Browsing by Author "Mezzano, Diego"

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    A review of platelet secretion assays for the diagnosis of inherited platelet secretion disorders
    (2015) Mumford, Andrew D.; Frelingerm III, Andrew L.; Gachet, Christian; Gresele, Paolo; Noris, Patrizia; Harrison, Paul; Mezzano, Diego
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    An adenine insertion in exon 6 of human GP6 generates a truncated protein associated with a bleeding disorder in four Chilean families
    (2013) Matus Ritter, Valeria; Valenzuela, G.; Sáez S., Claudia; Hidalgo, P.; Lagos Lucero, Marcela; Aranda Lauriani, Eduardo Javier; Panes Becerra, Olga Teresa; Pereira Garcés, Jaime Ignacio; Pillois, X.; Nurden, A.; Mezzano, Diego
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    Atorvastatin Prevents the Proadhesive and Prothrombotic Endothelial Cell Phenotype Induced by Cocaine and Plasma from Cocaine Consumers in Vitro
    (2014) Sáez, C.; Pereira Flores, K.; Ebensperger González, Roberto Alejandro; Panes Becerra, Olga Teresa; Massardo, T.; Hidalgo, P.; Mezzano, Diego; Pereira Garcés, Jaime Ignacio
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    La atorvastatina no modifica el incremento agudo de los niveles de p-selectina y fibrinógeno inducido con esfuerzo físico máximo
    (2010) Lindefjeld, Dante; Acevedo B., Mónica; Chamorro S., Gastón; Mezzano, Diego; Panes Becerra, Olga Teresa; Aranis, C.; Oporto, J.
    Introducción: Las estatinas han demostrado disminuir los eventos cardiovasculares en sujetos con y sin enfermedad aterosclerótica establecida. Se ha demostrado, que sus efectos benéficos no sólo dependen de la reducción del colesterol, sino que también podrían ser secundarios a otros efectos de las estatinas, como su efectos de reducción de inflamación y/ o trombogénesis entre otros. Sin embargo, no existen trabajos que demuestren que las estatinas sean capaces de frenarla activación de la cascada de inflamación y/o trombogénesis. Objetivos: Determinar el efecto de la administración oral de atorvastatina por 7 días sobre los niveles plasmáticos de proteína C- reactiva ultrasensible (PCR us), fibrinógeno y P-selectina, pre y post prueba de esfuerzo máximo inmediato y a las 24 horas de su ejecución. Métodos: Ensayo clínico en 50 hombres sanos (18 a 50 años), randomizado atorvastatina 80 mg/día - placebo por 7 días, doble ciego. Muestras tomadas en sangre para PCRus, fibrinógeno y P-selectina, perfil lipídico, creatin kinasa y transaminasas hepáticas, pre y post test de esfuerzo, y a las 24 horas. Los resultados para datos continuos se expresan como medias ± desviación estándar, test de student para muestras independientes, ANOVA para muestras repetidas. Programa estadístico SPSS 14.0. Resultados: Un grupo de 44 sujetos completaron el estudio: atorvastatina 80 mg (n=24) o placebo (n=20). En el grupo atorvastatina, después de una semana de tratamiento, los niveles de LDLc disminuyeron en 38% (LDL basal: 97 ± 27 mg/dL vs LDL post: 62 ± 31 mg/dL, p < 0.001). Sin embargo, no se observaron cambios en ese mismo período en los niveles de PCRus, fibrinógeno y P-selectina con respecto a placebo. Los niveles de fibrinógeno se elevaron 8% entre la etapa pre y post ejercicio inmediato (341 ± 56 mg/dL vs 368 ± 65 mg/dL, p<0.001), retornando a los niveles básales a las 24 horas; no hubo diferencias entre atorvastatina - placebo. Los niveles de P-selectina aumentaron 9.5% entre la etapa pre y post ejercicio inmediato (25 ± 1.5 ng/dL vs 28 ±1.7 ng/dL, p = 0.01), retornando a los niveles basales a las 24 horas; no hubo diferencias entre atorvastatina - placebo. El ejercicio no indujo elevación de PCRus. Los niveles plasmáticos de CKtotal se elevaron significativamente en ambos grupos post ejercicio (Atorvastatina 43% aumento, p = 0.004 versus nivel basal y placebo 12% aumento, p = 0.005 versus nivel basal). Sin embargo, no se encontró diferencias estadísticamente significativas entre el grupo atorvastatina versus placebo. Conclusiones: La administración de atorvastatina oral 80 mg/día por 7 días en sujetos sanos no inhibió la elevación de los niveles plasmáticos de fibrinógeno y P-selectina inducida por ejercicio.
