Studio dell'aggregazione piastrinica con aggregometro ad elettrodi multipli (multiplate) e della disfunzione endoteliale con tecnica ecocolorDoppler in soggetti trombofilici

Background: the link between venous thromboembolism (VTE) and arterial thromboembolic events (ATE) is still uncertain. In 2003 Prandoni et al published the first study that reported a connection, in term of etiopathogenesis between VTE and atherosclerosis. During the last few years several other study confirm this association, that could be attributed to common risk factors for the two conditions. The contribution of thrombophilic defects to the link between VTE and ATE has yet to be defined. Thrombophilic conditions (hereditary deficiencies of protein S, protein C and antithrombin) have been recognized as most potent thrombophilic conditions for VTE. Whether hereditary protein S, Protein C or antithrombin deficiency also are involved in the development of ATE need to be confirmed and the evidence of a possible association has been showed mainly from case reports. Blood haemostasis is a complex mechanism influenced from coagulation factors, aggregation proteins, blood cells (platelets, leucocytes) and vascular endothelium. Most of biochemical tests focused on coagulation system asses only a part of this complex mechanism and, in particular, the laboratory tests analyze only the coagulations cascade. But the role of platelets and vascular endothelium is not clear. The contribution of thrombophilic defects as common risk factor between VTE and ATE has yet to be defined compared with nondeficient family members. Moreover in this study the endothelial dysfunction could be the real cause for both conditions VTE and ATE. There are no data concerning the role of platelets function or vascular endothelium function in this thrombophilic patients population. The aim of the study is to define, in thrombophilic patients (Prot C, Prot S and antithrombin defects) compared with non-deficient family members. the role of platelets function using a new analyzer named Multiplate® whole blood aggregometry that evaluated platelets aggregations in whole blood and to define also the possible implication of endothelial function, by the non-invasive assessment of flow mediated dilatation (FMD) of the brachial artery, by B-mode ultrasonography, using a standardized procedure Material and Methods: after signing an informed consent, we enrolled patients with thrombophilic defects (cases) and create three subgroups (cases with deficit of protein C, protein S and antithrombin) with and without a history of thromboembolic disease, and subjects without thrombophilic defects (controls). We collected baseline data of all (cases and controls) on previous episodes of VTE and ATE, risk factors for atherosclerosis (i.e. hypertension, diabetes mellitus, cigarette smoking; hyperlipidemia) All patients were tested for thrombophilic defects in addition to their index deficiencies (FV Leiden, G20210 A prothrombin, lupus anticoagulant; PC and PS, AT). Moreover, we study platelets aggregations with a new analyzer named Multiplate® whole blood aggregometry that evaluated platelets aggregations in whole blood with thrombin inibitor (irudin); this instrument identify the electrical impedance (as area under curve, AUC) caused from platelets aggregation. The platelets aggregation was triggered by different activators: adenosine-5 diphosphate (ADP test), arachidonic acid (ASPI test) and thrombin receptor activatin peptide (TRAP -6) All cases and controls underwent evaluation of endothelial function by the non-invasive assessment of flow mediated dilatation (FMD) of the brachial artery, by B-mode ultrasonography, using a standardized procedure. Results: patients with thromphilic defects versus controls have similar demographical charatistics. The valutation of the platelets aggregation by Multiplate® with different tests (ASPI, ADP and TRAP) show a different in the two groups but it is no statistically significant; we observed the same results if analyze the three subgroups (Protein C defects, Protein S and antithrombin deficiency) protein separately. The ultrasonography evaluation of endothelial function show that there is a reduction of the flow mediated dilatation (FMD) in patients with thrombophilic defects versus controls. The FMD calculated in thrombophilic patients is statistically significant (3.7±0.5% vs 5.2±0.6% ,p value = 0.015) compared the controls. Discussion: Our preliminary data show that in patients with thrombophilic deficiency there is increased of platelets aggregation but it’s no statically significant. This results is confirm also in all different subgroups of thromphilic deficiency (Prot C, S, and AT deficiency ). However an endothelial dysfunction is showed in thrombophilic patients compared the controls. Although we speculated with this data, as other study have reported, that endothelial dysfunction rather than coagulation disorders is the main actor in the link between VTE and ATE in thrombophilic subjects. It is yet unclear the role of the different actors (endothelium dysfunction, platelet aggregation and coagulation factors) in the development on VTE and ATE, but this study can show that endothelium dysfunction can be one of the most important trigger factor in the thrombophilic patient

