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The social confinement resulting from the COVID-19 crisis temporarily reduced greenhouse gas emissions. Although experts contend that the decrease in pollution rates was not drastic, some surveys detect growth in social concern about the climate. In this new climate-conscious environment, municipalities and local governments are promoting a new way of living and caring for cities, even before they can regain national and international freedom of movement. This work analyzes the connections between new climate awareness arising from the COVID-19 crisis, proposals of sustainable citizenship around the world, and its communication on Twitter to educate the new eco-conscious audience. The methodology mixes quantitative and qualitative analysis, using the Twitonomy Premium tool and the Twitter research tool with data extracted at the end of December 2020. Among the top ten most influential and active accounts, the results show educational institutions, local institutions, companies, neighborhoods, associations, and influencers. The impossibility of living in the city has not prevented citizen education and commitment to make real change for when that city and its citizens return to normality. However, this new normality must be different: more ecological, more responsible, more sustainable, and practiced from early childhood.

BackgroundWe previously showed that, by activating innate immune receptors Toll‐like 4 (TLR4), adolescent intermittent ethanol (EtOH) exposure causes neuroinflammation, myelin damage, and behavioral dysfunctions. Recent findings reveal that clinically used opioid antagonists naltrexone (NT) and naloxone (NX) inhibit opioid‐induced TLR4 signaling and that NT, NX, and nalmefene (NF), the 6‐methylene derivative of NX, are able to reduce alcohol drinking escalation.MethodsNF (0.1 mg/kg, intraperitoneally) was injected 1 hour prior to EtOH (3 g/kg, intraperitoneally) following intermittent treatment in female (PND35) adolescent mice. Inflammatory molecules, myelin proteins, and apoptotic markers were assessed in the prefrontal cortex (PFC) and striatum/nucleus accumbens (STR/NAcc). The effect of NF on alcohol drinking preference was evaluated in both the wild‐type and TLR4 knockout (KO) adolescent mice. Using astroglial cells, the inhibitory potential of NT, NX, and NF on lipopolysaccharide (LPS), or the EtOH‐triggered TLR4 response, was compared.ResultsOur findings indicate that NF prevents the up‐regulation of cytokines (IL‐1β, IL‐17A, TNF‐α), chemokines (MCP‐1, MIP‐1, KC), and pro‐inflammatory mediators (iNOS, COX‐2), along with myelin damage and apoptotic events, in both PFC and STR/NAcc. NF also abolishes EtOH‐induced escalation of alcohol preference/consumption, but has no effect when administered to TLR4‐KO mice. In vitro experiments indicate that NX and NF inhibit TLR4 activation upon LPS or EtOH stimulation. Immunofluorescence studies and lipid rafts isolation show that NF is able to prevent TLR4 translocation to lipid rafts/caveolae in astrocytes.ConclusionsThese results suggest that NF prevents neuroinflammation and brain damage by blocking the TLR4 response and also support the role of central pro‐inflammatory immune signaling in the modulation of alcohol consumption/addiction.

AbstractThe co‐occurrence of chronic pain and alcohol use disorders (AUDs) involves complex interactions between genetic and neurophysiological aspects, and the research has reported mixed findings when they both co‐occur. There is also an indication of a gender‐dependent effect; males are more likely to use alcohol to cope with chronic pain problems than females. Recently, a new conceptualization has emerged, proposing that the negative affective component of pain drives and maintains alcohol‐related behaviors. We studied in a longitudinal fashion alterations in alcohol drinking patterns and pain thresholds in a mouse model of chronic neuropathic pain in a sex‐dependent manner. Following partial denervation (spared nerve injury [SNI]), stimulus‐evoked pain responses were measured before chronic alcohol consumption, during drinking, during a deprivation phase, and following an episode of excessive drinking. During the course of alcohol drinking, we observed pronounced sex differences in pain thresholds. Male mice showed a strong increase in pain thresholds, suggesting an analgesic effect induced by alcohol over time, an effect that was not observed in female mice. SNI mice did not differ from sham‐operated controls in baseline alcohol consumption. However, following a deprivation phase and the reintroduction of ethanol, male SNI mice but not female mice showed more pronounced excessive drinking than controls. Finally, we observed decreased central ethanol sensitivity in male SNI mice but not in females. Together with our finding, that ethanol is able to decrease a pain‐induced negative affective memory we come to following conclusion. We propose that a lower sensitivity to the intoxicating effects of alcohol together with the ability of alcohol to reduce the negative affective component of pain may explain the higher co‐occurrence of AUD in male chronic pain patients.

