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[Display omitted] Multidrug-resistant (MDR) bacteria-infected wound healing remains greatly challenging, especially in diabetic patients. Herein, a novel nano-drug delivery based on endogenous glucose-driven cascade reaction is proposed for boosting MDR bacteria-infected diabetic wound healing with high efficacy by improving wound microenvironment and enhancing photodynamic antibacterial activity. The composite nanoagent is first self-assembled by integrating berberine (B BR) and epigallocatechin gallate (E GCG) from natural plant extracts, named as BE NPs , which is successively coated with manganese dioxide nanoshells (M nO 2 NSs) and glucose oxidase (G OX) to form the final BEMG NPs. The cascade reaction is triggered by glucose at the wound site of diabetes which is specifically catalyzed by GOX in the BEMG NPs to produce gluconic acid and hydrogen peroxide (H 2 O 2). That is subsequently to decompose MnO 2 NSs in the BEMG NPs to generate oxygen (O 2). The BEMG NPs as photosensitizers effectively produce reactive oxygen species (ROS) to enhance the eradication of bacteria with the assistance of O 2. Under the synergistic function of the cascaded reaction, the BEMG NPs present excellent antibacterial efficacy even for MDR bacteria. The in vivo experiments explicitly validate that the constructed nano-drug delivery can augment the MDR bacteria-infected diabetic wound healing with excellent biosafety. The as-proposed strategy provides an instructive way to combat ever-threatening MDR bacteria, which particularly is beneficial for diabetic patients. [ABSTRACT FROM AUTHOR]

The majority of patients are diagnosed when ovarian cancer (OC) has metastasized, making surgery and chemotherapy less effective. Thus, there is an urgent need to elucidate the mechanisms underlying metastasis and to further explore novel diagnostic biomarkers of OC metastasis. Here, we conducted a genome-wide CRISPR-Cas9 screen for anoikis resistance to identify key genes associated with OC metastasis. Further, bioinformatic analysis was performed using TCGA and GTEx datasets to explore the genes associated with OC progression and prognosis. After integrated analysis, the V-set and transmembrane domain-containing protein 2-like (VSTM2L) was identified as a crucial gene closely associated with OC metastasis, progression, and prognosis. Further validation using a patient-based cohort suggested that VSTM2L expression was significantly higher in metastatic lesions than in primary lesions. Subsequently, an in vitro assay showed that VSTM2L silencing increased SKOV3 cell death and hampered spheroid formation. Mechanistically, GSEA highlighted that epithelial-mesenchymal transition (EMT)-related pathways was positively associated with VSTM2L expression. Consistently, the validation based on the VSTM2L silence suggested the involvement of VSTM2L in EMT-related TGF-β and NF-κB signaling. Meanwhile, the addition of VSTM2L-containing medium did not provoke those signaling, indicating VSTM2L functions as an intracellular protein to activate TGF-β and NF-κB signaling. In summary, our study revealed that VSTM2L is a novel player involved in anoikis resistance and is a promising biomarker of OC metastasis and prognosis. • Genome-wide screening combined with bioinformatics identified VSTM2L as a promising biomarker for ovarian cancer. • VSTM2L regulates TGF-β and NF-κB signaling and promotes anoikis resistance. • VSTM2L functions as an intracellular protein to regulate EMT-related signaling. [ABSTRACT FROM AUTHOR]

[Display omitted] • Copper indium sulfide QDs are emerging as versatile visible-light photocatalysts. • Different synthesis methods determine the properties and performances. • Modification strategies such as heterojunction formation improve the activity. • Excellent results in photocatalytic degradation, H 2 production and CO 2 reduction. • Promising prospects for future development and wider applications. Since the advent of photocatalytic technology, scientists have been searching for semiconductor materials with high efficiency in solar energy utilization and conversion to chemical energy. Recently, the development of quantum dot (QD) photocatalysts has attracted much attention because of their unique characteristics: small size, quantum effects, strong surface activity, and wide photoresponse range. Among ternary chalcogenide semiconductors, CuInS 2 QDs are increasingly examined in the field of photocatalysis due to their high absorption coefficients, good matching of the absorption range with sunlight spectrum, long lifetimes of photogenerated electron-hole pairs and environmental sustainability. In this review paper, the structural and electronic properties, synthesis methods and various photocatalytic applications of CuInS 2 QDs are systematically expounded. The current research status on the photocatalytic properties of materials based on CuInS 2 QD is discussed combined with the existing modification approaches for the enhancement of their performances. Future challenges and new development opportunities of CuInS 2 QDs in the field of photocatalysis are then prospected. [ABSTRACT FROM AUTHOR]

