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

Mecanismos de sinalização celular activados pela interleucina - IB, em condrócitos articulares : implicações na expressão da isoforma indutíval da síntase do monóxido de azoto.

Tese de doutoramento em Farmácia (Farmacologia) apresentada à Fac. de Farmácia da Univ. de CoimbraGrande parte dos efeitos catabólicos e inflamatórios que a citocina pró-inflamatória interleucina-1 (IL-1) origina nas articulações artríticas é mediada pelo monóxido de azoto (NO) sintetizado em grandes quantidades pela isoforma indutível da sintase do NO (NOS II). Este trabalho pretendeu contribuir para um melhor conhecimento dos mecanismos celulares envolvidos nas respostas do condrócito articular à IL-1, nomeadamente na regulação da expressão da NOS II. Os resultados obtidos mostraram que as espécies reactivas de oxigénio (ROS), particularmente o anião superóxido, as “cinases de resíduos de tirosina” e a “cinase de proteínas activada por mitogénios” p38 são indispensáveis para a activação do factor de transcrição Factor Nuclear-kapaB (NF-kB) e para a expressão subsequente da NOS II induzidas pela IL-1, em condrócitos articulares. A Diacereína e o seu metabolito activo, a Reína, inibem eficazmente estas respostas à IL-1, o mesmo acontecendo com o próprio NO. A activação do factor de transcrição Proteína Activadora-1 (AP-1) requer também a produção de ROS e NO, mas a expressão da NOS II, induzida pela IL-1, é independente da actividade deste factor. Tendo em conta o papel do NF-kB e do AP-1 na expressão de genes cujas proteínas, incluindo a NOS II, contribuem para a inflamação e degradação da cartilagem, estes resultados permitem concluir que a inibição da produção celular de ROS e de NO pode constituir uma estratégia terapêutica simultaneamente anti-inflamatória e condroprotectora. Além disso, estes resultados evidenciam duas acções opostas do NO: por um lado, a sua capacidade para activar o AP-1 e, por outro, a sua eficácia como inibidor do NF-kB. Esta dualidade de acções que o NO exerce no condrócito articular levanta algumas questões quanto ao seu real papel na fisiopatologia das doenças artríticas. A visão clássica de que pequenas quantidades de NO, produzidas pelas isoformas constitutivas, estão envolvidas em processos fisiológicos, enquanto concentrações elevadas, produzidas pela NOS II, originam respostas patológicas, é claramente insuficiente para explicar os mecanismos moleculares que regulam a síntese e acções biológicas do NO

Physiology and Pathophysiology of Musculoskeletal Aging

We live in a world with an ever-increasing aging population. This aging population is predicted to place a huge financial burden on healthcare systems around the world. Understanding healthy ageing is a key research priority, along with a better understanding of the pathophysiology of ageing that occurs in a number of age related diseases, such as arthritis. By gaining a better understanding of healthy musculoskeletal ageing we can provide better care and new therapies for common musculoskeletal problems. This Research Topic is intended to bring together basic researchers and clinicians working in the broad area of musculoskeletal ageing. The topic includes mechanisms of healthy ageing in the musculoskeletal system, which we define as skeletal muscle and the synovial joint, particularly constituent structures including articular cartilage, subchondral bone tendon and ligament. A particular focus of this Research Topic is dietary modulation of musculoskeletal ageing

Monoterpenes as Sirtuin-1 Activators: Therapeutic Potential in Aging and Related Diseases

Sirtuin 1 (SIRT) is a class III, NAD+-dependent histone deacetylase that also modulates the activity of numerous non-histone proteins through deacylation. SIRT1 plays critical roles in regulating and integrating cellular energy metabolism, response to stress, and circadian rhythm by modulating epigenetic and transcriptional regulation, mitochondrial homeostasis, proteostasis, telomere maintenance, inflammation, and the response to hypoxia. SIRT1 expression and activity decrease with aging, and enhancing its activity extends life span in various organisms, including mammals, and improves many age-related diseases, including cancer, metabolic, cardiovascular, neurodegenerative, respiratory, musculoskeletal, and renal diseases, but the opposite, that is, aggravation of various diseases, such as some cancers and neurodegenerative diseases, has also been reported. Accordingly, many natural and synthetic SIRT1 activators and inhibitors have been developed. Known SIRT1 activators of natural origin are mainly polyphenols. Nonetheless, various classes of non-polyphenolic monoterpenoids have been identified as inducers of SIRT1 expression and/or activity. This narrative review discusses current information on the evidence that supports the role of those compounds as SIRT1 activators and their potential both as tools for research and as pharmaceuticals for therapeutic application in age-related diseases

Mecanismos de sinalização celular activados pela interleucina - IB, em condrócitos articulares : implicações na expressão da isoforma indutíval da síntase do monóxido de azoto.