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    Blood Cells Cholinesterase Activity in Early Stage Alzheimer's Disease and Vascular Dementia
    (2005) Bernhardi Montgomery, Rommy von; Mezzano, Diego; Inestrosa Cantín, Nibaldo
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    Changes in regional cerebral blood flow are associated with endothelial dysfunction markers in cocaine-dependent patients under recent abstinence
    (2015) Massardo, T.; Quintana Fresno, Juan Carlos; Jaimovich, Rodrigo; Sáez S., Claudia; Cabreras, M.J.; Pereira-Flores, K.; Ibanez, C.; Pallavicini, J.; Veliz, J.; Mezzano, Diego; Pereira Garcés, Jaime Ignacio
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    Complementary effects of Mediterranean diet and moderate red wine intake on haemostatic cardiovascular risk factors
    (NATURE PUBLISHING GROUP, 2001) Mezzano, Diego; Leighton Puga, Federico; Martínez, Carlos; Marshall Rivera, Guillermo; Cuevas Marín, Ada Marisa; Castillo Valenzuela, Oscar; Panes Becerra, Olga Teresa; Rozowski Narkunska, Samuel Jaime; Pérez Pons, Druso Diego; Mizón Costa, Claudio Luis Enrique; San Martin, Alejandra; Pereira Pereira, J. Marcello
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    Daño endotelial y activación del sistema hemostático asociado al uso crónico de cocaína: estudios ex vivo e in vitro
    (2010) Pereira Garcés, Jaime Ignacio; Sáez, C.; Olivares, P.; Moreno, N.; Cabrera, M. J.; Panes Becerra, Olga Teresa; Belmont, S.; Hidalgo, P.; Massardo, T.; Pallavicini, J.; Mezzano, Diego
    Antecedentes: Usuarios crónicos de cocaína tienen riesgo aumentado de presentar infarto de miocardio, angina, muerte súbita y accidentes cerebrovasculares. Aunque la patogenia del daño vascular es mayormente desconocida, se ha encontrado arterieesclerosis prematura y formación de trombos intravasculares. Objetivo: Demostrar evidencia de daño endotelial y activación del sistema hemostático en usuarios crónicos de cocaína. Métodos: Un grupo de 23 pacientes con criterios de dependencia a cocaína DSM-IV; 19 hombres (edad promedio 32 a), con exposición a la droga dentro de 72 h del estudio. Disfunción endotelial se evaluó por enumeración de las células endoteliales circulantes (CEC) y nivel de sICAM . Para activación del sistema hemostático se incluyó: complejos trombina-antitrombina (TAT) y generación de trombina; NAP-2 y RANTES para activación plaquetaria. In vitro, CE en cultivo (HUVEC), se expusieron a plasma de consumidores o controles. Se midió factor von Willebrand (FVW) en el medio y expresión de FvW y factor tisú lar (FT) sobre las CE. adhesion plaquetaria estática se evaluó por microscopía. Resultados: En usuarios de cocaína, con respecto a controles, las CEC estaban significativamente elevadas (63±28 vs 7±5 células/mL; p<0. 0001), así como los niveles plasmáticos de sICAM (360±92 vs 261 ±34 ng/mL, respectivamente; p<0. 01). TAT en pacientes y controles fueron 2. 7±0. 7 y 0. 7±0. 4µg/L; p<0. 06). NAP-2 (129±8. 4 ng/mL) y RANTES (4. 01 ±2. 12 ng/mL) significativamente aumentados comparados con controles (87. 1 ±8. 6 añd 2. 12±0. 35, respectivamente; p< 0. 01). El plasma de usuarios de cocaína indujo mayor liberación de FVW desde las HUVEC comparado con plasma control (5. 64±4. 0 vs 1. 4±0. 8 UI/dL; p ≤ 0. 001). Las HUVEC expuestas a estos mismos plasmas, mostraron aumento significativo en la expresión de FT, FVW y mayor capacidad de adherir plaquetas. Conclusiones: Consumidores crónicos de cocaína evidencian disfunción endotelial y activación del sistema hemostático. En conjunto con las observaciones in vitro del efecto de los plasmas sobre las CE, estos resultados sugieren que la aterotrombosis puede jugar un papel importante en la patogenia del daño vascular asociado al uso de cocaína.
