203 research outputs found
A protective device for monorenal subjects or subjects with renal disease
No full textThere is described a protective device (1) for monorenal subjects or subjects with renal disease comprising : - a garment (2) wearable by a subject (P) at least at a lumbar region (L) of the subject (P) - at least one protective element (4) installed on said garment (2) at a portion thereof configured to be positioned at the lumbar region (L) of the subject (P) when the garment (2) is worn by the subject (P) - a belt element (6) configured to at least partially encircle the torso of the subject (P) in the lumbar region (L) and to exert a compressive action of the at least one protective element (4) against the lumbar region (L) of the subject (P)
A mathematical model of healthy and dystrophic skeletal muscle biomechanics
No full textDuchenne Muscular Dystrophy (DMD) is a common X-linked disease, caused by mutations in the gene encoding dystrophin and characterized by widespread muscle damage that invariably leads to paralysis and death. Lack of dystrophin in the muscles of DMD patients determines an increased fragility of muscle fibers, leading to repeated cycles of necrosis and regeneration that result in failed regeneration, increased fibrosis and progressive loss of muscle function. In this work, we propose a three-dimensional chemo-mechanical mathematical model of skeletal muscle in DMD. This model is based on stress-strain mechanical data of the muscle and studies of changes in fiber structure and interaction aiming to shade light into the biophysical mechanisms regulating muscle contraction. The results show that the model is able to reproduce the experimental data of maximum isometric force, maximum contraction velocity and concentric normalized F-V curve for the healthy and dystrophic muscle. Furthermore, the model is capable of predicting the force-velocity response of the muscle to eccentric loading without explicitly imposing its functional form in the formulation, and it is able to reproduce the concentric normalized F-V curve of the healthy fiber, as an additional proof of the predictive capabilities of the model. The resulting model represents a novel approach to study DMD pathogenesis by providing insights into the underlying mechanisms of muscle response to force associated with the impaired muscle functionality. Moreover, it could be an innovative tool for researchers to predict muscle response under conditions that are not possible to explore in the laboratory and an important step towards a new paradigm of in-silico trials that could allow identifying novel therapies bypassing the use of animal models
Metodo per stimare in tempo reale la probabilità di successo di un intervento di trombectomia
No full textMetodo per stimare in tempo reale la probabilità di successo di un intervento di trombectomia, comprendente le seguenti fasi: creare un database di dati generati da modelli di trombectomia e allenare un algoritmo predittivo con tali dati mediante un’unità di elaborazione associata al database; acquisire immagini cliniche relative a vasi occlusi di un paziente ed estrarre da tali immagini cliniche parametri geometrici dei vasi occlusi e parametri di composizione dell’occlusione; generare un modello tridimensionale dei vasi occlusi e dell’occlusione elaborando, mediante l’unità di elaborazione, i parametri geometrici dei vasi occlusi e i parametri di composizione dell’occlusione; selezionare parametri indicatori relativi all’intervento di trombectomia mediante elaborazione del modello tridimensionale dei vasi occlusi e dell’occlusione; calcolare la probabilità di successo dell’intervento di trombectomia con rimozione dell’occlusione elaborando i parametri indicatori mediante l’algoritmo predittivo
In silico approaches for transcatheter aortic valve replacement inspection
No full textIntroduction: Increasing applications of transcatheter aortic valve replacement (TAVR) to treat high- or medium-risk patients with aortic diseases have been proposed in recent years. Despite its increasing use, many influential factors are still to be understood. Furthermore, innovative applications of TAVR such as in bicuspid aortic valves or in low-risk patients are emerging in clinical use. Numerical analyses are increasingly used to reproduce clinical treatments. The future trends in this area are foreseen for in silico trials and personalized medicine. Areas covered: This review paper analyzes the recent years (Jan 2018–Aug 2020) of in silico studies simulating the behavior of transcatheter aortic valves with emphasis on the addressed clinical question and the used modeling strategies. The manuscripts are firstly classified based on their clinical hypothesis. A second classification is based on the adopted modeling approach in terms of patient domain, device modeling, and inclusion or exclusion of the fluid domain. Expert opinion: The TAVR can be virtually performed in numerous vessel geometries and with different devices. This versatility allows a rapid evaluation of the feasibility of different implantation approaches for specific patients, and patient populations, resulting in faster and safer introduction or optimization of new treatments or devices
Influence of the Stimulation Current on the Differences between Cell and Tissue Electrophysiological Simulations
