Development of a pitching control for a flapping wing MAV

The main purpose of this project is to develop a pitching control for MAVs with flapping wings. This is one of the first issues that needs to be assessed in the flapping wing technology due to the unsteadiness of the aerodynamic forces. In order to achieve this goal, we define the specific objectives defined in 2.1, 2.2 and 2.3. A brief description of the available methods and tools is presented in 2.4.Ingeniería Aeroespacia

Blood stasis imaging predicts cerebral microembolism during acute myocardial infarction

Background: Cardioembolic stroke is a major source of mortality and disability worldwide. The authors hypothesized that quantitative characterization of intracardiac blood stasis may be useful to determine cardioembolic risk in order to personalize anticoagulation therapy. The aim of this study was to assess the relationship between image-based metrics of blood stasis in the left ventricle and brain microembolism, a surrogate marker of cardiac embolism, in a controlled animal experimental model of acute myocardial infarction (AMI). -- Methods: Intraventricular blood stasis maps were derived from conventional color Doppler echocardiography in 10 pigs during anterior AMI induced by sequential ligation of the mid and proximal left anterior descending coronary artery (AMI-1 and AMI-2 phases). From these maps, indices of global and local blood stasis were calculated, such as the average residence time and the size and ratio of contact with the endocardium of blood regions with long residence times. The incidence of brain microemboli (high-intensity transient signals [HITS]) was monitored using carotid Doppler ultrasound. -- Results: HITS were detected in 0%, 50%, and 90% of the animals at baseline and during AMI-1 and AMI-2 phases, respectively. The average residence time of blood in the left ventricle increased in parallel. The residence time performed well to predict microemboli (C-index = 0.89, 95% CI, 0.75–1.00) and closely correlated with the number of HITS (R = 0.87, P < .001). Multivariate and mediation analyses demonstrated that the number of HITS during AMI phases was best explained by stasis. Among conventional echocardiographic variables, only apical wall motion score weakly correlated with the number of HITS (R = 0.3, P = .04). Mural thrombosis in the left ventricle was ruled out in all animals. -- Conclusions: The degree of stasis of blood in the left ventricle caused by AMI is closely related to the incidence of brain microembolism. Therefore, stasis imaging is a promising tool for a patient-specific assessment of cardioembolic risk.This study was supported by grant PI15/02211, Rio Hortega (CM17/00144), and Juan Rodés fellowships (JR15/00039) from Instituto de Salud Carlos III; grant DPI2016-75706-P and a Juan de la Cierva fellowship (IJCI-2014-19507) from Ministerio de Economía y Competitividad; synergy grant Y2018/BIO-4858-PREFI-CM from Comunidad Autónoma de Madrid; the European Union - European Regional Development Fund; by the Spanish Society of Cardiology (ISBI-DCM); by the University of California,San Diego, CTRI Galvanizing Engineering and Medicine Program; American Heart Association grant 16GRNT27250262; and National Institutes of Health UC CAI grant CII4560. P.M.-L. was also funded by CIBERCV. P.M.-L., L.R., J.C.A., and J.B. are inventors of a method for quantifying intracardiac stasis from imaging data under a Patent Cooperation Treaty patent application (WO2017091746A1)

Assessment Of Blood Flow Transport In The Left Ventricle Using Ultrasound. Validation Against 4-D Flow Cardiac Magnetic Resonance

Four-dimensional flow cardiac magnetic resonance (CMR) is the reference technique for analyzing blood transport in the left ventricle (LV), but similar information can be obtained from ultrasound. We aimed to validate ultrasound-derived transport in a head-to-head comparison against 4D flow CMR. In five patients and two healthy volunteers, we obtained 2D + t and 3D + t (4D) flow fields in the LV using transthoracic echocardiog-raphy and CMR, respectively. We compartmentalized intraventricular blood flow into four fractions of end -dia-stolic volume: direct flow (DF), retained inflow (RI), delayed ejection flow (DEF) and residual volume (RV). Using ultrasound we also computed the properties of LV filling waves (percentage of LV penetration and percent-age of LV volume carried by E/A waves) to determine their relationships with CMR transport. Agreement between both techniques for quantifying transport fractions was good for DF and RV (Ric [95% confidence inter-val]: 0.82 [0.33, 0.97] and 0.85 [0.41, 0.97], respectively) and moderate for RI and DEF (Ric= 0.47 [-0.29, 0.88] and 0.55 [-0.20, 0.90], respectively). Agreement between techniques to measure kinetic energy was variable. The amount of blood carried by the E-wave correlated with DF and RV (R = 0.75 and R = 0.63, respectively). There-fore, ultrasound is a suitable method for expanding the analysis of intraventricular flow transport in the clinical setting. (E-mail: [email protected]) (c) 2022 The Author(s). Published by Elsevier Inc. on behalf of World Federation for Ultrasound in Medicine &amp; Biology.Funding Agencies|Comunidad de Madrid [Y2018/BIO-4858 PREFI-CM]; Instituto de Salud Carlos III [DTS/1900063, PI15/02211]; Spanish Society of Cardiology (ISBIDCM); Ministerio de Economia y Competitividad, Spain [BES-2017-079924]; Swedish Research Council [2018-04454]; Swedish Heart and Lung Foundation [20210441]; EU-European Regional Development Fund</p

The Biological Bases of Group 2 Pulmonary Hypertension

Pulmonary hypertension (PH) is a potentially fatal condition with a prevalence of around 1% in the world population and most commonly caused by left heart disease (PH-LHD). Usually, in PH-LHD, the increase of pulmonary pressure is only conditioned by the retrograde transmission of the left atrial pressure. However, in some cases, the long-term retrograde pressure overload may trigger complex and irreversible biomechanical and biological changes in the pulmonary vasculature. This latter clinical entity, designated as combined pre- and post-capillary PH, is associated with very poor outcomes. The underlying mechanisms of this progression are poorly understood, and most of the current knowledge comes from the field of Group 1-PAH. Treatment is also an unsolved issue in patients with PH-LHD. Targeting the molecular pathways that regulate pulmonary hemodynamics and vascular remodeling has provided excellent results in other forms of PH but has a neutral or detrimental result in patients with PH-LHD. Therefore, a deep and comprehensive biological characterization of PH-LHD is essential to improve the diagnostic and prognostic evaluation of patients and, eventually, identify new therapeutic targets. Ongoing research is aimed at identify candidate genes, variants, non-coding RNAs, and other biomarkers with potential diagnostic and therapeutic implications. In this review, we discuss the state-of-the-art cellular, molecular, genetic, and epigenetic mechanisms potentially involved in PH-LHD. Signaling and effective pathways are particularly emphasized, as well as the current knowledge on -omic biomarkers. Our final aim is to provide readers with the biological foundations on which to ground both clinical and pre-clinical research in the field of PH-LHD