Osservazioni

di Calogero Piro. Convertire la realtà che ci circonda in immagini, è stata fin dai primordi dell’essere umano un’atavica necessità. Ancora oggi nella nostra cultura visiva è tutto basato sull’utilizzo dell’immagine per conoscere la realtà che ci circonda. Con la scoperta della fotografia, la riflessione intorno alla natura si fa sempre più interessante. Il ruolo della macchina fotografica in questo progetto per raccontare l’ambiente, la struttura, gli oggetti, i segni, i colori e le atmosfere che caratterizzano il centro del CNR di capo Granitola ha trovato prepotentemente in questi giovani allievi della cattedra di fotografia dell’Accademia di Belle Arti di Palermo, diretta dal Professore Sandro Scalia, momenti di grande professionalità, realizzando un grande reportage con tutti gli aspetti essenziali della struttura e delle articolazioni primarie del linguaggio fotografico. Questa esperienza extradidattica difficile ed impegnativa non soltanto per la necessità del confronto col “nuovo” in termini organizzativi, ma anche per la necessità di descrivere attraverso la fotografia il tema della Biodiversità, è stato affrontato brillantemente. Mettendo in primo piano, siti naturali, siti storici come: Mozia e Selinunte, i laboratori del centro di ricerche, la Flora e la Fauna, sono riusciti a raggiungere con acuta osservazione ottimi risultati visibili in questo catalogo, e con la tangibile riprova di cosa possa e debba essere una educazione estetica assolutamente “libera” da condizionamenti, viatico ineludibile perché l’espressione artistica, sotto qualunque forma, sia artefice dei grandi processi di vera maturazione culturale, si avverte in questi giovani artisti la purezza e la consapevolezza dei propri messaggi ancora privi, e speriamo sempre, di qualunque tipo di inquinamento tendenzioso

Spazio pubblico, arte, identità. Per una strategia di rigenerazione urbana

La riflessione al centro del volume “Spazio pubblico, arte e identità. Per una strategia di rigenerazione urbana”, che fa proprio l’interrogativo su quali siano le modalità di interazione tra spazio pubblico e pratica artistica, si contestualizza in un processo di approfondimento e di confronto, a tutto campo e multiscalare, dal contesto internazionale a quello nazionale, sul ruolo imprescindibile dello spazio pubblico, e più in generale della città pubblica, quale componente strutturale delle strategie di rigenerazione urbana riferite, in particolar modo, a contesti urbani e territoriali connotati da una significativa compresenza di componenti del patrimonio culturale. Tale riflessione consente di mettere a fuoco alcuni nodi tematici, che si configurano come significativi ambiti di innovazione disciplinare, centrali negli obiettivi e nelle politiche urbane europee, che da anni rivestono un ruolo rilevante nelle attività di ricerca e di sperimentazione, di disseminazione e di formazione che il Dipartimento di Pianificazione, Design, Tecnologia dell’Architettura, della Sapienza Università di Roma, sta svolgendo quale interprete proattivo e propulsivo delle istanze sociali, culturali, economiche e politiche, che scaturiscono dalle profonde trasformazioni indotte negli ultimi decenni nei territori delle città italiane ed europee dai processi di metropolizzazione del territori

Urban regeneration and new welfare. For a reconfiguration of the Network of public services for health

The metropolization processes of the contemporary city show a complex scenario: the contradictions induced by globalization effects, physical degradation, socioeconomic marginality, environmental fragility, new population instances, overlap the genetic anomalies of Italian cities, highlighting a new urban question. That question underlies generalised conditions of marginality, social inequality and poverty and in the current health emergency require a new urban welfare to guarantee fundamental rights to local communities, including the right to health, becoming the goal of an integrated and inter-scalar strategy. The regeneration strategy assumes the public city both as a physical matrix of reference, network of tangible and intangible networks, to guarantee a capillary territorial distribution, and as a framework of the coherence for structural choices. In this context, the paper presents some reflections starting from research activities carried out by the authors, who face, in term not merely emergency, the urgency of a reconfiguration of the public city components structure within the Network of public services for health. In contrast with the current organizational model and in coherence with the interactive and inclusive connotation of the new concept for urban welfare construction, that reconfiguration considers physical-territorial dimension as a structural framework. At the same time it requires new indicators, tools, implementation mechanisms, to substantiate the urban regeneration notion and implement a concrete policy of planning and production of services

