117,816 research outputs found
Urban Heat Island Mitigation and Urban Green Spaces: Testing a Model in the City of Padova (Italy)
No full textThe urban heat island (UHI) is a critical issue in most urbanised areas. Spatial variation of urban air temperature and humidity influences human thermal comfort, the settling rate of atmospheric pollutants, and the energy demand for cooling. UHIs can be particularly harmful to human health and there are numerous studies that link mortality and morbidity with extreme thermal events, that can be worsened by UHIs. The temperature difference between city centres and the surrounding countryside, which is accentuated in the summer months and at night, is the result not only of a greater production of anthropogenic heat but is mainly due to the properties of urban surfaces. The use of vegetation, and in particular urban tree planting, is one of possible strategies to contrast the heat island effects. In order to analyse the mitigation effects produced by green spaces in the city of Padova, a municipality in the northeast of Italy, simulations of the air temperature variations and their spatial distribution were carried out using the i-Tree Cool Air model. High-resolution RGBir aerial photos were processed to produce a tree canopy and a permeability map and the model was applied on a 10 m × 10 m grid over the entire city, producing a raster map of the aboveground air temperatures. A particularly hot July day with recorded air temperatures of 35 °C at 3 p.m. and 28 °C at 10 p.m. at a reference weather station was chosen for the test. In the daytime, the results show temperature differences up to almost 10 °C between urban open spaces with impervious cover (squares, streets) and green areas under tree canopy. At night, the simulated air temperatures are only slightly cooler in areas with tree cover than those recorded at the reference station, while urban areas with sealed surfaces maintain air temperatures 4.4 °C higher. The study was aimed at testing the applicability of the model as a tool for predicting air temperatures in relation to land use and canopy cover. The results show that the model can potentially be used to compare different urban forest and urban greening planning scenarios, however, further research is necessary to assess the reliability of the temperature predictions
New association of surfactants for the production of food and cosmetic nanoemulsions: preliminary development and characterization
No full textA new nanoemulsifing system has been developed. This study refers to an innovative association of polysorbate 80 and palmitic ester of l-ascorbic acid for the production of good stability and very thin nanostructured emulsions with average micellar diameter size ranging from 100 to 300 nm. This system has showed to be very performing to create nanoemulsions with moderate stirring rate and warming regimen thanks to the high efficiency of the association between ascorbyl palmitate and polysorbate-80 (PS-80). This nanoemulsified system is very easy to achieve and shows a very good capability to encapsulate several substrates of both nutritional and cosmetic usage such as melatonin, resveratrol, essential oils and steroidic terpenes such as boswellic acids and others. This system has been optimally applied to nutraceutical and cosmetic formulations and particularly to develop sprayable sublingual delivery systems for melatonin and the aforesaid molecules. This study describes developing and analytical characterization of this system containing melatonin
How are green spaces effective in urban heat island mitigation? A case study in northeastern Italy
No full textThe urban heat island (UHI) is an important and current issue in most urbanized areas. It can be particularly harmful to human health and there are numerous studies that link mortality and morbidity with extreme thermal events, that can be worsen by UHI. The temperature difference between city centers and the surrounding countryside, which is accentuated in the summer months and at night, is the result not only of a greater production of anthropogenic heat but also and above all is linked to the materials cities are made from. The use of vegetation, and in particular urban tree planting, constitutes one of the most effective strategies in contrasting the heat island effects. In order to analyze the mitigation effects produced by green spaces in the city center of Padua, a municipality in the northeast of Italy, simulations of the air temperature trends and their spatial distribution were carried out using the i-Tree CoolAir model. The extreme conditions for maximum summer temperatures, the UHI effects become more critical, were considered in the study. A particularly hot July day was chosen, with recorded air temperatures respectively of 35°C at 3 pm and 28°C at 10 pm, at a reference weather station. The results of the simulation show temperature differences up to almost 10°C in the daytime (3 pm) between urban open spaces with impervious cover (squares, streets) and green areas. These differences are related to the shading effect of the tree canopy. Although at night (10 pm), the air temperature differences are less evident. Once again, impervious open spaces maintain air temperatures 4°C higher than those recorded at the weather station, while in areas with tree cover temperatures are about 2°C lower
Anatomical and morphological microfeaturesof the leaf in Salix L. species and their physioecological significance
No full textPLANMAP - Morphostratigraphic map of Rembrandt basin (Mercury)
No full textMorphostratigraphic map of Rembrandt basin, as part of PLANMAP deliverable D2.2.
