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Myeloid-derived suppressor cells (MDSCs) are heterogeneous myeloid cell populations with immunosuppressive capacity, which contribute to immune regulation and tolerance induction. We previously reported impaired MDSC function in patients with primary Sjögren’s syndrome (pSS) and mice with experimental SS (ESS). However, the molecular mechanisms underlying MDSCs dysfunction remain largely unclear. In this study, we first found that aryl hydrocarbon receptor (AhR) was highly expressed by human and murine polymorphonuclear MDSCs (PMN-MDSCs). Indole-3-propionic acid (IPA), a natural AhR ligand produced from dietary tryptophan, significantly promoted PMN-MDSC differentiation and their suppressive function on CD4+ T cells. In contrast, feeding tryptophan-free diet resulted in decreased PMN-MDSC response, a phenotype that could be reversed by IPA supplementation. The functional importance of PMN-MDSCs was demonstrated in ESS mice by cell-depletion approach. Notably, AhR expression was reduced in PMN-MDSCs during ESS development, while AhR antagonism resulted in exacerbated ESS pathology and dysregulated T effector cells, which could be phenocopied by tryptophan-free diet. Interferon regulatory factor 4 (IRF4), a repressive transcription factor, was upregulated in PMN-MDSCs during ESS progression. Chromatin immunoprecipitation analysis revealed the binding capacity of IRF4 to the promoter region of AhR, while IRF4 deficiency markedly enhanced AhR-mediated PMN-MDSC responses. Furthermore, dietary supplementation of IPA markedly ameliorated salivary glandular pathology in ESS mice with restored MDSC immunosuppressive function. Together, our results identify a novel function of AhR in modulating PMN-MDSC response and demonstrate the therapeutic potential of targeting AhR for the treatment of pSS.

Consumption of a modern Western-type high-fat low-fiber diet increases the risk of obesity. However, how a host responds to such a diet, especially during the early period of dietary transition from a previous low-fat and fiber-rich diet, remains poorly explored.Wild-type C57BL/6 mice were fed a normal chow diet or a high-fat diet. Enteric glial cell (EGC) activation was detected through quantitative real-time PCR (qRT-PCR), immunoblotting and immunohistology analysis. Fluorocitrate or genetic deletion of glial fibrillary acidic protein (GFAP)-positive glial-intrinsic myeloid differentiation factor 88 (Myd88) was used to inhibit EGC activation, and the effect of a high-fat diet on obesity was further investigated. The role of MYD88-dependent sensing of commensal products in adipocyte was observed to analyze the effect of obesity.A dietary shift from a normal chow diet to a high-fat diet in mice induced a transient early-phase emergence of a GFAP-positive EGC network in the lamina propria of the ileum, accompanied with an increase in glial-derived neurotrophic factor production. Inhibition of glial cell activity blocked this response. GFAP-positive glial Myd88 knockout mice gained less body weight after high-fat diet (HFD) feeding than littermate controls. In contrast, adipocyte deletion of Myd88 in mice had no effect on weight gain but instead exacerbated glucose intolerance. Furthermore, short-term fluorocitrate intervention during HFD feeding attenuated body weight gain.Our findings indicate that EGCs are early responders to intestinal ecosystem changes and the GFAP-positive glial Myd88 signaling participates in regulating obesity.

Propofol is the most commonly used sedative in gastrointestinal endoscopic procedures, but is associated with cardiorespiratory suppression, particularly in elderly patients. Remimazolam is a new short-acting GABA(A) receptor agonist with minimal impact on cardiorespiratory suppression, and may be a viable alternative in elderly patients undergoing endoscopic procedures.This multicenter, randomized controlled trial was conducted between September 2020 and September 2021. Elderly patients (65-85 years of age) scheduled to undergo upper gastrointestinal endoscopy were randomized in 1:1 ratio to receive remimazolam tosilate (300 mg/h) or propofol (3 g/h) in addition to 50-μg fentanyl, until the Modified Observer's Assessment of Alertness/Sedation Scale (MOAA/S) reached ≤1. MOAA/S was maintained at 0 or 1 throughout the procedure using 2.5 mg remimazolam or 0.5 mg/kg propofol boluses in the two groups, respectively. The primary outcome was the rate of hypotension (defined as systolic blood pressure at ≤90 mmHg or 30% decline vs. the baseline). Bradycardia was defined as heart rate ≤50 per minute; respiratory depression was defined as respiratory rate8 per minute and/or SpOA total of 400 patients (161 men and 239 women; 70.4 ± 4.6 years of age) were enrolled (200 patients per group). Average body mass index was 22.2 ± 2.4 kg/mRemimazolam was associated with a lower rate of hypotension in elderly patients undergoing upper gastrointestinal endoscopy under deep sedation/anaesthesia than propofol.

Evidence for transcatheter aortic valve implantation (TAVI) is scarce among patients with non-calcific aortic stenosis, and it is not known whether aortic valve calcification is associated with new cerebral ischemic lesions (CILs) that are detected by diffusion-weighted magnetic resonance imaging. So, our study enrolled 328 patients who underwent transfemoral TAVI using a self-expanding valve between December 2016 and June 2021 from the TORCH registry (NCT02803294). A total of 34 patients were finally confirmed as non-calcific AS and the remaining 294 patients were included in the calcific AS group. Incidence of new CILs (70.6% vs. 85.7%,ip/i= 0.022), number of lesions (2.0 vs. 3.0,ip/i= 0.010), and lesions volume (105.0 mmsup3/supvs. 200.0 mmsup3/sup,ip/i= 0.047) was significantly lower in the non-calcific AS group. However, the maximum and average lesion volumes were comparable between two groups. Non-calcific AS was associated with lower risk for developing new CILs by univariate logistic regression analysis [Odds ratio (OR): 0.040, 95% confident interval (CI): 0.18-0.90,ip/i= 0.026] and multivariate analysis (OR: 0.031, 95% CI: 0.13-0.76,ip/i= 0.010). In summary, non-calcific AS patients had a lower risk of developing new cerebral ischemic infarction after TAVI compared to calcific AS patients. However, new ischemic lesions were still found in over 70% of patients.

