Browsing by Author "Mezzano, D."

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    ACCUMULATION OF 5-HYDROXYTRYPTAMINE BY AGING PLATELETS - STUDIES IN A MODEL OF SUPPRESSED THROMBOPOIESIS IN DOGS
    (GEORG THIEME VERLAG KG, 1994) Aranda, E.; Pizarro, M.; Pereira, J.; Mezzano, D.
    Thrombocytopenia was induced in healthy, male mongrel dogs by intramuscular injection of a single dose of estradiol valerate (1 mg/kg). A steady, almost linear decay of the blood platelet count starting about day 6 post-estradiol and attaining a mean value of 14 x 10(3) platelets/mu l one week later was observed. Thrombocytopenia is explained mainly by suppression of thrombocytopoiesis, as established by two independent ways: 1. Megakaryocytes in the bone marrow were markedly reduced. 2. Kinetic studies with In-111 labeled autologous platelets revealed a nearly linear decay of the radioactivity and mean survival times within the expected range. The progressive reduction in the platelet count is associated with an increase in the mean age of the platelets still circulating. Following estradiol injection, platelet 5-hydroxytryptamine (5-HT) increased from a basal value of 130 +/- 30 ng/10(8) platelets (platelet count of 351 +/- 53 x 10(3) platelets/mu l) to 343 +/- 100 ng/10(8) platelets eleven days latter, when the platelet count dropped to 32 +/- 18 x 10(3) platelets/mu l. No significant changes in the number or affinity of the 5-HT uptake receptors could be demonstrated in platelets exposed in vitro and in vivo to estradiol. Our results indicate that aging platelets accumulate 5-HT, probably by a sustained exposure to the monoamine in plasma, confirming previous observations based on models in which thrombopenia was induced by immune and mechanical means.
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    Inherited disorders of platelet function and challenges to diagnosis of mucocutaneous bleeding
    (2010) Israels, S. J.; El-Ekiaby, M.; Quiroga, T.; Mezzano, D.
    Platelets play a pivotal role in the arrest of bleeding at sites of vascular injury. Following endothelial damage, they respond rapidly by adhesion to subendothelial matrix proteins resulting in platelet activation, spreading, aggregation, secretion and recruitment of additional platelets to form the primary haemostatic plug. This mass provides a surface for thrombin generation and fibrin mesh formation that stabilizes the clot. Careful study of patients with inherited platelet disorders and, subsequently, of informative animal models, has identified structural platelet abnormalities that have enhanced our understanding of platelet function. The investigations of rare, but severe, inherited platelet disorders have led us to the discovery of causative molecular defects. One of the most informative is the rare autosomal recessive disorder Glanzmann thrombasthenia, caused by defect or deficiency in the platelet integrin alpha IIb beta 3, resulting in absent platelet aggregation and a significant clinical bleeding diathesis. Our new challenge is to understand the mechanisms underlying more common, but less well-defined, mucocutaneous bleeding (MCB) disorders. Present diagnostic testing for platelet function disorders and von Willebrand's Disease often fails to identify the cause of bleeding in individuals with inherited MCB.
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    Mediterranean food and diets, global resource for the control of metabolic syndrome and chronic diseases.
    (2008) Urquiaga, I.; Echeverría, G.; Polic, G.; Castillo, O.; Liberona, Y.; Rozowski, J.; Perez, D.; Martinez, C.; Vasquez, L.; Strobel, P.; Mezzano, D.; Leighton, F.
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    Serotonin- and Dopamine-Related Gene Expression in db/db Mice Islets and in MIN6 beta-Cells Treated with Palmitate and Oleate
    (2016) Cataldo Bascuñan, Luis Rodrigo; Busso, Dolores; Olmos Coelho, Pablo Roberto; Galgani Fuentes, José; Valenzuela, R.; Mezzano, D.; Aranda, E.; Cortés Mora, Víctor Antonio; Santos Martín, José Luis
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    Trombofilia primaria: detección y manifestación clínica en 105 casos
    (SOC MEDICA SANTIAGO, 2004) Srur, E.; Vargas, C.; Salas, S.; Parra, J.A.; Bianchi, V.; Mezzano, D.; Munoz, B.; Vasquez, M.; Pacheco, E.
    Background: Thrombophilia is defined as an altered hemostasis that predisposes to thrombosis. It can be primary when there is a family clustering of the disease or secondary, when it is associated to an acquired risk factor. Aim: to report clinical features in a series of patients with primary thrombophilia. Material and methods: Review of clinical records of patients with thrombotic episodes that lead to the suspicios of primary thrombophilia. Analysis of asymptomatic adult close relatives of these patients. Results: We repot 93 subjects (56 females, age range 14-77 years) with repeated episodes of thrombosis and a family history of thrombosis. Twenty four percent had protein C deficiency, 24% had antithrombin III deficiency, 18% had resistance to activated C protein by factor V Leiden, 10% had protein S deficiency, and 10% had the G20210 mutation of prothrombin gene. Among acquired defects studied simultaneously, 30% had lupus anticoagulent and 11% had hyperhomocysteinemia. Twenty four percent of cases had more than one thrombophilic risk factor. Among asymptomatic relatives, five had factor V Leiden, four had protein C deficiency and three had the G20210 mutation of prothrombin gene. Conclusions: Thrombophilia must be suspected in young subjects with thrombotic episode and a family history. the type of coagulation defect will determine prognosis, and the type of treatment (Rev Med Chile 2004; 132: 1466-73).