2,061 research outputs found

    How new technologies can promote an active and healthy city. Digital platform to identify areas of informal sport practise in the city of Malaga

    Get PDF
    La investigación realizada se ha llevado a cabo en el marco de la Cátedra Tecnologías Emergentes para la Ciudadanía, Red de Cátedras Estratégicas del Vicerrectorado de Proyectos Estratégicos, Universidad de Málaga, y el Polo Digital, Ayuntamiento de Málaga.In recent years the urban public space has become the largest casual sports infrastructure in cities and suburbs. WHO establishes a direct relationship between the Active Healthy City, social cohesion of communities and public space. This approach provides a framework for research and work on the design of the city and urban space as support for this sport practice. Moreover, new technologies provide an opportunity to promote the sport in the city. “Malaga Activa” digital platform project is an initiative that wants to promote the informal sport practice on the urban public space (outside the regulated sports facilities) and healthy living in the neighborhoods of the city of Malaga. This paper presents the results of the first phase of the project identifying the active sport areas -those in which physical and casual sport activities take place-. It also includes a methodology and a performance test of the created digital platform, as well as an assessment of the experience and possible improvements to be incorporated in the successive phases of the project.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

    UNA HABITACIÓN PROPIA Y APOYO MUTUO. Proyecto de vivienda social compartida para mujeres víctimas de violencia de género y sus hijas/os

    Get PDF
    El presente trabajo y proyecto de intervención social inspirado en el libro titulado: “Una habitación propia” de la escritora feminista Virginia Wolf, pretende ser un acercamiento a la problemática de la vivienda y en concreto a la situación de las mujeres que han sufrido malos tratos a manos de sus parejas o ex parejas y que tienen difícil el acceso a una vivienda, bien porque la perdieron en su día como consecuencia de procesos de deuda hipotecaria, de desahucios por impago en el alquiler o por el complicado acceso a la vivienda dada la escasez de ingresos con los que cuentan, consecuencia tanto del propio empobrecimiento emocional y económico al que se ve abocada la mujer víctima de violencia de género y sus hijas e hijos, como de los propios procesos de exclusión social y residencial. Para ello, se comienza introduciendo algunos conceptos relacionados con las políticas de vivienda: derecho a la vivienda, alquiler social, deuda hipotecaria, dación en pago, lanzamientos y desahucios, y cómo la legislación tiene en consideración a estos colectivos de mujeres víctimas de violencia de género, especialmente vulnerables. También se hace una reflexión sobre el informe que hace la Relatora Especial de las Naciones Unidas, respecto a vivienda y mujer. En el segundo apartado hablaremos del concepto de violencia de género, sus tipos, los mitos y las teorías explicativas sobre los motivos que mantienen a las mujeres víctimas de violencia de género en esa situación. Detallamos las ayudas económicas que contempla la legislación al respecto, así como los recursos de alojamiento que se ponen en funcionamiento para proteger a las mujeres víctimas de violencia de género y a sus hijas e hijos. En tercer lugar, se ponen en valor algunos proyectos de intervención en materia de vivienda social que lleva a cabo el Ayuntamiento de Zaragoza, a través de la Sociedad Municipal Zaragoza Vivienda, en colaboración con la Casa de la Mujer, como ejemplo local de política que une estos dos aspectos Para finalizar, se realiza la planificación novedosa de un Proyecto de intervención social en red sobre vivienda compartida y apoyo mutuo destinado a este colectivo de mujeres víctimas de violencia de género y sus hijas e hijos

    Root exudates from citrus plants subjected to abiotic stress conditions have a positive effect on rhizobacteria

    Get PDF
    Plants are constantly releasing root exudates to the rhizosphere. These compounds are responsible for different (positive or negative) interactions with other organisms, including plants, fungi or bacteria. In this work, the effect of root exudates obtained from in vitro cultured citrus plants on two rhizobacteria (Pseudomonas putida KT2440 and Novosphingobium sp. HR1a) was evaluated. Root exudates were obtained from two citrus genotypes differing in their sensitivity to salt and heat stress and differentially affected the growth of both rhizobacteria. Root exudates from salt-stressed plants of C. macrophylla (salt tolerant) induced an increase in bacterial growth higher than that obtained from Carrizo citrange exudates (salt sensitive). Root exudates from heat-stressed plants also had a positive effect on bacterial growth, which was more evident in the heat-sensitive C. macrophylla. These results reveal that the growth of these rhizobacteria can be modulated through citrus root exudates and can change depending on both the stress conditions as well as the genotype. Biosensors P. putida KT2442 (pMIS5) and Novosphingobium sp. HR1a (pPAH) were used to test the presence of proline and salicylates in root exudates by measuring β-galactosidase activity. This activity increased in the presence of root exudates obtained from stressed plants to a higher extent in the case of exudates obtained from the genotype resistant to each particular stress, indicating that those root exudates contain larger quantities of proline and salicylates, as it has been described previously. Our data reveals that both P. putida KT2442 (pMIS5) and Novosphingobium sp. HR1a (pPAH), could be used as biosensors of plant stress

