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The purpose of this study was to investigate the influence of increasing sulfate concentrations on chromium removal, to evaluate the effect of the presence of Cr(VI) on sulfate removal by Streptomyces sp. MC1 and to analyze the differential protein expression profile in the presence of this metal for the identification of proteins repressed or overexpressed. In the presence of Cr(VI) but in the absence of sulfate ions, bacterial growth was negligible, showing the Cr(VI) toxicity for this bacterium. However, the sulfate presence stimulated bacterium growth and Cr(VI) removal, regardless of its concentrations. Streptomyces sp. MC1 showed ability to remove chromium and sulfate simultaneously. Also, the sulfate presence favored the decrease of total chromium concentration from supernatants reaching a decrease of 50% at 48 h. In presence of chromium, seven proteins were down‐expressed and showed homology to proteins involved in protein biosynthesis, energy production and free radicals detoxification while two proteins involved in oxidation‐reduction processes identified as dihydrolipoamide dehydrogenase and S‐adenosyl‐l‐methionine synthase were overexpressed.

The COVID-19 pandemic has tremendously affected the whole of human society worldwide. Travel patterns have greatly changed due to the increased risk perception and the governmental interventions regarding COVID-19. This study aimed to identify contributing factors to the changes in public and private transportation mode choice behavior in China after COVID-19 based on an online questionnaire survey. In the survey, travel behaviors in three periods were studied: before the outbreak (before 27 December 2019), the peak (from 20 January to 17 March 2020), and after the peak (from 18 March to the date of the survey). A series of random-parameter bivariate Probit models was developed to quantify the relationship between individual characteristics and the changes in travel mode choice. The key findings indicated that individual sociodemographic characteristics (e.g., gender, age, ownership, occupation, residence) have significant effects on the changes in mode choice behavior. Other key findings included (1) a higher propensity to use a taxi after the peak compared to urban public transportation (i.e., bus and subway); (2) a significant impact of age on the switch from public transit to private car and two-wheelers; (3) more obvious changes in private car and public transportation modes in more developed cities. The findings from this study are expected to be useful for establishing partial and resilient policies and ensuring sustainable mobility and travel equality in the post-pandemic era.

Hepatic steatosis is a key initiating event in the pathogenesis of alcohol-associated liver disease (ALD), the most detrimental organ damage resulting from alcohol use disorder. However, the mechanisms by which alcohol induces steatosis remain incompletely understood. We have previously found that alcohol binging impairs brain insulin action, resulting in increased adipose tissue lipolysis by unrestraining sympathetic nervous system (SNS) outflow. Here, we examined whether an impaired brain-SNS-adipose tissue axis drives hepatic steatosis through unrestrained adipose tissue lipolysis and increased lipid flux to the liver.We examined the role of lipolysis, and the brain-SNS-adipose tissue axis and stress in alcohol induced hepatic triglyceride accumulation in a series of rodent models: pharmacological inhibition of the negative regulator of insulin signaling protein-tyrosine phosphatase 1β (PTP1b) in the rat brain, tyrosine hydroxylase (TH) knockout mice as a pharmacogenetic model of sympathectomy, adipocyte specific adipose triglyceride lipase (ATGL) knockout mice, wildtype (WT) mice treated with β3 adrenergic agonist or undergoing restraint stress.Intracerebral administration of a PTP1b inhibitor, inhibition of adipose tissue lipolysis and reduction of sympathetic outflow ameliorated alcohol induced steatosis. Conversely, induction of adipose tissue lipolysis through β3 adrenergic agonism or by restraint stress worsened alcohol induced steatosis.Brain insulin resistance through upregulation of PTP1b, increased sympathetic activity, and unrestrained adipose tissue lipolysis are key drivers of alcoholic steatosis. Targeting these drivers of steatosis may provide effective therapeutic strategies to ameliorate ALD.

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.

ABSTRACTPrenatal ethanol exposure causes a variety of cognitive deficits that have a persistent impact on quality of life, some of which may be explained by ethanol-induced alterations in interneuron function. Studies from several laboratories, including our own, have demonstrated that a single binge-like ethanol exposure during the equivalent to the third trimester of human pregnancy leads to acute apoptosis and long-term loss of interneurons in the rodent retrosplenial cortex (RSC). The RSC is interconnected with the hippocampus, thalamus, and other neocortical regions and plays distinct roles in visuospatial processing and storage, as well as retrieval of hippocampal-dependent episodic memories. Here we used slice electrophysiology to characterize the acute effects of ethanol on GABAergic neurotransmission in the RSC of neonatal mice, as well as the long-term effects of neonatal ethanol exposure on parvalbumin-interneuron mediated neurotransmission in adolescent mice. Mice were exposed to ethanol using vapor inhalation chambers. In postnatal day (P) 7 mouse pups, ethanol unexpectedly failed to potentiate GABAAreceptor-mediated synaptic transmission. Binge-like ethanol exposure of P7 mice expressing channel rhodopsin in parvalbumin-positive interneurons enhanced the peak amplitudes, asynchronous activity and total charge, while decreasing the rise-times of optically-evoked GABAAreceptor-mediated inhibitory postsynaptic currents in adolescent animals. These effects could partially explain the learning and memory deficits that have been documented in adolescent and young adult mice exposed to ethanol during the third trimester-equivalent developmental period.

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.

Nearly three billion people in low- and middle-income countries (LMICs) rely on polluting fuels, resulting in millions of avoidable deaths annually. Polluting fuels also emit short-lived climate forcers and greenhouse gases (GHGs). Liquefied petroleum gas (LPG) and grid-based electricity are scalable alternatives to polluting fuels but have raised climate and health concerns. Here, we compare emissions and climate impacts of a business-as-usual household cooking fuel trajectory to four large-scale transitions to gas and/or grid electricity in 77 LMICs. We account for upstream and end-use emissions from gas and electric cooking, assuming electrical grids evolve according to the 2022 World Energy Outlook’s “Stated Policies” Scenario. We input the emissions into a reduced-complexity climate model to estimate radiative forcing and temperature changes associated with each scenario. We find full transitions to LPG and/or electricity decrease emissions from both well-mixed GHG and short-lived climate forcers, resulting in a roughly 5 millikelvin global temperature reduction by 2040. Transitions to LPG and/or electricity also reduce annual emissions of PM2.5 by over 6 Mt (99%) by 2040, which would substantially lower health risks from Household Air Pollution. Primary input data was collected from the following sources: Baseline household fuel choices - WHO household energy database (https://www.nature.com/articles/s41467-021-26036-x) End-use emissions - US EPA lifecycle assessment of household fuels (https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=339679&Lab=NRMRL&simplesearch=0&showcriteria=2&sortby=pubDate&timstype=Published+Report&datebeginpublishedpresented) Upstream emissions - Argonne National Labs GREET Model (https://greet.es.anl.gov/index.php) Current and future population estimates - UNECA (http://data.un.org/Explorer.aspx?d=EDATA) Input data was processed by defining household fuel choice scenarios, estimating national household fuel consumption based on these scenarios, and applying fuel-specific emission factors to create country-specific emission pathways. These emission pathways were input into the FaIR model (https://zenodo.org/record/5513022#.Yt_jfHbMLb0) which generated additional data for each scenario including time series of pollution concentrations, radiative forcing, and temperature changes. All data is provided in CSV format. Nothing proprietary is required.