Endothelial dysfunction in patients with spontaneous venous thromboembolism

Background and Objectives A high incidence of atherosclerotic lesions and cardiovascular events has been reported in patients with spontaneous venous thromboembolism. Endothelial dysfunction is an early marker of atherosclerosis and has predictive value for ischemic events. We have evaluated endothelial function in patients with a history of spontaneous venous thromboembolism.Design and Methods Patients with a history of symptomatic, objectively confirmed, spontaneous venous thromboembolism were included in a case-control study. Exclusion criteria were any known risk factors for cardiovascular diseases, other conditions associated with endothelial dysfunction, estro-progestinic therapy or pregnancy. Controls were age-(±5 years) and sex-matched subjects with the same exclusion criteria but without previous venous thromboembolism. Endothelial function was evaluated by the non-invasive measurement of flow-mediated vasodilation of the brachial artery and of plasma markers of endothelium activation; platelet activation parameters were also measured.Results Twenty-eight cases (8 females; mean age 59±15 years) and 28 controls (8 females; mean age 58±15) were studied. Flow-mediated vasodilation was 3.5±0.6% in cases (95% CIs: 2.2 to 4.8) and 5.7±0.6% (4.2 to 6.8) in controls (p=0.015). Brachial artery blood flow and hyperemic blood flow did not differ between the two groups. Plasma von Willebrand factor and soluble P-selectin levels were significantly higher in patients with venous thromboembolism, while plasma soluble CD40 ligand and urinary 11-dehydro-TxB2 levels were similar in cases and controls.Interpretation and Conclusions Patients with spontaneous venous thromboembolism have endothelial dysfunction, unlike age- and sex- matched controls. This finding suggests that spontaneous venous thromboembolism may be a condition associated with an enhanced risk of atherosclerosis

The late Pleistocene Po River lowstand wedge in the Adriatic Sea : Controls on architecture variability and sediment partitioning

The authors dedicate this study to their colleague Giovanni Bortoluzzi, who passed away in 2015. A special tanks is due to Marco Ligi and Nevio Zitellini for geophysical data acquisition and processing; Marco Pastore and Filippo D'Oriano for their support during the cruise LSD2014 and processing of geophysical data. Elisabetta Campiani provided additional support for processing the multibeam bathymetry. A particular thank goes to Cpt. Emanuele Gentile and the crew of the R/V Urania during cruise LSD 2014. We thank Ronald Steel and an anonymous Reviewer for their constructive comments. This project was funded by ExxonMobil Upstream Research Company and by the Flagship Project RITMARE–The Italian Research for the Sea. We acknowledge the European Union Project PROMESS-1 (contract EVR1-2001-41) for borehole PRAD 1-2. This is ISMAR-CNR contribution number 1959.Peer reviewedPostprin

La renovación de la palabra en el bicentenario de la Argentina : los colores de la mirada lingüística

