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33 results on '"Radu, Claudia M."'

3. Comparison of assays measuring extracellular vesicle tissue factor in plasma samples: communication from the ISTH SSC Subcommittee on Vascular Biology

Author

Bonifay, Amandine, Mackman, Nigel, Hisada, Yohei, Sachetto, Ana Teresa Azevedo, Hau, Chi, Gray, Elaine, Hogwood, John, Aharon, Anat, Badimon, Lina, Barile, Lucio, Baudar, Justine, Beckmann, Lennart, Benedikter, Birke, Bolis, Sara, Bouriche, Tarik, Brambilla, Marta, Burrello, Jacopo, Camera, Marina, Campello, Elena, Ettelaie, Camille, Faille, Dorothée, Featherby, Sophie, Franco, Corentin, Guldenpfennig, Maite, Hansen, John-Bjarne, Judicone, Coralie, Kim, Yohan, Kristensen, Soren Risom, Laakmann, Katrin, Langer, Florian, Latysheva, Nadezhda, Lucien, Fabrice, de Menezes, Erika Marques, Mullier, François, Norris, Philip, Nybo, Jette, Orbe, Josune, Osterud, Bjarne, Paramo, Jose A., Radu, Claudia M., Roncal, Carmen, Samadi, Nazanin, Snir, Omri, Suades, Rosa, Wahlund, Casper, Chareyre, Corinne, Abdili, Evelyne, Martinod, Kimberly, Thaler, Johannes, Dignat-George, Françoise, Nieuwland, Rienk, and Lacroix, Romaric

Published
2024
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4. Profiling plasma alterations of extracellular vesicles in patients with acutely decompensated cirrhosis and bacterial infection.

Author

Campello, Elena, Zanetto, Alberto, Radu, Claudia M., Toffanin, Serena, Shalaby, Sarah, Gavasso, Sabrina, Rizzo, Stefania, Perin, Nicola, Angeli, Paolo, Burra, Patrizia, Senzolo, Marco, and Simioni, Paolo

Subjects
BACTERIAL diseases, EXTRACELLULAR vesicles, CIRRHOSIS of the liver, HOSPITAL patients, ELECTRON microscopy
Abstract

Background: Extracellular vesicles (EVs) modulate inflammation, coagulation and vascular homeostasis in decompensated cirrhosis. Aim: To characterize the profile of plasmatic EVs in patients with decompensated cirrhosis and bacterial infections and evaluate the association between EVs and the development of hemostatic complications. Methods: We measured the levels of EVs using high-sensitivity flow cytometry and phospholipid-dependent clotting time (PPL) in a prospective cohort of hospitalized patients with acutely decompensated cirrhosis with versus without bacterial infections. A separate cohort of patients with bacterial infections without cirrhosis was also enrolled. We measured endothelium-, tissue factor (TF)-bearing, platelet- and leukocyte-derived EVs. In patients with infections, EVs were reassessed upon resolution of infection. Bleeding and thrombotic complications were recorded during 1-year follow-up. Results: Eighty patients with decompensated cirrhosis were recruited (40 each with and without bacterial infections). Electron microscopy confirmed the presence of plasma EVs. Despite no difference in total EVs and PPL, patients with cirrhosis and infection had significantly higher TF+ EVs, P-Selectin+ EVs (activated platelet-derived), CD14+ EVs (monocyte/macrophages derived) and CD14+ TF+ EVs versus those with cirrhosis without infection. Upon infection resolution, levels of these EVs returned to those without infection. Patients with infections showed a significant association between reduced P-Selectin+ EVs and bleeding complications (HR 8.0 [95%CI 1.3-48.1]), whereas high levels of leukocyte-derived EVs (CD45+) and CD14+ EVs were significantly associated with thrombotic complications (HR 16.4 [95%CI 1.7-160] and 10.9 [95%CI 1.13-106], respectively). Results were confirmed in a validation cohort. Conclusion: Bacterial infections are associated with particular alterations of plasma EVs profile in decompensated cirrhosis. Bacterial infections trigger the release of EVs originating from various cell types, which may tip the precarious hemostatic balance of patients with acutely decompensated cirrhosis towards hyper- or hypocoagulability. [ABSTRACT FROM AUTHOR]

Published
2024
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6. In vitroand ex vivorescue of a nonsense mutation responsible for severe coagulation factor V deficiency

Author

Todaro, Alice M., Radu, Claudia M., Ciccone, Maria, Toffanin, Serena, Serino, M. Luisa, Campello, Elena, Bulato, Cristiana, Lunghi, Barbara, Gemmati, Donato, Cuneo, Antonio, Hackeng, Tilman M., Simioni, Paolo, Bernardi, Francesco, and Castoldi, Elisabetta

Abstract

Coagulation factor V (FV) deficiency is a rare bleeding disorder that is usually managed with fresh-frozen plasma. Patients with nonsense mutations may respond to treatment with readthrough agents.