The metabolic alterations of amino acid metabolism are closely associated with inflammatory response. However, relatively little is known about the roles of phenylalanine (Phe)/tyrosine (Tyr) catabolites during inflammation. Nitisinone (NTBC) is an orphan drug used to treat hereditary tyrosinemia type I potentially by changing Phe/Tyr metabolic flow. In this study, we used NTBC as a tool to investigate the potential role of the Phe/Tyr catabolic pathway in inflammatory responses. We found that NTBC was effective in tempering the bacterial endotoxin lipopolysaccharide (LPS)-induced septic shock in mice. Mechanistically, the protective effect was related to the accumulation of a Phe/Tyr catabolic intermediate, 4-hydroxyphenylpyruvate (4-HPP), induced by the NTBC treatment. 4-HPP could inhibit NLRP3 inflammasome priming and activation processes and therefore reduce IL-1β release and pyroptosis. Like NTBC, 4-HPP was also effective in attenuating endotoxic shock in mice. Our results suggest the Phe/Tyr catabolic pathway as a potential immunoregulatory hub that may be exploited therapeutically to alleviate inflammation.

Recent progress indicates that the gut microbiota plays important role in regulating the host's glucose homeostasis. However, the mechanisms remain unclear. Here, we reported that one integral member of the murine gut microbiota, the protozoan

The herpes virus entry mediator (HVEM) is an immune checkpoint molecule regulating immune response, but its role in tissue repair remains unclear. Here, we reported that HVEM deficiency aggravated hepatobiliary damage and compromised liver repair after 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-induced injury. A similar phenotype was observed in B and T lymphocyte attenuator (BTLA)-deficient mice. These were correlated with impairment of neutrophil accumulation in the liver after injury. The hepatic neutrophil accumulation was regulated by microbial-derived secondary bile acids. HVEM-deficient mice had reduced ability to deconjugate bile acids during DDC-feeding, suggesting a gut microbiota defect. Consistently, both HVEM and BTLA deficiency had dysregulated intestinal IgA responses targeting the gut microbes. These results suggest that the HVEM-BTLA signaling may restrain liver injury by regulating the gut microbiota.

Background Tyrosine kinase inhibitors (TKIs) can significantly prolong overall survival for patients with advanced non‐small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR)‐mutation or anaplastic lymphoma kinase (ALK)‐rearrangement. However, the real‐world evaluation status of ALK/EGFR in China remains unclear. Methods We conducted a prospective study including 1134 patients with cytologically or histologically confirmed advanced NSCLC (stage IIIb–IV) at 12 Chinese hospitals. Results The most common evaluation methods were amplification‐refractory mutation system for EGFR status and immunohistochemistry targeting D5F3 for ALK status. Among patients with non‐squamous, the EGFR mutation rate was 44.1% and the ALK rearrangement rate was 10.0%. Among patients with squamous cell carcinoma, the EGFR mutation rate was 8.3% and the ALK rearrangement rate was 3.7%. Among all patients, gender (HR = 1.7, 95%CI = 1.2–2.4, P = 0.006), smoking history (HR = 1.8, 95%CI = 1.3–2.7, P = 0.001), histology (HR = 5.0, 95%CI = 2.4–10.1, P < 0.001), and brain metastases (HR = 1.5, 95%CI = 1.1–2.2, P = 0.017) were independent predictors of EGFR mutation, while age (HR = 2.6, 95%CI = 1.7–4.1, P < 0.001) was an independent predictor of ALK rearrangement. The median time from tumor diagnosis to EGFR or ALK status confirmation was 7 and 5 days, respectively. Targeted therapy rate was 73.8% in EGFR‐positive patients and 51.4% in ALK‐positive patients. There was a negative correlation between the first‐line targeted therapy rate and the EGFR mutation detection period (r = −0.152, P = 0.02), while no significant correlation among patients with ALK rearrangement (r = −0.179, P = 0.076). Conclusion Squamous NSCLC patients should also be routinely tested to determine their EGFR/ALK statuses. The first‐line targeted therapy rate remains low in Chinese patients with NSCLC.

In this study, zein, a renewable natural biopolymer from corn, was used to prepare a new biodegradable material with poly(butylene adipate-terephthalate) (PBAT) by reactive blending in the presence of poly(ethylene glycol diglycidyl ether) (PEGDGE). The effects of blending temperature and zein content on the morphology and mechanical and thermal properties of PBAT/zein blends with or without PEGDGE were investigated. Because of the high reactivity of the epoxy group in PEGDGE, the interfacial compatibility between zein and PBAT was improved greatly, and zein exhibited as a spheral phase with smaller size and finer dispersion in the PBAT matrix after the introduction of PEGDGE. Therefore, PEGDGE served as a plasticizer and reactive compatibilizer in the PBAT/zein blending system. Both the tensile strength and elongation at break of the blends with PEGDGE were improved greatly compared with those of the blends without PEGDGE but decreased gradually with the increase of zein content. These findings may provide a feasible way to utilize zein widely, and the new biodegradable blends with excellent stretchability could be used as packing materials in the future.