The aim of this paper is to apply the modified potential well method and some new differential inequalities to study the asymptotic behavior of solutions to the initial homogeneous Neumann problem of a nonlinear diffusion equation driven by the p (x) -Laplace operator. Complete classification of global existence and blow-up in finite time of solutions is given when the initial data satisfies different conditions. We first obtain a threshold result for the solution to exist globally or to blow up in finite time when the initial energy is subcritical or critical. We also establish a decay rate of the L 2 norm for global solutions. Furthermore, we provide some sufficient conditions for the existence of global and blow-up solutions for supercritical initial energy. We finally give two-sided estimates of asymptotic behavior when the diffusion term dominates the source. This is a continuation of our previous work [17]. [ABSTRACT FROM AUTHOR]

Antibiotic contamination and excessive nitrate loads are generally concurrent in aquatic ecosystems. However, little is known about the effects of nitrate input on the biodegradation of antibiotics. In this study, the effects of nitrate input on microbial degradation of erythromycin, a typical macrolide antibiotic widely detected in lake sediments, were investigated. The results showed that the nitrate input significantly inhibited the erythromycin removal and such an inhibitory effect was strengthened with the increased input dosages. Nitrate input significantly increased sediment nitrite concentration, indicating enhanced denitrification under high nitrate pressure. Bacterial network module and keystone species analysis showed that nitrate input enriched the keystone species involved in denitrification (e.g., Simplicispira and Denitratisoma). In contrast, some potential erythromycin-degrading bacteria (e.g., Desulfatiglandales, Pseudomonadales, Nitrospira) were inhibited by nitrate input. The variations in dominant bacterial groups implied competition between denitrification and erythromycin degradation in response to nitrate input. Based on the partial least squares path modeling analysis, keystone species (total effect: 0.419) and bacterial module (total effect: 0.403) showed strong association with erythromycin removal percentage. This indicated that the inhibitory effect of nitrate input on erythromycin degradation was mainly explained by bacterial network modules and keystone species. These findings will help us to assess the bioremediation potential of antibiotic-contaminated sediments suffering from excessive nitrogen discharge concurrently. [Display omitted] • Nitrate input inhibited erythromycin biodegradation by enhancing denitrification. • Denitrification may compete for electrons with erythromycin reduction. • Nitrate inhibited potential erythromycin-degrading bacteria (e.g., Nitrospira). • Denitrifying bacteria (e.g., Denitratisoma) were enriched by nitrate input. • Nitrate inhibitory effect was mainly explained by keystone species and modules. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) are unstable metabolites produced during cellular respiration that can cause extensive damage to the body. Here we report a unique structural metalloprotein called RSAP p for the first time, which exhibits robust ROS-scavenging activity, high thermostability, and stress resistance. RSAP p is a previously uncharacterized DUF2935 (domain of unknown function, accession number: cl12705) family protein from Paenibacillus , containing a highly conserved four-helix bundle with binding sites for variable-valence metal ions (Mn2+/Fe2+/Zn2+). Enzymatic characterization results indicated that RSAP p displays the functionality of three different antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD). In particular, RSAP p exhibits a significant SOD-like activity that is remarkably effective in eliminating superoxide radicals (up to k cat / K M = 2.27 × 1011 mol−1 s−1), and maintains the catalytical active in a wide range of temperatures (25–100 °C) and pH (pH 2.0–9.0), as well as resistant to high temperature, alkali and acidic pH, and 55 different concentrations of detergent agents, chemical solvents, and inhibitors. These properties make RSAP p an attractive candidate for various industrial applications, including cosmetics, food, and pharmaceuticals. [Display omitted] • A novel ROS-scavenging metalloprotein (RSAP) from Paenibacillus was identified. • Its highly conserved 4-helix region endows a compact, stable and scalable structure. • RSAP can mimic catalytic activity of superoxide dismutase, catalase and peroxidase. • RSAP significantly tolerates high-temperature, extreme pH, and chemical agents. • Unique RSAP holds great expansibility and potential for industrial applications. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is a major cause of death and disability that involves brain dysfunction due to external forces. Here, we found lower levels of Ubiquinol-cytochrome c reductase, complex III subunit XI (Uqcr11) expression in the cerebral cortex of TBI mice. A neuronal damage model was constructed using H 2 O 2 or hypoxia reoxygenation (H/R) in vitro. We found that Uqcr11 overexpression attenuated the H 2 O 2 -or H/R-induced damage by preventing oxidative stress and neuronal apoptosis in HT22 cells. Moreover, up-regulated Uqcr11 contributed to the restoration of motor, learning, and memory in C57BL/6 mice after TBI, and its underlying mechanism may be associated with promoting neuron survival and inhibited oxidative stress. Collectively, our findings demonstrated that oxidative stress as well as neuronal apoptosis can be ameliorated post-TBI by Uqcr11 overexpression, which provides a potential therapeutic target for TBI. • Uqcr11 alleviates oxidative stress and apoptosis after H2O2 or H/R treatment. • Uqcr11 improved neurobehavioral function in mice after TBI. • Uqcr11 suppressed apoptosis and promoted neuronal survival in mice after TBI. [ABSTRACT FROM AUTHOR]

