Evaluation di adotta una tigre triestina, progetto di citizen science a scuola

Mentre c\u2019\ue8 chi si ostina a proclamare che \u201cla scienza non \ue8 democratica\u201d e che \ue8 patrimonio di pochi eletti, la realt\ue0 dei fatti procede su una strada diversa e vede la sempre maggiore diffusione della cosiddetta citizen science, ovvero la scienza fatta dai cittadini. L\u2019attivit\ue0 di osservazione e raccolta dati \ue8 oggi davvero alla portata di tutti, grazie agli strumenti tecnologici e di condivisione delle informazioni, che permettono a chiunque di contribuire attivamente alla ricerca di base e applicata. In particolare, sta assumendo oggi un ruolo sempre pi\uf9 determinante la partecipazione attiva e volontaria dei cittadini nella ricerca e nello sviluppo di politiche ambientali a supporto dei decisori. I cittadini, infatti, esprimono crescente interesse e preoccupazione per l\u2019impatto umano sull\u2019ambiente che necessariamente comporta il peggioramento della qualit\ue0 della vita. Attraverso la loro partecipazione attiva in campagne e progetti di citizen science (da ora CS), i cittadini accrescono, dunque, la conoscenza del territorio in cui abitano e stimolano le agenzie di controllo ambientale ad effettuare monitoraggi pi\uf9 estesi e accurati. I dati prodotti, messi a disposizione della comunit\ue0 attraverso internet, vanno ad arricchire la gamma dei cosiddetti open data. La CS, tuttavia, non \ue8 esente da critiche e problematiche. Dal punto di vista degli scienziati utilizzare dati reperiti attraverso il pubblico laico \ue8 rischioso e fa emergere il problema della qualit\ue0 e validazione del dato. Dall\u2019altra parte, perch\ue9 si possa parlare davvero di scienza dei cittadini, \ue8 necessario che i non professionisti ricevano qualcosa di tangibile come compenso per il loro apporto. Un terzo problema riguarda la dimensione etica della propriet\ue0 del dato: i membri del gruppo diventano co-produttori delle informazioni, co-proprietari dei dati, si pone allora la questione del diritto di autore e della titolarit\ue0 del dato. Un\u2019ultima criticit\ue0 riguarda la valutazione dei progetti di CS: innanzitutto \ue8 importante riuscire a definire dei criteri standard che individuino ci\uf2 che \ue8 un progetto di CS da ci\uf2 che non lo \ue8 e, secondariamente, \ue8 fondamentale impostare un processo valutativo per misurare l\u2019efficacia del progetto. Molto spesso la valutazione non viene effettuata per mancanza di fondi o di tempo, creando, tuttavia, un vuoto informativo circa le possibili azioni di miglioramento da mettere in campo..

Oxidative stress in DNA repeat expansion disorders: a focus on NRF2 signaling involvement

DNA repeat expansion disorders are a group of neuromuscular and neurodegenerative diseases that arise from the inheritance of long tracts of nucleotide repetitions, located in the regulatory region, introns, or inside the coding sequence of a gene. Although loss of protein expression and/or the gain of function of its transcribed mRNA or translated product represent the major pathogenic effect of these pathologies, mitochondrial dysfunction and imbalance in redox homeostasis are reported as common features in these disorders, deeply affecting their severity and progression. In this review, we examine the role that the redox imbalance plays in the pathological mechanisms of DNA expansion disorders and the recent advances on antioxidant treatments, particularly focusing on the expression and the activity of the transcription factor NRF2, the main cellular regulator of the antioxidant response

Oxidative stress in Duchenne muscular dystrophy: focus on the NRF2 redox pathway

Oxidative stress is involved in the pathogenesis of Duchenne muscular dystrophy (DMD), an X-linked genetic disorder caused by mutations in the dystrophin gene and characterized by progressive, lethal muscle degeneration and chronic inflammation. In this study, we explored the expression and signaling pathway of a master player of the anti-oxidant and anti-inflammatory response, namely NRF2, in muscle biopsies of DMD patients. We classified DMD patients in two age groups (Class I, 0-2 years and Class II, 2-9 years), in order to evaluate the antioxidant pathway expression during the disease progression. We observed that altered enzymatic antioxidant responses, increased levels of oxidized glutathione and oxidative damage are differently modulated in the two age classes of patients and well correlate with the severity of pathology. Interestingly, we also observed a modulation of relevant markers of the inflammatory response, such as heme oxygenase 1 and IL-6, suggesting a link between oxidative stress and chronic inflammatory response. Of note, using a transgenic mouse model, we demonstrated that IL-6 overexpression parallels the antioxidant expression profile and the severity of dystrophic muscle observed in DMD patients. This study advances our understanding of the pathogenic mechanisms underlying DMD and defines the critical role of oxidative stress on muscle wasting with clear implications for disease pathogenesis and therapy in human

