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As concerns about plastic pollution are rising, the number of remediation technologies to clean up plastic from the environment or prevent it from dispersing more is also increasing. Therefore, sorting and assessing these technological innovations to combat plastic pollution is fundamental. Our study provides additional insights on the current state of the art of plastic remediation technologies, offers an overview of deployed, tested, and conceptual remediation technologies and their characteristics (e.g., field of application, developmental stage), and assesses possible challenges and opportunities. We have created an overview of plastic remediation technologies by combining information retrieved from a systematic and non-systematic review. The systematic literature review, executed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and performed on the electronic database Scopus, allowed us to find remediation technologies described in the scientific literature and evaluate the current state of the art. The non-systematic web review was performed using predefined search terms to acquire additional remediation technologies and characteristics. In addition, we investigated the strengths, weaknesses, opportunities, and threats (SWOT) of plastic clean-up technologies for ports and inland waterways. Our overview, listing 124 individual remediation technologies, shows that the majority (60%) of the technologies are suitable to be deployed in inland waterways and, as indicated by the SWOT analysis, despite the challenges, technologies for these fields of application offer extensive opportunities (e.g., new jobs, raising awareness). Although there are still knowledge gaps, such as the potential environmental impact of these technologies, 56% of the studies published on plastic remediation technologies were published in the past three years, indicating a growing interest from the scientific community. Given the increased concern of the public and policymakers on plastic pollution and its consequences, our study provides crucial information on rising technological innovations to tackle this persistent pollutant. Also see: https://micro2022.sciencesconf.org/427076/document, In MICRO 2022, Online Atlas Edition: Plastic Pollution from MACRO to nano

Despite an increasing research conducted on ocean plastic pollution over the last decade, there are still large knowledge gaps in our current understanding of how floating plastic debris accumulating in subtropical oceanic gyres may harm the surface-associated pelagic community known as neuston. Removing floating plastic debris from the surface ocean can minimize potentially adverse effects of plastic pollution on the neuston, as well as prevent the formation of large quantities of secondary micro- and nanoplastics. However, due to the scarcity of observational data from remote and difficult to access offshore waters, neuston dynamics in subtropical oceanic gyres and thus the potential impacts of plastic pollution as well as of cleanup activities on the neuston remain uncertain. Here, we provide rare observational data of the relative distribution of floating plastic debris (0.05–5 cm in size) and members of the neuston in the eastern North Pacific Ocean. Our results reveal that the dominant neustonic species co-occurring with high concentrations of floating plastic debris in the North Pacific Garbage Patch (NPGP) such as Porpita porpita, Halobates spp., pteropods, isopods, heteropods, and crabs depict either a low atmospheric drag due to physical attributes or a potential plastic-associated fitness benefit such as increased surface area for oviposition and structure for habitat. We further observe relatively higher plastic to organism ratios inside the NPGP for most target species compared to waters outside the NPGP. The findings presented here provide a first observational baseline to develop ecological models that can help evaluate the long-term risks of plastic pollution and of offshore cleanup activities for neuston in the eastern North Pacific Ocean. We further suggest that offshore mitigation strategies aiming at removing floating plastic debris from the ocean surface need to evaluate both, the direct impact of neuston bycatch during plastic removal on neuston population dynamics, as well as the potential benefits of reducing the negative effects of plastic pollution on the neuston.

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Hypoxia is a hallmark of several solid tumors and it is often associated with chemotherapy resistance. The O2 levels decrease induces the activation of Hypoxia-inducible factor 1 (HIF-1) which coordinates cellular adaptive changes and metabolic reprogramming. Under normoxic conditions, HIF-1α subunit has a high turnover strictly regulated by the activation of prolyl hydroxylases (PHDs). At low oxygen levels, PHDs activity is inhibited and HIF-1α is stabilized and migrates into the nucleus where it bounds the HIF-1β exerting its transcriptional activity. Our research group has demonstrated that the lack of respiratory complex I (CI) imbalances the α-ketoglutarate (αKG)/succinate (SA) ratio towards αKG, metabolites that regulate the PHDs activity. The chronic activation of PHDs leads to HIF-1α destabilization even when O2 is available, a condition that we termed pseudonormoxia, and hampered tumor growth in vitro and in vivo. We hypothesized that pseudonormoxia may be induced by unbalancing the αKG/SA ratio mimicking a normoxic condition and leading to the block of tumor progression. In this context, the aim of this PhD project was to prove that HIF-1α destabilization and pseudonormoxia can be pharmacologically induced by increasing αKG levels using CI inhibitors (indirect approach) or cell permeable αKG ester derivatives (direct approach) in order to identify novel and safe adjuvant therapeutic agents for aggressive cancers. We screened a panel of compounds, composed by molecules that potentially may act as CI inhibitors and seven αKGlogues, for their ability to specifically destabilize HIF-1α in cancer cells, while being not toxic for their non-cancer counterpart. From these experiments, we identified four promising compounds that fit these criteria and that will be used for further investigations. The link between HIF-1α stabilization and mitochondrial function opens to new metabolic-based therapeutic approaches for cancers for which adaptation to hypoxia is a step that must be overcome to progress toward malignancy.