Diabetes is a serious, costly, and major health problem worldwide. Whereas diabetes could be alleviated by medication, this disease could not be fully cured at the present time due to the lack of effective therapeutic treatment for β-cell loss and/or dysfunction. Increased β-cell mass or volume could be achieved via differentiation of embryonic stem (ES) cells or pluripotent stem cells or through β-cell renewal, including proliferation, redifferentiation, and transdifferentiation. Data cumulated over the past several years suggest that increased β-cell dedifferentiation plays a crucial role in the progression of diabetes, shedding new light on potential targets for β-cell replacement therapy. In this review, we summarize current views on β-cell dedifferentiation, redifferentiation, and transdifferentiation. We also discuss potential mechanisms regulating these key processes to maintain β-cell homeostasis. Understanding pancreatic β-cell differentiation and dedifferentiation could be provide important information on developing effective strategies to cure diabetes. [ABSTRACT FROM AUTHOR]

Cadmium is a highly ubiquitous environmental pollutant that poses a serious threat to human health. In this study, we assessed the cardiotoxicity of Cd exposure and explored the possible mechanisms by which Cd exerts its toxic effects. The results demonstrated that exposure to Cd via drinking water containing CdCl 2 10 mg/dL for eight consecutive weeks induced cardiac injury in C57BL/6J mice. The histopathological changes of myocardial hemolysis, widening of myocardial space, and fracture of myocardial fiber were observed. Meanwhile, elevated levels of cardiac enzyme markers and up-regulation of pro-apoptotic genes also indicated cardiac injury after Cd exposure. Non-targeted lipidomic analysis demonstrated that Cd exposure altered cardiac lipid metabolism, resulted in an increase in pro-inflammatory lipids, and changed lipid distribution abundance. In addition, Cd exposure affected the secretion of inflammatory cytokines by activating the NF-κB signaling pathway, leading to cardiac inflammation in mice. Taken together, results of our present study expand our understanding of Cd cardiotoxicity at the lipidomic level and provide new experimental evidence for uncovering the association of Cd exposure with cardiovascular diseases. [Display omitted] • Cd exposure induced myocardial damage. • Cd exposure altered myocardial lipid profile. • Pro-inflammatory lipids increased after Cd exposure. • Cd exposure evoked myocardial inflammation. [ABSTRACT FROM AUTHOR]

