Hallazgos fundamentales sobre las renuncias al procedimiento judicial por violencia de género

En primer lugar se expondrán los resultados del análisis exploratorio realizado con el objetivo de recoger la información necesaria para el diseño de la herramienta a utilizar durante la fase de recogida de datos. Seguidamente se expondrán los resultados obtenidos en esta segunda fase de administración de los cuestionarios a las mujeres inmersas en el procedimiento judicial

Metabotropic Ca2+ channel-induced Ca2+ release and ATP-dependent facilitation of arterial myocyte contraction

Voltage-gated Ca2_ channels in arterial myocytes can mediate Ca2_ release from the sarcoplasmic reticulum and, thus, induce contraction without the need of extracellular Ca2_ influx. This metabotropic action of Ca2_ channels (denoted as calcium-channelinduced calcium release or CCICR) involves activation of G proteins and the phospholipase C-inositol 1,4,5-trisphosphate pathway. Here, we show a form of vascular tone regulation by extracellular ATP that depends on the modulation of CCICR. In isolated arterial myocytes, ATP produced facilitation of Ca2_-channel activation and, subsequently, a strong potentiation of CCICR. The facilitation of L-type channel still occurred after full blockade of purinergic receptors and inhibition of G proteins with GDP_S, thus suggesting that ATP directly interacts with Ca2_ channels. The effects of ATP appear to be highly selective, because they were not mimicked by other nucleotides (ADP or UTP) or vasoactive agents, such as norepinephrine, acetylcholine, or endothelin-1. We have also shown that CCICR can trigger arterial cerebral vasoconstriction in the absence of extracellular calcium and that this phenomenon is greatly facilitated by extracellular ATP. Although, at low concentrations, ATP does not induce arterial contraction per se, this agent markedly potentiates contractility of partially depolarized or primed arteries. Hence, the metabotropic action of L-type Ca2_ channels could have a high impact on vascular pathophysiology, because, even in the absence of Ca2_ channel opening, it might mediate elevations of cytosolic Ca2_ and contraction in partially depolarized vascular smooth muscle cells exposed to small concentrations of agonists

Urocortin induces positive inotropic effect in rat heart

9 páginas, 6 figuras.Aims The aim of this study is to evaluate the positive inotropic effect of urocortin (Ucn) and to characterize its signalling pathways. Methods and results Contractility was measured in ex vivo Langendorff-perfused hearts isolated from Wistar rats. Isolated ventricular cardiomyocytes were used to analyse intracellular calcium ([Ca2+]i) transients evoked by electrical stimulation and L-type Ca2+ current by confocal microscopy and whole-cell patch-clamping, respectively. The application of Ucn to perfused hearts induced progressive, sustained, and potent inotropic and lusitropic effects that were dose-dependent with an EC50 of approximately 8 nM. Ucn effects were independent of protein kinase A (PKA) activation but were significantly reduced by protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) inhibitors and by brefeldin A, an antagonist of guanine nucleotide exchange factor, suggested to be an inhibitor of exchange protein activated by cAMP (Epac). These whole-organ effects were correlated with the inotropic effects observed in isolated cells: Ucn increased ICaL density, [Ca2+]i transients, cell shortening and Ca2+ content of sarcoplasmic reticulum. Conclusion Our results show that Ucn evokes potent positive inotropic and lusitropic effects mediated, at least in part, by an increase in ICaL and [Ca2+]i transient amplitude. These effects may involve the activation of Epac, PKC, and MAPK signalling pathways.This study was supported by ‘Red Cardiovascular RECAVA’ of Instituto Carlos III (grant number: RD06-0014-0020, RD06-0014-0007, PI06-0133), Consejerías de Salud, de Innovación Ciencia y Empresa de la Junta de Andalucía (grant numbers: 174/2006, P06-CTS-01711), Inserm, and by Agence Nationale pour la Recherche (grant: Physio2006Epac). T.S is a ‘Ramon y Cajal’ Researcher and E.C is a fellow student from RECAVA.Peer reviewe

TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling

Calcium is an important second messenger required not only for the excitation-contraction coupling of the heart but also critical for the activation of cell signaling pathways involved in the adverse cardiac remodeling and consequently for the heart failure. Sustained neurohumoral activation, pressure-overload, or myocardial injury can cause pathologic hypertrophic growth of the heart followed by interstitial fibrosis. The consequent heart’s structural and molecular adaptation might elevate the risk of developing heart failure and malignant arrhythmia. Compelling evidences have demonstrated that Ca2+ entry through TRP channels might play pivotal roles in cardiac function and pathology. TRP proteins are classified into six subfamilies: TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPA (ankyrin), TRPML (mucolipin), and TRPP (polycystin), which are activated by numerous physical and/or chemical stimuli. TRP channels participate to the handling of the intracellular Ca2+ concentration in cardiac myocytes and are mediators of different cardiovascular alterations. This review provides an overview of the current knowledge of TRP proteins implication in the pathologic process of some frequent cardiac diseases associated with the adverse cardiac remodeling such as cardiac hypertrophy, fibrosis, and conduction alteration.Spanish Ministry of Economy and Competitiveness BFU2016–74932-C2Institute of Carlos III PI15/00203; PI16/00259; CB16/11/00431Andalusia Government PI-0313-201

Orai1 and TRPC1 Proteins Co-localize with CaV1.2 Channels to Form a Signal Complex in Vascular Smooth Muscle Cells