Published
2024
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11. Partial F8 gene duplication (factor VIII Padua) associated with high factor VIII levels and familial thrombophilia

Author

Simioni, Paolo, primary, Cagnin, Stefano, additional, Sartorello, Francesca, additional, Sales, Gabriele, additional, Pagani, Luca, additional, Bulato, Cristiana, additional, Gavasso, Sabrina, additional, Nuzzo, Francesca, additional, Chemello, Francesco, additional, Radu, Claudia M., additional, Tormene, Daniela, additional, Spiezia, Luca, additional, Hackeng, Tilman M., additional, Campello, Elena, additional, and Castoldi, Elisabetta, additional

Published
2021
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13. Immunization with Pentraxin3 prevents transition from subclinical to clinical lupus nephritis in lupus-prone mice: Insights from renal ultrastructural findings

Author

Gatto, Mariele, primary, Radu, Claudia M., additional, Luisetto, Roberto, additional, Ghirardello, Anna, additional, Bonsembiante, Federico, additional, Trez, Davide, additional, Valentino, Sonia, additional, Bottazzi, Barbara, additional, Simioni, Paolo, additional, Cavicchioli, Laura, additional, and Doria, Andrea, additional

Published
2020
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16. Partial F8gene duplication (factor VIII Padua) associated with high factor VIII levels and familial thrombophilia

Author

Simioni, Paolo, Cagnin, Stefano, Sartorello, Francesca, Sales, Gabriele, Pagani, Luca, Bulato, Cristiana, Gavasso, Sabrina, Nuzzo, Francesca, Chemello, Francesco, Radu, Claudia M., Tormene, Daniela, Spiezia, Luca, Hackeng, Tilman M., Campello, Elena, and Castoldi, Elisabetta

Abstract

High coagulation factor VIII (FVIII) levels comprise a common risk factor for venous thromboembolism (VTE), but the underlying genetic determinants are largely unknown. We investigated the molecular bases of high FVIII levels in 2 Italian families with severe thrombophilia. The proband of the first family had a history of recurrent VTE before age 50 years, with extremely and persistently elevated FVIII antigen and activity levels (>400%) as the only thrombophilic defects. Genetic analysis revealed a 23.4-kb tandem duplication of the proximal portion of the F8gene (promoter, exon 1, and a large part of intron 1), which cosegregated with high FVIII levels in the family and was absent in 103 normal controls. Targeted screening of 50 unrelated VTE patients with FVIII levels ≥250% identified a second thrombophilic family with the same F8rearrangement on the same genetic background, suggesting a founder effect. Carriers of the duplication from both families showed a twofold or greater upregulation of F8messenger RNA, consistent with the presence of open chromatin signatures and enhancer elements within the duplicated region. Testing of these sequences in a luciferase reporter assay pinpointed a 927-bp region of F8intron 1 associated with >45-fold increased reporter activity in endothelial cells, potentially mediating the F8transcriptional enhancement observed in carriers of the duplication. In summary, we report the first thrombophilic defect in the F8gene (designated FVIII Padua) associated with markedly elevated FVIII levels and severe thrombophilia in 2 Italian families.

Published
2021
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18. Dual polarization of human alveolar macrophages progressively increases with smoking and COPD severity

Author

Bazzan, Erica, primary, Turato, Graziella, additional, Tinè, Mariaenrica, additional, Radu, Claudia M., additional, Balestro, Elisabetta, additional, Rigobello, Chiara, additional, Biondini, Davide, additional, Schiavon, Marco, additional, Lunardi, Francesca, additional, Baraldo, Simonetta, additional, Rea, Federico, additional, Simioni, Paolo, additional, Calabrese, Fiorella, additional, Saetta, Marina, additional, and Cosio, Manuel G., additional

Published
2017
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29. Endocytosis of exogenous factor V by ex-vivo differentiated megakaryocytes from patients with severe parahaemophilia.

Author

Radu, Claudia M., Spiezia, Luca, Bulato, Cristiana, Gavasso, Sabrina, Campello, Elena, Sartorello, Francesca, Castoldi, Elisabetta, and Simioni, Paolo

Subjects
*HEMOPHILIA treatment, *MEGAKARYOCYTE differentiation, *BLOOD coagulation factor V, *ENDOCYTOSIS, *BLOOD transfusion, *STEM cell culture, *BLOOD donors
Abstract

Although human megakaryocytes can synthesize factor V ( FV), platelet FV derives largely from endocytosis of plasma FV. Recently, it has been shown that plasma transfusions can replenish the platelet FV pool in parahaemophilic patients. Here we corroborate this finding by showing FV endocytosis by ex vivo differentiated megakaryocytes derived from patients with inherited parahaemophilia. Mononuclear stem cells isolated from peripheral blood of healthy subjects and of three patients with severe parahaemophilia were cultured in the presence of thrombopoietin and interleukin-3 and differentiated into CD41-positive polynucleated megakaryocytes. Exogenous purified FV was added to the culture medium to evaluate FV endocytosis. Immunofluorescence staining revealed abundant FV expression in megakaryocytes derived from healthy donors, but no FV expression in those derived from patients with severe parahaemophilia. However, after the addition of purified FV to the culture medium, megakaryocytes from parahaemophilia patients became positive upon FV immunostaining, suggesting endocytosis of exogenous FV. Endocytosed FV retained factor Xa-co-factor activity as assessed by a prothrombin time-based functional test in megakaryocyte lysates. Addition of exogenous FV to culture medium can restore the FV content of megakaryocytes derived from patients with severe FV defects. This rescue mechanism can have important clinical implications in the management of parahaemophilia patients. [ABSTRACT FROM AUTHOR]

Published
2016
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