The package contains map layouts, base data and vector files in geopackage format
This dataset is included in the publication:
Semenzato, A., Massironi, M., Ferrari, S., Galluzzi, V., Rothery, D. A., Pegg, D. L., Pozzobon, R., & Marchi, S. (2020). An Integrated Geologic Map of the Rembrandt Basin, on Mercury, as a Starting Point for Stratigraphic Analysis. Remote Sensing, 12(19), 3213. https://doi.org/10.3390/rs1219321
FORMAZIONE DI COMPLESSI DELLA PROTEINA MITOCONDRIALE OPA 1 NEL MIOCARDIO ESPOSTO A STRESS OSSIDATIVO E CARATTERIZZAZIONE DI MUTANTI IN RESIDUI CISTEINICI
No full textThe heart is especially vulnerable to mitochondrial derangements. In fact, many cardiomyopathies are caused by anomalous mitochondrial metabolism or alterations of mitochondrial bioenergetics. The involvement of mitochondria in cardiac diseases is likely to be extended to structural changes, since mitochondrial activity and cellular signaling are tightly linked with mitochondrial morphology. A major example of this link is provided by the relationship between mitochondrial fragmentation and the progression of apoptosis. Among the proteins involved in mitochondrial dynamics, the dynamin-like GTPase Optic Atrophy 1 (OPA 1) is required for mitochondrial inner membrane fusion and maintenance of normal cristae structure. The research activity of this thesis was aimed at both investigating whether OPA 1 is altered in hearts subjected to ischemia and reperfusion and elucidating the relationships between OPA 1 changes and alterations in mitochondrial morphology. Due to the established role of mitochondria in generating reactive oxygen species, oxidative stress was investigated as a crucial mechanism altering OPA 1 structure and function.The susceptibility of OPA 1 to oxidation was initially characterized in intact hearts, cardiomyoblasts and isolated mitochondria. In isolated rat hearts perfused with hydrogen peroxide (H2O2) or subjected to ischemia and reperfusion OPA 1 was found to undergo the formation of high molecular weight (HMW) bands that were barely detectable in normoxic hearts. Since these HMW bands were only observed in electrophoreses carried out under non-reducing conditions, their formation reflected the oxidation of vicinal cysteinyl residues resulting in the generation of disulphide cross-bridges.
In mitochondria isolated from heart perfused with H2O2, Blue Native-PAGE (BN-PAGE) analysis displayed the aggregation of OPA 1 in various complexes with high molecular weight (ranging from xx to xx). These complexes were not present in mitochondria isolated from normoxic rat hearts. Then OPA 1 complex formation was analyzed both in HL-1, a proliferating atrial cardiomyocites derived from mouse AT-1 cells, and in mouse embryonic fibroblasts (MEFs), as a model cell line. Oxidative stress caused by incubation with H2O2 resulted in the formation of OPA 1 complexes that disappeared under reducing conditions, confirming the presence of intermolecular cross-bridges. Notably, under the same experimental condition causing OPA 1 aggregation (i.e., incubation with increasing concentration of H2O2) a fragmentation of mitochondrial network was observed in HL-1 cells suggesting that oxidation of cysteine residues might hamper the ability of OPA 1 to favour mitochondrial fusion.