Efficient capture of radioactive iodine (129I, 131I) is of great significance in spent fuel treatment. In this paper, a new adsorbent named Catechin@ACF was successfully prepared through interface assembly of specific recognition gripper with plant polyphenols (catechin) on activated collagen fiber (ACF), and the catechin membrane with specific grip on iodine was successfully constructed on the surface of ACF. The results showed that the adsorbent assembled catechin membrane was rich in aromatic rings, hydroxyl groups and imine adsorption sites, and possessed specific recognition and capture characteristics of iodine. Moreover, the as-prepared Catechin@ACF showed excellent capture capacity for iodine vapor and iodine in organic solution with the maximum capture capacity of 2122.68 mg/g and 258.29 mg/g, respectively. In iodine-cyclohexane solution, the adsorption process was in according with the Pseudo first order kinetic and Langmuir isothermal model. In addition, the specific recognition and capture mechanism analysis indicated that the aromatic rings, phenolic hydroxyl groups and imine groups in the catechin membrane were the specific and effective grippers for iodine, and finally iodine formed a stable conjugated system with the adsorbent in the form of I- and I3-. Therefore, the as-prepared specific iodine capturer Catechin@ACF was expected to play a vital role in the capture of radioactive iodine in spent fuel off-gas because of its specific recognition, high capture capacity, large-scale preparation, and environment-friendly.

Extraction uranium from complicated aqueous solutions (seawater and nuclear wastewater) has been promoting the development of multi-functional adsorbents with high adsorption capacities and high selectivity. Here, we proposed a co-immobilization approach to preparing uranium adsorbents. Due to specific recognition and binding between functional groups, bayberry tannin (BT) and hydrous titanium oxide (HTO) were co-immobilized onto nano collagen fibrils (NCFs). The adsorption performances of NCFs-HTO-BT to uranium were systematically investigated in two aqueous systems, including nuclear wastewater and seawater. Results proved that NCFs-HTO-BT possessed the remarkable adsorption capacities and affinities for uranium in wastewater (393.186 mg g−1) and spiked seawater (14.878 mg g−1) with the uranium concentration of 320 mg g−1 and 8 mg g−1, respectively. Based on characteristic analysis of the adsorbent before and after uranium adsorption, the hydroxyl groups of HTO, the adjacent phenolic hydroxyl groups of BT, and nitrogen-containing and oxygen-containing functional groups of NCFs were active sites for uranium adsorption.

A significant breakthrough in the field of obesity research was the demonstration that an obese phenotype could be manipulated by modulating the gut microbiota. An important next step is to elucidate a human-relevant "map'' of microbiota-host interactions that regulate the metabolic health of the host. An improved understanding of this crosstalk is a prerequisite for optimizing therapeutic strategies to combat obesity. Intestinal mucosal barrier dysfunction is an important contributor to metabolic diseases and has also been found to be involved in a variety of other chronic inflammatory conditions, including cancer, neurodegeneration, and aging. The mechanistic basis for intestinal barrier dysfunction accompanying metabolic disorders remains poorly understood. Understanding the molecular and cellular modulators of intestinal barrier function will help devise improved strategies to counteract the detrimental systemic consequences of gut barrier breakage. Changes in the composition and function of the gut microbiota, i.e., dysbiosis, are thought to drive obesity-related pathogenesis and may be one of the most important drivers of mucosal barrier dysfunction. Many effects of the microbiota on the host are mediated by microbiota-derived metabolites. In this review, we focus on several relatively well-studied microbial metabolites that can influence intestinal mucosal homeostasis and discuss how they might affect metabolic diseases. The design and use of microbes and their metabolites that are locally active in the gut without systemic side effects are promising novel and safe therapeutic modalities for metabolic diseases.

Background Well-designed mobile health (mHealth) interventions support a positive user experience; however, a high rate of disengagement has been reported as a common concern regarding mHealth interventions. To address this issue, it is necessary to summarize the design features that improve user engagement based on research over the past 10 years, during which time the popularity of mHealth interventions has rapidly increased due to the use of smartphones. Objective The aim of this review was to answer the question “Which design features improve user engagement with mHealth interventions?” by summarizing published literature with the purpose of guiding the design of future mHealth interventions. Methods This review followed the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) checklist. Databases, namely, PubMed, Web of Science, Cochrane Library, Ovid EMBASE, and Ovid PsycINFO, were searched for English and Chinese language papers published from January 2009 to June 2019. Thematic analysis was undertaken to assess the design features in eligible studies. The Mixed Methods Appraisal Tool was used to assess study quality. Results A total of 35 articles were included. The investigated mHealth interventions were mainly used in unhealthy lifestyle (n=17) and chronic disease (n=10) prevention programs. Mobile phone apps (n=24) were the most common delivery method. Qualitative (n=22) and mixed methods (n=9) designs were widely represented. We identified the following 7 themes that influenced user engagement: personalization (n=29), reinforcement (n=23), communication (n=20), navigation (n=17), credibility (n=16), message presentation (n=16), and interface aesthetics (n=7). A checklist was developed that contained these 7 design features and 29 corresponding specific implementations derived from the studies. Conclusions This systematic review and thematic synthesis identified useful design features that make an mHealth intervention more user friendly. We generated a checklist with evidence-based items to enable developers to use our findings easily. Future evaluations should use more robust quantitative approaches to elucidate the relationships between design features and user engagement.

