Beam-ion transport dependence on Magnetic Perturbations spectrum and plasma helicity in the ASDEX Upgrade tokamak

EUROfusion Consortium 63305

Improving mechanical performance of thermoplastic adhesion joints by atmospheric plasma

Polyethylene (PE) is characterized by low surface energy as a consequence of its non-polar nature. This characteristic is responsible for poor adhesion properties on polyethylene substrates. It is well known that some industrial applications such as coating, painting and formation of adhesion joints require high surface energy to promote good anchorages, so that, the use of polyethylene in these applications needs a previous surface treatment. In this work atmospheric plasma has been used to promote surface activation on polyethylene substrates for improved adhesion properties. The work has been focused on analyzing the influence of some variables (treatment rate and nozzle-sample distance) on mechanical performance of PE¿PE adhesion joints subjected to shear and T-peel tests.This work is a part of the project IPT-310000-2010-037, ''ECO-TEXCOMP: Research and development of textile structures useful as reinforcement of composite materials with marked ecological character.'' funded by the "Ministerio de Ciencia e Innovacion", with an aid of 189540.20 euros, within the "Plan Nacional de Investigacion Cientifica, Desarrollo e Innovacion Tecnologica 2008-2011" and funded by the European Union through FEDER funds, Technology Fund 2007-2013, Operational Programme on R + D + i for and on behalf of the companies. Also, microscopy services at UPV are acknowledged for SEM and AFM support.Fombuena, V.; Balart Gimeno, JF.; Boronat, T.; Sánchez-Nácher, L.; García-Sanoguera, D. (2013). Improving mechanical performance of thermoplastic adhesion joints by atmospheric plasma. Materials and Design. 47:49-56. doi:10.1016/j.matdes.2012.11.031S49564

Chapter 3: Pathophysiology

The hallmark pathophysiologic feature of dilated cardiomyopathy is systolic dysfunction. Several pathogenetic mechanisms appear to be operative. These include increased hemodynamic overload, ventricular remodeling, excessive neurohumoral stimulation, abnormal myocyte calcium cycling, excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis, and genetic mutations. Although beneficial in the early stages of heart failure, these compensatory mechanisms eventually lead to a vicious cycle of worsening heart failure. Genetic causes account for 30\u201340% of DCM and involve genes that encode a heterogeneous group of molecules that participate in force generation, force transmission, sarcomere integrity, cytoskeletal and nuclear architecture, electrolyte homeostasis, mitochondrial function, and transcription. Additional research will improve our understanding of the complex and longitudinal molecular changes that lead from gene mutation to clinical expressio