Nuova questione urbana e nuovo welfare. La città pubblica per il diritto alla salute

I processi di metropolizzazione, il degrado fisico, la marginalità socioeconomica, la fragilità ambientale, l’invecchiamento della popolazione, il cambiamento della struttura delle famiglie, la pressione dei flussi migratori, il mutamento del sistema dei valori e dei modelli comportamentali della popolazione, si sovrappongono alle anomalie genetiche delle città italiane, evidenziando l’emergere di una nuova questione urbana. Una questione urbana che richiede la messa in campo di un nuovo welfare urbano per garantire alle comunità locali i diritti alla salute, all’istruzione, all’ambiente, alla mobilità pubblica, all’abitare, alla città. In questo quadro, la complessità dello scenario, che l’attuale pandemia ha fatto emergere acuisce le patologie della città contemporanea, sottolineandone le carenze in termini di organizzazione, gestione e funzionamento, nonché le ricadute, in negativo, indotte sulle comunità insediate, in termini di benessere, qualità della vita e dell’ambiente urbano, privandole dei diritti fondamentali, tra cui quello alla salute. Questo richiama l’urgenza di una riflessione che, sotto un profilo strutturale e non meramente emergenziale, affronti la riconfigurazione dell’assetto delle componenti della città pubblica che afferiscono alla Rete dei servizi pubblici per la salute, contestualizzandola nell’ambito della strategia di rigenerazione urbana, per la realizzazione del nuovo welfar

Molecular evidence for the involvement of PPAR-δ and PPAR-γ in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spinal cord trauma

Abstract Background Palmitoylethanolamide (PEA) is an endogenous fatty acid amide displaying anti-inflammatory and analgesic actions. Moreover, several data have suggested that PEA reduced inflammation and tissue injury associated with spinal cord trauma and showed a regulatory role for peroxisome proliferator-activated receptor (PPAR)-α signaling in the neuroprotective effect of PEA. However, several other mechanisms could explain the anti-inflammatory and anti-hyperalgesic effects of PEA, including the activation of PPAR-δ and PPAR-γ. The aim of the present study was to carefully investigate the exact contribution of PPAR-δ and PPAR-γ in addition to PPAR-α, in the protective effect of PEA on secondary inflammatory damage associated with an experimental model of spinal cord injury (SCI). Methods SCI was induced in mice through a spinal cord compression by the application of vascular clips (force of 24 g) to the dura via a four-level T5 to T8 laminectomy, and PEA (10 mg/kg, intraperitoneally, 1 and 6 hours after SCI) was injected into wildtype mice and into mice lacking PPAR-α (PPAR-αKO). To deepen the ability of specific PPAR-δ and PPAR-γ antagonists to reverse the effect of PEA, mice were administered GSK0660 or GW9662, 30 minutes before PEA injection. Results Genetic ablation of PPAR-α in mice exacerbated spinal cord damage, while PEA-induced neuroprotection seemed be abolished in PPARαKO mice. Twenty-four hours after spinal cord damage, immunohistological and biochemical studies were performed on spinal cord tissue. Our results indicate that PPAR-δ and PPAR-γ also mediated the protection induced by PEA. In particular, PEA was less effective in PPAR-αKO, GSK0660-treated or GW9662-pretreated mice, as evaluated by the degree of spinal cord inflammation and tissue injury, neutrophil infiltration, proinflammmatory cytokine, inducible nitric oxide synthase expression and motor function. PEA is also able to restore PPAR-δ and PPAR-γ expression in spinal cord tissue. Conclusion This study indicates that PPAR-δ and PPAR-γ can also contribute to the anti-inflammatory activity of PEA in SCI.</p