Immune and nervous system sensing are two important ways of detecting inner and outer environmental changes. Immune cell activation in the gut can promote metabolic disorders. However, whether enteric nervous system sensing and activities are also important in metabolic syndromes is not clear. Enteric glial cells (EGCs) are thought to have sensing ability, but little is known about the potential connections between EGC and metabolic disorders. Consuming a modern Western-type high-fat low-fiber diet increases the risk of obesity. Here, we reported that dietary shift from a normal chow diet to a high-fat diet in wild-type (WT) C57BL/6 mice induced a transient emergence of glial fibrillary acidic protein (GFAP)-positive EGC network in the ileal lamina propria, accompanied by an increase of glial-derived neurotrophic factors production. Inhibition of EGC metabolic activity via gliotoxin fluorocitrate or glial-intrinsic deletion of myeloid differentiation factor 88 (Myd88) in mice blocked this dietary change-induced activity. Furthermore, we found a different role of MYD88 in glial cells versus adipocyte in diet-induced obesity. The glial Myd88 knockout mice gained less body weight after HFD feeding compared to the littermate controls. In contrast, adipocyte deletion of Myd88 in mice had no impact on the weight gain but had exacerbated glucose metabolic disorders. Pharmacological interventions of glial activities by fluorocitrate prevented body weight gain in a dietary type- and glial MYD88-independent manner. Collectively, our data reveal a previously unappreciated function of EGC in sensing a dietary shift-induced perturbation and glial activities as a whole may play roles in diet-induced obesity.New & NoteworthyIt is known that obesity and its related metabolic syndrome can damage the neuronal system. However, whether the neuronal system also participates in the development of obesity is unclear. Diet is an important contributing factor to obesity. Our study reveals that consuming a high-fat diet can induce a transient enteric glial cell response via its intrinsic sensing molecule(s). Inhibiting overall glial cell activities may have an impact on the development of the metabolic syndrome.

BACKGROUND Well-designed mobile health (mHealth) interventions support a positive user experience; however, a high rate of disengagement has been reported as a common concern regarding mHealth interventions. To address this issue, it is necessary to summarize the design features that improve user engagement based on research over the past 10 years, during which time the popularity of mHealth interventions has rapidly increased due to the use of smartphones. OBJECTIVE The aim of this review was to answer the question “Which design features improve user engagement with mHealth interventions?” by summarizing published literature with the purpose of guiding the design of future mHealth interventions. METHODS This review followed the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) checklist. Databases, namely, PubMed, Web of Science, Cochrane Library, Ovid EMBASE, and Ovid PsycINFO, were searched for English and Chinese language papers published from January 2009 to June 2019. Thematic analysis was undertaken to assess the design features in eligible studies. The Mixed Methods Appraisal Tool was used to assess study quality. RESULTS A total of 35 articles were included. The investigated mHealth interventions were mainly used in unhealthy lifestyle (n=17) and chronic disease (n=10) prevention programs. Mobile phone apps (n=24) were the most common delivery method. Qualitative (n=22) and mixed methods (n=9) designs were widely represented. We identified the following 7 themes that influenced user engagement: personalization (n=29), reinforcement (n=23), communication (n=20), navigation (n=17), credibility (n=16), message presentation (n=16), and interface aesthetics (n=7). A checklist was developed that contained these 7 design features and 29 corresponding specific implementations derived from the studies. CONCLUSIONS This systematic review and thematic synthesis identified useful design features that make an mHealth intervention more user friendly. We generated a checklist with evidence-based items to enable developers to use our findings easily. Future evaluations should use more robust quantitative approaches to elucidate the relationships between design features and user engagement.

Objective Goal of this work is to assess the feasibility to perform COVID-19 RNA tests within hospitals and communities experiencing SARS-CoV-2 virus outbreaks, to ultimately provide recommendations for hospitals with so-called fever clinics. In China, these specialised clinics within a hospital, specifically receive outpatients who have fever symptoms.Methods A team with expertise in the Exposure Analysis of Critical Control Points (EACCP) framework first identified potential infection routes during the testing for SARS-CoV-2, then constructed and tested flow diagrams, which were confirmed under actual conditions, demonstrating the feasibility to be carried out in hospitals with fever clinics. The team determined critical control points to mitigate the exposure risks at each control point.Findings The sampling and inactivation steps of clinical samples in fever clinics appeared to be associated with particularly high risk levels of exposure to SARS-CoV-2. Moderate levels of exposure were associated with storage and transportation of samples for inactivation; Low risk levels were associated with the transportation, storage and detection steps after inactivation.Conclusion To minimise risks of infection for personnel, optimised processes to carry out SARS-CoV-2 RNA tests in hospitals with fever clinics in China are proposed. The high risk of SARS-CoV-2 exposure during procedures preceding testing are the sampling and biological inactivation, which can be reduced by using full personal protective equipment and the use of BSL2 facilities in fever clinics or mobile BSL2 platforms. The implementation of the Exposure Analysis of Critical Control Points framework could facilitate rapid responses to outbreaks of emerging infectious diseases.