Studies suggested that greenness could reduce death risks related to ambient exposure to particulate matter (PM), while the available evidence was mixed across the globe and substantially exiguous in low- and middle-income countries. By conceiving an individual-level case-crossover study in central China, this analysis primarily aimed to quantify PM-mortality associations and examined the modification effect of greenness on the relationship. We investigated a total of 177,058 nonaccidental death cases from 12 counties in central China, 2008–2012. Daily residential exposures to PM 2.5 (aerodynamic diameter <2.5 µm), PM c (aerodynamic diameter between 2.5 and 10 µm), and PM 10 (aerodynamic diameter <10 µm) were assessed at a 1 × 1-km resolution through satellite-derived machine-learning models. Residential surrounding greenness was assessed using satellite-derived enhanced vegetation index (EVI) and normalized difference vegetation index (NDVI) at multiple buffer sizes (250, 500, and 1000 m). To quantify the acute mortality risks associated with short-term exposure to PM 2.5 , PM c , and PM 10 , a time-stratified case-crossover design was utilized in conjunction with a conditional logistic regression model in our main analyses. To investigate the effect modification of greenness on PM-mortality associations, we grouped death cases into low, medium, and high greenness levels using cutoffs of 25th and 75th percentiles of NDVI or EVI exposure, and examined potential effect heterogeneity in PM-related mortality risks among these groups. Mean concentrations (standard deviation) on the day of death were 73.8 (33.4) μg/m3 for PM 2.5 , 43.9 (17.3) μg/m3 for PM c , and 117.5 (44.9) μg/m3 for PM 10. Size-fractional PM exposures were consistently exhibited significant associations with elevated risks of nonaccidental and circulatory mortality. For every increase of 10-μg/m3 in PM exposure, percent excess risks of nonaccidental and circulatory mortality were 0.271 (95% confidence interval [CI]: 0.010, 0.533) and 0.487 (95% CI: 0.125, 0.851) for PM 2.5 at lag-01 day, 0.731 (95% CI: 0.108, 1.359) and 1.140 (95% CI: 0.267, 2.019) for PM c at lag-02 day, and 0.271 (95% CI: 0.010, 0.533) and 0.386 (95% CI: 0.111, 0.662) for PM 10 at lag-01 day, respectively. Compared to participants in the low-level greenness areas, those being exposed to higher greenness were found to be at lower PM-associated risks of nonaccidental and circulatory mortality. Consistent evidence for alleviated risks in medium or high greenness group was observed in subpopulations of female and younger groups (age <75). Short-term exposure to particulate air pollution was associated with elevated risks of nonaccidental and circulatory death, and individuals residing in higher neighborhood greenness possessed lower risk of PM-related mortality. These findings emphasized the potential public health advantages through incorporating green spaces into urban design and planning. • Impact of greenness on PM-mortality association was explored in central China. • Elevated risks of acute mortality associated with PM 2.5 , PM c , and PM 10 exposure. • Exposure to higher residential greenness could lower risks of PM-related mortality. • Same effect modification of greenness was observed in female and adults aged <75. [ABSTRACT FROM AUTHOR]