Grande parte dos efeitos catabólicos e inflamatórios que a citocina pró-inflamatória interleucina-1 (IL-1) origina nas articulações artríticas é mediada pelo monóxido de azoto (NO) sintetizado em grandes quantidades pela isoforma indutível da sintase do NO (NOS II). Este trabalho pretendeu contribuir para um melhor conhecimento dos mecanismos celulares envolvidos nas respostas do condrócito articular à IL-1, nomeadamente na regulação da expressão da NOS II. Os resultados obtidos mostraram que as espécies reactivas de oxigénio (ROS), particularmente o anião superóxido, as “cinases de resíduos de tirosina” e a “cinase de proteínas activada por mitogénios” p38 são indispensáveis para a activação do factor de transcrição Factor Nuclear-kapaB (NF-kB) e para a expressão subsequente da NOS II induzidas pela IL-1, em condrócitos articulares. A Diacereína e o seu metabolito activo, a Reína, inibem eficazmente estas respostas à IL-1, o mesmo acontecendo com o próprio NO. A activação do factor de transcrição Proteína Activadora-1 (AP-1) requer também a produção de ROS e NO, mas a expressão da NOS II, induzida pela IL-1, é independente da actividade deste factor. Tendo em conta o papel do NF-kB e do AP-1 na expressão de genes cujas proteínas, incluindo a NOS II, contribuem para a inflamação e degradação da cartilagem, estes resultados permitem concluir que a inibição da produção celular de ROS e de NO pode constituir uma estratégia terapêutica simultaneamente anti-inflamatória e condroprotectora. Além disso, estes resultados evidenciam duas acções opostas do NO: por um lado, a sua capacidade para activar o AP-1 e, por outro, a sua eficácia como inibidor do NF-kB. Esta dualidade de acções que o NO exerce no condrócito articular levanta algumas questões quanto ao seu real papel na fisiopatologia das doenças artríticas. A visão clássica de que pequenas quantidades de NO, produzidas pelas isoformas constitutivas, estão envolvidas em processos fisiológicos, enquanto concentrações elevadas, produzidas pela NOS II, originam respostas patológicas, é claramente insuficiente para explicar os mecanismos moleculares que regulam a síntese e acções biológicas do NO.Tese de doutoramento em Farmácia (Farmacologia) apresentada à Fac. de Farmácia da Univ. de Coimbr

Editorial: The Physiology of Inflammation-The Final Common Pathway to Disease

Healthy Aging 2020: CENTRO-01-0145-FEDER-000012 and POCI-01-0145-FEDER-028424 supported by Programa Operacional Competitividade e Internacionalização (COMPETE 2020) through FEDER and by the Portuguese Foundation for Science and Technolog

The “Journal of Functional Morphology and Kinesiology” Journal Club Series: Highlights on Recent Papers in Exercise-Induced Immune Response

We are glad to introduce the ninth Journal Club. This edition is focused on several relevant studies published in the last few years in the field of Exercise-Induced Immune Response, chosen by our Editorial Board members and their colleagues. We hope to stimulate your curiosity in this field and to share with you the passion for sport seen also from the scientific point of view. The Editorial Board members wish you an inspiring lecture

Elucidation of the Mechanism Underlying the Anti-Inflammatory Properties of (S)-(+)-Carvone Identifies a Novel Class of Sirtuin-1 Activators in a Murine Macrophage Cell Line

The signaling pathways involved in age-related inflammation are increasingly recognized as targets for the development of preventive and therapeutic strategies. Our previous study elucidated the structure-activity relationship of monoterpene compounds derived from p-menthane as potential anti-inflammatory drugs and identified (S)-(+)-carvone as the most potent among the compounds tested. This study aims at identifying the molecular mechanism underlying the anti-inflammatory properties of (S)-(+)-carvone. The murine macrophage cell line, Raw 264.7, was stimulated with bacterial lipopolysaccharide (LPS) to simulate inflammation. Western blot was used to assess protein levels and post-translational modifications. The subcellular localization of NF-κB/p65 was visualized by immunocytochemistry. An in vitro fluorometric assay was used to measure Sirtuin-1 (SIRT1) activity. (S)-(+)-carvone inhibited LPS-induced JNK1 phosphorylation, but not that of p38 and ERK1/2 and also did not affect the phosphorylation and degradation of the NF-κB inhibitor, IκB-α. Accordingly, (S)-(+)-carvone did not affect LPS-induced phosphorylation of NF-κB/p65 on Ser536 and its nuclear translocation, but it significantly decreased LPS-induced IκB-α resynthesis, a NF-κB-dependent process, and NF-κB/p65 acetylation on lysine (Lys) 310. Deacetylation of that Lys residue is dependent on the activity of SIRT1, which was found to be increased by (S)-(+)-carvone, while its protein levels were unaffected. Taken together, these results show that (S)-(+)-carvone is a new SIRT1 activator with the potential to counteract the chronic low-grade inflammation characteristic of age-related diseases