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In recent years, research has witnessed an increasing interest in the bidirectional relationship between emotion and sleep. Sleep seems important for restoring daily functioning, whereas deprivation of sleep makes us more emotionally aroused and sensitive to stressful stimuli and events. Sleep appears to be essential to our ability to cope with emotional stress in everyday life. However, when daily stress is insufficiently regulated, it may result in mental health problems and sleep disturbances too. Not only does emotion impact sleep, but there is also evidence that sleep plays a key role in regulating emotion. Emotional events during waking hours affect sleep, and the quality and amount of sleep influences the way we react to these events impacting our general well-being. Although we know that daytime emotional stress affects sleep by influencing sleep physiology, dream patterns, dream content and the emotion within a dream, its exact role is still unclear. Other effects that have been found are the exaggeration of the startle response, decrease in dream recall and elevation of awakening thresholds from rapid eye movement (REM), REM-sleep, increased or decreased latency to REM-sleep, increase in percentage of REM-density, REM-sleep duration, as well as the occurrence of arousals in sleep as a marker of sleep disruption. Equally, the way an individual copes with emotional stress, or the way in which an individual regulates emotion may modulate the effects of emotional stress on sleep. The research presented here supports the idea that adaptive emotion regulation benefits our follow-up sleep. We thus conclude the current review with a call for future research in order to clarify further the precise relationship between sleep, emotion and emotion regulation, as well as to explain further how sleep dissolves our emotional stress.

Background Excesses of antibiotic resistance genes (ARGs), which are regarded as emerging environmental pollutants, have been observed in various environments. The incidence of ARGs in drinking water causes potential risks to human health and receives more attention from the public. However, ARGs harbored in drinking water remain largely unexplored. In this study, we aimed at establishing an antibiotic resistome catalogue in drinking water samples from a wide range of regions and to explore the potential hosts of ARGs. Results A catalogue of antibiotic resistome in drinking water was established, and the host-tracking of ARGs was conducted through a large-scale survey using metagenomic approach. The drinking water samples were collected at the point of use in 25 cities in mainland China, Hong Kong, Macau, Taiwan, South Africa, Singapore and the USA. In total, 181 ARG subtypes belonging to 16 ARG types were detected with an abundance range of 2.8 × 10 −2 to 4.2 × 10 −1 copies of ARG per cell. The highest abundance was found in northern China (Henan Province). Bacitracin, multidrug, aminoglycoside, sulfonamide, and beta-lactam resistance genes were dominant in drinking water. Of the drinking water samples tested, 84% had a higher ARG abundance than typical environmental ecosystems of sediment and soil. Metagenomic assembly-based host-tracking analysis identified Acidovorax , Acinetobacter , Aeromonas , Methylobacterium , Methyloversatilis , Mycobacterium , Polaromonas , and Pseudomonas as the hosts of ARGs. Moreover, potential horizontal transfer of ARGs in drinking water systems was proposed by network and Procrustes analyses. Conclusions The antibiotic resistome catalogue compiled using a large-scale survey provides a useful reference for future studies on the global surveillance and risk management of ARGs in drinking water. Graphical abstract .

Several recent studies have shown the presence of genes for the key enzyme associated with archaeal methane/alkane metabolism, methyl-coenzyme M reductase (Mcr), in metagenome-assembled genomes (MAGs) divergent to existing archaeal lineages. Here, we study the mcr -containing archaeal MAGs from several hot springs, which reveal further expansion in the diversity of archaeal organisms performing methane/alkane metabolism. Significantly, an MAG basal to organisms from the phylum Thaumarchaeota that contains mcr genes, but not those for ammonia oxidation or aerobic metabolism, is identified. Together, our phylogenetic analyses and ancestral state reconstructions suggest a mostly vertical evolution of mcrABG genes among methanogens and methanotrophs, along with frequent horizontal gene transfer of mcr genes between alkanotrophs. Analysis of all mcr -containing archaeal MAGs/genomes suggests a hydrothermal origin for these microorganisms based on optimal growth temperature predictions. These results also suggest methane/alkane oxidation or methanogenesis at high temperature likely existed in a common archaeal ancestor. Methane metabolism by some lineages of Archaea contributes to the cycling of carbon on Earth. Here, the authors show high diversity of methyl-coenzyme M reductase (Mcr), a key enzyme associated with archaeal methane/alkane metabolism, in hot spring Archaea, and investigate their ecological roles and evolution.

