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Simple Summary: Microbial communities living at a depth of 450 m in a granitoid massif (Krasnoyarsk Krai, Russia), potentially suitable for the construction of a radioactive waste storage facility, were studied. It has been established that their activation by organic matter, molecular hydrogen, can cause copper corrosion, which is significantly accelerated in the presence of sulfate ions. Microbial biofilms including sulfate-reducing and fermentative bacteria are resistant to copper ions and can reduce their toxicity during the formation of sulfide minerals. This paper presents the results of microbial corrosion tests on M0-grade copper under conditions simulating a geological repository for radioactive waste at the Yeniseisky site (Krasnoyarsk Krai, Russia). The work used a microbial community sampled from a depth of 450 m and stimulated with glucose, hydrogen and sulfate under anaerobic conditions. It was shown that the maximum corrosion rate, reaching 9.8 µm/y, was achieved with the addition of sulfate (1 g/L) with the participation of microorganisms from the families Desulfomicrobiaceae, Desulfovibrionaceae and Desulfuromonadaceae. It was noted that the most important factor leading to copper corrosion was the accumulation of hydrogen sulfide during the activation of sulfate-reducing microorganisms of the genera Desulfomicrobium, Desulfovibrio and Desulfuromonas. During the development of the microbial community under these conditions, the content of copper can have a significant toxic effect at a concentration of more than 250 mg/L. [ABSTRACT FROM AUTHOR]

Macrophages play a key role in ozone-induced lung injury by regulating both the initiation and resolution of inflammation. These distinct activities are mediated by pro-inflammatory and anti-inflammatory/proresolution macrophages which sequentially accumulate in injured tissues. Macrophage activation is dependent, in part, on intracellular metabolism. Herein, we used RNA-sequencing (seq) to identify signaling pathways regulating macrophage immunometabolic activity following exposure of mice to ozone (0.8 ppm, 3 h) or air control. Analysis of lung macrophages using an Agilent Seahorse showed that inhalation of ozone increased macrophage glycolytic activity and oxidative phosphorylation at 24 and 72 h post-exposure. An increase in the percentage of macrophages in S phase of the cell cycle was observed 24 h post ozone. RNA-seq revealed significant enrichment of pathways involved in innate immune signaling and cytokine production among differentially expressed genes at both 24 and 72 h after ozone, whereas pathways involved in cell cycle regulation were upregulated at 24 h and intracellular metabolism at 72 h. An interaction network analysis identified tumor suppressor 53 (TP53), E2F family of transcription factors (E2Fs), cyclin-dependent kinase inhibitor 1A (CDKN1a/p21), and cyclin D1 (CCND1) as upstream regulators of cell cycle pathways at 24 h and TP53, nuclear receptor subfamily 4 group a member 1 (NR4A1/Nur77), and estrogen receptor alpha (ESR1/ERα) as central upstream regulators of mitochondrial respiration pathways at 72 h. To assess whether ERα regulates metabolic activity, we used ERα−/− mice. In both air and ozone-exposed mice, loss of ERα resulted in increases in glycolytic capacity and glycolytic reserve in lung macrophages with no effect on mitochondrial oxidative phosphorylation. Taken together, these results highlight the complex interaction between cell cycle, intracellular metabolism, and macrophage activation which may be important in the initiation and resolution of inflammation following ozone exposure. [ABSTRACT FROM AUTHOR]

Recent studies have identified exposure to environmental levels of ozone as a risk factor for the development of acute respiratory distress syndrome (ARDS), a severe form of acute lung injury (ALI) that can develop in humans with sepsis. The aim of this study was to develop a murine model of ALI to mechanistically explore the impact of ozone exposure on ARDS development. Mice were exposed to ozone (0.8 ppm, 3 h) or air control followed 24 h later by intravenous administration of 3 mg/kg lipopolysaccharide (LPS) or PBS. Exposure of mice to ozone + LPS caused alveolar hyperplasia; increased BAL levels of albumin, IgM, phospholipids, and proinflammatory mediators including surfactant protein D and soluble receptor for advanced glycation end products were also detected in BAL, along with markers of oxidative and nitrosative stress. Administration of ozone + LPS resulted in an increase in neutrophils and anti-inflammatory macrophages in the lung, with no effects on proinflammatory macrophages. Conversely, the numbers of resident alveolar macrophages decreased after ozone + LPS; however, expression of Nos2 , Arg1 , Cxcl1 , Cxcl2 , Ccl2 by these cells increased, indicating that they are activated. These findings demonstrate that ozone sensitizes the lung to respond to endotoxin, resulting in ALI, oxidative stress, and exacerbated pulmonary inflammation, and provide support for the epidemiologic association between ozone exposure and ARDS incidence. [ABSTRACT FROM AUTHOR]