    The Thyroid Hormone Receptors Modulate the Skin Response to Retinoids

    Get PDF
    [Background]: Retinoids play an important role in skin homeostasis and when administered topically cause skin hyperplasia, abnormal epidermal differentiation and inflammation. Thyroidal status in humans also influences skin morphology and function and we have recently shown that the thyroid hormone receptors (TRs) are required for a normal proliferative response to 12-O-tetradecanolyphorbol-13-acetate (TPA) in mice. [Methodology/Principal Findings]: We have compared the epidermal response of mice lacking the thyroid hormone receptor binding isoforms TRα1 and TRβ to retinoids and TPA. Reduced hyperplasia and a decreased number of proliferating cells in the basal layer in response to 9-cis-RA and TPA were found in the epidermis of TR-deficient mice. Nuclear levels of proteins important for cell proliferation were altered, and expression of keratins 5 and 6 was also reduced, concomitantly with the decreased number of epidermal cell layers. In control mice the retinoid (but not TPA) induced parakeratosis and diminished expression of keratin 10 and loricrin, markers of early and terminal epidermal differentiation, respectively. This reduction was more accentuated in the TR deficient animals, whereas they did not present parakeratosis. Therefore, TRs modulate both the proliferative response to retinoids and their inhibitory effects on skin differentiation. Reduced proliferation, which was reversed upon thyroxine treatment, was also found in hypothyroid mice, demonstrating that thyroid hormone binding to TRs is required for the normal response to retinoids. In addition, the mRNA levels of the pro-inflammatory cytokines TNFα and IL-6 and the chemotactic proteins S1008A and S1008B were significantly elevated in the skin of TR knock-out mice after TPA or 9-cis-RA treatment and immune cell infiltration was also enhanced. [Conclusions/significance]: Since retinoids are commonly used for the treatment of skin disorders, these results demonstrating that TRs regulate skin proliferation, differentiation and inflammation in response to these compounds could have not only physiological but also therapeutic implications.This work was supported by grants BFU2007-62402 and SAF2008-00121 from Ministerio de Ciencia e Innovación, RD06/0020/0036 and RD06/0020/0029 from the Fondo de Investigaciones Sanitarias and by the European Grant CRESCENDO (FP-018652).Peer reviewe

    Desarrollo de la motivacion de alumnos universitarios de turismo mediante el analisis basado en problemas

    Get PDF
    Hasta hace relativamente poco tiempo el concepto de aprendizaje era sinónimo de clases expositivas y magistrales únicamente donde la interacción del alumno con el profesor y con la materia era nula, actualmente las metodologías de aprendizaje están sufriendo un gran cambio para adaptarse a la nueva realidad. En este estudio se analiza la motivación del alumno hacia la materia y la asignatura con una metodología de aprendizaje participativa y sobre todo diferente basada en el Aprendizaje Basado en Problemas (en adelante ABP), se pretende la resolución de un problema siguiendo unas fases ya preestablecidas y que debe de ser resuelta por el alumno. El estudio empírico se realiza en la Universidad de Málaga, en la Facultad de Turismo, donde se pretende analizar el grado de motivación hacia la asignatura cambiando la metodología de aprendizaje. Este trabajo forma parte de un programa de Innovación educativa donde quiere poner de relieve la adaptación de las metodologías de aprendizaje según su naturaleza, sujeto, contexto, cultura, ect…Los resultados indican que existen diferencias significativas en la motivación y la percepción de la asignatura por parte de los alumnos, inmediatamente después de aplicar la metodología ABP, siendo un elemento fundamental para el cambio en el alumno.Universidad de Málaga. Campus de excelencia Internacional Andalucía Tec

