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Protection of β2GPI-Deficient Mice from Thrombosis Reflects a Defect in PAR3-facilitated Platelet Activation.
Blood
January 2025
Cleveland Clinic, Cleveland, Ohio, United States.
Antibodies to β2-glycoprotein I (β2GPI) cause thrombosis in antiphospholipid syndrome, however the role of β2GPI in coagulation in vivo is not understood. To address this issue, we developed β2GPI-deficient mice (Apoh-/-) by deleting exon 2 and 3 of Apoh using CRISPR/Cas9 and compared the development of thrombosis in wild-type (WT) and Apoh-/- mice using rose bengal and FeCl3-induced carotid thrombosis, laser-induced cremaster arteriolar injury, and inferior vena cava (IVC) stasis models. We also compared tail bleeding times and activation of platelets from WT and Apoh-/- mice in the absence and presence of β2GPI.
View Article and Find Full Text PDFDedicator of Cytokinesis 2 regulates cytoskeletal actin dynamics and is essential for platelet biogenesis and functions.
Cardiovasc Res
January 2025
Department of Pharmacology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Aims: Dedicator of Cytokinesis 2 (DOCK2), a member of the DOCK family of Guanine nucleotide exchange factors that specifically act on the Rho GTPases including Rac and Cdc42, plays pivotal roles in the regulation of leukocyte homeostasis. However, its functions in platelets remain unknown.
Methods And Results: Using mice with genetic deficiency of DOCK2 (Dock2-/-), we showed that Dock2-/-mice exhibited a macrothrombocytopenic phenotype characterized as decreased platelet count and enlarged platelet size by transmission electron microscopy.
Integrating biomarkers for hemostatic disorders into computational models of blood clot formation: A systematic review.
Math Biosci Eng
December 2024
Laboratory of Optimization, Design, and Advanced Control, School of Chemical Engineering, Universidade Estadual de Campinas, Campinas, São Paulo, Brazil.
In the pursuit of personalized medicine, there is a growing demand for computational models with parameters that are easily obtainable to accelerate the development of potential solutions. Blood tests, owing to their affordability, accessibility, and routine use in healthcare, offer valuable biomarkers for assessing hemostatic balance in thrombotic and bleeding disorders. Incorporating these biomarkers into computational models of blood coagulation is crucial for creating patient-specific models, which allow for the analysis of the influence of these biomarkers on clot formation.
View Article and Find Full Text PDFEndothelial tip-cell position, filopodia formation and biomechanics require BMPR2 expression and signaling.
Commun Biol
January 2025
Freie Universität Berlin, Institute for Chemistry and Biochemistry, Thielallee 63, 14195, Berlin, Germany.
Blood vessel formation relies on biochemical and mechanical signals, particularly during sprouting angiogenesis when endothelial tip cells (TCs) guide sprouting through filopodia formation. The contribution of BMP receptors in defining tip-cell characteristics is poorly understood. Our study combines genetic, biochemical, and molecular methods together with 3D traction force microscopy, which reveals an essential role of BMPR2 for actin-driven filopodia formation and mechanical properties of endothelial cells (ECs).
View Article and Find Full Text PDFLong-Term Success of Dental Implants in Atrophic Maxillae: A 3-Year Case Series Using Hydroxyapatite and L-PRF.
Bioengineering (Basel)
November 2024
Clinical Research Laboratory, Dentistry School, Universidade Federal Fluminense, Niteroi 24220-140, Brazil.
Dental implants are essential for the prosthetic rehabilitation of edentulous patients, requiring adequate bone volume and density for osseointegration and load support. The posterior region of the maxilla, commonly deficient in bone quality and quantity, represents a clinical challenge. This case series reports an analysis involving 69 dental implants in the atrophic maxilla of nine patients.
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