Search

With the rapid growth of energy consumption in the building sector and the consequent necessity to develop energy efficiency strategies, the application of heat pump systems seems to be a competitive solution to improve energy efficiency. In particular, air-source heat pump (ASHP) systems assisted by solar energy have drawn great attention, owing to their great feasibility in buildings for space heating/cooling and hot ater production purposes. The complementation system between solar and air energy can solve the poor performance of the air source heat pump under low-temperature conditions and can also make up for the shortcoming of the solar collector as an unstable energy source. Both solar energy technologies and air source heat pumps (ASHP) are widely used renewable energy sources at the moment. The former has the advantages of low utilization cost, simple technology, easy access, and no pollution, while the latter has the advantages of high efficiency, energy-saving, and good environmental benefits. Among emerging technologies coupled to heat pump systems, PV/T hybrid solar collectors are estimated to have a high potential and a fast-growing market. The PV performance of PV/T collectors increases slightly compared with a panel with PV cells since the operating temperatures of the PV cells are reduced due to the cooling effect of the heat extraction. Solar-assisted heat pump systems for DHW and space heating purposes have been studied by several researchers. Both experimental investigations and numerical studies aimed to assess the potential and performance of various system designs under different climatic boundaries. The aim of the present thesis is the investigation of the energy performance of systems based on the coupling of air to water heat pumps with PV/T hybrid solar collectors for producing domestic hot water (DHW). The gains from using these two currently promising technologies and the benefits of their integration are investigated by analising different configurations of these integrated systems. Comparisons with more traditional technologies were performed both in terms of thermal and electrical power production and energy savings. In particular, investigations were performed in order to identify the optimal number of modules that make up the solar plant and the most performing technology with the purpose of this thesis among PV, PV/T, and ST collectors. Furthermore, two different integration configurations were analysed depending on the different functions of the thermal contribution of the PV/T string within the entire system. The simulations were performed both for the context of the mainland, considering the climate of Palermo (Italy), both for the context of the minor Mediterranean islands, with particular reference to Lampedusa (Italy). For the latter case, in particular, the impact of the substitution of existing fuel-based technologies with heat pump systems eventually coupled to a photovoltaic (PV), solar thermal plant (ST), and hybrid photovoltaic-thermal (PV/T) systems was analysed.