El libro reúne trabajos en los que se exponen resultados de investigaciones presentadas por investigadores de Argentina, Chile, Brasil, España, Italia y Alemania en el XII Congreso de la Sociedad Argentina de Lingüística (SAL), Bicentenario: la renovación de la palabra, realizado en Mendoza, Argentina, entre el 6 y el 9 de abril de 2010. Las temáticas abordadas en los 167 capítulos muestran las grandes líneas de investigación que se desarrollan fundamentalmente en nuestro país, pero también en los otros países mencionados arriba, y señalan además las áreas que recién se inician, con poca tradición en nuestro país y que deberían fomentarse. Los trabajos aquí publicados se enmarcan dentro de las siguientes disciplinas y/o campos de investigación: Fonología, Sintaxis, Semántica y Pragmática, Lingüística Cognitiva, Análisis del Discurso, Psicolingüística, Adquisición de la Lengua, Sociolingüística y Dialectología, Didáctica de la lengua, Lingüística Aplicada, Lingüística Computacional, Historia de la Lengua y la Lingüística, Lenguas Aborígenes, Filosofía del Lenguaje, Lexicología y Terminología

Studio dell'aggregazione piastrinica con aggregometro ad elettrodi multipli (multiplate) e della disfunzione endoteliale con tecnica ecocolorDoppler in soggetti trombofilici

