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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.

Each of 4 male alcoholic subjects received 0.7 mg/kg calcium carbimide (CC) orally 12 hr before ingestion of 0.25 gm/kg ethanol on 3 separate occasions. The CC-ethanol interaction consisted of increased blood acetaldehyde level and elevated heart rate. For each individual there was small variability in the area under the curve (AUC) values of the blood ethanol level--time course profiles for the 3 experiments, indicating a consistent extent of ethanol absorption. For subjects 1, 2, and 3 there was appreciable intraindividual variability in the AUC and the peak blood acetaldehyde levels of the blood acetaldehyde level--time course curves; the variation in these parameters was small for subjects 4. The intraindividual variability in the peak heart rate response was small for subjects 1 and 2 and appreciable for subjects 3 and 4. Regression analysis of the blood acetaldehyde level--heart rate data for each of the 3 experiments conducted on the 4 subjects revealed that there were positive, linear correlations. There was appreciable intraindividual variability in the slope values for the 3 experiments. The results of this study, conducted on 4 male alcoholics, suggest that for other alcoholic subjects there could be appreciable intraindividual variability in the intensity of the CC-ethanol interaction.

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.

Background:  We previously found that activation of the glial cell line‐derived neurotrophic factor (GDNF) pathway in the ventral tegmental area (VTA) reduces ethanol‐drinking behaviors. In this study, we set out to assess the contribution of endogenous GDNF or its receptor GFRα1 to the regulation of ethanol‐related behaviors.Methods:  GDNF and GFRα1 heterozygote mice (HET) and their wild‐type littermate controls (WT) were used for the studies. Ethanol‐induced hyperlocomotion, sensitization, and conditioned place preference (CPP), as well as ethanol consumption before and after a period of abstinence were evaluated. Blood ethanol concentration (BEC) was also measured.Results:  We observed no differences between the GDNF HET and WT mice in the level of locomotor activity or in sensitization to ethanol‐induced hyperlocomotion after systemic injection of a nonhypnotic dose of ethanol and in BEC. However, GDNF and GFRα1 mice exhibited increased place preference to ethanol as compared with their WT littermates. The levels of voluntary ethanol or quinine consumption were similar in the GDNF HET and WT mice, however, a small but significant increase in saccharin intake was observed in the GDNF HET mice. No changes were detected in voluntary ethanol, saccharin or quinine consumption of GFRα1 HET mice as compared with their WT littermates. Interestingly, however, both the GDNF and GFRα1 HET mice consumed much larger quantities of ethanol after a period of abstinence from ethanol as compared with their WT littermates. Furthermore, the increase in ethanol consumption after abstinence was found to be specific for ethanol as similar levels of saccharin intake were measured in the GDNF and GFRα1 HET and WT mice after abstinence.Conclusions:  Our results suggest that endogenous GDNF negatively regulates the rewarding effect of ethanol and ethanol‐drinking behaviors after a period of abstinence.

To discuss current evidence of global climate change and its implications for allergic rhinitis and other allergic respiratory diseases.Global climate change is evidenced by increasing average earth temperature, increasing anthropogenic greenhouse gas levels, and elevated pollen levels. Pollutants of interest include carbon dioxide (CO2), ozone (O3), and nitrous oxide (NO2) because they can enhance the allergic response and lead to increased symptoms of allergic respiratory diseases. Heightened CO2 levels stimulate pollen production via photosynthesis and increased growth in multiple plant species investigated. Although worsened air quality appears to increase prevalence of allergic rhinitis, the effects of increased temperature are less certain. The findings of increased aeroallergen levels likely contribute to increases in presentation of allergic diseases, although more healthcare impact studies are necessary.Although recent literature indicates and strongly supports changes in temperature, pollution levels, and aeroallergen levels, more longitudinal epidemiologic surveillance of allergic diseases in relation to climate change as well as pathophysiologic studies on changing aeroallergen effects on allergic diseases are needed.

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.