Voltage-dependent CaV1.2 L-type Ca2 channels (LTCC) are the main route for calcium entry in vascular smooth muscle cells (VSMC). Several studies have also determined the relevant role of store-operated Ca2 channels (SOCC) in vascular tone regulation. Nevertheless, the role of Orai1- and TRPC1-dependent SOCC in vascular tone regulation and their possible interaction with CaV1.2 are still unknown. The current study sought to characterize the co-activation of SOCC and LTCC upon stimulation by agonists, and to determine the possible crosstalk between Orai1, TRPC1, and CaV1.2. Aorta rings and isolated VSMCobtained from wild type or smooth muscle-selective conditional CaV1.2 knock-out (CaV1.2KO) mice were used to study vascular contractility, intracellular Ca2 mobilization, and distribution of ion channels. We found that serotonin (5-HT) or store depletion with thapsigargin (TG) enhanced intracellular free Ca2 concentration ([Ca2 ]i) and stimulated aorta contraction. These responses were sensitive to LTCC and SOCC inhibitors. Also, 5-HT- and TG-induced responses were significantly attenuated in CaV1.2KO mice. Furthermore, hyperpolarization induced with cromakalim or valinomycin significantly reduced both 5-HT and TG responses, whereas these responses were enhanced with LTCC agonist Bay-K-8644. Interestingly, in situ proximity ligation assay revealed that CaV1.2 interacts with Orai1 and TRPC1 in untreated VSMC. These interactions enhanced significantly after stimulation of cells with 5-HT and TG. Therefore, these data indicate for the first time a functional interaction between Orai1, TRPC1, and CaV1.2 channels in VSMC, confirming that upon agonist stimulation, vessel contraction involves Ca2 entry due to co-activation of Orai1- and TRPC1-dependent SOCC and LTCC.Ministerio de Economía y Competitividad BFU2013-45564-C2-1-PMinisterio de Economía y Competitividad BFU2013-45564-C2-2-PInstituto de Salud Carlos III RD12/0042/ 0041Cardiovascular Network “RIC” PI12/00941Junta de Andalucía PI-0108-2012Junta de Andalucía P12- CTS-196

Método y kit de diagnóstico para la determinación cuantitativa de la expresión del canal maxi-K

Método y kit de diagnóstico para la determinación cuantitativa de la expresión del canal maxi-K. La presente invención se refiere a un método y kit de diagnóstico para la determinación cuantitativa en leucocitos de sangre periférica de una muestra de sangre total de la expresión de los genes KCNM implicados en la hipertensión arterial humana. En concreto de la expresión, de los niveles de ARNm y/o proteínas, de las subunidades alfa y beta1 del canal iónico maxi-K, es decir, de los genes KCNMA1 y KCNMB1.Españ

Approximation to the economic cost of healthcare for hypertensive patients diagnosed with COVID-19

IntroductionMany researchers have focused their studies on hypertension due to its over-representation among COVID-19 patients. Both retrospective and observational studies conducted close to the Wuhan area have reported that hypertension is the most common comorbidity observed in patients affected by COVID-19.ObjectiveOur objective is that patients with arterial hypertension have a worse prognosis in terms of evolution leading to higher costs.MethodsA retrospective cross-sectional study was conducted. A total of 3,581 patients from La Paz University Hospital (LPUH) during the period between 15 July 2020 and 31 July 2020 were included in this study.ResultsIt should be noted that 40.71% of the patients were hypertensive. As expected, hypertension was associated with men, among whom we observed a higher prevalence and a higher age (median age of 77 years (IQI: 65–85) versus 52 years (IQI: 37–64), p-value < 0.001). Hypertensive patients had a higher prevalence of dyspnea (52.14% vs. 47.15%, p-value = 0.004) and altered awareness (14.89% vs. 4.30%, p-value <0.001). The non-parametric Kaplan–Meier curve estimates the survival of patients in the two study groups. We can see how patients with hypertension have a higher associated mortality, with the difference being statistically significant, p-value (log-rank) = 0.004. Only for the appearance of complications during hospitalization, the group of hypertensive patients reached the figure of €1,355,901.71 compared to the total of 421,403.48 € for normotensive patients.ConclusionOur study shows the worse clinical evolution of patients with COVID-19 in terms of associated morbidity and mortality. It also shows that the cost of managing patients with hypertension is greater than that of managing normotensive patients

Healthcare workers hospitalized due to COVID-19 have no higher risk of death than general population. Data from the Spanish SEMI-COVID-19 Registry

Aim To determine whether healthcare workers (HCW) hospitalized in Spain due to COVID-19 have a worse prognosis than non-healthcare workers (NHCW). Methods Observational cohort study based on the SEMI-COVID-19 Registry, a nationwide registry that collects sociodemographic, clinical, laboratory, and treatment data on patients hospitalised with COVID-19 in Spain. Patients aged 20-65 years were selected. A multivariate logistic regression model was performed to identify factors associated with mortality. Results As of 22 May 2020, 4393 patients were included, of whom 419 (9.5%) were HCW. Median (interquartile range) age of HCW was 52 (15) years and 62.4% were women. Prevalence of comorbidities and severe radiological findings upon admission were less frequent in HCW. There were no difference in need of respiratory support and admission to intensive care unit, but occurrence of sepsis and in-hospital mortality was lower in HCW (1.7% vs. 3.9%; p = 0.024 and 0.7% vs. 4.8%; p<0.001 respectively). Age, male sex and comorbidity, were independently associated with higher in-hospital mortality and healthcare working with lower mortality (OR 0.211, 95%CI 0.067-0.667, p = 0.008). 30-days survival was higher in HCW (0.968 vs. 0.851 p<0.001). Conclusions Hospitalized COVID-19 HCW had fewer comorbidities and a better prognosis than NHCW. Our results suggest that professional exposure to COVID-19 in HCW does not carry more clinical severity nor mortality