Prolyl oligopeptidase inhibition ameliorates experimental pulmonary fibrosis both in vivo and in vitro

Abstract Background Pulmonary fibrosis is a progressive disease characterized by lung remodeling due to excessive deposition of extracellular matrix. Although the etiology remains unknown, aberrant angiogenesis and inflammation play an important role in the development of this pathology. In this context, recent scientific research has identified new molecules involved in angiogenesis and inflammation, such as the prolyl oligopeptidase (PREP), a proteolytic enzyme belonging to the serine protease family, linked to the pathology of many lung diseases such as pulmonary fibrosis. Therefore, the aim of this study was to investigate the effect of a selective inhibitor of PREP, known as KYP-2047, in an in vitro and in an in vivo model of pulmonary fibrosis. Methods The in vitro model was performed using human alveolar A549 cells. Cells were exposed to lipopolysaccharide (LPS) 10 μg/ml and then, cells were treated with KYP-2047 at the concentrations of 1 μM, 10 μM and 50 μM. Cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) bromide colorimetric assay, while inflammatory protein expression was assessed by western blots analysis. The in vivo model was induced in mice by intra-tracheal administration of bleomycin (1 mg/kg) and then treated intraperitoneally with KYP-2047 at doses of 1, 2.5 and 5 mg/kg once daily for 12 days and then mice were sacrificed, and lung tissues were collected for analyses. Results The in vitro results demonstrated that KYP-2047 preserved cell viability, reduced inflammatory process by decreasing IL-18 and TNF-α, and modulated lipid peroxidation as well as nitrosative stress. The in vivo pulmonary fibrosis has demonstrated that KYP-2047 was able to restore histological alterations reducing lung injury. Our data demonstrated that KYP-2047 significantly reduced angiogenesis process and the fibrotic damage modulating the expression of fibrotic markers. Furthermore, KYP-2047 treatment modulated the IκBα/NF-κB pathway and reduced the expression of related pro-inflammatory enzymes and cytokines. Moreover, KYP-2047 was able to modulate the JAK2/STAT3 pathway, highly involved in pulmonary fibrosis. Conclusion In conclusion, this study demonstrated the involvement of PREP in the pathogenesis of pulmonary fibrosis and that its inhibition by KYP-2047 has a protective role in lung injury induced by BLM, suggesting PREP as a potential target therapy for pulmonary fibrosis. These results speculate the potential protective mechanism of KYP-2047 through the modulation of JAK2/STAT3 and NF-κB pathways. Graphical abstrac

Traumatic brain injury leads to development of Parkinson’s disease related pathology in mice

Traumatic brain injury (TBI) is a major health and socio-economic problem that affects all societies. This condition results from the application of external physical strength to the brain that leads to transitory or permanent structural and functional impairments. Moreover, TBI is a risk factor for neurodegeneration and can e.g. increase the risk for Parkinson’s disease (PD), a late-onset neurodegenerative disorder with loss of dopaminergic neurons in substantia nigra.In this study, we wanted to explore the possible development of PD-related pathology within the context of an experimental model of TBI.Traumatic brain injury was induced in mice by controlled cortical impact. At different time points behavioral tests (open field, elevated plus maze tests and Barnes maze) were performed: The animals were sacrificed 30 days after the impact and the brains were processed for Western blot and immunohistochemical analyses. Following TBI there was a significant decrease in expression of tyrosine hydroxylase and dopamine transporter in the substantia nigra as well as significant behavioral alterations. In addition, a strong increase in neuroinflammation was evident, as shown by increased levels of cyclooxygenase-2 and inducible nitric oxide synthase as well as IκB-α degradation and nuclear-κB translocation. Moreover, neurotrophic factors such as brain-derived neurotrophic factor, neurotrophin-3, nerve growth factor, and glial cell line-derived neurotrophic factor were decreased 30 days post-TBI. Interestingly, we observed a significant accumulation of α-synuclein in microglia compared to astrocytes. This study suggests that PD-related molecular events can be triggered upon TBI. The biological mechanisms linking brain trauma and neurodegenerative diseases need to be further investigated

