(Re) Solving Repair After Myocardial Infarction

Cardiovascular diseases, including myocardial infarction and its complications such as heart failure, are the leading cause of death worldwide. To date, basic and translational research becomes necessary to unravel the mechanisms of cardiac repair post-myocardial infarction. The local inflammatory tissue response after acute myocardial infarction determines the subsequent healing process. The diversity of leukocytes such as neutrophils, macrophages and lymphocytes contribute to the clearance of dead cells while activating reparative pathways necessary for myocardial healing. Cardiomyocyte death triggers wall thinning, ventricular dilatation, and fibrosis that can cause left ventricular dysfunction and heart failure. The ultimate goal of cardiac repair is to regenerate functionally viable myocardium after myocardial infarction to prevent cardiac death. Current therapies for heart failure after myocardial infarction are limited and non-curative. At the moment in clinic, conventional surgical interventions such as coronary artery bypass graft or percutaneous coronary interventions are only able to partially restore heart function, with a minor improvement in the left ventricular ejection fraction. The goal of this review is to provide an overview of endogenous myocardial repair mechanisms possibly transferable to future treatment strategies. Among the innovative factors identified as essential in cardiac healing, we highlight specialized pro-resolving mediators as the emerging factors that provide the key molecular signals for the activation of the reparative cells in the myocardium

(Re) Solving Repair After Myocardial Infarction

Cardiovascular diseases, including myocardial infarction and its complications such as heart failure, are the leading cause of death worldwide. To date, basic and translational research becomes necessary to unravel the mechanisms of cardiac repair post-myocardial infarction. The local inflammatory tissue response after acute myocardial infarction determines the subsequent healing process. The diversity of leukocytes such as neutrophils, macrophages and lymphocytes contribute to the clearance of dead cells while activating reparative pathways necessary for myocardial healing. Cardiomyocyte death triggers wall thinning, ventricular dilatation, and fibrosis that can cause left ventricular dysfunction and heart failure. The ultimate goal of cardiac repair is to regenerate functionally viable myocardium after myocardial infarction to prevent cardiac death. Current therapies for heart failure after myocardial infarction are limited and non-curative. At the moment in clinic, conventional surgical interventions such as coronary artery bypass graft or percutaneous coronary interventions are only able to partially restore heart function, with a minor improvement in the left ventricular ejection fraction. The goal of this review is to provide an overview of endogenous myocardial repair mechanisms possibly transferable to future treatment strategies. Among the innovative factors identified as essential in cardiac healing, we highlight specialized proresolving mediators as the emerging factors that provide the key molecular signals for the activation of the reparative cells in the myocardium

Bayesian Inference of Model Error in Imprecise Models

International audienceModern science makes use of computer models to reproduce and predict complex physical systems. Every model involves parameters, which can be measured experimentally (e.g., mass of a solid), or not (e.g., coefficients in the k − ε turbulence model). The latter parameters can be inferred from experimental data, through a procedure called calibration of the computer model. However, some models may not be able to represent reality accurately, due to their limited structure : this is the definition of model error. The "best value" of the parameters of a model is traditionnally defined as the best fit to the data. It depends on the experiment, the quantities of interest considered, and also on the supposed underlying statistical structure of the error. Bayesian methods allow the calibration of the model by taking into account its error. The fit to the data is balanced with the complexity of the model, following Occam's principle. Kennedy and O'Hagan's innovative method [1] to represent model error with a Gaussian process is a reference in this field. Recently, Tuo and Wu [3] proposed a frequentist addition to this method, to deal with the identifiability problem between model error and calibration error. Plumlee [2] applied the method to simple situations and demonstrated the potential of the approach. In this work, we compare Kennedy and O'Hagan's method with its frequentist version, which involves an optimization problem, on several numerical examples with varying degrees of model error. The calibration provides estimates of the model parameters and model predictions, while also inferring model error within observed and not observed parts of the experimental design space. The case of non-linear costly computer models is also considered, and we propose a new algorithm to reduce the numerical complexity of Bayesian calibration techniques

