Dark Coupling and Gauge Invariance

We study a coupled dark energy-dark matter model in which the energy-momentum exchange is proportional to the Hubble expansion rate. The inclusion of its perturbation is required by gauge invariance. We derive the linear perturbation equations for the gauge invariant energy density contrast and velocity of the coupled fluids, and we determine the initial conditions. The latter turn out to be adiabatic for dark energy, when assuming adiabatic initial conditions for all the standard fluids. We perform a full Monte Carlo Markov Chain likelihood analysis of the model, using WMAP 7-year data.Comment: 16 pages, 2 figures, version accepted for publication in JCA

Fibrosis in hypertensive heart disease: role of the renin-angiotensin-aldosterone system

Structural homogeneity of cardiac tissue is governed by mechanical and humoral factors that regulate cell growth, apoptosis, phenotype, and extracellular matrix turnover. ANGII has endocrine, autocrine, and paracrine properties that influence the behavior of cardiac cells and matrix by AT1 receptor binding. Various paradigms have been suggested, including ANGII-mediated up-regulation of collagen types I and III formation and deposition in cardiac conditions, such as HHD. A growing body of evidence, however, deals with the potential role of aldosterone, either local or systemic, in inducing cardiac fibrosis. Aldosterone might also mediate the profibrotic actions of ANGII. To reduce the risk of heart failure that accompanies HHD, its adverse structural remodeling (eg, myocardial hypertrophy and fibrosis) must be targeted for pharmacologic intervention. Cardioprotective agents must reverse not only the exaggerated growth of cardiac cells, but also regress existing abnormalities in fibrillar collagen. Available experimental and clinical data suggest that agents interfering with ACE, the AT1 receptor, or the mineralocorticoid receptor may provide such a cardioprotective effect

Myocardial fibrosis in arterial hypertension

It is now accepted that, in addition to left ventricular hypertrophy, hypertensive heart disease is characterized by alterations in myocardial structure, leading to loss of tissue homogeneity and pathological remodelling. It is time to recognize that, in hypertensive heart disease, it is not only the quantity but also the quality of the myocardium that is responsible for adverse cardiovascular events. The data reviewed here indicate that, in patients with hypertensive heart disease, myocardial fibrosis predisposes to an enhanced risk for diastolic and/or systolic ventricular dysfunction, symptomatic heart failure, ischaemic heart disease and arrhythmias

Estudio ecocardiográfico y de la concentración de NT-proBNP en pacientes diabéticos tipo 2 con y sin cardiopatía isquémica

The aim of this study was to determine whether there are differences in echocardiographic findings or in the level of a biochemical marker (i.e. N-terminal probrain natriuretic peptide [NT-proBNP]) between controls and type-2 diabetic patients with or without ischemic heart disease. Echocardiography was used to assess left ventricular function and morphology. In addition, the plasma NT-proBNP concentration was measured. The prevalence of diastolic dysfunction was greater in diabetics without ischemic heart disease than in controls (88% vs. 74%, respectively; P< .001) and the NT-proBNP concentration was higher (350.6+/-197.8 vs. 281.7+/-190.4 fmol/mL; P< .001). Diabetics with ischemic heart disease had a higher NT-proBNP concentration than those without (720.4+/-278.1 vs. 350.6+/-197.8 fmol/mL, respectively; P< .001). An NT-proBNP concentration >490 fmol/mL had a sensitivity of 84% and a specificity of 75% for detecting ischemic heart disease in diabetics

Accuracy of a method based on atomic absorption spectrometry to determine inorganic arsenic in food : Outcome of the collaborative trial IMEP-41

Peer reviewedPublisher PD

Myocardial Response to Biomechanical Stress

Biomechanical stress of the myocardium is the situation resulting from hypoxia, hypertension, and other forms of myocardial injury, that invariably lead to increased demands for cardiac work and/or loss of functional myocardium. As a consequence of biomechanical stress a number of responses develop involving all the myocardial cells, namely cardiomyocytes. As a result some myocardial phenotypic changes develop that are initially compensatory (i.e., hypertrophy) but which may mediate the eventual decline in myocardial function that occurs with the transition from hypertrophy to failure in conditions of persistent stress (i.e., apoptosis and fibrosis). This review focuses on the steps involved in the response of the myocardium to biomechanical stress and highlights the most recent developments in the molecular mechanisms involved in the development of heart failure