Abstract Harmine, a useful botanical compound, has demonstrated insecticidal activity against some pests. However, harmine's mechanism of action has not been thoroughly elucidated to date. To preliminarily explore harmine's insecticidal mechanisms, the cytotoxicity of harmine against Spodoptera frugiperda Sf9 cells was comprehensively investigated. Our results indicated that harmine induced apoptosis in Sf9 cells, as evidenced by cellular and nuclear morphological changes, DNA laddering and increases in caspase-3-like activities. In addition, activation of the mitochondrial apoptotic pathway by harmine was confirmed by the generation of ROS, opening of mitochondrial permeability transition pores (MPTPs), increase in cytosolic Ca2+, changes in mRNA expression levels of genes involved in the mitochondrial apoptotic pathway and increase and release of Cytochrome c. Furthermore, lysosomal membrane permeabilization, release of cathepsin L from the lysosome into the cytosol and cleavage of caspase-3 were also triggered, which indicated that lysosomes were involved in this physiological process. Moreover, the effect of harmine on DNA topoisomerase I activity was investigated by in vivo and molecular docking experiments. These data not only verified that harmine induced apoptosis via comprehensive activation of the mitochondrial and lysosomal pathways and inhibition of DNA topoisomerase I activity in Sf9 cells but also revealed a mechanism of harmine insecticidal functions for pest control. Graphical abstract Unlabelled Image Highlights • Harmine induced apoptosis in Spodoptera frugiperda Sf9 cells. • Harmine activated mitochondrial apoptotic pathway in Sf9 cells. • Harmine activated lysosomal apoptotic pathway in Sf9 cells. • Harmine inhibited DNA topoisomerase I activity. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a well-known environmental pollutant with high toxicity. Despite a variety of studies have demonstrated that Cd exposure induces multiple organ damages in humans, there is still a lack of knowledge of Cd induced skeletal muscle impairment. Exercise is a non-invasive, effective intervention to improve human health and combat diseases. In this study, we aimed to evaluate the toxic effects of Cd exposure on skeletal muscle function and explore the possibility of exercise for attenuating skeletal muscle toxicity of chronic Cd exposure. C57BL/6J mice were exposed to Cd via drinking water containing CdCl 2 10 mg/dL for 8 weeks while a moderate exercise was daily induced by a motorized treadmill to mice. It was found that Cd exposure significantly reduced the ratio of gastrocnemius and body weight, decreased mouse exercise capacity, weakened muscle strength, promoted lipid accumulation and up-regulated pro-apoptotic genes in the skeletal muscle. Non-targeted lipidomics analysis indicated that Cd exposure disturbed lipid metabolism, altered lipid signatures and elevated pro-inflammatory lipid species in the skeletal muscle. Moreover, Cd exposure evoked an intense inflammatory response in the skeletal muscle by up-regulating pro-inflammatory cytokine production such as Eotaxin (CCL11), TNF-α, IL-1β, IL-6, RANTES (CCL5) and so on. Notably, treadmill exercise effectively protected against Cd induced skeletal muscle impairment indicated by the effects of inhibiting lipid metabolism disturbance, suppressing pro-inflammatory cytokine production and preserving skeletal muscle function. These results demonstrated that environment relevant Cd exposure impairs skeletal muscle function and exercise effectively antagonizes the Cd toxicity in the skeletal muscle and preserves skeletal muscle function. This study provided the novel evidence for unraveling Cd toxicity on the skeletal muscle function and highlighted the possibility of considering exercise as a countermeasure for Cd induced skeletal muscle impairment at population level. • Cd exposure impairs skeletal muscle function. • Cd exposure alters lipid profile by increasing pro-inflammatory lipids. • Cd exposure induces muscular inflammation by elevating pro-inflammatory cytokines. • Exercise attenuates Cd induced skeletal muscle impairment by suppressing lipid disturbances and reducing inflammation. [ABSTRACT FROM AUTHOR]

Arsenic (As) speciation in the phloem sap of rice plants and its role in As accumulation in rice grains remain largely uncharacterized. In the present study, we tested As chemical species in the phloem exudates of rice treated with arsenate [As(V)], arsenite [As(III)], monomethylarsonic acid [MMA(V)], or dimethylarsinic acid [DMA(V)]. As(V) was the main species (58%) in the phloem exudates of As(V)-exposed rice, whereas As(III) predominated (69%) in As(III)-exposed rice. A large proportion of As(V) (41–45%) was observed in the phloem exudates when rice was treated with methylated As species. High concentrations of phytochelatins were detected in the phloem exudates when the As(V) treatment level was increased. The role of phloem transport was analyzed by applying a ±stem-girdling treatment to the rice plants, limiting phloem transport to the grain in rice pulsed with As(III), As(V), MMA(V), or DMA(V). The findings of the present study indicate that organic As is more mobile than inorganic As during phloem transport. Phloem transport accounted for 54% of As(III), 56% of As(V), 100% of MMA(V), and 89% of DMA(V) transport to the grain. The total As concentration and As(III) percentage in rice phloem and grain were significantly affected by increasing the phosphate concentration in the medium. [ABSTRACT FROM AUTHOR]