Le malattie neurodegenerative sono caratterizzate da disfunzione e perdita di specifiche popolazioni neuronali in risposta ad invecchiamento o eventi tossici o traumatici. Tuttavia, recentemente, è diventato chiaro che la disfunzione astrocitica ha un ruolo importante nei processi degenerativi. Infatti, gli astrociti rappresentano la popolazione cellulare maggiore del Sistema Nervoso Centrale (SNC) e costituiscono l’elemento principale per la sua omeostasi. Alterazioni biochimiche e strutturali degli astrociti durante la neuroinfiammazione rappresentano una risposta fisiologica a danni a carico del SNC per minimizzare e riparare il danno iniziale. Tuttavia, danni cerebrali prolungati forniscono segnali dannosi che possono compromettere le funzioni di astrociti e neuroni e causare neuroinfiammazione cronica. La neuroinfiammazione è un processo caratterizzato da attivazione gliale, che sottende ad un ciclo continuo di eventi infiammatori in cui si ha rilascio di citochine infiammatorie ed altri mediatori neurotossici che causano stress ossidativo e impediscono il ripristino funzionale del parenchima cerebrale. Un altro meccanismo implicato nelle malattie neurodegenerative è rappresentato dalla disfunzione mitocondriale. I mitocondri sono organelli dinamici. In particolare, i processi della dinamica mitocondriale (che coinvolgono cicli alternati di fissione/fusione e il loro trasporto assonale) e della biogenesi sono cruciali per l’omeostasi neuronale e la funzionalità sinaptica. Inoltre, un’alterazione dell’equilibrio tra processi di fissione e fusione può determinare il destino delle cellule neuronali. Queste informazioni supportano l’ipotesi che la disfunzione mitocondriale abbia un ruolo importante nel processo degenerativo, a causa dell’alta richiesta di energia da parte delle cellule neuronali per svolgere le loro funzioni, tra cui neurogenesi e differenziamento neuronale. Ad oggi, la correlazione tra neuroinfiammazione, disfunzione mitocondriale e neurodegenerazione è stata poco studiata. In questo lavoro, abbiamo descritto gli effetti di un certo numero di molecole antiossidanti naturali nel ripristinare la funzionalità astrocitica e la sopravvivenza neuronale in modelli in-vitro di astrogliosi reattiva. Tutte le molecole antiossidanti testate hanno rivelato la capacità di ridurre la proliferazione degli astrociti e ripristinare la sopravvivenza di astrociti e neuroni ed i livelli basali di specie reattive dell’ossigeno (ROS) mediante una differente modulazione di NF-kB in colture cellulari di astrociti e neuroni, suggerendo che NF-kB svolga un ruolo cruciale nel controllo della sopravvivenza neuronale e nelle risposte anti-infiammatorie. Inoltre, in un modello cellulare di differenziamento indotto da Nerve Growth Factor (NGF), abbiamo dimostrato che la differenziazione è accompagnata da un incremento del rimodellamento mitocondriale che richiede la modulazione di fissione/fusione e mitofagia, e l’induzione di proteine e fattori di trascrizione che regolano la biogenesi e il metabolismo mitocondriale, per aumentarne l’efficienza e soddisfare requisiti energetici più elevati. Questo studio ha rivelato un nuovo meccanismo di modulazione della funzionalità mitocondriale dipendente da NGF, importante nella neurogenesi e rigenerazione cerebrale. Nel complesso, i nostri dati identificano i mitocondri come elemento centrale a due meccanismi cruciali nel processo neurodegenerativo: neuroinfiammazione e neurogenesi. Inoltre, morfologia e attività mitocondriale possono essere modulate da un complesso crosstalk di eventi molecolari controllati da NGF o molecole antiossidanti. L’importanza della disfunzione mitocondriale e della sua correlazione a processi di neuroinfiammazione nella patologie neurodegenerative è attualmente oggetto di studio in un modello animale di Parkinson basato sulla neurotossicità di 6-OHDA, come anche il potenziale terapeutico di NGF e molecole antiossidanti. Neurodegenerative disorders are characterized by dysfunction and loss of specific neuronal populations in response to age-related, or toxic and traumatic events. Recently, it has become clear that astrocytic dysfunction plays a relevant role in neurodegenerative processes. In fact, astrocytes represent the main type of glia in the central nervous system (CNS) and constitute the principal element of the brain homeostatic system. Biochemical and structural changes of astrocytes during neuroinflammation represent a physiological response to CNS injury to minimize and repair the initial damage. Nevertheless, prolonged brain insults provide detrimental signals that can compromise astrocytic and neuronal functions and lead to chronic neuroinflammation. In fact, neuroinflammation is characterized by sustained glial activation (reactive astrogliosis) and the generation of an inflammatory loop, through the release of cytokines and other neurotoxic mediators that cause oxidative stress and limit functional repair of brain parenchyma. Another hallmark of neurodegenerative disorders is represented by mitochondrial dysfunction. Mitochondria are very dynamic organelles. In particular, mitochondrial dynamic processes (involving alternation of fission/fusion cycles and their axonal transport) and biogenesis are crucial for neuronal homeostasis and synaptic function. Moreover, alteration of the balance between fission and fusion can determine the fate of neuronal cells. This knowledge supports the hypothesis that alteration of mitochondrial function and metabolism plays an important role in the neurodegenerative process because neuronal cells require high levels of energy to perform their functions, such as during neuronal differentiation. So far, the correlation between neuroinflammation, mitochondrial dysfunction and neurodegeneration has been poorly investigated. In this study, we describe the effects of a number of natural anti-oxidants in rescuing astrocytic function and neuronal viability following glial activation. All tested dietary antioxidants were able to reduce astrocyte proliferation and restore astrocytic and neuronal survival and basal levels of reactive oxygen species (ROS), via differential modulation of NF-kB binding activity in cell cultures of neurons and astrocytes, suggesting that NF-kB plays a crucial role in the modulation of neuronal survival and anti-inflammatory responses. In addition, in a cellular model of neuronal NGF-induced differentiation, we demonstrated that this mechanism is accompanied by increased mitochondrial remodeling involving modulation of fission and fusion proteins, mitophagy and induction of proteins and transcription factors that regulate mitochondria biogenesis and metabolism to increase their efficiency and meet higher energy requirements. These data revealed a new NGF-dependent modulation of mitochondrial function that appear be important in both neurogenesis and nerve regeneration following brain injury. Overall, our data identify mitochondria as the “core” element of two relevant mechanisms underlying neurodegenerative disorders: neuroinflammation and neurogenesis. Moreover, we show that modulation of their morphology and activity can be achieved by a complex interplay of molecular events that can be controlled by both NGF and dietary factors. The relevance of mitochondrial dysfunction and its connection to neuroinflammation in neurodegenerative diseases is under investigation in the animal model of Parkinson based on 6-hydroxydopamine (6-OHDA) neurotoxicity. This model will be also used to assess the therapeutic potential of NGF and antioxidant molecules.