    Clinical management and acute exacerbations in patients with idiopathic pulmonary fibrosis in Spain: results from the OASIS study

    Get PDF
    Clinical management; Acute exacerbations; Early treatmentGestión clínica; Exacerbaciones agudas; Tratamiento precozGestió clínica; Exacerbacions agudes; Tractament precoçBackground Idiopathic pulmonary fibrosis (IPF) is a progressive disease associated with decline in lung function and poor prognosis entailing significant impairment in quality of life and high socioeconomic burden. The aim of this study was to characterize clinical management and resources utilization of patients with IPF in Spain, according to predicted forced vital capacity (FVC) % at baseline. Methods Prospective, non-interventional, multicentric real-world data study in patients with IPF in Spain with 12-months follow-up. Clinical management and resources utilization during study period were recorded and compared between groups. FVC decline and acute exacerbations occurrence and associated healthcare resource use were also analysed. FVC decline after 12 months was estimated as relative change. Results 204 consecutive patients with IPF were included and divided according to baseline FVC % predicted value. At baseline, patients with FVC  10% in the more preserved lung function groups than in the FVC < 50% group, because of their already deteriorated condition. Conclusions We observed a significantly higher annual IPF-related resource use in patients with more impaired lung function at baseline. Since FVC decreases irrespective of FVC% predicted at baseline, slowing IPF progression to maintain patients at early disease stages is relevant to improve IPF management and to optimize resource use.The study was supported and funded by Boehringer Ingelheim España

    Mechanistic investigation of Ca2+ alternans in human heart failure and its modulation by fibroblasts

