHTR), a life-threatening complication in sickle cell disease (SCD), is characterized by marked hemoglobin drop with destruction of both transfused and autologous red blood cells (RBCs) exacerbation SCD symptoms. One mechanism RBCs auto-antibody production secondary to transfusion. As rituximab specifically targets circulating B cells, we thought that it could be beneficial preventing this immune-mediated complication. We report the case patient who...

10.3324/haematol.12074 article EN cc-by-nc Haematologica 2007-11-30

Activation of protein kinase C (PKC) inhibits cell cycle progression at the G1/S and G2/M transitions. We found that phorbol 12‐myristate 13‐acetate (PMA) induced upregulation p21, not only in MCF‐7 cells arrested G1 phase as previously shown, but also delayed G2 phase. This increase p21 accumulated phases after PMA treatment was inhibited by PKC inhibitor GF109203X. indicates activity is required for PMA‐induced arrest cycle. To further assess role PKC‐induced independently its arrest, we...

10.1016/s0014-5793(99)00022-8 article EN FEBS Letters 1999-02-05

Autoimmune hemolytic anemia (AIHA) due to warm-acting IgA autoantibodies is rare. We explored the pathogenic mechanisms underlying destruction of red blood cells (RBCs) in a patient with severe AIHA mediated exclusively by polymeric immunoglobulin A (pIgA) anti-Band 3 autoantibodies. The follow-up period was 17 months. RBCs were not destroyed complement activation as no deposition observed on patient's RBCs. pIgA eluted from did induce RBC through phagocytosis monocytes or antibody-dependent...

10.1182/blood-2010-03-276162 article EN cc-by Blood 2010-07-20

Polymerization of the sickle hemoglobin (HbS) is a key determinant cell disease (SCD), an inherited blood disorder. Fetal (HbF) major modulator severity by both decreasing HbS intracellular concentration and inhibiting its polymerization. However, heterocellular distribution HbF common in SCD. For polymerization inhibition, hypothesis "HbF per red (HbF/RBC) threshold" requires accurate measurement individual RBC. To date, detection methods are limited to qualitative RBC populations...

10.1002/ajh.25937 article EN American Journal of Hematology 2020-07-18

Background Pneumococcal hemolytic uremic syndrome ( P ‐ HUS ) is a rare but severe complication of invasive pneumococcal disease IPD in young children. Consensual biologic diagnosis criteria are currently lacking. Study Design and Methods A prospective study was conducted on 10 children with culture‐confirmed . Five presented full‐blown , three had an incomplete form anemia mild or no uremia HA ), two neither nor T homsen‐ F riedenreich h, Tk cryptantigens sialic acid expression were...

10.1111/trf.12981 article EN Transfusion 2014-12-30

Microtubule damages induced by paclitaxel inhibit proteasome-dependent degradation of cyclin B, resulting in a sustained activation B/cdc2 kinase and cell cycle arrest mitosis. It has been previously shown that this activity is also required for paclitaxel-induced apoptosis. We found here increased cdc2 mRNA protein levels led to an accumulation the active dephosphorylated form NIH-OVCAR-3 cells. The addition cycloheximide inhibited increase level, further indicating stimulates synthesis....

10.1002/1097-0215(20000915)87:6<779::aid-ijc3>3.0.co;2-4 article EN International Journal of Cancer 2000-01-01

BACKGROUND Delayed hemolytic transfusion reaction (DHTR) is a life‐threatening condition in sickle cell disease (SCD) patients that frequently complicated by hyperhemolysis. Antibodies resulting from antigen disparity between donors of European ancestry and African are common, but situations involving antibodies not classically clinical significance also encountered. Anti‐HI generally considered to be an innocuous naturally occurring antibody. STUDY DESIGN AND METHODS We describe two cases...

10.1111/trf.13611 article EN Transfusion 2016-05-03

BACKGROUND The transfusion of red blood cell (RBC) concentrates is the main treatment for acute vaso‐occlusive symptoms in sickle disease (SCD). Units packed RBCs (pRBCs) must retain optimal characteristics throughout storage period. Transfused interact with plasma and endothelium that lines vessels may be target immune‐hematologic conflict if patient produces antibodies against RBCs. Questions remain concerning benefit‐risk balance RBC transfusions, particular about shelf‐life units. STUDY...

10.1111/trf.13636 article EN Transfusion 2016-05-17

BACKGROUND Red blood cell (RBC) Thomsen‐Friedenreich antigen exposure (T activation) in infants with necrotizing enterocolitis (NEC) has occasionally been associated posttransfusional intravascular hemolysis thought to be due anti‐T antibodies the donor plasma. STUDY DESIGN AND METHODS We describe an infant NEC and Clostridium perfringens infection complicated by severe after plasma transfusion. After this case, confirmed were prospectively evaluated for T activation. checked patients...

10.1111/trf.14196 article EN Transfusion 2017-06-22

Background and Objectives Intravascular haemolytic reactions are reported in red‐cell T‐activated patients after blood transfusion. The relationship between T antigen antibodies present normal plasma these remains unclear. In this study, we assessed the activity of vitro comparison with anti‐A/B antibodies. Materials Methods We established a haemolysis assay based on treating target red‐blood‐cells (RBCs) 2‐aminoethylisothiouronium bromide (AET). Two hundred seven donor sera were analysed...

10.1111/j.1423-0410.2010.01450.x article EN Vox Sanguinis 2010-11-30

BACKGROUND Red blood cell (RBC) storage in banks is not exempt from cellular injury. Alterations observed on RBCs freshly isolated units can rapidly appear circulation. The transfusion of old units, even if this a controversial issue, could therefore have adverse effects the recipient. We wanted to determine respective duration and recipient plasma for into patients with severe sepsis. STUDY DESIGN AND METHODS Eleven stored RBC were sampled at various time points, approximately Days 3 8...

10.1111/trf.14170 article EN Transfusion 2017-05-31

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10.3324/haematol.2017.175976 article FR cc-by-nc Haematologica 2017-10-12

Blood transfusion remains a key treatment for managing occlusive episodes and painful crises in sickle-cell disease (SCD). In that clinical context, red blood cells (RBCs) from donors transfused to patients, may be affected by plasma components the recipients' blood. Senescence lesion markers appear on after transfusion, shortening RBC lifespan circulation. specific context of SCD, senescence signals can also trigger events, typical disease. This work follows through our previous data...

10.3390/biom11070963 article EN cc-by Biomolecules 2021-06-30
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