Our current understanding of the host-microbiota interaction in the gut is dominated by studies focused primarily on prokaryotic bacterial communities. However, there is an underappreciated symbiotic eukaryotic protistic community that is an integral part of mammalian microbiota. How commensal protozoan bacteria might interact to form a stable microbial community remains poorly understood. Here, we describe a murine protistic commensal, phylogenetically assigned as Tritrichomonas musculis, whose colonization in the gut resulted in a reduction of gut bacterial abundance and diversity in wild-type C57BL/6 mice. Meanwhile, dietary nutrient and commensal bacteria also influenced the protozoan’s intestinal colonization and stability. While mice fed a normal chow diet had abundant T. musculis organisms, switching to a Western-type high-fat diet led to the diminishment of the protozoan from the gut. Supplementation of inulin as a dietary fiber to the high-fat diet partially restored the protozoan’s colonization. In addition, a cocktail of broad-spectrum antibiotics rendered permissive engraftment of T. musculis even under a high-fat, low-fiber diet. Furthermore, oral administration of Bifidobacterium spp. together with dietary supplementation of inulin in the high-fat diet impacted the protozoan’s intestinal engraftment in a bifidobacterial species-dependent manner. Overall, our study described an example of dietary-nutrient-dependent murine commensal protozoan-bacterium cross talk as an important modulator of the host intestinal microbiome. IMPORTANCE Like commensal bacteria, commensal protozoa are an integral part of the vertebrate intestinal microbiome. How protozoa integrate into a commensal bacterium-enriched ecosystem remains poorly studied. Here, using the murine commensal Tritrichomonas musculis as a proof of concept, we studied potential factors involved in shaping the intestinal protozoal-bacterial community. Understanding the rules by which microbes form a multispecies community is crucial to prevent or correct microbial community dysfunctions in order to promote the host’s health or to treat diseases.

The physiologic signals that regulate beige adipogenesis remain incompletely understood, especially those that limit browning and prevent overexpenditure of energy. In this study, the TNF family member cytokine lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT), also known as TNF super family protein 14 (TNFSF14), can inhibit adipose precursor differentiation into beige adipocytes. In acute cold stress, LIGHT deficiency in mice accelerated browning in the subcutaneous white adipose tissue (scWAT). Further experiments showed that LIGHT interacting with lymphotoxin-β receptor (LTβR) on adipose precursors blocked beige fat biogenesis. LTβR signals attenuated the JNK pathway, which contributed to their antibeiging effect. Blocking JNK activation using a small molecular inhibitor prevented cold-induced scWAT beiging. Furthermore, LIGHT/LTβR signals acted as an attenuator of white adipogenesis. LIGHT deficiency in mice promoted obesity during high-fat diet feeding. These findings identify the LIGHT axis as a regulator of adipose tissue homeostasis and suggest that LIGHT signaling functions as a mechanism to divert energy in favor of immune activation.-Kou, Y., Liu, Q., Liu, W., Sun, H., Liang, M., Kong, F., Zhang, B., Wei, Y., Liu, Z., Wang, Y. LIGHT/TNFSF14 signaling attenuates beige fat biogenesis.

The efficient capture of radioactive iodine (I-129, I-131) and radon (Rn-222) is crucial to the development of nuclear energy in spent fuel treatment. Herein, we successfully synthesized a new type of three-dimensional hydrolyzed collagen aerogel immobilized with catechin (Catechin@3DCF aerogel) as an effective adsorbent to remove iodine and radon through enzymatic hydrolysis, dialysis, freeze-drying, immobilization, and cross-linking. The as-prepared adsorbent was systematically characterized by FE-SEM, EDX, FT–IR, and XPS, showing that the adsorbent possesses ultra-high porosity, high content flake structure, and abundant adsorption sites on the surface of adsorbent. The results show that Catechin@3DCF aerogel exhibited excellent capture capacity for iodine and radon, with the maximum capture capacity of 222.67 wt% (88.5 wt% for 3DCF aerogel) and 44,877.9 Bq/Kg, respectively. Through the active group-shielding experiment analysis, the phenolic hydroxyl groups on the surface of adsorbent played a major role in iodine capture, followed by the -NHR group. In addition, mechanism studies have shown that the capture of iodine is mainly by chemical adsorption, while the capture of radon is mainly through physical adsorption, which is related to the numerous mesopores and flake structure of the adsorbent. Furthermore, Catechin@3DCF aerogel still maintains excellent adsorption capacity for iodine and radon under 60Co γ-ray irradiation at a total dose ranging from 10 to 350 kGy, indicating that it has excellent radiation resistance stability. Advantages such as novelty, ultra-high porosity, high-radiation stability, ultra-high capture capacity, environment-friendly, and low-cost indicate that biomass-derived Catechin@3DCF aerogel plays a role in the capture of radioactive iodine and radon from airborne effluents.

Bifidobacterium inhabiting the human and animal intestinal tract is known for its health-promoting effect. Tolerance to acid stress is crucial for bifidobacteria to survive and then exert their beneficial effects in the gut. A long-term adaptation in successive batch cultures was used as evolutionary engineering strategy to improve acid stress tolerance in an industrial probiotic strain, B. longum JDM301. Its derivative, JDM301AR showed higher resistance to several stress conditions, including acid stress than the parental strain, JDM301. To better understand bifidobacterial acid stress response, the changes of fatty acid (FA) in cell membrane of these two strains were determined. A shift in the production of FA in cell membrane, characterized by increased C14:0 was found, when JDM301AR was exposed to low-pH environment. It was implied that the increased production of C14:0 is associated with the acquisition of acid-tolerant phenotype for JDM301AR. High-throughput RNA-sequencing was performed to analyze the changes of gene expression profile after acid-exposure. The transcriptional profiles of JDM301AR and JDM301 under normal condition and acid stress were compared to reveal the different acid response between them. A total of 5 genes involved in FA metabolism were upregulated and no downregulated genes were found in response to acid stress in JDM301AR. The up-regulated BLJ_0565 and BLJ_1105 may play important roles in the modification of membrane FA composition of JDM301AR after acid exposure. Overall, these results suggested that successive batch cultures induced the acid stress tolerance of B. longum involved in transcriptional and physiological responses, including modification of cell wall and cell membrane, metabolism of amino acid and neutralization of internal pH by strengthening NH3 production and transport.