    Full text link
    [EN] Heart failure (HF) is characterized, among other factors, by a progressive loss of contractile function and by the formation of an arrhythmogenic substrate, both aspects partially related to intracellular Ca2+ cycling disorders. In failing hearts both electrophysiological and structural remodeling, including fibroblast proliferation, contribute to changes in Ca2+ handling which promote the appearance of Ca2+ alternans (Ca-alt). Ca-alt in turn give rise to repolarization alternans, which promote dispersion of repolarization and contribute to reentrant activity. The computational analysis of the incidence of Ca2+ and/or repolarization alternans under HF conditions in the presence of fibroblasts could provide a better understanding of the mechanisms leading to HF arrhythmias and contractile function disorders. Methods and findings The goal of the present study was to investigate in silico the mechanisms leading to the formation of Ca-alt in failing human ventricular myocytes and tissues with disperse fibroblast distributions. The contribution of ionic currents variability to alternans formation at the cellular level was analyzed and the results show that in normal ventricular tissue, altered Ca2+ dynamics lead to Ca-alt, which precede APD alternans and can be aggravated by the presence of fibroblasts. Electrophysiological remodeling of failing tissue alone is sufficient to develop alternans. The incidence of alternans is reduced when fibroblasts are present in failing tissue due to significantly depressed Ca2+ transients. The analysis of the underlying ionic mechanisms suggests that Ca-alt are driven by Ca2+-handling protein and Ca2+ cycling dysfunctions in the junctional sarcoplasmic reticulum and that their contribution to alternans occurrence depends on the cardiac remodeling conditions and on myocyte-fibroblast interactions. Conclusion It can thus be concluded that fibroblasts modulate the formation of Ca-alt in human ventricular tissue subjected to heart failure-related electrophysiological remodeling. Pharmacological therapies should thus consider the extent of both the electrophysiological and structural remodeling present in the failing heart.This work was partially supported by the Plan Estatal de Investigación Científica y Técnica y de Innovación 2013 2016" from the Ministerio de Economía, Industria y Competitividad of Spain and Fondo Europeo de Desarrollo Regional (FEDER) DPI2016-75799-R (AEI/FEDER, UE), and by the Programa de Ayudas de Investigación y Desarrollo (PAID-01-17) from the Universitat Politècnica de València. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Mora-Fenoll, MT.; Gomez, JF.; Morley, G.; Ferrero De Loma-Osorio, JM.; Trenor Gomis, BA. (2019). Mechanistic investigation of Ca2+ alternans in human heart failure and its modulation by fibroblasts. PLoS ONE. 14(6):1-19. https://doi.org/10.1371/journal.pone.0217993S119146Glukhov, A. V., Fedorov, V. V., Kalish, P. W., Ravikumar, V. K., Lou, Q., Janks, D., … Efimov, I. R. (2012). Conduction Remodeling in Human End-Stage Nonischemic Left Ventricular Cardiomyopathy. Circulation, 125(15), 1835-1847. doi:10.1161/circulationaha.111.047274Lou, Q., Fedorov, V. V., Glukhov, A. V., Moazami, N., Fast, V. G., & Efimov, I. R. (2011). Transmural Heterogeneity and Remodeling of Ventricular Excitation-Contraction Coupling in Human Heart Failure. Circulation, 123(17), 1881-1890. doi:10.1161/circulationaha.110.989707Gomez, J. F., Cardona, K., & Trenor, B. (2015). Lessons learned from multi-scale modeling of the failing heart. Journal of Molecular and Cellular Cardiology, 89, 146-159. doi:10.1016/j.yjmcc.2015.10.016Kohl, P., & Gourdie, R. G. (2014). Fibroblast–myocyte electrotonic coupling: Does it occur in native cardiac tissue? Journal of Molecular and Cellular Cardiology, 70, 37-46. doi:10.1016/j.yjmcc.2013.12.024Gaudesius, G., Miragoli, M., Thomas, S. P., & Rohr, S. (2003). Coupling of Cardiac Electrical Activity Over Extended Distances by Fibroblasts of Cardiac Origin. Circulation Research, 93(5), 421-428. doi:10.1161/01.res.0000089258.40661.0cKohl, P., Camelliti, P., Burton, F. L., & Smith, G. L. (2005). Electrical coupling of fibroblasts and myocytes: relevance for cardiac propagation. Journal of Electrocardiology, 38(4), 45-50. doi:10.1016/j.jelectrocard.2005.06.096Camelliti, P., Green, C. R., LeGrice, I., & Kohl, P. (2004). Fibroblast Network in Rabbit Sinoatrial Node. Circulation Research, 94(6), 828-835. doi:10.1161/01.res.0000122382.19400.14Rook, M. B., van Ginneken, A. C., de Jonge, B., el Aoumari, A., Gros, D., & Jongsma, H. J. (1992). Differences in gap junction channels between cardiac myocytes, fibroblasts, and heterologous pairs. American Journal of Physiology-Cell Physiology, 263(5), C959-C977. doi:10.1152/ajpcell.1992.263.5.c959Mahoney, V. M., Mezzano, V., Mirams, G. R., Maass, K., Li, Z., Cerrone, M., … Morley, G. E. (2016). Connexin43 contributes to electrotonic conduction across scar tissue in the intact heart. Scientific Reports, 6(1). doi:10.1038/srep26744Quinn, T. A., Camelliti, P., Rog-Zielinska, E. A., Siedlecka, U., Poggioli, T., O’Toole, E. T., … Kohl, P. (2016). Electrotonic coupling of excitable and nonexcitable cells in the heart revealed by optogenetics. Proceedings of the National Academy of Sciences, 113(51), 14852-14857. doi:10.1073/pnas.1611184114Rubart, M., Tao, W., Lu, X.-L., Conway, S. J., Reuter, S. P., Lin, S.