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Sustainable development goals (SDGs) adopted in 2015 are geared toward sustainable development through various pathways, one being reducing inequality as covered in SDG 10. Inequalities are a threat to health and wellbeing of populations and a planet Earth in which we live. This rapid review aims to identify key issues that are likely to exacerbate inequalities around the six SDGs directly related to One Health, which are SDG 3, 6, 11, 13, 14 and 15, and suggest some actions that may help to address them using inclusive governance taking into account the coronavirus disease of 2019 (COVID-19) pandemic. Informed by the literature on SDGs and using the “inclusive development concept” by Gupta and Vegelin, literature search was done in Google Scholar, PubMed Central, as well as, searching of references in the relevant articles identified using search terms from the six SDGs that are directly related to One Health. In the context of the SDGs, in order to achieve One Health through inclusive governance, and tackle inequalities, the following needs to be considered and addressed: increasing number of armed conflicts; ongoing COVID-19 pandemic; ensuring availability of water and sanitation facilities; improving city and urban areas planning to cope with climate change; improving governance arrangements for addressing climate change factoring gender and human rights; multisectoral planning for conservation of oceans, seas, and marine resources; balancing trade regulation of wildlife trade with conservation efforts; need for a research collaborative involving experts from environmental sciences, wildlife, agriculture and human health to study and develop scientific evidence on contribution of changes in land use practices to occurrence of zoonotic diseases; and need of a legislation for promoting animal welfare to protect public health. Also, inclusion of people with disabilities in the use of digital technologies is critical.

Although extreme weather events have played a constant role in human history, heatwaves (HWs) have become more frequent and intense in the past decades, causing concern especially in light of the increasing evidence on climate change. Despite the increasing number of reviews suggesting a relationship between heat and health, these reviews focus primarily on mortality, neglecting other important aspects. This systematic review of reviews gathered the available evidence from research syntheses conducted on HWs and health. Following the PRISMA guidelines, 2232 records were retrieved, and 283 reviews were ultimately included. Information was extracted from the papers and categorized by topics. Quantitative data were extracted from meta-analyses and, when not available, evidence was collected from systematic reviews. Overall, 187 reviews were non-systematic, while 96 were systematic, of which 27 performed a meta-analysis. The majority evaluated mortality, morbidity, or vulnerability, while the other topics were scarcely addressed. The following main knowledge gaps were identified: lack of a universally accepted definition of HW; scarce evidence on the HW-mental health relationship; no meta-analyses assessing the risk perception of HWs; scarcity of studies evaluating the efficacy of adaptation strategies and interventions. Future efforts should meet these priorities to provide high-quality evidence to stakeholders.

Abstract Aims Despite a general decline in tobacco use in the last decades, the prevalence of tobacco smoking in individuals with alcohol use disorder (AUD) remains substantial (45–50%). Importantly, the co-use of both substances potentiates the adverse effects, making it a significant public health problem. Substantial evidence suggests that AUD and Tobacco use disorder (TUD) may share common mechanisms. Targeting these mechanisms may therefore provide more effective therapy. Numerous studies describe a potential role of the endogenous opioid system in both AUD and TUD. Reviewing this literature, we aim to evaluate the efficacy of molecules that target the opioid system as promising therapeutic interventions for treating alcohol and tobacco co-use disorders. Methods We provide a synthesis of the current epidemiological knowledge of alcohol and tobacco co-use disorders. We evaluate clinical and preclinical research that focuses on the regulation of the endogenous opioid system in alcohol, nicotine, and their interactions. Results The epidemiological data confirm that smoking stimulates heavy drinking and facilitates alcohol craving. Pharmacological findings suggest that treatments that are efficacious in the dual addiction provide a beneficial treatment outcome in comorbid AUD and TUD. In this regard, MOP, DOP and NOP-receptor antagonists show promising results, while the findings prompt caution when considering KOP-receptor antagonists as a treatment option in alcohol and tobacco co-use disorders. Conclusions Existing literature suggests a role of the opioid system in sustaining the high comorbidity rates of AUD and TUD. Molecules targeting opioid receptors may therefore represent promising therapeutic interventions in ‘heavy drinking smokers.’

Abstract Radiation damage in biological systems is initiated by free radicals and progresses with time through a variety of mechanisms. The time-scale and details of these mechanisms are briefly reviewed. Because of the variety of mechanisms of radio-biological damage, any single radio-protective or therapeutic agent can be only partially effective. The potential of and need for simultaneously using several radio-protective and therapeutic agents, including sulfhydryl compounds, superoxide dismutase, antioxidant proteins, and DNA repair enzymes, are examined, based on a priori considerations of the consequences of radiation exposure.