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    Diagnosis of inherited platelet function disorders : Guidance from the SSC of the ISTH
    (2015) Gresele, P.; Harrison, P.; Gachet, C.; Hayward, C.; Kenny, D.; Mezzano, Diego; Mumford, A.; Nugent, D.; Cattaneo, M.
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    Fibrin and D-dimer bind to monomeric GPVI
    (2017) Onselaer, M. B.; Hardy, A. T.; Wilson, C.; Sánchez, X.; Babar, A. K.; Miller, J. L. C.; Watson, C. N.; Watson, S. K.; Bonna, A.; Mezzano, Diego; Philippou, H.; Herr, A. B.; Ariens, R. A. S.; Watson, S. P.
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    Fluoxetine Impairs Insulin Secretion without Modifying Extracellular Serotonin Levels in MIN6 β-cells
    (2015) Cataldo Bascuñan, Luis Rodrigo; Cortés Mora, Víctor Antonio; Mizgier Rojas, María Luisa; Aranda, E.; Mezzano, Diego; Olmos Coelho, Pablo Roberto; Galgani Fuentes, José; Suazo, J.; Santos Martín, José Luis
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    Human platelet interaction with E-coli O111 promotes tissue-factor-dependent procoagulant activity, involving Toll like receptor 4
    (2017) Matus, V.; Valenzuela, J.; Hidalgo, P.; Pozo, L.; Panes Becerra, Olga Teresa; Wozniak Banchero, Aniela; Mezzano, Diego; Pereira Garcés, Jaime Ignacio; Sáez, Claudia G.
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    Immobilized fibrinogen activates human platelets through glycoprotein VI
    (2018) Mangin, P.; Onselaer, M.; Receveur, N.; Le Lay, N.; Hardy, A.; Wilson, C.; Sanchez, X.; Loyau, S.; Dupuis, A.; Mezzano, Diego
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    Increased activation of protein C, but lower plasma levels of free, activated protein C in uraemic patients : relationship with systemic inflammation and haemostatic activation
    (BLACKWELL SCIENCE LTD, 2001) Mezzano, Diego; Quiroga Gutiérrez, Sara Teresita; Panes Becerra, Olga Teresa; Pereira Garcés, Jaime Ignacio; Pais, Edgar; Marshall Rivera, Guillermo; Tagle, Rodrigo; Downey Concha, Patricio; Cáceres, Soledad; González, Fernando
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    Increased RhoA/Rho-Kinase Activity and Markers of Endothelial Dysfunction in Young Adult Subjects with Metabolic Syndrome
    (2015) Leguina-Ruzzi, Alberto; Pereira Garcés, Jaime Ignacio; Pereira-Flores, Karla; Valderas Igor, Juan Patricio; Mezzano, Diego; Velarde Aliaga, María Victoria; Sáez S., Claudia
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    Inhibition of angiogenesis by platelets in systemic sclerosis patients
    (2015) Hirigoyen Pérez, Daniela María.; Burgos, Paula I.; Mezzano, Veronica.; Durán, Josefina; Barrientos, Magaly.; Sáez, Claudia G.; Panes Becerra, Olga Teresa; Mezzano, Diego; Iruretagoyena B., Mirentxu
    Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.
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    Inhibition of platelet activation and thrombus formation by adenosine and inosine : studies on their relative contribution and molecular modeling
    (2014) Fuentes, E.; Pereira Garcés, Jaime Ignacio; Mezzano, Diego; Alarcon, M.; Caballero, J.; Palomo, I.
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    Laboratory monitoring of P2Y12 inhibitors : communication from the SSC of the ISTH
    (2018) Frelinger III, A.L.; Gachet, C.; Mumford, A.D.; Noris, P.; Mezzano, Diego; Harrison, P.; Gresele, P.
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    Mediterranean diet, but not red wine, is associated with beneficial changes in primary haemostasis
    (2003) Mezzano, Diego; Leighton, Federico; Marshall Rivera, Guillermo; Pereira Garcés, Jaime Ignacio