The Prognostic Value of Pentraxin-3 in COVID-19 Patients: A Systematic Review and Meta-Analysis of Mortality Incidence

Over the last three years, humanity has been facing one of the most serious health emergencies due to the global spread of Coronavirus disease (COVID-19). In this scenario, the research of reliable biomarkers of mortality from COVID-19 represents a primary objective. Pentraxin 3 (PTX3), a highly conserved protein of innate immunity, seems to be associated with a worse outcome of the disease. Based on the above, this systematic review and meta-analysis evaluated the prognostic potential of PTX3 in COVID-19 disease. We included 12 clinical studies evaluating PTX3 in COVID-19 patients. From our research, we found increased PTX3 levels compared to healthy subjects, and notably, PTX3 was even more augmented in severe COVID-19 rather than non-severe cases. Moreover, we performed a meta-analysis to establish if there were differences between ICU and non-ICU COVID-19 patients in PTX3-related death. We combined 5 studies for a total of 543 ICU vs. 515 non-ICU patients. We found high significative PTX3-related death in ICU COVID-19 hospitalized individuals (184 out of 543) compared to non-ICU (37 out of 515), with an overall effect OR: 11.30 [2.00, 63.73]; p = 0.006. In conclusion, we probed PTX3 as a reliable marker of poor outcomes after COVID-19 infection as well as a predictor of hospitalized patients’ stratification

The association of adelmidrol with sodium hyaluronate displays beneficial properties against bladder changes following spinal cord injury in mice.

The disruption of coordinated control between the brain, spinal cord and peripheral nervous system caused by spinal cord injury (SCI) leads to several secondary pathological conditions, including lower urinary tract dysfunction. In fact, urinary tract dysfunction associated with SCI is urinary dysfunction could be a consequence of a lack of neuroregeneration of supraspinal pathways that control bladder function. The object of the current research was to explore the effects of adelmidrol + sodium hyaluronate, on bladder damage generated after SCI in mice. Spinal cord was exposed via laminectomy, and SCI was induced by extradural compression at T6 to T7 level, by an aneurysm clip with a closing force of 24 g. Mice were treated intravesically with adelmidrol + sodium hyaluronate daily for 48 h and 7 days after SCI. Adelmidrol + sodium hyaluronate reduced significantly mast cell degranulation and down-regulated the nuclear factor-κB pathway in the bladder after SCI both at 48 h and 7days. Moreover, adelmidrol + sodium hyaluronate reduced nerve growth factor expression, suggesting an association between neurotrophins and bladder pressure. At 7 days after SCI, the bladder was characterized by a marked bacterial infection and proteinuria; surprisingly, adelmidrol + sodium hyaluronate reduced significantly both parameters. These data show the protective roles of adelmidrol + sodium hyaluronate on bladder following SCI, highlighting a potential therapeutic target for the reduction of bladder changes

Adenosine Targeting as a New Strategy to Decrease Glioblastoma Aggressiveness

Glioblastoma is the most commonly malignant and aggressive brain tumor, with a high mortality rate. The role of the purine nucleotide adenosine and its interaction with its four subtypes receptors coupled to the different G proteins, A1, A2A, A2B, and A3, and its different physiological functions in different systems and organs, depending on the active receptor subtype, has been studied for years. Recently, several works have defined extracellular adenosine as a tumoral protector because of its accumulation in the tumor microenvironment. Its presence is due to both the interaction with the A2A receptor subtype and the increase in CD39 and CD73 gene expression induced by the hypoxic state. This fact has fueled preclinical and clinical research into the development of efficacious molecules acting on the adenosine pathway and blocking its accumulation. Given the success of anti-cancer immunotherapy, the new strategy is to develop selective A2A receptor antagonists that could competitively inhibit binding to its endogenous ligand, making them reliable candidates for the therapeutic management of brain tumors. Here, we focused on the efficacy of adenosine receptor antagonists and their enhancement in anti-cancer immunotherapy