Background: the link between venous thromboembolism (VTE) and arterial thromboembolic events (ATE) is still uncertain. In 2003 Prandoni et al published the first study that reported a connection, in term of etiopathogenesis between VTE and atherosclerosis. During the last few years several other study confirm this association, that could be attributed to common risk factors for the two conditions. The contribution of thrombophilic defects to the link between VTE and ATE has yet to be defined. Thrombophilic conditions (hereditary deficiencies of protein S, protein C and antithrombin) have been recognized as most potent thrombophilic conditions for VTE. Whether hereditary protein S, Protein C or antithrombin deficiency also are involved in the development of ATE need to be confirmed and the evidence of a possible association has been showed mainly from case reports. Blood haemostasis is a complex mechanism influenced from coagulation factors, aggregation proteins, blood cells (platelets, leucocytes) and vascular endothelium. Most of biochemical tests focused on coagulation system asses only a part of this complex mechanism and, in particular, the laboratory tests analyze only the coagulations cascade. But the role of platelets and vascular endothelium is not clear. The contribution of thrombophilic defects as common risk factor between VTE and ATE has yet to be defined compared with nondeficient family members. Moreover in this study the endothelial dysfunction could be the real cause for both conditions VTE and ATE. There are no data concerning the role of platelets function or vascular endothelium function in this thrombophilic patients population. The aim of the study is to define, in thrombophilic patients (Prot C, Prot S and antithrombin defects) compared with non-deficient family members. the role of platelets function using a new analyzer named Multiplate® whole blood aggregometry that evaluated platelets aggregations in whole blood and to define also the possible implication of endothelial function, by the non-invasive assessment of flow mediated dilatation (FMD) of the brachial artery, by B-mode ultrasonography, using a standardized procedure Material and Methods: after signing an informed consent, we enrolled patients with thrombophilic defects (cases) and create three subgroups (cases with deficit of protein C, protein S and antithrombin) with and without a history of thromboembolic disease, and subjects without thrombophilic defects (controls). We collected baseline data of all (cases and controls) on previous episodes of VTE and ATE, risk factors for atherosclerosis (i.e. hypertension, diabetes mellitus, cigarette smoking; hyperlipidemia) All patients were tested for thrombophilic defects in addition to their index deficiencies (FV Leiden, G20210 A prothrombin, lupus anticoagulant; PC and PS, AT). Moreover, we study platelets aggregations with a new analyzer named Multiplate® whole blood aggregometry that evaluated platelets aggregations in whole blood with thrombin inibitor (irudin); this instrument identify the electrical impedance (as area under curve, AUC) caused from platelets aggregation. The platelets aggregation was triggered by different activators: adenosine-5 diphosphate (ADP test), arachidonic acid (ASPI test) and thrombin receptor activatin peptide (TRAP -6) All cases and controls underwent evaluation of endothelial function by the non-invasive assessment of flow mediated dilatation (FMD) of the brachial artery, by B-mode ultrasonography, using a standardized procedure. Results: patients with thromphilic defects versus controls have similar demographical charatistics. The valutation of the platelets aggregation by Multiplate® with different tests (ASPI, ADP and TRAP) show a different in the two groups but it is no statistically significant; we observed the same results if analyze the three subgroups (Protein C defects, Protein S and antithrombin deficiency) protein separately. The ultrasonography evaluation of endothelial function show that there is a reduction of the flow mediated dilatation (FMD) in patients with thrombophilic defects versus controls. The FMD calculated in thrombophilic patients is statistically significant (3.7±0.5% vs 5.2±0.6% ,p value = 0.015) compared the controls. Discussion: Our preliminary data show that in patients with thrombophilic deficiency there is increased of platelets aggregation but it’s no statically significant. This results is confirm also in all different subgroups of thromphilic deficiency (Prot C, S, and AT deficiency ). However an endothelial dysfunction is showed in thrombophilic patients compared the controls. Although we speculated with this data, as other study have reported, that endothelial dysfunction rather than coagulation disorders is the main actor in the link between VTE and ATE in thrombophilic subjects. It is yet unclear the role of the different actors (endothelium dysfunction, platelet aggregation and coagulation factors) in the development on VTE and ATE, but this study can show that endothelium dysfunction can be one of the most important trigger factor in the thrombophilic patientsIntroduzione: La correlazione tra malattia trombo embolica venosa e patologia arteriosa è un dato che ormai affascina e riscuote l’interesse di molti studiosi. Già nel 2003 Prandoni et al misero in evidenza tale possibile correlazione; molti altri studi hanno successivamente consolidato tale dato dimostrando anche la condivisione di numerosi fattori di rischio (diabete, ipertensione arteriosa, dislipidemia, fumo di sigaretta). Il complesso meccanismo coagulativo è influenzato da molteplici attori: fattori della coagulazione, cellule ematiche (leucociti, piastrine) e dall’endotelio vascolare. Molte delle indagini tuttora utilizzate per la