Chronic fluoride exposure can cause developmental neurotoxicity, however the precise mechanisms remain unclear. To explore the mechanism of mitophagy in fluoride-induced developmental neurotoxicity, specifically focusing on PRKAA1 in regulating the PINK1/Parkin pathway, we established a Sprage Dawley rat model with continuous sodium fluoride (NaF) exposure and an NaF-treated SH-SY5Y cell model. We found that NaF exposure increased the levels of LC3-Ⅱ and p62, impaired autophagic degradation, and subsequently blocked autophagic flux. Additionally, NaF exposure increased the expression of PINK1, Parkin, TOMM-20, and Cyt C and cleaved PARP in vivo and in vitro, indicating NaF promotes mitophagy and neuronal apoptosis. Meanwhile, phosphoproteomics and western blot analysis showed that NaF treatment enhanced PRKAA1 phosphorylation. Remarkably, the application of both 3-methyladenosine (3-MA; autophagy inhibitor) and dorsomorphin (DM; AMPK inhibitor) suppressed NaF-induced neuronal apoptosis by restoring aberrant mitophagy. In addition, 3-MA attenuated an increase in p62 protein levels and NaF-induced autophagic degradation. Collectively, our findings indicated that NaF causes aberrant mitophagy via PRKAA1 in a PINK1/Parkin-dependent manner, which triggers neuronal apoptosis. Thus, regulating PRKAA1-activated PINK1/Parkin-dependent mitophagy may be a potential treatment for NaF-induced developmental neurotoxicity. [Display omitted] • NaF exposure caused developmental neurotoxicity. • NaF-induced neuronal apoptosis results from aberrant mitophagy. • PRKAA1 regulates PINK1/Parkin-dependent neuronal mitophagy. • Targeted intervention of PRKAA1-mediated mitophagy alleviates NaF-induced neuronal apoptosis. [ABSTRACT FROM AUTHOR]

Excessive fluoride exposure can cause liver injury, but the specific mechanisms need further investigation. We aimed to explore the role of impaired lysosomal biogenesis and defective autophagy in fluoride-induced hepatotoxicity and its potential mechanisms, focusing on the role of transcription factor E3 (TFE3) in regulating hepatocyte lysosomal biogenesis. To this end, we established a Sprague-Dawley (SD) rat model exposed to sodium fluoride (NaF) and a rat liver cell line (BRL3A) model exposed to NaF. The results showed that NaF exposure diminished liver function and led to apoptosis as well as autophagosome accumulation and impaired autophagic degradation. In addition, NaF exposure caused compromised lysosome biogenesis and decreased lysosomal degradation, and inhibited TFE3 nuclear translocation. Notably, the mTOR inhibitors rapamycin (RAPA) and Ad-TFE3 promoted lysosomal biogenesis and enhanced lysosomal degradation function. Furthermore, RAPA and Ad-TFE3 reduced NaF-induced apoptosis by alleviating impaired autophagic degradation. In conclusion, NaF impairs lysosomal biogenesis by inhibiting TFE3 nuclear translocation, decreasing lysosomal degradation function, resulting in impaired autophagic degradation, and ultimately inducing apoptosis. Therefore, TFE3 may be a promising therapeutic target for fluoride-induced hepatotoxicity. [Display omitted] • NaF-induced apoptosis in hepatocytes is caused by impaired autophagic degradation. • Lysosomal biogenesis disorders induce a decrease in lysosomal degradation function. • TFE3 is a key factor in the regulation of lysosomal biogenesis. • TFE3 nuclear translocation and overexpression alleviate NaF-induced apoptosis. [ABSTRACT FROM AUTHOR]