Che rapporto intercorre tra un’opera letteraria e una sua interpretazione? Che cosa fa sì che la prima supporti la seconda? Come possiamo discernere un’interpretazione valida da una che non lo è ? Come può una stessa opera avere interpretazioni differenti e a volte incompatibili tra loro? Assumendo come punto di partenza la proposta di Nelson Goodman di qualificare l’opera letteraria come allografica e, quindi, di definire l’identità dell’opera sulla base della sua compitazione, cercare un risposta alle domande proposte implica un riflessione tanto sul linguaggio, quale strumento simbolico, quanto sulle modalità di riferimento proprie delle opere letterarie. In particolare, di fronte al dissolversi del mondo nella molteplicità delle versioni che il linguaggio può offrire di esso, una peculiare concezione della metafora, intesa come proiezione di un regno del linguaggio su un altro regno dello stesso, si qualifica come un buon modello per la comprensione del rapporto che lega opere letterarie e loro interpretazioni. In tal modo l’opera stessa non solo diviene significativa, ma, attraverso tale significazione, riesce anche a farsi produttiva, modificando, ampliando, ristrutturando la versione dal mondo dalla quale l’interprete-lettore prende le mosse. Ciascuna lettura di un’opera letteraria può infatti essere concepita come una via attraverso la quale ciò che nell’opera è detto viene proiettato sulla visione del mondo propria dell’interprete e di quanti possono condividerne il punto di vista. In tal modo le interpretazioni pongono le opere cui si riferiscono nelle condizioni di fornire un apporto significativo tanto alla comprensione quanto alla costituzione della nostra versione del mondo. E se ciò può avvenire in diversi modi, mutando le interpretazioni a seconda di chi le produce e delle circostanze in cui sorgono, l’opera evita la dissoluzione in virtù della compitazione che la identifica., What is the relationship between a literary work and its interpretation? What makes the first support the second one? How can we discern a valid interpretation from one that is not? How can the same work have different interpretations, sometimes incompatible with each other? Taking as starting point the Nelson Goodman’s proposal to qualify literary works as allografic, and, therefore, to define the works identity based on their spelling, look for a response to posed questions implies a reflection both on language, as symbolic tool, and on the ways of reference of literary works. In particular, after the world dissolution in the multiplicity of versions that the language can offer of it, a peculiar conception of metaphor, understood as the projection of a realm to another of language, qualifies as a good model for the understanding of the relationship between literary works and their interpretations. In this way, the work itself not only becomes significant, but, by meaning, is also successful to get productive, changing, expanding, renovating the world version from which the reader-interpreter starts. Each reading of a literary work can in fact be seen as a way in which what is said in the work is projected onto the interpreter's own world vision and those whose can share his point of view. In this way, the interpretations put the works to which they refer in a position to make a significant contribution both to the understanding and to the constitution of our version of the world. And if this can be done in several ways, changing interpretations depending on who produces them and on the circumstances in which they arise, the work avoids the dissolution by virtue of spelling that identifies it.