This study evaluated compliance with the comprehensive smoke-free law in public indoor places introduced in Shanghai in March 2017. Observations and PM2.5 monitoring over 30 min intervals in 8 types of the venue were conducted three times: within a month before implementation and 3- and 12-months post implementation. Observations of evidence of smoking decreased from 66.2% before legislation to 52.8% three months after (p = 0.002) and 49.7% one year after (p &lt, 0.001). The density of lit cigarettes also reduced significantly after implementation (p &lt, 0.001). When adjusting for outdoor, indoor PM2.5 levels were significantly lower after the legislation, but only by a small amount (three months later: &minus, 0.27, p = 0.08, one year later: &minus, 0.12, p = 0.03). Evidence of compliance was weakest in farmer&rsquo, s markets and bars, and smoking in male toilets did not change significantly. The reduction in smoking was affected by the management performance of their obligations. The comprehensive smoke-free law led to modest reductions in smoking and PM2.5 levels as a result, but from levels suggesting quite high levels of pre-compliance. However, compliance was limited in some areas, suggesting more effort is required on management to gain better compliance in some places like farmer&rsquo, s markets, bars, and toilets.

Objective: The aim of this study was to identify the potential psychological mechanism of well-being in migrants in Shanghai, China. Methods: A cross-sectional study was conducted in 2018. First, a literature review was conducted to understand the salutogenesis of migrants in China. Then, 2573 random participants were recruited from six workplaces and public places in six districts of Shanghai. The Chinese versions of the Patient Health Questionnaire-9 (PHQ-9), the Personal Wellbeing Index (PWI), and the Sense of Coherence (SOC) Scale were used to evaluate the depression, subjective well-being (SWB), and SOC of migrants. The t-test, ANOVA, and multiple linear regression and structural equation models (SEM) were used to analyze the correlations and paths among generalized resistant resources (GRRs), SOC, PHQ, and SWB. Results: The subjects were aged between 18 and 58 (mean, 28.17, SD, 6.99). SOC showed a positive correlation with SWB (r = 0.46, p &lt, 0.001) and a negative correlation to PHQ (r = &ndash, 0.53, p &lt, 0.001). After controlling for the demographic characteristics, we found that PHQ, SOC (comprehensibility, manageability, meaningfulness), and GRRs (income ratio, marital status) contributed 33.3% of the variance in SWB, and their linear regression coefficients were: &minus, 0.32 (p &lt, 0.001), 0.09 (p &lt, 0.001), 0.15 (p &lt, 0.001), 0.06 (p &lt, 0.05), and 0.16 (p &lt, 0.05), respectively. These findings not only confirmed the direct association among SOC, PHQ and SWB, but also verified two underlying mechanisms regarding the mediating effect of SOC by using SEM: (1) GRRs (income ratio, marital status) are positively associated with a higher SOC, which further contributes to favorable SWB, and (2) PHQ is negatively associated with poor SWB indirectly via SOC. Conclusion: Migrant workers with low SOC and high PHQ are vulnerable to poor well-being levels. Meanwhile, GRRs (income ratio, marital status) may strengthen the SOC level, and can be regarded as the basis of intervention. Further investigation may be needed to focus on external psychological support factors.

Injury to the biliary epithelium triggers cholangiopathies. However, factors involved in regulating the pathogenesis remains incompletely understood. Here, we report that the gut microbiota is important in regulating hepatobiliary fibroproliferative regenerative process. In helminth Clonorchis sinensis-induced bile duct injury model, wild-type mice showed more extensive peribiliary fibroproliferative responses than non-littermate IL-33-deficient mice. However, these reactions could be attenuated by co-housing of the animals together. In the meantime, the relatively fibroproliferative-resistant IL-33-deficient mice could become fibroproliferative-responsive especially in large intrahepatic bile duct by antibiotics treatment. Furthermore, microbiota-derived metabolite butyrate was able to inhibit biliary organoid expansion in vitro and temper 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced biliary fibrosis in vivo. Together, our data implies a potential way of management of hepatobiliary diseases by modulating gut microbiota.

Nano-scale zero-valent iron (NZVI) is easy to be agglomerated and passivated in the process of U(VI) reduction and fixation. Herein, a facile one-step process for titanium modified beaded segments like nano-zero-valent iron nanoparticles (FTNP) was designed and prepared for U(VI) adsorption-reduction from aqueous solution. The as-prepared NZVI, FTNP were characterized by Fourier transform infrared Spectroscopy (FT-IR), X-ray diffraction (XRD), X-Ray photoelectron spectra (XPS), Scanning electron microscope (SEM), Transmission electron microscope (TEM) and Energy dispersive X-ray spectrum (EDS). Results indicated that the beaded segments like FTNP were successful prepared. Furthermore, the uranium removal performance of FTNP with the effect of adsorption and reduction were investigated and showed excellent adsorption and reducibility for U(VI) from aqueous solution. Batch adsorption for U(VI) shown the U(VI) adsorption capacity of FTNP reached 734.4 mg g–1 (pH = 5.0). In the Fe-U reaction system, Fe2+ was generated as the primary reducing agent to reduce U(VI) from Fe0. Therefore, part of U(VI) was removed and reduced to U(IV), while others was precipitation hydrolyzed to schoepite, which also reduced to U(IV) and precipitated. This study may provide a novel and significant method for using nano-zero-valent iron to develop for wastewater decontamination.