This hypothesis was validated by identifying which residues of cysteine were involved in the formation of disulfides cross-bridges.
Since NMR and crystallographic structure of OPA 1 is not available, 3D structure information were obtained by means of homology modeling. In a collaborative effort with Prof. S. Moro (Faculty of Pharmacy, University of Study of Padova), analyses were carried out aimed at identifying the cysteine residues exposed on the protein surface that is also the region involved in OPA 1 dimerization. As a result of this study, cysteines 853, 856 and 874 were indicated as the residues that more likely contribute to the formation of OPA 1 complexes.
This hypothesis was verified by performing site-directed mutagenesis experiments on the expression construct containing wild-type Opa1 isoform 1. By substituting the native cysteine residues with serine. This approach allowed us obtaining the following mutants: (i) the double mutant in C853-6S; (ii) the single mutants in C853S or in C874S. New clones have been sequenced to ensure fidelity. Lentiviral vectors containing the mutated cysteine plasmids were produced in order to transfect OPA 1-/- MEF cell line (kindly given by Prof. L. Scorrano). Both C853S and C853-6S expressed detectable level of OPA 1, while cells containing OPA 1 mutated in the single residue C874S were not obtained.
Cells harbouring the OPA 1 mutants were assessed for mitochondrial morphology. Under control conditions C853-6S cells displayed punctuate mitochondria that is similar to the mitochondrial phenotype displayed by OPA 1-/- MEF cells; conversely, the expression of the C853S mutant restored the fusion morphology.
Cells were incubated with H2O2 in order to elucidate the relationship between OPA 1 aggregation and disulphide crossbridge formation. OPA 1 complex formation was inhibited in both cell lines.
To investigate the correlation between OPA 1 aggregation and mitochondrial fission, C853S cells were treated with H2O2. In C853S mutants the time required for completing the fission process was doubled with respect of MEF wild type cells.
In conclusion these findings highlight the relevance of cysteine 853 in maintaining the role of OPA 1 in mitochondrial fusion, and especially in the derangement of this function caused by oxidative stress. In fact, when cells expressing the mutant C853S were exposed to a severe oxidative stress, OPA 1 aggregation was prevented along with a significant delay in the occurrence of mitochondrial fission.Il cuore è particolarmente soggetto a disfunzioni mitocondriali e numerose cardiomiopatie sono associate ad un anomalo metabolismo mitocondriale o ad alterazioni bioenergetiche mitocondriali.
Studi recenti hanno messo in evidenza come l’attività dei mitocondri e le vie di trasduzione del segnale cellulare influenzino la morfologia dei mitocondri, ad esempio, la frammentazione della rete mitocondriale è correlata al processo di apoptosi. La proteina OPA 1, GTPasi appartenente alla famiglia delle dinamine, è coinvolta nel processo di fusione della membrana interna mitocondriale e nel mantenimento della struttura delle cristae interne mitocondriali. Tuttavia sono necessari maggiori studi atti a contribuire ad una maggiore comprensione delle proteine e dei meccanismi alla base delle funzionalità di OPA 1. Nel presente lavoro di tesi è stato studiato l’effetto dello stress ossidativo sulla proteina mitocondriale OPA 1 nel cuore, dato che i mitocondri sono sede di produzione e bersaglio delle specie reattive dell’ossigeno (ROS).
Inizialmente, utilizzando cuori di ratto isolati e perfusi ex-vivo, è stato valutato l’effetto di ischemia/riperfusione e perfusione con perossido di idrogeno (H2O2) sulla proteina OPA 1. Nei campioni trattati è stata osservata la formazione di complessi ad alto peso molecolare (high molecular weight, HMW) della proteina in esame. In condizioni riducenti, tali complessi vengono disgregati. Questi risultati indicano che in condizioni di forte stress ossidativo con H2O2 si ha l’aggregazione di OPA 1 e che nella formazione dell’aggregato è coinvolta la formazione di ponti disolfuro.