Variation in food resources can result in dramatic fluctuations in the body condition of animals dependent on those resources. Decreases in body mass can disrupt patterns of energy allocation and impose stress, thereby altering immune function. In this study we investigated links between changes in body mass of captive cane toads (Rhinella marina), their circulating white blood cell populations, and their performance in immune assays. Captive toads that lost weight over a 3-month period had increased levels of monocytes and heterophils and reduced levels of eosinophils. Basophil and lymphocyte levels were unrelated to changes in mass. Because individuals that lost mass had higher heterophil levels but stable lymphocyte levels, the ratio of these cell types was also higher, partially consistent with a stress response. Phagocytic ability of whole blood was higher in toads that lost mass, due to increased circulating levels of phagocytic cells. Other measures of immune performance were unrelated to mass change. These results highlight the challenges faced by invasive species as they expand their range into novel environments which may impose substantial seasonal changes in food availability that were not present in the native range. Individuals facing energy restrictions may shift their immune function towards more economical and general avenues of combating pathogens.

Twenty-minute neighbourhoods highlight the importance of well-connected and mixed-used neighbourhoods and communities with proximate access to employment, essential services, public transport, and open spaces. Shorter distances together with re-prioritised public spaces encourage more active transport choices, resulting in public health benefits and reduced environmental pollution. Higher liveability brought about by mixed-use developments enables people to have equitable access to local facilities, amenities, and employment opportunities, promoting vibrancy, social cohesion, and intergenerational connections. The attributes of 20-minute neighbourhoods also combine to create places, that are acknowledged as friendly for all ages, address changing needs across the life course, and provide better support for the ageing population. Furthermore, there are indications that 20-minute neighbourhoods may be more resilient against many of the negative impacts of stringent public health protocols such as those implemented in periods of lockdown during the Covid-19 pandemic. In this article, we evaluate and compare planning policies and practices aimed at establishing 20-minute neighbourhoods in Melbourne (Australia) and Scotland (the UK). Using case studies, we discuss similarities and differences involved in using place-based approaches of 20-minute neighbourhoods to address 21st-century challenges in key areas of health and wellbeing, equity, environmental sustainability, and community resilience.

Public awareness of the alcohol-cancer link is low. Provision of this information could reduce alcohol consumption and related harms. The Spread campaign is a multi-media education campaign implemented in Western Australia to inform people about the carcinogenic properties of alcohol and associated harms. The aims of the present study were to (i) examine attitudinal and behavioural outcomes of the Spread campaign and (ii) identify demographic and drinking status factors associated with enactment of harm-reduction behaviours resulting from exposure.A cross sectional survey of Western Australian drinkers (consumed alcohol at least a few times in the previous 12 months, n = 760) examined campaign recognition, campaign perceptions, and behaviours resulting from campaign exposure. Chi-square analyses and a generalised linear model were used to identify demographic and alcohol-related factors associated with behavioural outcomes.Around two-thirds of respondents recognised the campaign (65%), and of these, 22% reported successfully reducing how often or how much they drank due to seeing the campaign. Three quarters (73%) of all respondents considered the campaign message about the alcohol-cancer link to be believable. Respondents drinking at levels above the Australian guideline were less likely to have positive perceptions of the campaign than those complying with the guideline, but were more likely to report enacting the assessed harm-reduction behaviours as a result of campaign exposure.The results suggest that provision of information about the alcohol-cancer link has the potential to motivate reduced alcohol consumption. Implementing such campaigns could constitute an effective alcohol harm-reduction strategy.

