Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Abstract Background Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries. Results In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries

Trypillia mega-sites of the Ukraine

No abstract available

Intracellular versus extracellular iron accumulation in freshwater periphytic mats across a mine water treatment lagoon

Despite the importance of periphyton–metal interactions in bioremediation schemes and in phosphorus (P) cycling, the processes controlling metal accumulation in periphytic mats are still poorly understood. Iron (Fe) accumulation in periphytic mats was examined across a Fe settlement lagoon receiving mine drainage in Scotland, UK, between March and June 2008. Quantification and mapping of intracellular and extracellular Fe concentrations in periphyton samples using scanning electron microscopy–energy dispersive spectroscopy suggested that Fe accumulation was dominated by the association of Fe-rich precipitates with the extracellular polymeric substances matrix, rather than biotic uptake. Intracellular Fe concentrations were significantly higher in periphyton samples exposed to the highest dissolved Fe concentrations. Neither intracellular nor extracellular Fe concentrations were significantly affected by light availability or cell density. While diatoms dominated the periphyton communities there was no significant association of diatom functional groups with Fe accumulation, indicating that community composition may not affect the function of periphytic mats with respect to Fe removal. Scale-up calculations based on the mean measured Fe accumulation rate by periphyton substrates of 0.021 g m−2 day−1 showed that exposure of large surface areas of periphyton substrate in the settlement lagoon would only increase the Fe removal efficiency of the lagoon by c.1%

Expression of Wild-Type CFTR Suppresses NF-kappa B-Driven Inflammatory Signalling

Mutation of the cystic fibrosis transmembrane-conductance regulator (CFTR) causes cystic fibrosis (CF) but not all CF aspects can easily be explained by deficient ion transport. CF-inflammation provides one example but its pathogenesis remains controversial. Here, we tested the simple but fundamental hypothesis that wild-type CFTR is needed to suppress NF-kappaB activity.In lung epithelial (H441) and engineered (H57) cell lines; we report that inflammatory markers are significantly suppressed by wild-type CFTR. Transient-transfection of wild-type CFTR into CFTR-naïve H441 cells, dose-dependently down-regulates both basal and Tumour Necrosis Factor-alpha evoked NF-kappaB activity when compared to transfection with empty vector alone (p<0.01, n>5). This effect was also observed in CFTR-naïve H57-HeLa cells which stably express a reporter of NF-kappaB activity, confirming that the CFTR-mediated repression of inflammation was not due to variable reporter gene transfection efficiency. In contrast, H57 cells transfected with a control cyano-fluorescent protein show a significantly elevated basal level of NF-kappaB activity above control. Initial cell seeding density may be a critical factor in mediating the suppressive effects of CFTR on inflammation as only at a certain density (1x10(5) cells/well) did we observe the reduction in NF-kappaB activity. CFTR channel activity may be necessary for this suppression because the CFTR specific inhibitor CFTR(inh172) significantly stimulates NF-kappaB activity by approximately 30% in CFTR expressing 16HBE14o- cells whereas pharmacological elevation of cyclic-AMP depresses activity by approximately 25% below baseline.These data indicate that CFTR has inherent anti-inflammatory properties. We propose that the hyper-inflammation found in CF may arise as a consequence of disrupted repression of NF-kappaB signalling which is normally mediated by CFTR. Our data therefore concur with in vivo and in vitro data from Vij and colleagues which highlights CFTR as a suppressor of basal inflammation acting through NF-kappaB, a central hub in inflammatory signalling

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field