-F., & Soonpaa, M. H. (2017). Electrical coupling between ventricular myocytes and myofibroblasts in the infarcted mouse heart. Cardiovascular Research, 114(3), 389-400. doi:10.1093/cvr/cvx163Miragoli, M., Gaudesius, G., & Rohr, S. (2006). Electrotonic Modulation of Cardiac Impulse Conduction by Myofibroblasts. Circulation Research, 98(6), 801-810. doi:10.1161/01.res.0000214537.44195.a3Jacquemet, V., & Henriquez, C. S. (2008). Loading effect of fibroblast-myocyte coupling on resting potential, impulse propagation, and repolarization: insights from a microstructure model. American Journal of Physiology-Heart and Circulatory Physiology, 294(5), H2040-H2052. doi:10.1152/ajpheart.01298.2007Li, Y., Asfour, H., & Bursac, N. (2017). Age-dependent functional crosstalk between cardiac fibroblasts and cardiomyocytes in a 3D engineered cardiac tissue. Acta Biomaterialia, 55, 120-130. doi:10.1016/j.actbio.2017.04.027Zlochiver, S., Muñoz, V., Vikstrom, K. L., Taffet, S. M., Berenfeld, O., & Jalife, J. (2008). Electrotonic Myofibroblast-to-Myocyte Coupling Increases Propensity to Reentrant Arrhythmias in Two-Dimensional Cardiac Monolayers. Biophysical Journal, 95(9), 4469-4480. doi:10.1529/biophysj.108.136473Nguyen, T. P., Xie, Y., Garfinkel, A., Qu, Z., & Weiss, J. N. (2011). Arrhythmogenic consequences of myofibroblast–myocyte coupling. Cardiovascular Research, 93(2), 242-251. doi:10.1093/cvr/cvr292Greisas, A., & Zlochiver, S. (2016). The Multi-Domain Fibroblast/Myocyte Coupling in the Cardiac Tissue: A Theoretical Study. Cardiovascular Engineering and Technology, 7(3), 290-304. doi:10.1007/s13239-016-0266-xSridhar, S., Vandersickel, N., & Panfilov, A. V. (2017). Effect of myocyte-fibroblast coupling on the onset of pathological dynamics in a model of ventricular tissue. Scientific Reports, 7(1). doi:10.1038/srep40985Gomez, J. F., Cardona, K., Martinez, L., Saiz, J., & Trenor, B. (2014). Electrophysiological and Structural Remodeling in Heart Failure Modulate Arrhythmogenesis. 2D Simulation Study. PLoS ONE, 9(7), e103273. doi:10.1371/journal.pone.0103273KODAMA, M., KATO, K., HIRONO, S., OKURA, Y., HANAWA, H., YOSHIDA, T., … AIZAWA, Y. (2004). Linkage Between Mechanical and Electrical Alternans in Patients with Chronic Heart Failure. Journal of Cardiovascular Electrophysiology, 15(3), 295-299. doi:10.1046/j.1540-8167.2004.03016.xRosenbaum, D. S., Jackson, L. E., Smith, J. M., Garan, H., Ruskin, J. N., & Cohen, R. J. (1994). Electrical Alternans and Vulnerability to Ventricular Arrhythmias. New England Journal of Medicine, 330(4), 235-241. doi:10.1056/nejm199401273300402Jordan, P. N., & Christini, D. J. (2006). Action Potential Morphology Influences Intracellular Calcium Handling Stability and the Occurrence of Alternans. Biophysical Journal, 90(2), 672-680. doi:10.1529/biophysj.105.071340Cherry, E. M. (2017). Distinguishing mechanisms for alternans in cardiac cells using constant-diastolic-interval pacing. Chaos: An Interdisciplinary Journal of Nonlinear Science, 27(9), 093902. doi:10.1063/1.4999354Groenendaal, W., Ortega, F. A., Krogh-Madsen, T., & Christini, D. J. (2014). Voltage and Calcium Dynamics Both Underlie Cellular Alternans in Cardiac Myocytes. Biophysical Journal, 106(10), 2222-2232. doi:10.1016/j.bpj.2014.03.048Nolasco, J. B., & Dahlen, R. W. (1968). A graphic method for the study of alternation in cardiac action potentials. Journal of Applied Physiology, 25(2), 191-196. doi:10.1152/jappl.1968.25.2.191Picht, E., DeSantiago, J., Blatter, L. A., & Bers, D. M. (2006). Cardiac Alternans Do Not Rely on Diastolic Sarcoplasmic Reticulum Calcium Content Fluctuations. Circulation Research, 99(7), 740-748. doi:10.1161/01.res.0000244002.88813.91Díaz, M. E., O’Neill, S. C., & Eisner, D. A. (2004). Sarcoplasmic Reticulum Calcium Content Fluctuation Is the Key to Cardiac Alternans. Circulation Research, 94(5), 650-656. doi:10.1161/01.res.0000119923.64774.72Zhou, X., Bueno-Orovio, A., Orini, M., Hanson, B., Hayward, M., Taggart, P., … Rodriguez, B. (2016). In Vivo and In Silico Investigation Into Mechanisms of Frequency Dependence of Repolarization Alternans in Human Ventricular Cardiomyocytes. Circulation Research, 118(2), 266-278. doi:10.1161/circresaha.115.307836Xie, L.-H., Sato, D., Garfinkel, A., Qu, Z., & Weiss, J. N. (2008). Intracellular Ca Alternans: Coordinated Regulation by Sarcoplasmic Reticulum Release, Uptake, and Leak. Biophysical Journal, 95(6), 3100-3110. doi:10.1529/biophysj.108.130955Cutler, M. J., Wan, X., Laurita, K. R., Hajjar, R. J., & Rosenbaum, D. S. (2009). Targeted SERCA2a Gene Expression Identifies Molecular Mechanism and Therapeutic Target for Arrhythmogenic Cardiac Alternans. Circulation: Arrhythmia and Electrophysiology, 2(6), 686-694. doi:10.1161/circep.109.863118Kanaporis, G., & Blatter, L. A. (2015). The Mechanisms of Calcium Cycling and Action Potential Dynamics in Cardiac Alternans. Circulation Research, 116(5), 846-856. doi:10.1161/circresaha.116.305404Pastore, J. M., Girouard, S. D., Laurita, K. R., Akar, F. G., & Rosenbaum, D. S. (1999). Mechanism Linking T-Wave Alternans to the Genesis of Cardiac Fibrillation. Circulation, 99(10), 1385-1394. doi:10.1161/01.cir.99.10.1385O’Hara, T., Virág, L., Varró, A., & Rudy, Y. (2011). Simulation of the Undiseased Human Cardiac Ventricular Action Potential: Model Formulation and Experimental Validation. PLoS Computational Biology, 7(5), e1002061. doi:10.1371/journal.pcbi.1002061Mora, M. T., Ferrero, J. M., Romero, L., & Trenor, B. (2017). Sensitivity analysis revealing the effect of modulating ionic mechanisms on calcium dynamics in simulated human heart failure. PLOS ONE, 12(11), e0187739. doi:10.1371/journal.pone.0187739Andrew MacCannell, K., Bazzazi, H., Chilton, L., Shibukawa, Y., Clark, R. B., & Giles, W. R. (2007). A Mathematical Model of Electrotonic Interactions between Ventricular Myocytes and Fibroblasts. Biophysical Journal, 92(11), 4121-4132. doi:10.1529/biophysj.106.101410Spach, M. S., Heidlage, J. F., Dolber, P. C., & Barr, R. C. (2000). Electrophysiological Effects of Remodeling Cardiac Gap Junctions and Cell Size. Circulation Research, 86(3), 302-311. doi:10.1161/01.res.86.3.302Kieval, R. S., Spear, J. F., & Moore, E. N. (1992). Gap junctional conductance in ventricular myocyte pairs isolated from postischemic rabbit myocardium. Circulation Research, 71(1), 127-136. doi:10.1161/01.res.71.1.127Gomez, J. F., Cardona, K., Romero, L., Ferrero, J. M., & Trenor, B. (2014). Electrophysiological and Structural Remodeling in Heart Failure Modulate Arrhythmogenesis. 