Che rapporto intercorre tra un’opera letteraria e una sua interpretazione? Che cosa fa sì che la prima supporti la seconda? Come possiamo discernere un’interpretazione valida da una che non lo è ? Come può una stessa opera avere interpretazioni differenti e a volte incompatibili tra loro? Assumendo come punto di partenza la proposta di Nelson Goodman di qualificare l’opera letteraria come allografica e, quindi, di definire l’identità dell’opera sulla base della sua compitazione, cercare un risposta alle domande proposte implica un riflessione tanto sul linguaggio, quale strumento simbolico, quanto sulle modalità di riferimento proprie delle opere letterarie. In particolare, di fronte al dissolversi del mondo nella molteplicità delle versioni che il linguaggio può offrire di esso, una peculiare concezione della metafora, intesa come proiezione di un regno del linguaggio su un altro regno dello stesso, si qualifica come un buon modello per la comprensione del rapporto che lega opere letterarie e loro interpretazioni. In tal modo l’opera stessa non solo diviene significativa, ma, attraverso tale significazione, riesce anche a farsi produttiva, modificando, ampliando, ristrutturando la versione dal mondo dalla quale l’interprete-lettore prende le mosse. Ciascuna lettura di un’opera letteraria può infatti essere concepita come una via attraverso la quale ciò che nell’opera è detto viene proiettato sulla visione del mondo propria dell’interprete e di quanti possono condividerne il punto di vista. In tal modo le interpretazioni pongono le opere cui si riferiscono nelle condizioni di fornire un apporto significativo tanto alla comprensione quanto alla costituzione della nostra versione del mondo. E se ciò può avvenire in diversi modi, mutando le interpretazioni a seconda di chi le produce e delle circostanze in cui sorgono, l’opera evita la dissoluzione in virtù della compitazione che la identifica., What is the relationship between a literary work and its interpretation? What makes the first support the second one? How can we discern a valid interpretation from one that is not? How can the same work have different interpretations, sometimes incompatible with each other? Taking as starting point the Nelson Goodman’s proposal to qualify literary works as allografic, and, therefore, to define the works identity based on their spelling, look for a response to posed questions implies a reflection both on language, as symbolic tool, and on the ways of reference of literary works. In particular, after the world dissolution in the multiplicity of versions that the language can offer of it, a peculiar conception of metaphor, understood as the projection of a realm to another of language, qualifies as a good model for the understanding of the relationship between literary works and their interpretations. In this way, the work itself not only becomes significant, but, by meaning, is also successful to get productive, changing, expanding, renovating the world version from which the reader-interpreter starts. Each reading of a literary work can in fact be seen as a way in which what is said in the work is projected onto the interpreter's own world vision and those whose can share his point of view. In this way, the interpretations put the works to which they refer in a position to make a significant contribution both to the understanding and to the constitution of our version of the world. And if this can be done in several ways, changing interpretations depending on who produces them and on the circumstances in which they arise, the work avoids the dissolution by virtue of spelling that identifies it.

Converting carcinomas in benign oncocytomas has been suggested as a potential anti-cancer strategy. One of the oncocytoma hallmarks is the lack of respiratory complex I (CI). Here we use genetic ablation of this enzyme to induce indolence in two cancer types, and show this is reversed by allowing the stabilization of Hypoxia Inducible Factor-1 alpha (HIF-1α). We further show that on the long run CI-deficient tumors re-adapt to their inability to respond to hypoxia, concordantly with the persistence of human oncocytomas. We demonstrate that CI-deficient tumors survive and carry out angiogenesis, despite their inability to stabilize HIF-1α. Such adaptive response is mediated by tumor associated macrophages, whose blockage improves the effect of CI ablation. Additionally, the simultaneous pharmacological inhibition of CI function through metformin and macrophage infiltration through PLX-3397 impairs tumor growth in vivo in a synergistic manner, setting the basis for an efficient combinatorial adjuvant therapy in clinical trials.

Converting carcinomas in benign oncocytomas has been suggested as a potential anti-cancer strategy. One of the oncocytoma hallmarks is the lack of respiratory complex I (CI). Here we use genetic ablation of this enzyme to induce indolence in two cancer types, and show this is reversed by allowing the stabilization of Hypoxia Inducible Factor-1 alpha (HIF-1α). We further show that on the long run CI-deficient tumors re-adapt to their inability to respond to hypoxia, concordantly with the persistence of human oncocytomas. We demonstrate that CI-deficient tumors survive and carry out angiogenesis, despite their inability to stabilize HIF-1α. Such adaptive response is mediated by tumor associated macrophages, whose blockage improves the effect of CI ablation. Additionally, the simultaneous pharmacological inhibition of CI function through metformin and macrophage infiltration through PLX-3397 impairs tumor growth in vivo in a synergistic manner, setting the basis for an efficient combinatorial adjuvant therapy in clinical trials.

Converting carcinomas in benign oncocytomas has been suggested as a potential anti-cancer strategy. One of the oncocytoma hallmarks is the lack of respiratory complex I (CI). Here we use genetic ablation of this enzyme to induce indolence in two cancer types, and show this is reversed by allowing the stabilization of Hypoxia Inducible Factor-1 alpha (HIF-1α). We further show that on the long run CI-deficient tumors re-adapt to their inability to respond to hypoxia, concordantly with the persistence of human oncocytomas. We demonstrate that CI-deficient tumors survive and carry out angiogenesis, despite their inability to stabilize HIF-1α. Such adaptive response is mediated by tumor associated macrophages, whose blockage improves the effect of CI ablation. Additionally, the simultaneous pharmacological inhibition of CI function through metformin and macrophage infiltration through PLX-3397 impairs tumor growth in vivo in a synergistic manner, setting the basis for an efficient combinatorial adjuvant therapy in clinical trials., Lack of respiratory complex I is a hallmark of oncocytomas. Here the authors show that inactivation of this complex via knockout of the NDUFS3 subunit or using metformin, converts tumors from an aggressive phenotype into low-proliferative oncocytomas, which can be further inhibited by targeting pro-tumorigenic macrophages.