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Copyright of Brazilian Journal of Law & International Relations / Relações Internacionais no Mundo is the property of Relacoes Internacionais no Mundo and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The tree has long been incorporated into human culture and is interpreted as compatible with a human being as a result of the man’ cognizing the world. Thus, the tree (and its elements) is used as a source of metaphor for describing all the spheres and domains of human activity. The prerequisites for the man-tree metaphor are the qualities of man and tree which can be matched: the physical configuration of the tree and the human body, which is vertically directed; local relations between trees and human relations; the visual image of the tree and the family tree concept. The cultural concept of the tree is implicit in personal names and idioms as lexical units. It manifests itself in the context of folklore texts (rhymes, ballads, verbalized superstitions, incantations, riddles) and classical works of fiction. The man-tree metaphor reflects the ancient ideas about man-tree kinship and man-tree isomorphism. The metaphorical transfer is reciprocal: the man can be endowed with the qualities of the tree, the tree can be endowed with the qualities of the man. The man-tree / tree-man metaphor is based both on the generic concept of the tree and its elements and on the concept of individual trees. The man-tree metaphors are verbalized through nouns (functions and status), verbs (activities), adjectives (qualities).

The Russian lexemes « dame » and « lady » which were borrowed from European languages to designate wealthy, educated and high society women became assimilated in the Russian language and culture. The words gave rise to culture-oriented colocations (кaвaлерственaя дaмa/ chivalry dame), and developed new connotations, which the lexeme «женщинa»/ woman does not have. In addition to neutral and positive connotations (“истиннaя леди”/ true lady), the lexemes acquired negative connotations like “дaмa полусветa”/ demimondaine dame, which indicate to the woman’s inferior social status (полковaя дaмa/ regimental dame), highlight women’s weaknesses not inherent to men (aвтоледи/ auto lady), and stereotypical ideas of women’s low intellect (дaмский ромaн/ love story). The inherent and adherent connotations of the lexemes «дaмa»/ dame and «леди»/ lady revealed through analysis are based on traditional stereotypical ideas about women’s social roles and imply evaluation of the woman’s performance in traditionally male spheres. Thereby, acquisition of negative and ironic connotations by the lexemes is conditioned in society denying women’s new functions and roles from feminist perspective.

Exposure to ozone causes decrements in pulmonary function, a response associated with alterations in lung lipids. Pulmonary lipid homeostasis is dependent on the activity of peroxisome proliferator activated receptor gamma (PPARγ), a nuclear receptor that regulates lipid uptake and catabolism by alveolar macrophages (AMs). Herein, we assessed the role of PPARγ in ozone-induced dyslipidemia and aberrant lung function in mice. Exposure of mice to ozone (0.8 ppm, 3 h) resulted in a significant reduction in lung hysteresivity at 72 h post exposure; this correlated with increases in levels of total phospholipids, specifically cholesteryl esters, ceramides, phosphatidylcholines, phosphorylethanolamines, sphingomyelins, and di- and triacylglycerols in lung lining fluid. This was accompanied by a reduction in relative surfactant protein-B (SP-B) content, consistent with surfactant dysfunction. Administration of the PPARγ agonist, rosiglitazone (5 mg/kg/day, i.p.) reduced total lung lipids, increased relative amounts of SP-B, and normalized pulmonary function in ozone-exposed mice. This was associated with increases in lung macrophage expression of CD36, a scavenger receptor important in lipid uptake and a transcriptional target of PPARγ. These findings highlight the role of alveolar lipids as regulators of surfactant activity and pulmonary function following ozone exposure and suggest that targeting lipid uptake by lung macrophages may be an efficacious approach for treating altered respiratory mechanics. [ABSTRACT FROM AUTHOR]

Two groups of facts have been established in previous drug development studies of the non-benzodiazepine anxiolytic fabomotizole. First, fabomotizole prevents stress-induced decrease in binding ability of the GABAA receptor's benzodiazepine site. Second, fabomotizole is a Sigma1R chaperone agonist, and exposure to Sigma1R antagonists blocks its anxiolytic effect. To prove our main hypothesis of Sigma1R involvement in GABAA receptor-dependent pharmacological effects, we performed a series of experiments on BALB/c and ICR mice using Sigma1R ligands to study anxiolytic effects of benzodiazepine tranquilizers diazepam (1 mg/kg i.p.) and phenazepam (0.1 mg/kg i.p.) in the elevated plus maze test, the anticonvulsant effects of diazepam (1 mg/kg i.p.) in the pentylenetetrazole-induced seizure model, and the hypnotic effects of pentobarbital (50 mg/kg i.p.). Sigma1R antagonists BD-1047 (1, 10, and 20 mg/kg i.p.), NE-100 (1 and 3 mg/kg i.p.), and Sigma1R agonist PRE-084 (1, 5, and 20 mg/kg i.p.) were used in the experiments. Sigma1R antagonists have been found to attenuate while Sigma1R agonists can enhance GABAARs-dependent pharmacological effects. [ABSTRACT FROM AUTHOR]