1D Simulation Study. PLoS ONE, 9(9), e106602. doi:10.1371/journal.pone.0106602Taggart, P., Sutton, P. M., Opthof, T., Coronel, R., Trimlett, R., Pugsley, W., & Kallis, P. (2000). Inhomogeneous Transmural Conduction During Early Ischaemia in Patients with Coronary Artery Disease. Journal of Molecular and Cellular Cardiology, 32(4), 621-630. doi:10.1006/jmcc.2000.1105Heidenreich E. Algoritmos para ecuaciones de reacción difusión aplicados a electrofisiología. Ph.D. Thesis. Universidad de Zaragoza. 2009. https://institutoi4.net/wp-content/uploads/2017/08/TesisEAH.pdfHeidenreich, E. A., Ferrero, J. M., Doblaré, M., & Rodríguez, J. F. (2010). Adaptive Macro Finite Elements for the Numerical Solution of Monodomain Equations in Cardiac Electrophysiology. Annals of Biomedical Engineering, 38(7), 2331-2345. doi:10.1007/s10439-010-9997-2Xie, Y., Garfinkel, A., Weiss, J. N., & Qu, Z. (2009). Cardiac alternans induced by fibroblast-myocyte coupling: mechanistic insights from computational models. American Journal of Physiology-Heart and Circulatory Physiology, 297(2), H775-H784. doi:10.1152/ajpheart.00341.2009Luo, C. H., & Rudy, Y. (1991). A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction. Circulation Research, 68(6), 1501-1526. doi:10.1161/01.res.68.6.1501Pruvot, E. J., Katra, R. P., Rosenbaum, D. S., & Laurita, K. R. (2004). Role of Calcium Cycling Versus Restitution in the Mechanism of Repolarization Alternans. Circulation Research, 94(8), 1083-1090. doi:10.1161/01.res.0000125629.72053.95Kanaporis, G., & Blatter, L. A. (2017). Membrane potential determines calcium alternans through modulation of SR Ca 2+ load and L-type Ca 2+ current. Journal of Molecular and Cellular Cardiology, 105, 49-58. doi:10.1016/j.yjmcc.2017.02.004Goldhaber, J. I., Xie, L.-H., Duong, T., Motter, C., Khuu, K., & Weiss, J. N. (2005). Action Potential Duration Restitution and Alternans in Rabbit Ventricular Myocytes. Circulation Research, 96(4), 459-466. doi:10.1161/01.res.0000156891.66893.83Walmsley, J., Rodriguez, J. F., Mirams, G. R., Burrage, K., Efimov, I. R., & Rodriguez, B. (2013). mRNA Expression Levels in Failing Human Hearts Predict Cellular Electrophysiological Remodeling: A Population-Based Simulation Study. PLoS ONE, 8(2), e56359. doi:10.1371/journal.pone.0056359Narayan, S. M., Bayer, J. D., Lalani, G., & Trayanova, N. A. (2008). Action Potential Dynamics Explain Arrhythmic Vulnerability in Human Heart Failure. Journal of the American College of Cardiology, 52(22), 1782-1792. doi:10.1016/j.jacc.2008.08.037Livshitz, L. M., & Rudy, Y. (2007). Regulation of Ca2+ and electrical alternans in cardiac myocytes: role of CAMKII and repolarizing currents. American Journal of Physiology-Heart and Circulatory Physiology, 292(6), H2854-H2866. doi:10.1152/ajpheart.01347.2006WILSON, L. D., WAN, X., & ROSENBAUM, D. S. (2006). Cellular Alternans: A Mechanism Linking Calcium Cycling Proteins to Cardiac Arrhythmogenesis. Annals of the New York Academy of Sciences, 1080(1), 216-234. doi:10.1196/annals.1380.018Wilson, L. D., Jeyaraj, D., Wan, X., Hoeker, G. S., Said, T. H., Gittinger, M., … Rosenbaum, D. S. (2009). Heart failure enhances susceptibility to arrhythmogenic cardiac alternans. Heart Rhythm, 6(2), 251-259. doi:10.1016/j.hrthm.2008.11.008Cutler, M. J., Wan, X., Plummer, B. N., Liu, H., Deschenes, I., Laurita, K. R., … Rosenbaum, D. S. (2012). Targeted Sarcoplasmic Reticulum Ca 2+ ATPase 2a Gene Delivery to Restore Electrical Stability in the Failing Heart. Circulation, 126(17), 2095-2104. doi:10.1161/circulationaha.111.071480Bayer, J. D., Narayan, S. M., Lalani, G. G., & Trayanova, N. A. (2010). Rate-dependent action potential alternans in human heart failure implicates abnormal intracellular calcium handling. Heart Rhythm, 7(8), 1093-1101. doi:10.1016/j.hrthm.2010.04.008Wang, L., Myles, R. C., De Jesus, N. M., Ohlendorf, A. K. P., Bers, D. M., & Ripplinger, C. M. (2014). Optical Mapping of Sarcoplasmic Reticulum Ca 2+ in the Intact Heart. Circulation Research, 114(9), 1410-1421. doi:10.1161/circresaha.114.302505Rovetti, R., Cui, X., Garfinkel, A., Weiss, J. N., & Qu, Z. (2010). Spark-Induced Sparks As a Mechanism of Intracellular Calcium Alternans in Cardiac Myocytes. Circulation Research, 106(10), 1582-1591. doi:10.1161/circresaha.109.213975Tomek, J., Tomková, M., Zhou, X., Bub, G., & Rodriguez, B. (2018). Modulation of Cardiac Alternans by Altered Sarcoplasmic Reticulum Calcium Release: A Simulation Study. Frontiers in Physiology, 9. doi:10.3389/fphys.2018.01306Hammer, K. P., Ljubojevic, S., Ripplinger, C. M., Pieske, B. M., & Bers, D. M. (2015). Cardiac myocyte alternans in intact heart: Influence of cell–cell coupling and β-adrenergic stimulation. Journal of Molecular and Cellular Cardiology, 84, 1-9. doi:10.1016/j.yjmcc.2015.03.012Majumder, R., Engels, M. C., de Vries, A. A. F., Panfilov, A. V., & Pijnappels, D. A. (2016). Islands of spatially discordant APD alternans underlie arrhythmogenesis by promoting electrotonic dyssynchrony in models of fibrotic rat ventricular myocardium. Scientific Reports, 6(1). doi:10.1038/srep24334Shiferaw, Y., & Karma, A. (2006). Turing instability mediated by voltage and calcium diffusion in paced cardiac cells. Proceedings of the National Academy of Sciences, 103(15), 5670-5675. doi:10.1073/pnas.0511061103Sato, D., Shiferaw, Y., Garfinkel, A., Weiss, J. N., Qu, Z., & Karma, A. (2006). Spatially Discordant Alternans in Cardiac Tissue. Circulation Research, 99(5), 520-527. doi:10.1161/01.res.0000240542.03986.e

