1,721,008 research outputs found
Inherited disorders and gene regulation of platelet signal transduction: the picture is expanding.
Inherited Platelet Function Disorders: Algorithms for Phenotypic and Genetic Investigation
Inherited platelet function disorders (IPFDs) manifest with mucocutaneous bleeding and are frequently difficult to diagnose due to their heterogeneity, the complexity of the platelet activation pathways and a lack of standardization of the platelet function laboratory assays and of their use for this purpose. A rational diagnostic approach to IPFDs should follow an algorithm where clinical examination and a stepwise laboratory evaluation play a crucial role. A streamlined panel of laboratory tests, with consecutive steps of increasing level of complexity, allows the phenotypic characterization of most IPFDs. A first-line diagnosis of a significant fraction of the IPFD may be made also at nonspecialized centers by using relatively simple tests, including platelet count, peripheral blood smear, light transmission aggregometry, measurement of platelet granule content and release, and the expression of glycoproteins by flow cytometry. Some of the most complex, second- and third-step tests may be performed only in highly specialized laboratories. Genotyping, including the widespread application of next-generation sequencing, has enabled discovery in the last few years of several novel genes associated with platelet disorders and this method may eventually become a first-line diagnostic approach; however, a preliminary clinical and laboratory phenotypic characterization nowadays still remains crucial for diagnosis of IPFDs
E-studium: blended e-learning for university education support
In the changing framework of education and training, the e-studium project proposes a dynamic and versatile education system, effectively managing the learning process and using Information and Communication Technologies (ICTs) to respond to the specific characteristics of a variety of different degree programmes and courses and, at the same time, to the individual needs of a wide audience of students disseminated throughout Italy. The organisation model adopted in e-studium is an integrated multiple instances e-learning system. At the kernel of e-studium is MetaLearn, a software integration component which connects the different information and authentication sources, such as the academic registrar (information about students) and faculties databases (data on lecturers and programmes) with the target multiple e-learning platforms. In the experiment the MetaLearn architecture has been implemented on top of a set of target Moodle Course Management System (CMS) instances, thus realising the blended e-learning approach. In this work the main architectural features of MetaLearn and the different phases of development and implementation of the e-studium project are presented. The results also include usage analysis and a discussion on the impact of the quality of teaching on students, and on the requirements posed on the academic members who participated in the project
Highly Active Antiretroviral Therapy-related Mechanisms of Endothelial and Platelets Function Alterations
Highly active antiretroviral therapy (HAART) has transformed human immunodeficiency virus (HIV) infection into a chronic condition, which has allowed the infected population to age and become prone to chronic degenerative diseases common to the general population, including atherosclerotic cardiovascular disease, and coronary artery disease (CAD). Possible causative mechanisms of HIV-associated CAD are related to classic cardiovascular risk factors, such as dyslipidemia, insulin resistance, and fat redistribution, which may be due to either HIV infection or to HAART-associated toxicity. However, other mechanisms are emerging as crucial for the cardiovascular complication of HIV and HAART. This article analyzes the effects of HIV and HAART on endothelial function, endothelium-leukocyte interactions, and platelets as possible mechanisms of enhanced cardiovascular risk
Intraplatelet signaling mechanisms of the priming effect of matrix metalloproteinase-2 on platelet aggregation
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