Toxin-antitoxin (TA) systems are widespread in bacteria and archaea. However, the roles of chromosomally encoded TA systems in bacterial physiology are still open to debate. In this study, a TA module-relBE in Bifidobacterium longum JDM301 (relBE(Bif)) was identified and its function in stress response was evaluated. Bioinformatics analysis of the whole genome sequences of JDM301 revealed a pair of linked genes encoding a RelBE-like TA system (RelBE(Bif)). Our results revealed a bicistronic operon formed by relBE(Bif) in JDM301. Over-expression of RelE(Bif) had a toxic effect on Escherichia coli, which could be neutralized by co-expression of its cognate antitoxin, RelB(Bif) Our data also demonstrated that RelE(Bif) is an mRNA interferase and that the activity of RelE(Bif) can be inhibited by RelB(Bif) These results suggest that RelE(Bif) is a toxic nuclease which arrests cell growth through mRNA degradation, and that the activity of RelE(Bif) can be abolished by co-expression of RelB(Bif) In addition, we also found that the expression of RelBE(Bif) is increased during osmotic stress, suggesting that RelBE(Bif) is activated under this adverse condition. Our results imply that the RelBE(Bif) TA module may represent a cell growth modulator which helps B. longum to deal with osmotic stress.

Additional file 1. List of genes involved in NH3 production, peptidoglycan synthesis, pantothenate and CoA biosynthesis and cell division and chromosome partitioning expressed differently in JDM301AR compared with JDM301 in normal condition.

Current evidence to support extensive use of probiotics in inflammatory bowel disease is limited and factors that contribute to the inconsistent effectiveness of clinical probiotic therapy are not completely known. Here, we used Bifidobacterium longum JDM 301 as a model probiotic to study potential factors that may influence the effect of probiotics in experimental colitis. We found that the effect of B. longum JDM 301 in tempering experimental colitis varied across individual mice even with the same genetic background. The probiotic efficacy was highly correlated with the host gut microbial community features. Consumption of a diet rich in fat could exacerbate mucosal injury-induced colitis but could not change the host responsiveness to B. longum JDM 301 treatment, suggesting of potential mechanistic differences between regulating colitis pathogenesis, and modulating probiotic efficacies by the gut microbiota. Together, our results suggest that personalized microbiome features may modify the probiotic therapeutic effect and support the idea of personalized probiotic medicine in inflammatory bowel disease.

Background Clostridium difficile (C. difficile) is a main cause of antibiotic-associated diarrhoea in humans. Several studies have been performed to reveal the prevalence rate of C. difficile in cats and dogs. However, little is known about the epidemiology of C. difficile in healthy pets in China. This study aimed to assess the burden of C. difficile shedding by healthy dogs and cats in China. Furthermore, the genetic diversity and antimicrobial susceptibility patterns of the recovered isolates were determined. Methods A total of 175 faecal samples were collected from 146 healthy dogs and 29 cats. C. difficile strains were isolated and identified from the feces of these pets. The characterized C. difficile strains were typed by multilocus sequence typing (MLST), and the MICs of the isolates were determined against ampicillin, clindamycin, tetracycline, moxifloxacin, chloramphenicol, cefoxitin, metronidazole and vancomycin by the agar dilution method. Results Overall, 3 faecal samples (1.7%) were C. difficile culture positive. One sample (0.7%) from a dog was C. difficile culture positive, while two cats (7.0%) yielded positive cultures. The prevalence rate differed significantly between cats and dogs. These isolates were typed into 3 MLST genotypes and were susceptible to chloramphenicol, tetracycline, metronidazole and moxifloxacin and resistant to ampicillin, clindamycin and cefoxitin. Notably, one strain, D141–1, which was resistant to three kinds of antibiotics and carried toxin genes, was recovered in the faeces of a healthy dog. Conclusion Our results suggest that common pets may be a source of pathogenic C. difficile, indicating that household transmission of C. difficile from pets to humans can not be excluded.

Current evidence to support extensive use of probiotics in inflammatory bowel disease is limited and factors contribute to the inconsistent effectiveness of clinical probiotic therapy are not completely known. Here, as a proof-of-concept, we utilized Bifidobacterium longum JDM 301, a widely used commercial probiotic strain in China, to study potential factors that may influence the beneficial effect of probiotics in experimental colitis. We found that the probiotic therapeutic effect was varied across individual mouse even with the same genetic background and consuming the same type of food. The different probiotic efficacy was highly correlated with different microbiome features in each mouse. Consumption of a diet rich in fat can change the host sensitivity to mucosal injury-induced colitis but did not change the host responsiveness to probiotic therapy. Finally, the host genetic factor TLR2 was required for a therapeutic effect of B. longum JDM 301. Together, our results suggest that personalized microbiome and genetic features may modify the probiotic therapeutic effect.

