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Unbalances in gain and phase of receiving chains as well as mutual coupling effects among radiating elements degrade the performance in direction of arrival estimations (DOA) in digital array radars (DAR). These effects can be described by an unknown distortion matrix by which the received signals are in fact multiplied. The calibration of the array consists then on finding an approximation to this matrix, so that is possible to compensate the received signals prior to their processing. This article presents the active calibration procedure used to improve the targets DOA estimations of a surface surveillance radar. The radar is a high range resolution system that performs the digital beamforming only on receive. To calibrate the system, an auxiliary rotating radiating source plus an electro-optical delay line are used. The waveform used in the calibration is the same that the system use in operation and the signal processing chain used by the system to detect targets is included In the calibration algorithm so it can be viewed as a whole-system calibration. Matched filtering and integration allow to obtain a high enough signal to noise ratio in the calibration process. Results are presented for both the calibration algorithm, using computer simulations, and for the calibration data set, to finally show the Improvements in DOA estimation using the monopulse technique after calibration.

This article introduces a new radar architecture, which implements a new signal processing scheme, with applications to the Intelligent Transportation Systems. The proposed solution exploits a well-known problem regarding low range radar systems, the Glint Effect, in order to improve previous results. For that purpose, the presented system is required to measure azimuth and Doppler of targets, for which it opts for a 2-channel Digital Array Receiver scheme working with a frequency-modulated continuous wave. This involves more complex hardware and signal processing software, comparing to the common mono-channel non coherent systems, nevertheless latest devices (radio frequency subsystems, field-programmable gate arrays, digitizers, etc) make it simple and affordable. The proposed system, with an easy-and-fast side-looking installation, exploits several advantages of its 2-channel synchronous architecture (e.g. clutter cancellation, Doppler history availability, etc) to achieve a better estimation of two key measurements: traffic flow (instantaneous and average) and vehicles speed.

Resumen Introduccion En descompensaciones por insuficiencia cardiaca (IC), tanto el dano renal agudo (DRA) como los niveles elevados de galectina-3 (Gal-3) se han asociado con una peor evolucion. Los niveles plasmaticos de Gal-3 se ven influidos por la funcion renal; sin embargo, el posible papel de la Gal-3 como predictor de DRA no esta establecido. Metodos Se midieron las concentraciones de Gal-3 al ingreso en 175 pacientes hospitalizados por IC y se registro la aparicion de DRA segun los criterios analiticos RIFLE. Resultados Durante el ingreso, 44 pacientes (25,1%) desarrollaron DRA, aunque solo 14 (8%) correspondian a los estadios mas avanzados, siendo en estos los niveles de Gal-3 al ingreso significativamente mayores, permaneciendo como predictor de DRA tras el ajuste multivariado por otras variables predictoras y por funcion renal basal. Conclusiones Los valores elevados de Gal-3 al ingreso se asocian a mayor riesgo de DRA durante la hospitalizacion por IC descompensada.

Introduction In decompensated heart failure (HF), both acute kidney injury (AKI) and high Galectina-3 (Gal-3) levels have been associated with poorer outcomes. Plasma Gal-3 levels are affected by renal function; however, the potential role of Gal-3 as a predictor of AKI has not been established. Methods We measured Gal-3 concentrations at admission for 175 patients hospitalized for HF and recorded the onset of AKI according to the Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) analytical criteria. Results During hospitalization, 44 patients (25.1%) developed AKI, although only 14 (8%) corresponded to more advanced stages. These 14 patients had significantly higher Gal-3 levels at admission, which remained a predictor of AKI after the multivariate adjustment by other predictors and by baseline renal function. Conclusions High Gal-3 levels at admission are associated with a higher risk of AKI during hospitalization for decompensated HF.

Diabetes & Metabolism - In Press.Proof corrected by the author Available online since mardi 7 novembre 2017

Left ventricular remodeling following myocardial infarction (MI) is related to adverse outcome. It has been shown that an up-regulation of plasma soluble ST2 (sST2) levels are associated with lower pre-discharge left ventricular (LV) ejection fraction, adverse cardiovascular outcomes and mortality outcome after MI. The mechanisms involved in its modulation are unknown and there is not specific treatment capable of lowering plasma sST2 levels in acute-stage HF. We recently identified Yin-yang 1 (Yy1) as a transcription factor related to circulating soluble ST2 isoform (sST2) expression in infarcted myocardium. However, the underlying mechanisms involved in this process have not been thoroughly elucidated. This study aimed to evaluate the pathophysiological implication of miR-199a-5p in cardiac remodeling and the expression of the soluble ST2 isoform. Myocardial infarction (MI) was induced by permanent ligation of the left anterior coronary artery in C57BL6/J mice that randomly received antimiR199a therapy, antimiR-Ctrl or saline. A model of biomechanical stretching was also used to characterize the underlying mechanisms involved in the activation of Yy1/sST2 axis. Our results show that the significant upregulation of miR-199a-5p after myocardial infarction increases pathological cardiac hypertrophy by upregulating circulating soluble sST2 levels. AntimiR199a therapy up-regulates Sirt1 and inactivates the co-activator P300 protein, thus leading to Yy1 inhibition which decreases both expression and release of circulating sST2 by cardiomyocytes after myocardial infarction. Pharmacological inhibition of miR-199a rescues cardiac hypertrophy and heart failure in mice, offering a potential therapeutic approach for cardiac failure. This study was supported by a grant from the Seneca Foundation-Agency of Science and Technology of the Region of Murcia (20652/JLI/18) and a grant from the Instituto de Salud Carlos III (PI19/00519) which is cofinanced through the European Union's European Regional Development Fund (FEDER). Dr. Lax is a Ramon and Cajal researcher at the Department of Medicine, University of Murcia. Sí