In this study, a new type of field-effect transistor (FET)-based biosensor is demonstrated to be able to overcome the problem of severe charge-screening effect caused by high ionic strength in solution and detect proteins in physiological environment. Antibody or aptamer-immobilized AlGaN/GaN high electron mobility transistors (HEMTs) are used to directly detect proteins, including HIV-1 RT, CEA, NT-proBNP and CRP, in 1X PBS (with 1%BSA) or human sera. The samples do not need any dilution or washing process to reduce the ionic strength. The sensor shows high sensitivity and the detection takes only 5 minutes. The designs of the sensor, the methodology of the measurement, and the working mechanism of the sensor are discussed and investigated. A theoretical model is proposed based on the finding of the experiments. This sensor is promising for point-of-care, home healthcare, and mobile diagnostic device.

Chromium, one of the top five toxic heavy metals ranked according to significance in public health by WHO, exists as Cr(III) which is naturally occurring or Cr(VI) which is anthropogenic in origin. The EPA specifies the maximum contaminant level in drinking water to be 10−6 M or 0.1 mg/L or 100 ppb for the total dissolved Cr. To ensure the water consumed by the population has these pollutants below the safe threshold, this report demonstrates a field effect transistor (FET) based sensor design incorporating a highly target specific ion-selective membrane combined with extended gate technology which manifests sensitivity exceeding the Nernst limit aided by the high field effect in the short gap region of extended gate technology. Characterization and repeated testing of the portable device revealed a commendable calibration sensitivity of 99 mV/log [Cr3+] and 71 mV/log [Cr6+] for Cr(III) and Cr(VI) respectively, well surpassing the Nernst limits of sensitivity and offering a detection limit lower than ion-selective electrodes (10−6 M), and comparable to the expensive benchtop laboratory instrument, ICP-MS. This report presents a robust, easy to fabricate, economic and efficient handheld biosensor to detect the chromium in a liquid sample whether it exists as Cr(III) or Cr(VI).

Abstract Background Thrombomodulin (TM) exerts anticoagulant and anti-inflammatory effects to improve the survival of patients with septic shock. Heat stroke resembles septic shock in many aspects. We tested whether TM would improve cognitive deficits and related causative factors in heat-stressed (HS) mice. Methods Adult male mice were exposed to HS (33°C for 2 hours daily for 7 consecutive days) to induce cognitive deficits. Recombinant human soluble TM (1 mg/kg, i.p.) was administered immediately after the first HS trial and then once daily for 7 consecutive days. We performed the Y-maze, novel objective recognition, and passive avoidance tests to evaluate cognitive function. Plasma levels of lipopolysaccharide (LPS), high-mobility group box 1 (HMGB1), coagulation parameters, and both plasma and tissue levels of inflammatory and oxidative stress markers were biochemically measured. The duodenum and hippocampus sections were immunohistochemically stained. The intestinal and blood-brain barrier permeability were determined. Results Compared with controls, HS mice treated with TM had lesser extents of cognitive deficits, exacerbated stress reactions, gut barrier disruption, endotoxemia, blood-brain barrier disruption, and inflammatory, oxidative, and coagulatory injury to heart, duodenum, and hippocampal tissues, and increased plasma HMGB1. In addition to reducing cognitive deficits, TM therapy alleviated all the abovementioned complications in heat-stressed mice. Conclusions The findings suggest that HS can lead to exacerbated stress reactions, endotoxemia, gut barrier disruption, blood-brain barrier disruption, hippocampal inflammation, coagulopathy, and oxidative stress, which may act as causative factors for cognitive deficits. TM, an anti-inflammatory, antioxidant, and anti-coagulatory agent, inhibited heat stress-induced cognitive deficits in mice.

