Search

The constant growth of solid and hazardous waste production is increasing the European concerns about the protection of the environment and natural resources. It is estimated that Europe produces up to 3 billion tons of waste every year. EU is promoting several waste management policies aiming to reduce the environmental impacts of waste and improve Europe's resource efficiency. In this context, public administration of numerous Italian regions are showing more attention in order to reducing the environmental impacts related to solid and hazardous waste management. Life cycle assessment (LCA) is a powerful tool to quantify environmental impacts and determine the potential management strategies to reduce these impacts. Nevertheless, the identification of Life Cycle Inventory (LCI) modelling framework to model multifunctionality could be a very critical point. This study analyzed the environmental performance of the waste management, including municipal solid waste and industrial waste, in the Emilia Romagna region (Italy) adopting attributional and consequential approaches. The influence of LCI modelling frameworks on the environmental results has been investigated. [ABSTRACT FROM AUTHOR]

Mini ORC power systems with the capability to deliver 3-50 kWe are receiving increased recognition for applications such as heat recovery from automotive engines, or distributed power generation from geothermal reservoirs and solar irradiation. Efficient and reliable expanders are the enabling components of such power systems, and all the related developments are currently at the research stage [1]. In the open literature experimental gas dynamic data is limited concerning the fluids and the flow conditions of interest for ORC expanders [2]. Therefore, CFD tools used for the fluid dynamic design of these components cannot be validated against reliable test cases. To bridge this gap, new experimental facilities are currently being built, such as the ORCHID setup [3]. The availability of proper experimental datasets is not, however, the sole requirement for validating a CFD code. Another precondition, equivalently important, is to define an appropriate validation methodology. This paper introduces the first steps towards the validation of a CFD solver for non-ideal compressible flows. Notably, a numerical procedure based on uncertainty quantification analysis has been conceived to assess the accuracy of the thermophysical sub-model of the code, i.e. the equation of state (EoS). Due to the lack of suitable experimental data, a synthetic dataset is generated and used to investigate the validity of the procedure. The associated validation exercise confirms the applicability of the proposed procedure, but also points out that the adopted validation metrics should be complemented with additional statistical indicators. [ABSTRACT FROM AUTHOR]

Currently, turbomachinery design optimization methodologies are mainly restricted to steady state approaches, due to the high computational cost associated with time-accurate shape optimization algorithms. However, the possibility to include unsteady effects in turbomachinery optimization can significantly increase the level of accuracy of the design predictions, leading to a more realistic representation of the actual performance and ultimately to a substantial increase in operating efficiency. Unsteady effects are particularly relevant in Organic Rankine Cycle turbines. A trade-off between high-fidelity time-accurate unsteady simulations of the flow solution and computational cost is therefore needed at design level. In this paper, a first application of the harmonic balance method to non-ideal compressible flows is presented. The methodology allows to solve the unsteady flow equations for a set of specified frequencies only, with significant computational time savings. An algorithm is proposed for non uniform time sampling in order to resolve frequencies that do not need to be integral multiple of one fundamental harmonic. This enables the solution of quasi-periodically forced non-linear flow problems, in combination with complex fluid models based on accurate equations of state. The method is applied to the unsteady analysis of a supersonic Organic Rankine Cycle stator with quasi-periodic inlet operating conditions, showing about one order magnitude lower computational cost compared to time-accurate simulations. [ABSTRACT FROM AUTHOR]

High temperature Organic Rankine Cycles power systems of low power capacity, i.e. 3-50 kW e , are receiving recognition for distributed and mobile energy generation applications. For this type of power plants, it is customary to adopt a radial-turbine as prime mover, essentially for their ability to cope with very large volumetric flow ratio with limited fluid-dynamic penalty. To date, the design of such turbines is based on design guidelines and loss models developed mainly for turbo-chargers, subsequently adapted by means of non-validated computational fluid-dynamic calculations. In the attempt to provide data sets for CFD validation and calibration of loss models, a mini-ORC radial inflow turbine delivering 10kW of mechanical power will be realized and tested in the Propulsion and Power Laboratory of TU-Delft. The fluid dynamic design and characterization of the machine is detailed in this paper. According to available models, the results indicate that the optimal layout of mini-ORC turbines can substantially differ from that of radial-inflow turbines utilized in more traditional applications, strengthening the need of experimental campaigns to support the conception of new design practices. [ABSTRACT FROM AUTHOR]