coagulazione valutano solo una parte di questa complessa cascata coagulativa, ma il ruolo svolto dalle piastrine e dall’endotelio non è ancora chiarito. In particolare, in uno specifico sottogruppo della popolazione, i soggetti trombofilici, i quali presentano un deficit degli inibitori naturali della coagulazione (proteina C, proteina S e antitrombina) e che manifestano una maggiore incidenza della malattia tromboembolica venosa e, anche se in misura differente, dell’aterotrombosi. Lo scopo del nostro studio è stato quello di valutare la funzione endoteliale, attraverso l’utilizzo di tecnica ecografica dell’arteria brachiale della dilatazione flusso mediata (FMD) e l’aggregazione piastrinica, attraverso l’uso di aggregometro basato sull’impedenziometria con elettrodi multipli (Multiplate®), in un gruppo di soggetti con difetto degli inibitori naturali della coagulazione rispetto ad un gruppo di volontari sani. Materiali e metodi: nel gruppo dei casi sono stati arruolati, dopo consenso informato, 68 soggetti con difetto noto degli inibitori della coagulazione (deficit di Prot C, Prot S o antitrombina) e nel gruppo dei controlli 59 soggetti volontari sani confrontabili per sesso ed età ( 3 anni). Sono stati esclusi dallo studio soggetti con età inferiore ai 18 aa, che si sono rifiutati di firmare il consenso informato, che assumevano terapia anticoagulante o antiaggregante piastrinica o con piastrinopenia (conta piastrinica 450 x109/L). Tutti i soggetti arruolati allo studio sono stati sottoposti a raccolta anamnestica dettagliata relativa a fattori di rischio e precedenti cardiovascolari o tromboembolici venosi; ciascuno di essi inoltre è stato sottoposto a prelievo di 18 ml di sangue venoso per esecuzione di test della coagulazione classica e studio ipercoagulabile (proteina C, proteina S, antitrombina, variante protrombinica, fattore V Leiden anticorpi antifosfolipidi). Su ogni campione di sangue veniva effettuato studio dell’ aggregazione piastrinica con aggregometro ad impedenza ad elettrodi multipli (Multiplate®), che eseguiva contemporaneamente più test (ASPItest, ADPtest e TRAPtest). Infine su ogni soggetto è stato eseguita valutazione ecografica della disfunzione endoteliale mediante valutazione della dilatazione flusso mediata (FMD) con misurazione dell’arteria brachiale prima e dopo iperemia. Risultati: i soggetti con difetto trombofilico presentavano caratteristiche demografiche sovrapponibili a quelle dei controlli sani. L’incidenza di eventi trombo embolici venosi e risultata ovviamente più elevata nel gruppo dei casi; mentre i soggetti trombofilici hanno mostrato di aver sviluppato in età più giovane eventi cardiovascolari. Nella valutazione dell’aggregazione piastrinica studiata con il Multiplate® , con differenti test di stimolazione (ASPI, ADP e TRAP) sono emerse differenze della AUC (area sotto la curva) che esprime in modo quantitativo l’aggregazione piastrinica che tuttavia non sono risultate statisticamente significative; il dato si è confermato anche nella valutazione dei casi, prendendo in considerazione singolarmente ogni difetto trombofilico. In relazione alla valutazione della disfunzione endoteliale mediante ecografia dell’arteria brachiale si è evidenziato un decremento statisticamente significativo della dilatazione flusso mediata (FMD) nei casi rispetto ai controlli (3.7±0.5% vs 5.2±0.6% , p value = 0.015), mentre sono risultati di dimensioni sovrapponibili il diametro e il flusso basale del vaso. Discussione: Per quanto riguarda la valutazione aggregometrica su sangue intero, i dati raccolti, non hanno evidenziato una differenza significativa dell’aggregazione piastrinica valutata con i test di induzione (TRAP, ADP, ASPI) nei soggetti trombofilici rispetto ai controlli. Tale dato potrebbe quindi essere interpretato come l’assenza di una “intrinseca” iperaggregabilità delle piastrine di questi soggetti che possa essere l’innesco della cascata trombotica a cui essi vanno più spesso incontro. In relazione allo studio della funzione endoteliale i dati hanno mostrato che esiste una riduzione della dilatazione dell’arteria brachiale post fase iperemica che in valore percentuale è significativamente piu bassa nei soggetti trombofilici rispetto ai controlli. Il dato quindi sembra confermare che nei soggetti con deficit degli inibitori della coagulazione, con noto incremento dell’incidenza di eventi tromboembolici, sia la disfunzione endoteliale a rappresentare il determinante capace di innescare tale process

3D Seismic Geomorphology: the Enigma Project, an Encounter Between Academia and Industry

not availabl

ABO blood group and the risk of post-thrombotic syndrome

Post-thrombotic syndrome (PTS) has been associated to DVT recurrence, increased FVIII, inflammatory biomarker plasma levels, and persistence of vein obstruction. These same features have also been widely reported in non-O blood type subjects. Our aim was to investigate the correlation between the incidence of PTS and ABO blood types. Consecutive patients referred to the Department of Medicine of University of Padua between January 2004 and January 2012 following the diagnosis of a first episode of proximal DVT were enrolled. The presence of PTS was assessed via the Villalta scale at predefined time points (3, 6, 12, 18, 24, 36\ua0months). Hazard ratio (HR) for PTS development was calculated in non-O (exposed) vs O blood (unexposed) type patients. Out of 671 eligible patients, 606 were enrolled. Overall, 192 (31.7%) patients developed PTS: 142 (34.5%) non-O and 50 (25.6%) O blood type patients. Individuals with non-O blood group were associated with a significantly higher risk to develop PTS (HR 1.53, 95% CI, 1.05-2.24; p\u2009=\u20090.028) than O group. Non-O blood type might be a risk factor for the development of PTS