Gut microbiota dysbiosis has been implicated in rheumatoid arthritis (RA) and influences disease progression. Although molecular and culture‐independent studies revealed RA patients harbored a core microbiome and had characteristic bacterial species, the lack of cultured bacterial strains had limited investigations on their functions. This study aimed to establish an RA‐originated gut microbial biobank (RAGMB) that covers and further to correlates and validates core microbial species on clinically used and diagnostic inflammation and immune indices. We obtained 3200 bacterial isolates from fecal samples of 20 RA patients with seven improved and 11 traditional bacterial cultivation methods. These isolates were phylogenetically identified and selected for RAGMB. The RAGMB harbored 601 bacterial strains that represented 280 species (including 43 novel species) of seven bacterial phyla. The RAGMB covered 93.2% at species level of medium‐ and high‐abundant (relative abundances ≥0.2%) RA gut microbes, and included four rare species of the phylum Synergistota. The RA core gut microbiome was defined and composed of 20 bacterial species. Among these, Mediterraneibacter tenuis and Eubacterium rectale were two species that statistically and significantly correlated with clinically used diagnostic indices such as erythrocyte sedimentation rate (ESR) and IL‐10. Thus, M. tenuis and E. rectale were selected for experimental validation using DSS‐treated and not DSS‐treated mice model. Results demonstrated both M. tenuis and E. rectale exacerbated host inflammatory responses, including shortened colon length and increased spleen weight, decreased IL‐10 and increased IL‐17A levels in plasma. Overall, we established the RAGMB, defined the RA core microbiome, correlated and demonstrated core microbial species effected on host inflammatory and immune responses. This work provides diverse gut microbial resources for future studies on RA etiology and potential new targets for new biomedical practices. Intensive collection of 3200 bacterial isolates from fecal samples of newly diagnosed rheumatoid arthritis (RA) patients resulted in an RA‐originated gut microbial biobank (RAGMB). This RAGMB has 601 strains that represent 280 bacterial species (including 43 novel species), and covers 93.2% of medium‐ and high‐abundant gut microbial species of the RA fecal samples. By integrating additional RA cohort metagenomic data, an RA core microbiome composing of 20 core microbial species were defined and correlated to RA clinical indices. Two RA core microbial species, Mediterraneibacter tenuis and Eubacterium rectale, were selected for experimental validation with mouse models and the results showed that both M. tenuis and E. rectale exacerbated host inflammatory and immune responses. Highlights An rheumatoid arthritis (RA)‐originated gut microbial biobank (RAGMB) was established, comprising 601 bacterial strains representing 280 species (including 43 novel species) across seven bacterial phyla. RAGMB covers 93.2% of medium‐ and high‐abundant RA gut microbe species from isolated samples. The RA core microbiome consists of 20 bacterial species, with Mediterraneibacter tenuis and Eubacterium rectale showing significant correlations with clinical indices such as ESR and IL‐10. RA core species Mediterraneibacter tenuis and Eubacterium rectale exacerbate inflammatory responses, including shortened colon length, enlarged spleen and altered plasma cytokine levels.

Introduction Postoperative delirium (POD) is a common postoperative complication and is associated with numerous adverse outcomes. Advanced age and hip surgery are high risk factors for POD. Both remimazolam tosilate for injection and sevoflurane can be used as sedatives for the maintenance of general anesthesia, but the comparison of their impacts on the incidence of POD has not been reported. This study aims to compare the effect of remimazolam tosilate vernus sevoflurane on the incidence of POD in older patients undergoing total hip arthroplasty. Methods and analysis This is a two-arm, parallel, prospective, multicenter, randomized controlled trial. A total of 456 older patients at six clinical trial centers in China will be randomly assigned in a 1:1 ratio to receive general anesthesia with remimazolam tosilate or sevoflurane as sedative. The primary outcome measure is the prevalence of POD during the first 4 postoperative days. Secondary outcomes include cognitive function [Mini-Mental State Examination (MMSE)], perioperative pain degree [Visual Analogue Scale (VAS)], postoperative nausea and vomiting (PONV) within 4 days after surgery, recovery time after drug withdrawal, the amount of vasoactive drugs used during operation, length of hospital stay, and in-hospital complications. Ethics and dissemination The Research Ethics Committee of Qilu Hospital of Shandong University has approved the study protocol (REF: KYLL-202206-25), which is applicable to all research centers. Participant recruitment begins in August 2022. Written informed consent will be obtained from each patient before randomization. The findings will be published in an international peer-reviewed medical journal. Trial registration The trial has been registered at the Chinese Clinical Trial Registry: ChiCTR2200062455; date of registration: 2022-08-08.