Mini ORC power systems with the capability to deliver 3-50 kWe are receiving increased recognition for applications such as heat recovery from automotive engines, or distributed power generation from geothermal reservoirs and solar irradiation. Efficient and reliable expanders are the enabling components of such power systems, and all the related developments are currently at the research stage [1]. In the open literature experimental gas dynamic data is limited concerning the fluids and the flow conditions of interest for ORC expanders [2]. Therefore, CFD tools used for the fluid dynamic design of these components cannot be validated against reliable test cases. To bridge this gap, new experimental facilities are currently being built, such as the ORCHID setup [3]. The availability of proper experimental datasets is not, however, the sole requirement for validating a CFD code. Another precondition, equivalently important, is to define an appropriate validation methodology. This paper introduces the first steps towards the validation of a CFD solver for non-ideal compressible flows. Notably, a numerical procedure based on uncertainty quantification analysis has been conceived to assess the accuracy of the thermophysical sub-model of the code, i.e. the equation of state (EoS). Due to the lack of suitable experimental data, a synthetic dataset is generated and used to investigate the validity of the procedure. The associated validation exercise confirms the applicability of the proposed procedure, but also points out that the adopted validation metrics should be complemented with additional statistical indicators. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea is a growing worldwide health problem. The landmark feature of OSA is a chronic intermittent hypoxia (CIH) responsible for multiple organ damages including heart diseases. CIH profoundly alters both visceral adipose tissue (VAT) and heart structures and functions, but little is known regarding their interactions in the context of CIH. We recently showed that VAT senescence drives myocardial alterations through the release of profibrotic factors in aged mice. Thus, we aim at demonstrating that CIH induces a premature vWAT senescent phenotype, responsible for subsequent heart dysfunction. In a first series of animals, ten-week old C57BL6 male mice (n = 10/group) were exposed to 14 days CIH protocol (8 hours daily, 5–21% cyclic inspired oxygen fraction, 60 seconds per cycle). In another series, mice were submitted to VAT surgical lipectomy or sham-surgery (n = 10/group) and then exposed to the same CIH protocol. VAT and heart were assessed by histology for fibrosis (Sirius red), cell hypertrophy (wheat-germ agglutinin) and reactive oxygen species (ROS) (4-HNE), and markers of senescence (p16, p21, p53), inflammation (CD68, Tnfa, Serpine1), fibrosis (Col1a1) and hypertrophy were also evaluated by RT-qPCR and western blot. CIH induced an increased macrophage infiltration in VAT, along with an increased expression of senescence markers, ROS production and gene expression of inflammatory and fibrogenic markers. This was associated with CIH-induced myocardial interstitial fibrosis and upregulation of profibrotic gene expression in myocardium. Interestingly, VAT lipectomy prevented CIH-induced myocardial fibrosis. Short-term exposure to CIH is sufficient to induce both VAT remodelling, characterized by oxidative stress, inflammation and fibrosis, and cardiac interstitial fibrosis that was prevented by VAT lipectomy. This strongly suggest a causal crosstalk between CIH-induced VAT senescence and cardiac remodeling. [ABSTRACT FROM AUTHOR]