Respuestas del miocardio al estrés biomecánico

El estrés biomecánico del miocardio hace referencia a la situación que se genera cuando, debido a la hipertensión, la hipoxia u otras formas de daño miocárdico, están aumentadas las demandas de trabajo cardíaco y/o se ha perdido miocardio funcionante. Como consecuencia del estrés biomecánico se producen diversas respuestas que afectan a todas las células miocárdicas, en particular a los cardiomiocitos. El resultado final de las mismas son distintas modificaciones fenotípicas que inicialmente son compensadoras (p. ej., hipertrofia), pero que si persiste el estrés pueden mediar la transición de la hipertrofia a la insuficiencia cardíaca (p. ej., apoptosis y fibrosis). Esta revisión se centra en la descripción de las distintas fases de las respuestas miocárdicas al estrés, así como en la consideración de los hallazgos más recientes sobre los mecanismos moleculares implicados en el desarrollo de insuficiencia cardíaca

Influence of Chemical Enhancers and Iontophoresis on the In Vitro Transdermal Permeation of Propranolol: Evaluation by Dermatopharmacokinetics

[EN] The aims of this study were to assess, in vitro, the possibility of administering propranolol transdermally and to evaluate the usefulness of the dermatopharmacokinetic (DPK) method in assessing the transport of drugs through stratum corneum, using propranolol as a model compound. Four chemical enhancers (decenoic and oleic acid, laurocapram, and R-(+)-limonene) and iontophoresis at two current densities, 0.25 and 0.5 mA/cm(2) were tested. R-(+)-limonene, and iontophoresis at 0.5 mA/cm(2) were proven to be the most efficient in increasing propranolol transdermal flux, both doubled the original propranolol transdermal flux. Iontophoresis was demonstrated to be superior than the chemical enhancer because it allowed faster delivery of the drug. The DPK method was sufficiently sensitive to detect subtle vehicle-induced effects on the skin permeation of propranolol. The shorter duration of these experiments and their ability to provide mechanistic information about partition between vehicle and skin and diffusivity through skin place them as practical and potentially insightful approach to quantify and, ultimately, optimize topical bioavailability.This research was funded by Ministerio de Ciencia e Innovación (AP2007-03456) and the Universidad CEU Cardenal Herrera.Calatayud-Pascual, M.; Sebastian-Morelló, M.; Balaguer-Fernandez, C.; Delgado-Charro, M.; Lopez-Castellano, A.; Merino Sanjuán, V. (2018). Influence of Chemical Enhancers and Iontophoresis on the In Vitro Transdermal Permeation of Propranolol: Evaluation by Dermatopharmacokinetics. Pharmaceutics. 10(4):1-15. https://doi.org/10.3390/pharmaceutics10040265S11510

Association of increased plasma cardiotrophin-1 with inappropriate left ventricular mass in essential hypertension

Inappropriate left ventricular mass is present when the value of left ventricular mass exceeds individual needs to compensate hemodynamic load imposed by increased blood pressure. The goal of this study was to investigate whether plasma concentration of cardiotrophin-1, a cytokine that induces exaggerated hypertrophy in cardiomyocytes with hypertensive phenotype, is related to inappropriate left ventricular mass in patients with essential hypertension. The study was performed in 118 patients with never-treated hypertension and without prevalent cardiac disease. The left ventricular mass prediction from stroke work (systolic blood pressurexDoppler stroke volume), sex, and height (in meters(2.7)) was derived. An observed left ventricular mass/predicted left ventricular mass value >128% defined inappropriate left ventricular mass. Plasma cardiotrophin-1 was measured by an enzyme-linked immunosorbent assay. The studies were repeated in a group of 45 patients after 1 year of antihypertensive treatment. At baseline 67 and 51 patients presented with appropriate and inappropriate left ventricular mass, respectively. Plasma cardiotrophin-1 was higher (P<0.001) in patients with inappropriate mass than in patients with appropriate mass and normotensive controls. A direct correlation was found between cardiotrophin-1 and observed left ventricular mass/predicted left ventricular mass ratio (r=0.330, P<0.001) in all hypertensive patients. After treatment, plasma cardiotrophin-1 decreased and increased in patients in which inappropriate left ventricular mass regressed and persisted, respectively, despite a similar reduction of blood pressure in the 2 subgroups of patients. Albeit descriptive in nature, these results suggest the hypothesis that an excess of cardiotrophin-1 may contribute to inappropriate left ventricular growth in hypertensive patients