Bark is frequently used in southern African traditional medicine to treat inflammation, yet it remains to be rigorously examined for its immunological and anti-inflammatory activity.Barks obtained from ten important and popular southern Africa plants were evaluated for their anti-inflammatory and immunomodulatory properties against the secretion of some pro-inflammatory cytokines (interleukin (IL)-1β, IL-6, tumour necrosis factor-α (TNF-α), and interferon-gamma (IFN-γ) as well as chemokines (monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein (MIP)-2) in murine RAW 264.7 macrophages.The inhibitory effects of aqueous and ethanol extracts were determined using cytokine multiplex-bead assays in lipopolysaccharide (LPS)-stimulated and unstimulated RAW 264.7 cells.Overall, the ethanol extracts were more potent cytokine inhibitors compared to the aqueous extracts. The LPS-stimulated cells treated with the ethanol extracts of Erythrina lysistemon Hutch., Pterocelastrus rostratus Walp. Syzygium cordatum Hochst. ex Krauss and Warburgia salutaris (G. Bertol.) Chiov., demonstrated significant (p < 0.005) inhibition up to 85% of IL-1β, IL-6, and TNF-α secretion compared to the LPS control. Additionally, P. rostratus and S. cordatum aqueous bark extracts substantially decreased the secretion of all the tested cytokines and chemokines. Chemical investigation of the S. cordatum extract resulted in the identification of four ellagic acid derivatives: ellagic acid 4-O-α-rhamnopyranoside (1), ellagic acid 4-O-α-4″-acetylrhamnopyranoside (2), 3-O-methylellagic acid 4'-O-α-3″-O-acetylrhamnopyranoside (3) and 3-O-methylellagic acid 4'-O-α-4″-O-acetylrhamnopyranoside (4), along with mixtures of ellagic acid 4-O-α-2″-acetylrhamnopyranoside (5), ellagic acid 4-O-α-3″-acetylrhamnopyranoside (6) and ellagic acid (7). Their structures were confirmed by mass spectrometry, NMR spectroscopy, and comparison with data from literature.The cytokine inhibition properties of most of the medicinal plants screened herein are reported for the first time. Our results provide insights into the mechanism of action by which the selected southern African medicinal plants regulate inflammation.

Neuroimaging studies have demonstrated gray matter (GM) volume abnormalities in substance users. While the majority of substance users are polysubstance users, very little is known about the relation between GM volume abnormalities and polysubstance use.In this study we assessed the relation between GM volume, and the use of alcohol, tobacco, cocaine and cannabis as well as the total number of substances used, in a sample of 169 males: 15 non-substance users, 89 moderate drinkers, 27 moderate drinkers who also smoke tobacco, 13 moderate drinkers who also smoke tobacco and use cocaine, 10 heavy drinkers who smoke tobacco and use cocaine and 15 heavy drinkers who smoke tobacco, cannabis and use cocaine.Regression analyses showed that there was a negative relation between the number of substances used and volume of the dorsal medial prefrontal cortex (mPFC) and the ventral mPFC. Without controlling for the use of other substances, the volume of the dorsal mPFC was negatively associated with the use of alcohol, tobacco, and cocaine. After controlling for the use of other substances, a negative relation was found between tobacco and cocaine and volume of the thalami and ventrolateral PFC, respectively.These findings indicate that mPFC alterations may not be substance-specific, but rather related to the number of substances used, whereas, thalamic and ventrolateral PFC pathology is specifically associated with tobacco and cocaine use, respectively. These findings are important, as the differential alterations in GM volume may underlie different cognitive deficits associated with substance use disorders.

Our previous studies showed that prenatal ethanol exposure (PEE) elevated blood total cholesterol (TCH) level in adult offspring rats. This study was aimed at elucidating the intrauterine programming mechanism of hypercholesterolemia in adult rats induced by PEE. Pregnant Wistar rats were intragastrically administered ethanol (4 mg/kg∙d) from gestational day (GD) 9 to 20. The offspring rats were euthanized at GD20 and postnatal week 24. Results showed that PEE decreased serum TCH and HDL-C levels (female and male) as well as LDL-C level (female only) in fetal rats but increased serum TCH level and the TCH/HDL-C and LDL-C/HDL-C ratios in adult rats. Furthermore, PEE elevated serum corticosterone levels but inhibited hepatic insulin-like growth factor 1 (IGF1) signaling pathway, cholesterol synthesis and output in fetal rats. The conversed changes were observed in adult rats. Moreover, histone acetylation (H3K9ac and H3K14ac) and expression of hepatic reverse cholesterol transport (RCT) related genes, scavenger receptor BI and low-density lipoprotein receptor were decreased before and after birth by PEE. In HepG2 cells, cortisol negatively regulated the IGF1 signaling pathway and cholesterol metabolic genes, but this inhibition of the cholesterol metabolic genes could be reversed by glucocorticoid receptor antagonist RU486, whereas exogenous IGF1 treatment only reversed the downregulation of RCT genes by cortisol. We confirmed a "two programming" mechanism for PEE-induced hypercholesterolemia in adult rats. The "first programming" was a glucocorticoid (GC)-induced persistent reduction of RCT genes by epigenetic modifications, and the "second programming" was the negative regulation of cholesterol synthesis and output by the GC-IGF1 axis.