No full textThis study compares stimulation waveforms for single-cell simulations. The alternatives include monophasic and biphasic current pulses, and a new waveform that resembles the transmembrane current responsible for conduction in tissue. Results indicate that the new stimulation produces the lowest mismatch between action potential markers simulated in cell and in tissue. In comparison with the monophasic stimulation, the new stimulation reduced cell-fiber differences by 99% for triangulation, by 95% for maximum transmembrane voltage, and by 76% for the maximum voltage slope. In conclusion, the new stimulation waveform could help to improve the trustworthiness of single-cell simulations in studies involving tissue-derived markers
Effect of myofibril architecture on the active contraction of dystrophic muscle. A mathematical model
No full textDuchenne muscular dystrophy (DMD) is a muscle degenerative disease caused by a mutation in the dystrophin gene. The lack of dystrophin leads to persistent inflammation, degeneration/regeneration cycles of muscle fibers, Ca2+ dysregulation, incompletely regenerated fibers, necrosis, fibrotic tissue replacement, and alterations in the fiber ultrastructure i.e., myofibril misalignment and branched fibers. This work aims to develop a comprehensive chemo-mechanical model of muscle-skeletal tissue accounting for dispersion in myofibrillar orientations, in addition to the disorders in sarcomere pattern and the fiber branching. The model results confirm a significant correlation between the myofibrillar dispersion and the reduction of isometric force in the dystrophic muscle and indicate that the reduction of contraction velocity in the dystrophic muscle seems to be associated with the local disorders in the sarcomere patterns of the myofibrils. Also, the implemented model can predict the force–velocity response to both concentric and eccentric loading. The resulting model represents an original approach to account for defects in the muscle ultrastructure caused by pathologies as DMD
An electrophysiologic computational model of the zebrafish heart
No full textIn recent years there has been a growing interest in the zebrafish thanks to its physiological characteristics similar to humans '. The following work aims to create a full electrophysiological computational model of the zebrafish heart with the ultimate purpose of assessing the influence of pathologies and drug administration. The model considers a full body and the two-chambers of a 3 days post fertilization zebrafish. A four-variable phenomenological Action Potential model is used to describe the action potential of different regions of the heart. Tissue conductivity has been calibrated in order to reproduce the activation sequence described in literature. This model allows the evaluation of the main electrophysiological parameters in terms of activation sequence and timing, AP morphology (i.e., APD{90}, AP amplitude, maximum and minimum AP derivatives), and ECG morphology (i.e., P-wave, T-wave, and QRS-complex amplitudes and durations)
Analysis of vulnerability to reentry in acute myocardial ischemia using a realistic human heart model
No full textElectrophysiological alterations of the myocardium caused by acute ischemia constitute a pro-arrhythmic substrate for the generation of potentially lethal arrhythmias. Experimental evidence has shown that the main components of acute ischemia that induce these electrophysiological alterations are hyperkalemia, hypoxia (or anoxia in complete artery occlusion), and acidosis. However, the influence of each ischemic component on the likelihood of reentry is not completely established. Moreover, the role of the His-Purkinje system (HPS) in the initiation and maintenance of arrhythmias is not completely understood. In the present work, we investigate how the three components of ischemia affect the vulnerable window (VW) for reentry using computational simulations. In addition, we analyze the role of the HPS on arrhythmogenesis. A 3D biventricular/torso human model that includes a realistic geometry of the central and border ischemic zones with one of the most electrophysiologically detailed model of ischemia to date, as well as a realistic cardiac conduction system, were used to assess the VW for reentry. Four scenarios of ischemic severity corresponding to different minutes after coronary artery occlusion were simulated. Our results suggest that ischemic severity plays an important role in the generation of reentries. Indeed, this is the first 3D simulation study to show that ventricular arrhythmias could be generated under moderate ischemic conditions, but not in mild and severe ischemia. Moreover, our results show that anoxia is the ischemic component with the most significant effect on the width of the VW. Thus, a change in the level of anoxia from moderate to severe leads to a greater increment in the VW (40 ms), in comparison with the increment of 20 ms and 35 ms produced by the individual change in the level of hyperkalemia and acidosis, respectively. Finally, the HPS was a necessary element for the generation of approximately 17% of reentries obtained. The retrograde conduction from the myocardium to HPS in the ischemic region, conduction blocks in discrete sections of the HPS, and the degree of ischemia affecting Purkinje cells, are suggested as mechanisms that favor the generation of ventricular arrhythmias
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