Mammalian respiratory complex I (CI) biogenesis requires both nuclear and mitochondria-encoded proteins and is mostly organized in respiratory supercomplexes. Among the CI proteins encoded by the mitochondrial DNA, NADH-ubiquinone oxidoreductase chain 1 (ND1) is a core subunit, evolutionary conserved from bacteria to mammals. Recently, ND1 has been recognized as a pivotal subunit in maintaining the structural and functional interaction among the hydrophilic and hydrophobic CI arms. A critical role of human ND1 both in CI biogenesis and in the dynamic organization of supercomplexes has been depicted, although the proof of concept is still missing and the critical amount of ND1 protein necessary for a proper assembly of both CI and supercomplexes is not defined. By exploiting a unique model in which human ND1 is allotopically re-expressed in cells lacking the endogenous protein, we demonstrated that the lack of this protein induces a stall in the multi-step process of CI biogenesis, as well as the alteration of supramolecular organization of respiratory complexes. We also defined a mutation threshold for the m.3571insC truncative mutation in mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 1 (MT-ND1), below which CI and its supramolecular organization is recovered, strengthening the notion that a certain amount of human ND1 is required for CI and supercomplexes biogenesis.

Osteoporosis affects the skeletal system and is characterized by a reduction in bone strength that predisposes one to an increased risk of fractures. In Italy, about 3.5 million women and 1 million men suffers from osteoporosis. These numbers are set to increase in the coming twenty years because the percentage of the Italian population over 65 will increase by 25%. The purpose of this study is to evaluate the general characteristics of a population of patients suffering from osteoporosis and the relation with comorbidity. A single site, open-label, investigator-initiated, retrospective trial was conducted at the Bone Metabolic Disease Clinic, Department of Physical Medicine and Rehabilitation, University Hospital “P. Giaccone”, Palermo (Italy). 1500 patients of Bone Metabolic Diseases Clinic were enrolled from January 2009 and September 2017. All the patients were evaluated by Hologic Discovery QDR and subjected to a questionnaire that investigated general characteristics, life style, clinical data, osteoporosis pharmacological treatment, completed physical therapy, and Bone Densitometry results. The subjects with increased fracture risk have a high mean age, a lower BMI, report practicing less physical activity and less sun exposure. They also have a higher CIRS-comorbidity index and report previous fragility fractures more often. The study demonstrated a statistically significant association between the risk of fragility fractures, T-Score ≤-1, and comorbidity. This study could contribute to develop a protocol for primary prevention of fragility fractures in the female population affected by osteoporosis demonstrating a correlation between comorbidity and fragility fractures incidences.

Deregulated metabolism is a well-established hallmark of cancer. At the hub of various metabolic pathways deeply integrated within mitochondrial functions, the α-ketoglutarate dehydrogenase complex represents a major modulator of electron transport chain activity and tricarboxylic acid cycle (TCA) flux, and is a pivotal enzyme in the metabolic reprogramming following a cancer cell’s change in bioenergetic requirements. By contributing to the control of α-ketoglutarate levels, dynamics, and oxidation state, the α-ketoglutarate dehydrogenase is also essential in modulating the epigenetic landscape of cancer cells. In this review, we will discuss the manifold roles that this TCA enzyme and its substrate play in cancer.

Mitochondrial respiratory function is now recognized as a pivotal player in all the aspects of cancer biology, from tumorigenesis to aggressiveness and chemotherapy resistance. Among the enzymes that compose the respiratory chain, by contributing to energy production, redox equilibrium and oxidative stress, complex I assumes a central role. Complex I defects may arise from mutations in mitochondrial or nuclear DNA, in both structural genes or assembly factors, from alteration of the expression levels of its subunits, or from drug exposure. Since cancer cells have a high-energy demand and require macromolecules for proliferation, it is not surprising that severe complex I defects, caused either by mutations or treatment with specific inhibitors, prevent tumor progression, while contributing to resistance to certain chemotherapeutic agents. On the other hand, enhanced oxidative stress due to mild complex I dysfunction drives an opposite phenotype, as it stimulates cancer cell proliferation and invasiveness. We here review the current knowledge on the contribution of respiratory complex I to cancer biology, highlighting the double-edged role of this metabolic enzyme in tumor progression, metastasis formation, and response to chemotherapy.