In seguito, mediante Blue Native-PAGE (BN-PAGE), è stata eseguita un’analisi dei complessi proteici a partire da mitocondri isolati da cuore di ratto in condizioni normossiche e da cuori perfusi con H2O2. L’analisi ha dimostrato che OPA 1 aggrega in complessi di diverso peso molecolare in condizioni native.
La formazione del complesso di OPA 1 è stata analizzata sia cellule HL-1, una linea di cardiomiociti da atrioma murino, che in fibroblasti embrionali murini (mouse embryonic fibroblasts, MEFs). Al fine di indurre stress ossidativo le cellule sono state incubate con 1 mM H2O2 per 2 ore. Il complesso di OPA 1 scompare in condizioni riducenti, confermando la formazione di ponti disolfuro intermolecolari. Inoltre, in cellule HL-1 incubate con concentrazioni crescenti di H2O2 è stata osservata frammentazione della rete mitocondriale.
Ci siamo proposti di individuare quali fossero i residui cisteinici coinvolti nella formazione del ponte disolfuro. La struttura della proteina OPA 1 non è stata determinata né mediante NMR né mediante tecnica cristallografica.
In collaborazione con il Prof. S. Moro (Facoltà di Farmacia, Università degli Studi di Padova) è stata ipotizzata la struttura 3D della proteina mediante homology modelling al fine di caratterizzare quali fossero i residui cisteinici esposti sulla superficie proteica. In questo modo le cisteine 853, 856 e 874 sono stati individuati come residui più probabilmente coinvolti nella formazione del complesso di OPA 1.
Per confermare questa ipotesi, sono stati eseguiti degli esperimenti di mutagenesi sito-diretta a partire da un costrutto plasmidico contenente la sequenza genica per l’isoforma 1 umana del gene OpaI. Mediante questa tecnica sono stati ottenuti plasmidi mutati a livello delle singole cisteine 853 (C853S) e 874 (C874S), ed un doppio mutante cisteina 853-6 (C853-6S). I cloni sono stati sequenziati per confermare le avvenute mutazioni. Sono stati prodotti vettori lentivirali contenenti i plasmidi mutagenizzati al fine di esprimere stabilmente la proteina di interesse nella linea cellulare MEF OPA 1-/- (gentilmente fornita dal Prof. L. Scorrano). Sono state ottenute linee cellulari esprimenti la proteina OPA 1 mutata a livello del singolo residuo cisteinico 853 e dei residui 853-6, mentre non è stata ottenuta la linea esprimente la proteina mutata in C874S.
È stata quindi valutata la morfologia mitocondriale nelle linee cellulari ottenute. Le cellule C853-6S presentano mitocondri disgregati con un fenotipo simile alla linea MEF OPA 1-/-; al contrario, nelle cellule esprimenti la proteina OPA 1 mutata a livello del residuo 853, si verifica il ripristino del fenotipo di fusione mitocondriale.
Al fine di chiarire la relazione tra l’aggregazione di OPA 1 e la formazione dei ponti disolfuro, le cellule sono state incubate con H2O2. La formazione del complesso di OPA 1 risulta inibita in ambedue le linee cellulari contenenti la proteina mutata. Le cellule C853S sono state trattate con H2O2 per verificare la correlazione tra l’aggregazione della proteina in esame e il processo di fissione mitocondriale. I cloni C853S completano il processo di fissione mitocondriale in un tempo doppio rispetto alla linea MEF WT.
Per concludere, in condizioni di elevato stress ossidativo la proteina OPA 1 è esposta ad ossidazione che ne modifica lo stato di aggregazione. Tale processo è correlato ad una diminuzione della fusione mitocondriale e, nelle cellule HL-1, ad un aumentato rilascio di citocromo c. Il meccanismo di aggregazione della proteina è stato stabilito mediante mutagenesi sito specifica che mette in luce il ruolo del residuo cisteinico 853
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