    Evaluación del manejo de los residuos sólidos de la asociación de productores agropecuarios de los Molinos Cajanleque - Chocope

    Get PDF
    El presente trabajo de investigación tuvo como objetivo realizar una evaluación de manejo de los residuos sólidos en la asociación de agropecuarios de los Molinos Cajanleque – Chocope, por tal motivo se realizaron varios instrumentos que nos ayudaron a recaudar información importante para su desarrollo. Esta investigación tipo básico con diseño no experimental – longitudinal, lo cual relacionamos a la variable manejo de residuos sólidos; por otro lado, como población se consideró a todos los residuos generados en la asociación. Los instrumentos utilizados fueron las checklist basadas en el D.S 016-2012-AG, el anexo del D.S 017-2012-AG, tablas de caracterización de residuos y matriz ambiental. Obteniendo como resultado que la asociación solo cumple con el 26.6% de la normativa vigente y que incumple con 26 infracciones según la normativa. Sin embargo, en relación a nuestros objetivos específicos, se elaboró una caracterización de residuos sólidos generando 12 214.7 kg en 3 meses; de acuerdo a la matriz ambiental se identificaron los principales procesos de impacto significativo, tales como: almacenamiento1, lavado, enligado, hidroenfriamiento, estibado, enzunchado, embolsado y paletizado2. Por último, se presentó una propuesta de manejo de los residuos sólidos con la búsqueda de minimizar los impactos ambientales y mejorar la salud de la población