Oxidative stress in Duchenne muscular dystrophy: focus on the NRF2 redox pathway

Oxidative stress is involved in the pathogenesis of Duchenne muscular dystrophy (DMD), an X-linked genetic disorder caused by mutations in the dystrophin gene and characterized by progressive, lethal muscle degeneration and chronic inflammation. In this study, we explored the expression and signaling pathway of a master player of the anti-oxidant and anti-inflammatory response, namely NRF2, in muscle biopsies of DMD patients. We classified DMD patients in two age groups (Class I, 0-2 years and Class II, 2-9 years), in order to evaluate the antioxidant pathway expression during the disease progression. We observed that altered enzymatic antioxidant responses, increased levels of oxidized glutathione and oxidative damage are differently modulated in the two age classes of patients and well correlate with the severity of pathology. Interestingly, we also observed a modulation of relevant markers of the inflammatory response, such as heme oxygenase 1 and IL-6, suggesting a link between oxidative stress and chronic inflammatory response. Of note, using a transgenic mouse model, we demonstrated that IL-6 overexpression parallels the antioxidant expression profile and the severity of dystrophic muscle observed in DMD patients. This study advances our understanding of the pathogenic mechanisms underlying DMD and defines the critical role of oxidative stress on muscle wasting with clear implications for disease pathogenesis and therapy in human

Targeting NRF2 for the treatment of Friedreich's ataxia: a comparison among drugs

NRF2 (Nuclear factor Erythroid 2-related Factor 2) signaling is impaired in Friedreich's Ataxia (FRDA), an autosomal recessive disease characterized by progressive nervous system damage and degeneration of nerve fibers in the spinal cord and peripheral nerves. The loss of frataxin in patients results in iron sulfur cluster deficiency and iron accumulation in the mitochondria, making FRDA a fatal and debilitating condition. There are no currently approved therapies for the treatment of FRDA and molecules able to activate NRF2 have the potential to induce clinical benefits in patients. In this study, we compared the efficacy of six redox-active drugs, some already adopted in clinical trials, targeting NRF2 activation and frataxin expression in fibroblasts obtained from skin biopsies of FRDA patients. All of these drugs consistently increased NRF2 expression, but differential profiles of NRF2 downstream genes were activated. The Sulforaphane and N-acetylcysteine were particularly effective on genes involved in preventing inflammation and maintaining glutathione homeostasis, the dimethyl fumarate, omaxevolone, and EPI-743 in counteracting toxic products accumulation, the idebenone in mitochondrial protection. This study may contribute to develop synergic therapies, based on a combination of treatment molecules

Ferroptosis in Friedreich’s ataxia: a metal-induced neurodegenerative disease

Ferroptosis is an iron-dependent form of regulated cell death, arising from the accumulation of lipid-based reactive oxygen species when glutathione-dependent repair systems are compromised. Lipid peroxidation, mitochondrial impairment and iron dyshomeostasis are the hallmark of ferroptosis, which is emerging as a crucial player in neurodegeneration. This review provides an analysis of the most recent advances in ferroptosis, with a special focus on Friedreich’s Ataxia (FA), the most common autosomal recessive neurodegenerative disease, caused by reduced levels of frataxin, a mitochondrial protein involved in iron–sulfur cluster synthesis and antioxidant defenses. The hypothesis is that the iron-induced oxidative damage accumulates over time in FA, lowering the ferroptosis threshold and leading to neuronal cell death and, at last, to cardiac failure. The use of anti-ferroptosis drugs combined with treatments able to activate the antioxidant response will be of paramount importance in FA therapy, such as in many other neurodegenerative diseases triggered by oxidative stress

Unraveling the Role of Heme in Neurodegeneration

Heme (iron-protoporphyrin IX) is an essential co-factor involved in several biological processes, including neuronal survival and differentiation. Nevertheless, an excess of free-heme promotes oxidative stress and lipid peroxidation, thus leading to cell death. The toxic properties of heme in the brain have been extensively studied during intracerebral or subarachnoid hemorrhages. Recently, a growing number of neurodegenerative disorders have been associated to alterations of heme metabolism. Hence, the etiology of such diseases remains undefined. The aim of this review is to highlight the neuropathological role of heme and to discuss the major heme-regulated pathways that might be crucial for the survival of neuronal cells. The understanding of the molecular mechanisms linking heme to neurodegeneration will be important for therapeutic purposes

Fibroblast Interaction with Different Abutment Surfaces: In Vitro Study

Background: Attaining an effective mucosal attachment to the transmucosal part of the implant could protect the peri-implant bone. Aim: To evaluate if chair side surface treatments (plasma of Argon and ultraviolet light) may affect fibroblast adhesion on different titanium surfaces designed for soft tissue healing. Methods: Grade 5 titanium discs with four different surface topographies were subdivided into 3 groups: argon-plasma; ultraviolet light, and no treatment. Cell morphology and adhesion tests were performed at 20 min, 24 h, and 72 h. Results: Qualitative observation of the surfaces performed at the SEM was in accordance with the anticipated features. Roughness values ranged from smooth (MAC Sa = 0.2) to very rough (XA Sa = 21). At 20 min, all the untreated surfaces presented hemispherical cells with reduced filopodia, while the cells on treated samples were more spread with broad lamellipodia. However, these differences in spreading behavior disappeared at 24 h and 72 h. Argon-plasma, but not UV, significantly increased the number of fibroblasts independently of the surface type but only at 20 min. Statistically, there was no surface in combination with a treatment that favored a greater cellular adhesion. Conclusions: Data showed potential biological benefits of treating implant abutment surfaces with the plasma of argon in relation to early-stage cell adhesion