Publications by authors named "C Bachelot-Loza"

Article Synopsis
  • The differentiation of megakaryocytes (Mks) from haematopoietic stem cells is influenced by mechanical forces, with PIEZO1 playing a key role in sensing these forces.
  • Gain-of-function mutations in PIEZO1 lead to hereditary xerocytosis, highlighting its importance in thrombosis and potentially affecting platelet formation.
  • This study demonstrated that activating PIEZO1 with YODA1 initially reduces Mk maturation but later promotes endomitosis and proplatelet formation, indicating a complex regulatory role for PIEZO1 in Mk development.
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Article Synopsis
  • Venoms contain enzymes that affect blood clotting, relying on calcium and phospholipids, while antivenoms vary in their ability to counteract these effects.
  • The study aimed to analyze the venom composition, assess their impact on blood coagulation through rotational thromboelastometry, and compare the effectiveness of four different antivenoms.
  • Both venoms caused increased coagulation, with one being fully dependent on calcium, while antivenoms showed varying effectiveness, particularly, Bothrofav performed best against the venoms despite differing clinical symptoms from bites.
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Anthracyclines, such as doxorubicin (Dox), are widely used chemotherapeutic agents for the treatment of solid tumors and hematologic malignancies. However, they frequently induce cardiotoxicity leading to dilated cardiomyopathy and heart failure. This study sought to investigate the role of the exchange protein directly activated by cAMP (EPAC) in Dox-induced cardiotoxicity and the potential cardioprotective effects of EPAC inhibition.

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Background: The circulating form of human endoglin (sEng) is a cleavage product of membrane-bound endoglin present on endothelial cells. Because sEng encompasses an RGD motif involved in integrin binding, we hypothesized that sEng would be able to bind integrin αIIbβ3, thereby compromising platelet binding to fibrinogen and thrombus stability.

Methods: In vitro human platelet aggregation, thrombus retraction, and secretion-competition assays were performed in the presence of sEng.

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Background: High on-treatment platelet reactivity has been reported in 30% of patients on clopidogrel and 50% in elderly patients; however, little is known about the mechanisms of this biological resistance. One hypothesis is an age-related impaired hepatic metabolism of the prodrug clopidogrel, leading to a lower formation of its active metabolite (clopidogrel-AM).

Objectives: To compare the levels of clopidogrel-AM formed using "old" and "young" human liver microsomes (HLMs) and their consequences on platelet functions.

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