Background In very preterm infants, white matter injury is a prominent brain injury, and hypoxic ischemia (HI) and infection are the two primary pathogenic factors of this injury. Microglia and microvascular endothelial cells closely interact; therefore, a common signaling pathway may cause neuroinflammation and blood–brain barrier (BBB) damage after injury to the immature brain. CXC chemokine ligand 5 (CXCL5) is produced in inflammatory and endothelial cells by various organs in response to insults. CXCL5 levels markedly increased in the amniotic cavity in response to intrauterine infection and preterm birth in clinical studies. The objective of this study is to determine whether CXCL5 signaling is a shared pathway of neuroinflammation and BBB injury that contributes to white matter injury in the immature brain. Methods Postpartum day 2 (P2) rat pups received lipopolysaccharide (LPS) followed by 90-min HI. Immunohistochemical analyses were performed to determine microglial activation, neutrophil infiltration, BBB damage, and myelin basic protein and glial fibrillary acidic protein expression. Immunofluorescence experiments were performed to determine the cellular distribution of CXCL5. Pharmacological tests were performed to inhibit or enhance CXCL5 activity. Results On P2, predominant increases in microglial activation and BBB damage were observed 24 h after LPS-sensitized HI induction, and white matter injury (decreased myelination and increased astrogliosis) was observed on P12 compared with controls. Immunohistochemical analyses revealed increased CXCL5 expression in the white matter 6 and 24 h after insult. Immunofluorescence experiments revealed upregulated CXCL5 expression in the activated microglia and endothelial cells 24 h after insult. CXCL5 inhibition by SB225002, a selective nonpeptide inhibitor of CXCR2, significantly attenuated microglial activation and BBB damage, increased myelination, and reduced astrogliosis in the white matter after LPS-sensitized HI. In addition, CXCL5-sensitized HI or CXCL5 alone significantly induced BBB damage and white matter injury in association with different neuroinflammation mechanisms. CXCL5-sensitized HI-induced microglial activation and neutrophil infiltration, whereas CXCL5 alone predominately caused neutrophil infiltration. Conclusions CXCL5 is a potential biomarker for white matter injury in preterm infants. Pharmacological blockade of CXCL5 signaling that attenuates dysregulated neuroinflammation can be used a therapeutic strategy against white matter injury in the immature brain.

Purpose - The purpose of this paper is to examine the antecedents of, and the relationships between, entrepreneurial opportunity recognition, and individual-level innovation performance.Design methodology approach - Questionnaire data were collected from 268 senior R&D project team members (response rate 64.58 percent) along with 83 R&D managers who evaluated their employees' innovative behaviors in one science park in Taiwan.Findings - The results show that an individual's self-efficacy, prior knowledge, social networks, and perception about the industrial environment on opportunities all had positive effects on entrepreneurial opportunity recognition. Also entrepreneurial opportunity recognition contributed significantly to individual-level innovation performance.Research limitations implications - The findings show that perception about the industrial environment on opportunities variable was the most important predictor among all four of the antecedents of entrepreneurial opportunity recognition. That is, individual characteristics and traits cannot fully explain the entrepreneurial opportunity recognition process. Because the data were limited to high technology industry, future studies need to validate these findings in other industries.Practical implications - Findings of this study suggest that to increase R&D employee's innovation performance, it is critical for high technology firms to invest in developing and enhancing employees' entrepreneurial opportunity recognition ability.Originality value - The process of entrepreneurial opportunity recognition has been viewed as a black box. Although the literature has explored various antecedents that influence entrepreneurial opportunity recognition, there is limited empirical research that has examined the linkage between entrepreneurial opportunity recognition and potential outcome variables.