Sodium-glucose co-transporter-2 inhibitors (SGLT2i) have shown to prevent heart failure progression, although the mechanisms remain poorly understood. Here we evaluated the effect of empagliflozin (EMPA, SGLT2i) in cardiac remodeling after myocardial infarction, the interplay with diabetes status and the role of cardiac GTP enzyme cyclohydrolase 1 (cGCH1). A rat model of diabetes (50 mg/kg streptozotocin, i.p.) was subjected to myocardial infarction and left ventricular systolic dysfunction, by ligation of the left anterior descending coronary artery. EMPA therapy significantly improved cardiac remodeling parameters and ameliorated processes of fibrosis and hypertrophy, in both non-diabetic and diabetic rats. This cardioprotective effect related with a significant increase in myocardial expression levels of cGCH1, which led to activation of nNOS and eNOS, and inhibition of iNOS, and subsequently resulted in increasing of NO levels and decreasing O2.- and nitrotyrosine levels. These effects were replicated in a cardiomyocyte biomechanical stretching diabetic model, where silencing cGCH1 blocked the preventive effect of EMPA. The beneficial effects were observed irrespective of diabetes status, although the magnitude was greater in presence of diabetes. Empagliflozin improves myocardial remodeling after myocardial infarction through overexpression of cGCH1, and irrespective of diabetes status. This study was supported by a grant from the Seneca Foundation-Agency of Science and Technology of the Region of Murcia (20652/JLI/18) and a grant from the Instituto de Salud Carlos III (PI19/00519). Sí

This paper presents a technological demonstrator with traffic applications, which carries out three typical intelligent transportation system (ITS) tasks: traffic flow measurement, speed estimation, and vehicles classification. The proposed system is a frequency-modulated continuous wave radar working at 24 GHz, with side-looking installation. Two signal-processing modes, 1-D and 2-D, are introduced as detection scheme. Unlike other existing commercial systems, this demonstrator makes use of phase information from target echoes in order to perform clutter cancellation and target speed measurement. To this end, two different speed-estimating methods are proposed and compared by means of experimental results obtained from a complex scenario.

BACKGROUND: Soluble ST2 (sST2), which is the soluble form of interleukin (IL)-1 receptor-like 1, identifies risk in acutely decompensated heart failure (ADHF). IL-1β is an inflammatory cytokine that has deleterious effects in myocardial remodeling and function. IL-1β inhibition has beneficial effects after acute myocardial infarction. However, the role of IL-1β in ADHF and its relationship to ST2 remain unclear. OBJECTIVES: This study sought to investigate the relationship between IL-1β and sST2, and the prognostic impact of such a relationship in patients with ADHF. METHODS: This study examined 316 consecutive patients who were hospitalized with ADHF (72 ± 12 years of age, 57% male, and left ventricular ejection fraction 45 ± 17%). Blood samples were collected at presentation, and IL-1β and sST2 levels were measured. All-cause mortality was obtained for all patients at 1 year. RESULTS: The IL-1β concentration at presentation was associated with prior HF hospitalizations, functional impairment, and higher N-terminal pro-B-type natriuretic peptide and high-sensitivity troponin T concentrations. IL-1β was higher in patients who died during the year after hospitalization (n = 52, 16.5%) (p = 0.005), and the optimal threshold was identified with levels over 49.1 pg/ml (hazard ratio: 2.5; 95% confidence interval: 1.43 to 4.49; p = 0.0014). Circulating IL-1β positively correlated with sST2 (ρ = 0.65; p < 0.001). Considering the prognostic thresholds of IL-1β (≥49.1 pg/ml) and sST2 (≥35.0 ng/ml) concentrations: all patients with low sST2 also presented with low IL-1β; among patients with high sST2, only those with also high IL-1β had a significantly higher risk of death (30% vs. 14%; hazard ratio: 2.52; 95% confidence interval: 1.40 to 4.56; p = 0.002). CONCLUSIONS: Circulating IL-1β concentrations are clinically meaningful in ADHF patients and interplay with the predictive ability of sST2. IL-1 axis-related inflammation signaling may represent a therapeutic target in ADHF. This work has been supported by grants PI14/01637 and PI17/01742 from "Instituto de Salud Carlos III," Madrid, Spain, and grant PI14/19334 from "Fundacion Seneca de Ciencia y Tecnologia de la Region de Murcia," Murcia, Spain. Dr. Pascual-Figal has received grant support from Roche Diagnostics; and has received educational fees from Novartis. Dr. Bayes-Genis has received speaker fees from Novartis, Roche, and Critical Diagnostics. Dr. Diez has received educational fees from Novartis. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Sí