We compare two mechanisms to implement a simple binary choice, e.g. adopt one of two proposals. We show that when neither alternative is ex ante preferred, simple majority voting cannot implement the first best outcome. We introduce a simple bidding mechanism where votes can be bought at a quadratic cost and voters receive rebates equal to the average of others' payments. This mechanism is budget-balanced, individually rational, and fully efficient in the limit. Moreover, the mechanism redistributes from those that gain from the outcome to those that lose and everyone is better off under bidding compared to voting. We test the two mechanisms in the lab using an environment with “moderate” and “extremist” voters. The observed efficiency losses under voting are close to theoretical predictions and significantly larger than under bidding. Because of redistribution, the efficiency gain from bidding benefits mostly the moderate voters. [ABSTRACT FROM AUTHOR]

Fluoride is capable of inducing developmental neurotoxicity; regrettably, the mechanism is obscure. We aimed to probe the role of lysosomal biogenesis disorder in developmental fluoride neurotoxicity—specifically, the regulating effect of the transient receptor potential mucolipin 1 (TRPML1)/transcription factor EB (TFEB) signaling pathway on lysosomal biogenesis. Sprague-Dawley rats were given fluoridated water freely, during pregnancy to the parental rats to 2 months after delivery to the offspring. In addition, neuroblastoma SH-SY5Y cells were treated with sodium fluoride (NaF), with or without mucolipin synthetic agonist 1 (ML-SA1) or adenovirus TFEB (Ad-TFEB) intervention. Our findings revealed that NaF impaired learning and memory as well as memory retention capacities in rat offspring, induced lysosomal biogenesis disorder, and decreased lysosomal degradation capacity, autophagosome accumulation, autophagic flux blockade, apoptosis, and pyroptosis. These changes were evidenced by the decreased expression of TRPML1, nuclear TFEB, LAMP2, CTSB, and CTSD, as well as increased expression of LC3-II, p62, cleaved PARP, NLRP3, Caspase1, and IL-1β. Furthermore, TRPML1 activation and TFEB overexpression both restored TFEB nuclear protein expression and promoted lysosomal biogenesis while enhancing lysosomal degradation capacity, recovering autophagic flux, and attenuating NaF-induced apoptosis and pyroptosis. Taken together, these results show that NaF promotes the progression of developmental fluoride neurotoxicity by inhibiting TRPML1/TFEB expression and impeding lysosomal biogenesis. Notably, the activation of TRPML1/TFEB alleviated NaF-induced developmental neurotoxicity. Therefore, TRPML1/TFEB may be promising markers of developmental fluoride neurotoxicity. [Display omitted] • NaF induces learning and memory as well as memory retention capacities impairment. • NaF induces autophagic flux blockade, apoptosis, and pyroptosis. • The TRPML1/TFEB mediates NaF-induced lysosomal biogenesis disorder. • The intervention of TRPML1/TFEB alleviates NaF-induced developmental neurotoxicity. [ABSTRACT FROM AUTHOR]

Fluoride can induce hepatotoxicity, but the mechanisms responsible are yet to be investigated. This study sought to investigate the role and mechanism of mitochondrial reactive oxygen species (mtROS), autophagy, and ferroptosis in fluoride-induced hepatic injury with a focus on the role of mtROS-mediated cross-talk between autophagy and ferroptosis. To this end, an in vivo Sprague-Dawley rat model and in vitro BRL3A cells were exposed to sodium fluoride (NaF). The results revealed that NaF exposure diminished the mitochondrial membrane potential, increased mtROS production and TOMM20 expression, and induced autophagic flux blockage and ferroptosis in vivo and in vitro. Furthermore, the autophagy activator (RAPA) enhanced GPX4 expression while inhibiting ACSL4 expression, reduced the accumulation of ferrous ions in BRL3A cells, and restored lipid peroxidation levels, thus inhibiting ferroptosis. Fer-1, a ferritinase inhibitor, downregulated the expression of LC3-II and p62, increased the number of autolysosomes while decreasing the number of autophagosomes, and alleviated the blockage of autophagic flux by improving autophagic degradation. These results suggest the occurrence of a cross-talk between autophagy and ferroptosis. The mtROS inhibitor (Mito-TEMPO) could alleviate autophagic flux blockage and inhibit ferroptosis in NaF-induced liver injury. In addition, the cross-talk between NaF-induced autophagy and ferroptosis was dependent on the mtROS pathway. [Display omitted] • NaF induces mitochondrial damage. • NaF induces autophagic flux blockage and ferroptosis. • Fer-1 effectively alleviates mtROS-dependent autophagic flux blockage. • RAPA is involved in the regulation of mtROS-dependent ferroptosis. • NaF-induced cross-talk of autophagy and ferroptosis is mtROS-dependent. [ABSTRACT FROM AUTHOR]