Today, strategies for emergency preparedness, in presence of accidental scenarios in high-risk plants with releases into the atmosphere, have become a priority. To achieve this goal, it is important to have forecast meteorological data in local areas to use in dispersion and transport models and so to respond in advance emergency situations. The paper reports results of research performed to develop a new tool, called FORCALM that is capable to elaborate European Centre for Medium-Range Forecasts (ECMWF) forecast data to use for simulations by CALMET/CALPUFF modeling system. A case study, relevant to an accident occurred in Mediterranean Refinery at Milazzo (Italy), has been examined to validate the procedure and the capacity to evaluate the transport and depositions pollutant in terms of forecast information. The results were compared with those obtained using CALMET/CALPUFF simulations based on measured meteorological, covering the area under study.

Aims: Mitochondria are very dynamic organelles. Mitochondrial dynamics (alternation of fission/fusion cycles and their axonal transport) and biogenesis are crucial for neuronal homeostasis and synaptic function; moreover, alteration of the balance between fission and fusion can determine the fate of neuronal cells. Fission processes require the intervention of Fis1 and the active form of Drp1, whereas fusion is primarily regulated by Opa1 and Mfn1/2. We here focused on correlation between oxidative stress and mitochondrial dynamics and biogenesis. Materials and Methods: We compared the effect of hydrogen peroxide and Rotenone (a neurotoxin that inhibits the Complex-I of electrons transport chain), on primary cortical neurons or models of neurodegeneration based on neuroblastoma or PC12 cells. Protein levels and distribution (cytoplasm, mitochondria or nuclei) were assessed by western blots and immunofluorescence imaging. Results: Exposure of neurons or neuroblastoma to Rotenone determined a dose-dependent (200-400-800 nM) decrease of P-Drp1 and a biphasic trend of Opa1 and Mfn2 in a time-dependent manner (1-3-6-24h). In PC12 cells, alterations of mitochondrial proteins in response to hydrogen peroxide was paralleled by differential distribution (cytoplasm/nuclei) of oxidative-stress sensors (DJ-1, Nrf2) and proteins regulating mitochondrial biogenesis (mtTFAM and PGC1a), while determining a dose- and time-dependent increase of ROS and ATP depletion. Interestingly, human fibroblasts showed similar changes in response to rotenone but a different trend in response to Amyloid-beta oligomers. Discussion/Conclusions: These studies suggest 1) the existence of a complex cross-talk underlying mitochondrial dynamics and biogenesis, 2) alteration of mitochondrial dynamic proteins as biomarkers of mitochondrial dysfunction in neurodegenerative processes.

Emergency response plans to mitigate the severity of the accidental release of hazardous compounds in the air have become a primary concern in view of the many adverse events occurred over the years in high-risk plants. To do this, an accurate estimate of forecast meteorological data to be used in dispersion models can be very useful to respond in advance to emergency situations. In this field, FORCALM is a new tool developed to elaborate European Centre for Medium-Range Weather Forecasts data on a 3D computational domain with a high-resolution grid. FORCALM data can be used to perform predictive simulations of impacts on local and regional levels by using CALPUFF modelling system. A case study relevant to an accident, occurred in the “Mediterranea” Refinery at Milazzo (Italy) in 2014, has been also examined for validation purposes. A comparison with results obtained by using CALMET modelling system and observed meteorological data, covering the area under study, is also described. The validation work has allowed confirming that predictive assessments, carried out with the help of FORCALM, lead to information regarding potential environmental impacts with a good degree of accuracy.

Neuronal differentiation involves extensive modification of biochemical and morphological properties to meet novel functional requirements. Reorganization of the mitochondrial network to match the higher energy demand plays a pivotal role in this process. Mechanisms of neuronal differentiation in response to nerve growth factor (NGF) have been largely characterized in terms of signaling, however, little is known about its impact on mitochondrial remodeling and metabolic function. In this work, we show that NGF-induced differentiation requires the activation of autophagy mediated by Atg9b and Ambra1, as it is disrupted by their genetic knockdown and by autophagy blockers. NGF differentiation involves the induction of P-AMPK and P-CaMK, and is prevented by their pharmacological inhibition. These molecular events correlate with modifications of energy and redox homeostasis, as determined by ATP and NADPH changes, higher oxygen consumption (OCR) and ROS production. Our data indicate that autophagy aims to clear out exhausted mitochondria, as determined by enhanced localization of p62 and Lysotracker-red to mitochondria. In addition, we newly demonstrate that NGF differentiation is accompanied by increased mitochondrial remodeling involving higher levels of fission (P-Drp1) and fusion proteins (Opa1 and Mfn2), as well as induction of Sirt3 and the transcription factors mtTFA and PPARγ, which regulate mitochondria biogenesis and metabolism to sustain increased mitochondrial mass, potential, and bioenergetics. Overall, our data indicate a new NGF-dependent mechanism involving mitophagy and extensive mitochondrial remodeling, which plays a key role in both neurogenesis and nerve regeneration.