    Immigrant IBD Patients in Spain Are Younger, Have More Extraintestinal Manifestations and Use More Biologics Than Native Patients

    Get PDF
    Crohn's disease; Immigrant; Inflammatory bowel diseaseEnfermedad de Crohn; Inmigrante; Enfermedad inflamatoria del intestinoMalaltia de Crohn; Immigrant; Malaltia inflamatòria intestinalBackground: Previous studies comparing immigrant ethnic groups and native patients with IBD have yielded clinical and phenotypic differences. To date, no study has focused on the immigrant IBD population in Spain. Methods: Prospective, observational, multicenter study comparing cohorts of IBD patients from ENEIDA-registry who were born outside Spain with a cohort of native patients. Results: We included 13,524 patients (1,864 immigrant and 11,660 native). The immigrants were younger (45 ± 12 vs. 54 ± 16 years, p < 0.001), had been diagnosed younger (31 ± 12 vs. 36 ± 15 years, p < 0.001), and had a shorter disease duration (14 ± 7 vs. 18 ± 8 years, p < 0.001) than native patients. Family history of IBD (9 vs. 14%, p < 0.001) and smoking (30 vs. 40%, p < 0.001) were more frequent among native patients. The most prevalent ethnic groups among immigrants were Caucasian (41.5%), followed by Latin American (30.8%), Arab (18.3%), and Asian (6.7%). Extraintestinal manifestations, mainly musculoskeletal affections, were more frequent in immigrants (19 vs. 11%, p < 0.001). Use of biologics, mainly anti-TNF, was greater in immigrants (36 vs. 29%, p < 0.001). The risk of having extraintestinal manifestations [OR: 2.23 (1.92-2.58, p < 0.001)] and using biologics [OR: 1.13 (1.0-1.26, p = 0.042)] was independently associated with immigrant status in the multivariate analyses. Conclusions: Compared with native-born patients, first-generation-immigrant IBD patients in Spain were younger at disease onset and showed an increased risk of having extraintestinal manifestations and using biologics. Our study suggests a featured phenotype of immigrant IBD patients in Spain, and constitutes a new landmark in the epidemiological characterization of immigrant IBD populations in Southern Europe
    corecore