Obesity is associated with remodeled and dysfunctional visceral white adipose tissue (vWAT). Recent studies suggest a cross-talk between vWAT and heart contributing to cardiac abnormalities. We hypothesized that adipose tissue macrophages (ATM) play a key role in the vWAT remodeling through a mechanism of premature senescence in high fat diet (HFD)-induced obesity. Establish the chronological order of events leading to vWAT premature senescence in the context of obesity and figure out the role of senescent ATM in the cross-talk between vWAT and heart. Two-month-old C57BL/6 male mice (n = 5/group) fed with HFD (60% fat, 7% sucrose) or chow diet (CD) for 2, 5, or 10 weeks underwent in vivo cardiac evaluation (echocardiography) and metabolic tests (glucose and insulin tolerance tests). Myocardial fibrosis, vWAT remodeling, ATM infiltration (CD68), senescence (p16 and p21) and inflammation were assessed. Body weight gain induced by HFD diverged from CD (CD: 29.6 ± 0.5 vs HFD: 35.0 ± 1.3, P < 0.01) after 5 weeks. Even preceding this, mice showed glucose intolerance and insulin resistance. These changes paralleled vWAT remodeling, i.e. increase in adipocyte size, ATM infiltration, and appearance of crown-like structures, a phenomenon of inflammatory adipocyte death. Classic pro-inflammatory markers, other than those involved in macrophage recruitment were unchanged. Two weeks of HFD sufficed to induce ATM senescence (p16 and p21). Myocardial function evaluated by strain rate was compromised by HFD as early as 2 weeks of diet (CD: 33.2 ± 1.2 vs HFD: 28.4 ± 0.2, P < 0.01). This was later followed by myocardial interstitial fibrosis. HFD disturbed glucose homeostasis, induced ATM senescence and myocardial dysfunction prior to body weight gain. These alterations preceded major inflammation and fibrotic remodeling both in vWAT and heart. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea is a growing health problem effecting almost 1 billion world population. The landmark feature of OSA is chronic intermittent hypoxia (CIH) responsible for multiple organ damages including heart. CIH profoundly alters both visceral white adipose tissue (vWAT) and heart structures and functions, but little is known regarding their interactions in context of CIH. We recently showed that vWAT senescence drives myocardial alterations through the release of profibrotic factors in aged mice. Here, we aim at demonstrating that CIH induces a premature vWAT senescent phenotype, responsible for subsequent heart dysfunction. In a 1st experiment, 10 weeks old C57BL6 male mice (n = 10/group) were exposed to 14 days CIH protocol (8 hours daily, 5-21% cyclic inspired oxygen fraction, 60 seconds per cycle). In a 2nd series, mice were submitted to either vWAT lipectomy or sham-surgery. Finally, we used p53 KO mice or littermates, also exposed to the same CIH protocol. vWAT and hearts were assessed for fibrosis, hypertrophy, DNA damage, oxidative stress, markers of senescence (p16, p21, p53) and inflammation by histology, RT-qPCR and western blot. CIH induced a "senescent-like" phenotype in vWAT, characterized by increased fibrosis, oxidative stress, DNA damage and inflammation (macrophage infiltration and inflammatory markers expression). This was associated with CIH-induced myocardial interstitial fibrosis and upregulation of profibrotic gene expression in myocardium. Interestingly, CIH did not induce vWAT remodeling in p53KO mice and CIH-induced myocardial interstitial fibrosis was prevented by both vWAT resection and p53 deletion. Short-term exposure to CIH is sufficient to induce vWAT premature senescence and cardiac interstitial fibrosis that was prevented by vWAT lipectomy and deletion of p53 senescence pathway. This strongly suggest a causal crosstalk between CIH-induced vWAT senescence and cardiac remodelling. [ABSTRACT FROM AUTHOR]

Objective: To analyse the content of the interventions reported in studies investigating the applicability and efficacy of Argentine tango in participants with Idiopathic Parkinson Disease.Methods: Independent reviewers searched databases (PubMed, CINAHL, EMBASE, PsycINFO, and PEDro) from their inception to November 2019. Eligible studies were randomised, controlled and uncontrolled clinical trials, and case reports.Main Outcome Measure: The Template for Intervention Description and Replication guidelines and checklist were used to assess quality and quantity of the content of Argentine tango interventions' description.Results: We found 21 papers investigating the applicability and efficacy of Argentine tango in participants with Idiopathic Parkinson Disease. Completeness of the reporting of intervention was satisfying. The intervention is intended to affect a variety of aspects of functioning relevant to individuals with Idiopathic Parkinson Disease. Detailed information on the intervention's procedure and dosing is usually provided. The delivery of the Tango dance program was predominantly extensive; however, the intervention has been provided with various approaches and showed to be very adaptable. Attrition- and adherence- rates described are acceptable. The Adapted Tango dance program is the earliest and most researched modality of tango intervention in participants with Idiopathic Parkinson Disease.Conclusions: Argentine tango is appropriately described in the studies investigating the applicability and efficacy of the intervention in participants with Idiopathic Parkinson Disease. However, the reporting could be ameliorated. [ABSTRACT FROM AUTHOR]

Introduction Modifiable lifestyle choices, such as physical activity, can favor metabolic health in aging and obesity. We demonstrated that endocardial fibrosis and cardiovascular dysfunction decrease in response to exercise in aged mice. Recent evidence suggests exercise may prevent high fat diet (HFD)-induced adipose tissue premature senescence and rescue cardio-metabolic function. Objective Our aim was to understand the role of white adipose tissue (WAT) bioenergetics in the accumulation of senescent cells during HFD and exercise. Method Thirty-two WT male mice (5 months old) were subjected to high-fat diet (HFD: 60% fat) and chow diet (CD: 13% fat). After 5 weeks on diets, animals were randomized to 4 weeks of sedentary or exercise protocol ( n = 8/group). Exercise consisted in forced swimming for 90 min/day for 5 days/week. Before and after the 4-week exercise/sedentary protocol, mice were evaluated for the cardio-metabolic profile. Histological, molecular and bioenergetic features of inguinal and epidydimal WAT (iWAT and eWAT, respectively) were evaluated. Results Short-term exercise is sufficient to attenuate obesity-induced cardiac interstitial fibrosis and dysfunction, WAT alterations and glucose intolerance, before major body weight reduction. Cardiac functional improvement was associated with decreased plasma leptin levels in HFD trained mice. Both fat depots, iWAT and eWAT, showed premature senescence in response to HFD, at time when inflammation and fibrosis were not in place yet, and exercise reversed it. Iterative testing in a supervised predictive model on the transcriptional profile of WAT under HFD confirmed differences in the depot response to diet and exercise. Conclusion We provide evidence that attenuation of cardiac dysfunction is associated with the response of WAT to exercise. Strategies targeting senescence could be of primary relevance to restore cardio-metabolic health in different pathophysiological conditions. [ABSTRACT FROM AUTHOR]