Probiotics might offer an attractive alternative to prevent and control Clostridium difficile (C. difficile) infection (CDI). Limited information is available on the ability of commercially used bifidobacterial strains to inhibit C. difficile. This study examined the anti-clostridial effects of Bifidobacterium longum JDM301, a widely used commercial probiotic strain in China, in vitro and in vivo. In vitro evaluation revealed a significant reduction in C. difficile counts when JDM301 was co-cultured with C. difficile, which was correlated with the significant decrease in clostridial toxin titres (TcdA and TcdB). Furthermore, the cell-free culture supernatants (CFS) of JDM301 inhibited C. difficile growth and degraded TcdA and TcdB. Notably, the results showed that acid pH promoted the degradation of TcdA by CFS from JDM301. Furthermore, comparative studies among 10 B. longum strains were performed, which showed that the inhibitory effect of CFS from JDM301 was similar with the other 8 B. longum strains and higher than strain BLY1. However, when it was neutralized, the significant different was lost. When present together, it was suggested that the acid pH induced by probiotics not only played important roles in the growth inhibition against C. difficile resulting in the reduction of toxins titres, but also directly promoted the degradation of clostridial toxin. In vivo studies proved that JDM301 partially relieved damage to tissues caused by C. difficile and also decreased the number of C. difficile and toxin levels. In summary, our results demonstrated that the commercial strain, JDM301 could be considered a probiotic able to exert anti-toxin capability and most of the CFS from Bifidobacterium were able to inhibit the growth of C. difficile, depending on acid pH. These results highlighted a potential that JDM301 could be helpful in preventing CDI and that most of the bifidobacterial strains could (at least partially) exert protective effects by reducing toxin titres through growth inhibition against toxigenic C. difficile.

Probiotics might offer an attractive alternative to prevent and control Clostridium difficile (C. difficile) infection (CDI). Limited information is available on the ability of commercially used bifidobacterial strains to inhibit C. difficile. This study examined the anti-clostridial effects of Bifidobacterium longum JDM301, a widely used commercial probiotic strain in China, in vitro and in vivo. In vitro evaluation revealed a significant reduction in C. difficile counts when JDM301 was co-cultured with C. difficile, which was correlated with the significant decrease in clostridial toxin titres (TcdA and TcdB). Furthermore, the cell-free culture supernatants (CFS) of JDM301 inhibited C. difficile growth and degraded TcdA and TcdB. Notably, the results showed that acid pH promoted the degradation of TcdA by CFS from JDM301. Furthermore, comparative studies among 10 B. longum strains were performed, which showed that the inhibitory effect of CFS from JDM301 was similar with the other 8 B. longum strains and higher than strain BLY1. However, when it was neutralized, the significant different was lost. When present together, it was suggested that the acid pH induced by probiotics not only played important roles in the growth inhibition against C. difficile resulting in the reduction of toxins titres, but also directly promoted the degradation of clostridial toxin. In vivo studies proved that JDM301 partially relieved damage to tissues caused by C. difficile and also decreased the number of C. difficile and toxin levels. In summary, our results demonstrated that the commercial strain, JDM301 could be considered a probiotic able to exert anti-toxin capability and most of the CFS from Bifidobacterium were able to inhibit the growth of C. difficile, depending on acid pH. These results highlighted a potential that JDM301 could be helpful in preventing CDI and that most of the bifidobacterial strains could (at least partially) exert protective effects by reducing toxin titres through growth inhibition against toxigenic C. difficile.

Bifidobacterium longum strain JDM301, a widely used commercial strain in China, encodes at least two MazEF-like modules and one RelBE-like toxin-antitoxin (TA) system in its chromosome, designated MazE 1 F 1 Bif , MazE 2 F 2 Bif , and RelBE Bif , respectively. Bacterial TA systems play an important role in several stress responses, but the relationship between these TA systems is largely unknown. In this study, the interactions between MazF 1 Bif and MazE 2 Bif or RelB Bif were assessed in B. longum strain JDM301. MazF 1 Bif caused the degradation of tufA Bif mRNA, and its toxicity was inhibited by forming a protein complex with its cognate antitoxin, MazE 1 Bif . Notably, MazF 1 Bif toxicity was also partially neutralized when jointly expressed with noncognate antitoxin MazE 2 Bif or RelB Bif . Our results show that the two noncognate antitoxins also inhibited mRNA degradation caused by MazF 1 Bif toxin. Furthermore, the physical interplay between MazF 1 Bif and its noncognate antitoxins was confirmed by immunoprecipitation. These results suggest that MazF 1 Bif can arrest cell growth and that MazF 1 Bif toxicity can be neutralized by its cognate and noncognate antitoxins. These results imply that JDM301 uses a sophisticated toxin-antitoxin interaction network to alter its physiology when coping with environmental stress. IMPORTANCE Although toxin-antitoxin (TA) systems play an important role in several stress responses, the regulatory mechanisms of multiple TA system homologs in the bacterial genome remain largely unclear. In this study, the relationships between MazE 1 F 1 Bif and the other two TA systems of Bifidobacterium longum strain JDM301 were explored, and the interactions between MazF 1 Bif and MazE 2 Bif or RelB Bif were characterized. In addition, the mRNA degradation activity of MazF 1 Bif was demonstrated. In particular, the interaction of the toxin with noncognate antitoxins was shown, even between different TA families (MazF 1 Bif toxin and RelB Bif antitoxin) in JDM301. This work provides insight into the regulatory mechanisms of TA systems implicated in the stress responses of bifidobacteria.