Indagini istologiche, immunoistochimiche e immunobiochimiche in capre clinicamente sane provenienti da un focolaio di scrapie

Nel corso del 2003, nell’ambito del piano di sorveglianza passiva sulle Encefalopatie Spongiformi Trasmissibili (TSEs), per la prima volta in Sardegna, è stata diagnosticata istologicamente ed immunoistochimicamente la scrapie in una capra. Il soggetto proveniva da un gregge nel quale da 2 anni si manifestava una patologia polimorfa caratterizzata talvolta da sintomi neurologici e da una mortalità intorno al 20%. Sulla base della legge attualmente in vigore in Italia si è proceduto all’abbattimento di tutte le capre presenti in allevamento (n = 93). Durante l’abbattimento venivano prelevati da ciascun capo obex, linfonodi retrofaringei e tonsille. L’esame istologico dell’obex non evidenziava quadri lesivi di tipo spongiforme mentre l’esame immunoistochimico del tessuto nervoso e linfatico evidenziava la presenza di cinque soggetti nello stato pre-clinico della malattia

Gambling at the time of COVID-19: results from interviews in an Italian sample of gamblers

© 2022 The Author(s). Published by Elsevier Ltd on behalf of International Society for the Study of Emerging Drugs. https://creativecommons.org/licenses/by/4.0/The coronavirus pandemic affected the life of those suffering from addic- tive behaviors often confined to prolonged periods of self-isolation. To explore the variation of symptoms related to gambling, 46 outpatients of the mental health services in the Trento Province were invited to take part in a phone interview at the start of the national lockdown. Although only 2.17% increased gambling activity during this period, half of the sample (50.00%) experienced irritability, mood fluctuation (43.48%) and anxiety (39.13%). Follow-up studies should assess modifications in their behaviors that occurred after the reopening of gambling venues.Peer reviewedFinal Published versio

Water planning and management in the Cornia river plain by means of the gis-integrated freewat platform

Coastal aquifer, Cornia valley, Tuscany, Managed Aquifer Recharge, FREEWAT platform

Impact of Vitamin D3 Deficiency on Phosphatidylcholine-/Ethanolamine, Plasmalogen-, Lyso-Phosphatidylcholine-/Ethanolamine, Carnitine- and Triacyl Glyceride-Homeostasis in Neuroblastoma Cells and Murine Brain

Vitamin D3 hypovitaminosis is associated with several neurological diseases such as Alzheimer’s disease, Parkinson’s disease or multiple sclerosis but also with other diseases such as cancer, diabetes or diseases linked to inflammatory processes. Importantly, in all of these dis eases lipids have at least a disease modifying effect. Besides its well-known property to modulate gene-expression via the VDR-receptor, less is known if vitamin D hypovitaminosis influences lipid homeostasis and if these potential changes contribute to the pathology of the diseases themselves. Therefore, we analyzed mouse brain with a mild vitamin D hypovitaminosis via a targeted shotgun lipidomic approach, including phosphatidylcholine, plasmalogens, lyso-phosphatidylcholine, (acyl- /acetyl-) carnitines and triglycerides. Alterations were compared with neuroblastoma cells cultivated in the presence and with decreased levels of vitamin D. Both in cell culture and in vivo, decreased vitamin D level resulted in changed lipid levels. While triglycerides were decreased, carnitines were increased under vitamin D hypovitaminosis suggesting an impact of vitamin D on energy metabolism. Additionally, lyso-phosphatidylcholines in particular saturated phosphatidylcholine (e.g., PC aa 48:0) and plasmalogen species (e.g., PC ae 42:0) tended to be increased. Our results suggest that vitamin D hypovitaminosis not only may affect gene expression but also may directly influence cellular lipid homeostasis and affect lipid turnover in disease states that are known for vitamin D hypovitaminosis