Results 61 to 70 of about 12,785,139 (351)
Global Journal of Transfusion Medicine, 2019 Introduction: Hemophilia is an X-linked congenital bleeding disorder caused by a deficiency of coagulation factor VIII (FVIII) in hemophilia A (HA) or factor IX (FIX) in hemophilia B (HB).
Sangita Darshan Shah +5 more
doaj +1 more source
Immunogenicity of Current and New Therapies for Hemophilia A
Pharmaceuticals, 2022 Anti-drug antibody (ADA) development is a significant complication in the treatment of several conditions. For decades, the mainstay of hemophilia A treatment was the replacement of deficient coagulation factor VIII (FVIII) to restore hemostasis, control,
Alessandra N. L. Prezotti +3 more
doaj +1 more source
CCT4 promotes tunneling nanotube formation
FEBS Letters, EarlyView.Tunneling nanotubes (TNTs) are membranous tunnel‐like structures that transport molecules and organelles between cells. They vary in thickness, and thick nanotubes often contain microtubules in addition to actin fibers. We found that cells expressing monomeric CCT4 generate many thick TNTs with tubulin.
Miyu Enomoto +3 more
wiley +1 more source
Tolerating Factor VIII: Recent Progress
Frontiers in Immunology, 2020 Development of neutralizing antibodies against biotherapeutic agents administered to prevent or treat various clinical conditions is a longstanding and growing problem faced by patients, medical providers and pharmaceutical companies.
Sebastien Lacroix-Desmazes +4 more
doaj +1 more source
Molecular Oncology, EarlyView.This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani +14 more
wiley +1 more source
Role of Factor VIII C2 Domain in Factor VIII Binding to Factor Xa [PDF]
Journal of Biological Chemistry, 1999 Factor VIII (FVIII) is activated by proteolytic cleavages with thrombin and factor Xa (FXa) in the intrinsic blood coagulation pathway. The anti-C2 monoclonal antibody ESH8, which recognizes residues 2248-2285 and does not inhibit FVIII binding to von Willebrand factor or phospholipid, inhibited FVIII activation by FXa in a clotting assay. Furthermore,
Kazuya Hosokawa +10 more
openaire +3 more sources
Molecular Oncology, EarlyView.This study investigates gene expression differences between two major pediatric acute lymphoblastic leukemia (ALL) subtypes, B‐cell precursor ALL, and T‐cell ALL, using a data‐driven approach consisting of biostatistics and machine learning methods. Following analysis of a discovery dataset, we find a set of 14 expression markers differentiating the ...
Mona Nourbakhsh +8 more
wiley +1 more source
Haematologica, 2010 Background Pregnancy in von Willebrand’s disease may carry a significant risk of bleeding. Information on changes in factor VIII and von Willebrand factor and pregnancy outcome in relation to von Willebrand factor gene mutations are very scanty.Design ...
Giancarlo Castaman +2 more
doaj +1 more source
Molecular Oncology, EarlyView.The COMBAT classification system, developed through multi‐omics integration, stratifies adult patients with B‐cell acute lymphoblastic leukemia(B‐ALL) into three molecular subtypes with distinct surface antigen patterns, immune landscape, methylation patterns, biological pathways and prognosis.
Yang Song +11 more
wiley +1 more source
In Vitro Modeling of the Influence of FVIII Activity and Heparin Induced Prolongation of APTT
Biomolecules & Biomedicine, 2008 Anticoagulant therapy is most commonly assessed by measuring the effect of the drug on global clotting assay, such as APTT. It is known that response of the APTT to hepa-rin may be decreased in patients with high levels of factor VIII.
Aida Mehmedagić +3 more
doaj +1 more source