Background The cardioprotective effects of metformin remain poorly defined. Interleukin (IL)-33/ST2L signaling is a novel cardioprotective pathway, which is antagonized by the soluble isoform sST2. No data exist about the regulation of ST2 expression. This study aimed to evaluate the pathophysiological implication of Yin-Yang 1 (Yy1) transcription factor in cardiac remodeling and the expression of the soluble ST2 isoform. Methods and results Myocardial infarction (MI) was induced in Wistar rats randomly receiving metformin or saline solution by permanent ligation of the left anterior coronary artery. In addition, a model of cardiomyocyte “biochemical strain” was used. Metformin administration improved post-MI cardiac remodeling, an effect that was associated with increased IL-33 and reduced sST2 levels in the myocardium. The anti-remodeling effects of metformin were also associated with a decrease in the transcription factor Yy1 intranuclear level and lower levels of phosphorylated HDAC4 within the cytoplasmic space. These effects were also observed in a cardiomyocyte biochemical strain model, where Yy1 silencing or HDAC4 inhibition blocked sST2 production in cardiomyocytes. Metformin blocked the HDAC4 phosphorylation induced by MI, preventing its export from the nucleus to the cytosol. The presence of dephosphorylated HDAC4 in the nucleus acted as a co-repressor of Yy1, repressing sST2 expression. Conclusion The transcription factor Yy1 regulates sST2 expression, and repression of Yy1 by metformin results in lower levels of sST2 that are associated with favorable myocardial remodeling. The manipulation of YY1 or its co-repressor HDAC4 emerge as new targets to modulate ST2/IL33 signaling and prevent adverse cardiac remodeling.

Background: Serum concentrations of ST2 (interleukin-1 receptor-like 1) represent a meaningful prognostic marker in cardiac diseases. Production of soluble ST2 (sST2) may be partially extracardiac. Identification of sST2 sources is relevant to design strategies for modulating its signaling. Methods and Results: An experimental model of ischemic heart failure was used. sST2, membrane-bound ST2 (ST2L), and IL-33 were measured in lungs, heart, kidney, and liver by quantifying mRNA and protein expression in tissue samples obtained at different times (1, 2, 4, and 24 weeks). Primary human type II pneumocyte cell cultures were subjected to strain. sST2 was measured in samples of bronchial aspirate and serum obtained from patients treated with invasive respiratory support. In the experimental model, sST2 increased significantly from the first week in both lungs and myocardium, whereas ST2L/IL-33 response was unfavorable in lungs (decrease) and favorable in myocardium (increase). No changes were observed in liver and kidneys. ST2 immunostaining was intensely observed in alveolar epithelium, and sST2 was secreted by primary human type II pneumocytes in response to strain. sST2 levels in lung aspirates were substantially higher in the presence of cardiogenic pulmonary edema (median, 228 [interquartile range, 28.4–324.0] ng/mL; P Conclusions: The lungs are a relevant source of sST2 in heart failure. These results may have implications for the progression of disease and the development of therapies targeting the ST2 system in patients with heart failure.

The protective effects of the antioxidants present in food are of great relevance for cardiovascular health. This study evaluates whether the extracts from reformulated meat products with a reduction in fat and/or sodium content exert a cardioprotective effect against ischemia-induced oxidative stress in cardiomyocytes, compared with non-meat foods. Ischemic damage caused loss of cell viability, increased reactive oxygen species and lipid peroxidation and decreased the antioxidant activity. Pretreatment for 24 h with digested or non-digested extracts from reformulated meat products led to protection against ischemia-induced oxidative damage: increased cell viability, reduced oxidative stress and restored the antioxidant activity. Similar results were obtained using extracts from tuna fish, but not with the extracts of green peas, salad or white beans. These results suggest that reformulated meat products have a beneficial impact in protecting cardiac cells against ischemia, and they may represent a source of natural antioxidants with benefits for cardiovascular health.

Sodium-glucose co-transporter-2 inhibitors (SGLT2i) have shown to prevent heart failure progression, although the mechanisms remain poorly understood. Here we evaluated the effect of empagliflozin (EMPA, SGLT2i) in cardiac remodeling after myocardial infarction, the interplay with diabetes status and the role of cardiac GTP enzyme cyclohydrolase 1 (cGCH1). A rat model of diabetes (50 mg/kg streptozotocin, i.p.) was subjected to myocardial infarction and left ventricular systolic dysfunction, by ligation of the left anterior descending coronary artery. EMPA therapy significantly improved cardiac remodeling parameters and ameliorated processes of fibrosis and hypertrophy, in both non-diabetic and diabetic rats. This cardioprotective effect related with a significant increase in myocardial expression levels of cGCH1, which led to activation of nNOS and eNOS, and inhibition of iNOS, and subsequently resulted in increasing of NO levels and decreasing O