Background and Aims: Alcohol-associated liver disease (ALD) accounts for 70% of liver-related deaths in Europe, with no effective approved therapies. Although mitochondrial dysfunction is one of the earliest manifestations of alcohol-induced injury, restoring mitochondrial activity remains a problematic strategy due to oxidative stress. Here, we identify methylation-controlled J protein (MCJ) as a mediator for ALD progression and hypothesize that targeting MCJ may help in recovering mitochondrial fitness without collateral oxidative damage. Approach and Results: C57BL/6 mice [wild-type (Wt)] Mcj knockout and Mcj liver-specific silencing (MCJ-LSS) underwent the NIAAA dietary protocol (Lieber-DeCarli diet containing 5% (vol/vol) ethanol for 10 days, plus a single binge ethanol feeding at day 11). To evaluate the impact of a restored mitochondrial activity in ALD, the liver, gut, and pancreas were characterized, focusing on lipid metabolism, glucose homeostasis, intestinal permeability, and microbiota composition. MCJ, a protein acting as an endogenous negative regulator of mitochondrial respiration, is downregulated in the early stages of ALD and increases with the severity of the disease. Whole-body deficiency of MCJ is detrimental during ALD because it exacerbates the systemic effects of alcohol abuse through altered intestinal permeability, increased endotoxemia, and dysregulation of pancreatic function, which overall worsens liver injury. On the other hand, liver-specific Mcj silencing prevents main ALD hallmarks, that is, mitochondrial dysfunction, steatosis, inflammation, and oxidative stress, as it restores the NAD+/NADH ratio and SIRT1 function, hence preventing de novo lipogenesis and improving lipid oxidation. Conclusions: Improving mitochondrial respiration by liver-specific Mcj silencing might become a novel therapeutic approach for treating ALD.

The continual spread of novel coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), posing a severe threat to the health worldwide. The main protease (Mpro, alias 3CLpro) of SARS-CoV-2 is a crucial enzyme for the maturation of viral particles and is a very attractive target for designing drugs to treat COVID-19. Here, we propose a multiple conformation-based virtual screening strategy to discover inhibitors that can target SARS-CoV-2 Mpro. Based on this strategy, nine Mpro structures and a protein mimetics library with 8960 commercially available compounds were prepared to carry out ensemble docking for the first time. Five of the nine structures are apo forms presented in different conformations, whereas the other four structures are holo forms complexed with different ligands. The surface plasmon resonance assay revealed that 6 out of 49 compounds had the ability to bind to SARS-CoV-2 Mpro. The fluorescence resonance energy transfer experiment showed that the biochemical half-maximal inhibitory concentration (IC50) values of the six compounds could hamper Mpro activities ranged from 0.69 ± 0.05 to 2.05 ± 0.92 μM. Evaluation of antiviral activity using the cell-based assay indicated that two compounds (Z1244904919 and Z1759961356) could strongly inhibit the cytopathic effect and reduce replication of the living virus in Vero E6 cells with the half-maximal effective concentrations (EC50) of 4.98 ± 1.83 and 8.52 ± 0.92 μM, respectively. The mechanism of the action for the two inhibitors were further elucidated at the molecular level by molecular dynamics simulation and subsequent binding free energy analysis. As a result, the discovered noncovalent reversible inhibitors with novel scaffolds are promising antiviral drug candidates, which may be used to develop the treatment of COVID-19.

This paper is devoted to study the electrochemical behavior of Pt catalyst in a polymer electrolyte fuel cell at various operating conditions and at different electric potential difference (also known as voltage) cycling applied in accelerated stress tests. The degradation of platinum is considered with respect to the Pt ion dissolution and the Pt oxide coverage of catalyst described by a one-dimensional model. In the model, degradation rate increases with temperature and decreasing particle diameter of Pt nano-particles. The theoretical study of the underlying diffusion system with the nonlinear reactions is presented by analytical methods and gives explicit solutions through a first integral of the ODE system. Numerical tests are obtained using a second order implicit-explicit scheme. The computer simulation shows that the lifetime of the catalyst depends on the voltage profile and the upper potential level. By this Pt mass loss is more significant at the membrane surface than at the gas diffusion layer.