Introduction Mitochondrial dysfunction in white adipose tissue has been demonstrated to play a role in metabolic disorders. Recent evidence indicates that carbon monoxide (CO) modulates mitochondria bioenergetic. However, whether CO promotes beneficial effects in adipocytes during metabolic disorders by affecting mitochondrial functions is currently unknown. Objective The aim of this study was to investigate the effects of CO on metabolism and insulin-sensitivity in adipocytes and evaluate the therapeutic impact of CORM-401, CO-releasing agent, on adipose tissue dysfunction in obese mice. Method 3T3-L1 adipocytes were treated with CORM-401 and cellular bioenergetic was determined by a seahorse analyzer while insulin-sensitivity was assessed by AKT-phosphorylation. Dietary induced obese mice were treated with CORM-401 three times a week for 8 weeks while maintained on a high fat diet. Glucose metabolism was assessed by metabolic tests and fasting blood glucose and insulin. Results We found that CORM-401 induced a simultaneous uncoupling of mitochondrial respiration and an increased in glycolysis in 3T3-L1 adipocytes in vitro as well as in mouse adipose tissue ex-vivo. This was accompanied by an increase of insulin-induced AKT-phosphorylation in adipocytes pre-treated with CORM-401 compared to untreated adipocytes suggesting that CO increases insulin-sensitivity in adipocytes. We confirmed these results in vivo by showing that mice pre-treated with CORM-401 displayed a higher insulin-sensitivity (lower glycemia after insulin injection) compared to untreated mice. Finally, we found that a prolonged treatment (8 weeks) of mice with CORM-401 improves glycemic profiles and insulin tolerance tests in high fat diet-induced obesity. Conclusion Our results demonstrate that CO prevents the dysfunction of adipose tissue metabolism during obesity and indicate that the beneficial effects of CO involve uncoupling of mitochondrial respiration and an increase in glycolysis. [ABSTRACT FROM AUTHOR]

Introduction L’obésité se caractérise par une accumulation excessive de masse grasse ainsi qu’un état inflammatoire chronique évoluant à bas bruit. Dans ce contexte, le stockage et le sensing nutritionnel représentent un véritable challenge métabolique au niveau systémique et cellulaire. Parmi les processus biologiques susceptibles de contribuer aux altérations méta-inflammatoires caractéristiques de l’obésité, nous étudions l’autophagie, processus lysosomal permettant la dégradation des organites cellulaires, lié au flux nutritionnel ainsi qu’à la régulation de la signalisation pro-inflammatoire. Patients et méthodes Nous avons analysé les variations du flux de dégradation autophagique dans des adipocytes isolés provenant de tissus adipeux prélevés chez des patients obèses, obèses traités par chirurgie bariatrique, ou non obèses, ainsi que dans des adipocytes en culture dans lesquels des vecteurs viraux permettent de moduler l’expression de protéines régulatrices. Résultats Nous observons une diminution de l’activité autophagique adipocy-taire des sujets obèses comparée aux sujets non obèses, et une corrélation inverse entre hypertrophie adipocytaire et activité autophagique suggérant un lien avec le stockage lipidique. Nous avons testé l’implication d’un candidat, la kinase DAPK2 (Death Associated Protein Kinase 2) exprimée préférentiellement dans les adipocytes et dont l’expression est fortement réduite dans le tissu adipeux des sujets obèses. L’inhibition de cette kinase induit une diminution de l’activité autophagique tandis qu’une surexpression augmente le processus dans des lignées adipocytaires. Nous observons également une restauration partielle et concomitante de l’activité autophagique et de l’expression génique de DAPK2 après perte de poids induite par chirurgie bariatrique chez les sujets obèses, ren-forçant le rôle de cette kinase dans la régulation de l’autophagie et l’homéostasie adipocytaire. Conclusion Nos résultats montrent un lien entre l’expression de DAPK2 et le niveau d’activité autophagique dans les adipocytes. Ils suggèrent qu’un défaut de régulation de l’activité de cette kinase pourrait contribuer à la dysfonction adipocytaire dans l’obésité. Déclaration d’intérêt Les auteurs déclarent ne pas avoir d’intérêt direct ou indirect (financier ou en nature) avec un organisme privé, industriel ou commercial en relation avec le sujet présenté. [ABSTRACT FROM AUTHOR]