In the meat industry, it is essential to monitor and identify meat freshness grades due to its impact on the safety of human diets. This study aimed to identify premium, sub-fresh, and spoiled lamb samples using visible and near-infrared (Vis-NIR) hyperspectral imaging (HSI) in the range of 400–1000 nm coupled with chemometrics methods. The two-dimensional correlation spectroscopy (2D-CS) was utilized to select effective wavelengths for simplifying the model and increasing the calculation speed. The capabilities of the four models including partial least squares discriminant analysis (PLS-DA), soft independent modelling of class analogy (SIMCA), back propagation neuron network (BP), decision tree (DT) and random forest (RF) were compared to select the best identification model. The results showed that the RF model generated excellent performance, the accuracies of the training and test sets were 93% and 91%, respectively. In summary, this study showed that it was feasible to rapidly and non-destructively identify and evaluate the freshness grades of lamb using Vis-NIR. • Vis-NIR spectroscopy and chemometrics were used to determine freshness grades of lamb. • Spectral preprocessing and wavelength selection were applied to optimize the models. • The 2D-CS-RF model provided fast recognition with 91% accuracy on the testing set. [ABSTRACT FROM AUTHOR]

One of transcription factors of the T-box family, Brachyury has been implicated in tumorigenesis of many types of cancers, regulating cancer cell proliferation, metastasis, invasion and epithelial-to-mesenchymal transition (EMT). However, the role of Brachyury in breast cancer cells has been scarcely reported. The present study aimed to investigate the expression and role of Brachyury in breast cancer. Brachyury expression was analyzed by qRT-PCR and Western blot. The correlations between Brachyury expression and clinicopathological factors of breast cancer were determined. Involvement of EMT stimulation and hypoxia-inducible factor-1α (HIF-1α) expression induction by Brachyury was also evaluated. Moreover, the effect of Brachyury on tumor growth and metastasis in vivo was examined in a breast tumor xenograft model. Brachyury expression was enhanced in primary breast cancer tissues and Brachyury expression was correlated with tumor stage and lymph node metastasis. Hypoxia enhanced Brachyury expression, the silencing of which blocked the modulation effect of hypoxia on E-cadherin and vimentin expression. Brachyury significantly augmented HIF-1alpha expression via PTEN/Akt signaling as well as accelerated cell proliferation and migration in vitro . Additionally, Brachyury accelerated breast tumor xenograft growth and increased lung metastasis in nude mice. In summary, our data confirmed that Brachyury might contribute to hypoxia-induced EMT of breast cancer and trigger HIF-1alpha expression via PTEN/Akt signaling. [ABSTRACT FROM AUTHOR]

Macrophages play an important role in the pathogenesis of proliferative vitreoretinopathy (PVR). M2 macrophages can promote tissue remodeling and repair. In this study, CD206 positive M2 type macrophages were found in preretinal fibrous membranes of the mouse model of PVR induced by the intravitreal injection of retinal pigment epithelial (RPE) cells. Notch signaling determines M2 macrophage polarization. The specific inhibition of Notch signaling pathway by the intravitreal injection of γ-secretase inhibitor DAPT attenuated RPE cells-induced PVR formation as demonstrated by the decreased expression of α-SMA, and inhibited M2 type macrophage infiltation as demonstrated by the decreased expression of Arg-1. Notch signaling may modulate PVR formation by regulating M2 type macrophage polarization. [ABSTRACT FROM AUTHOR]

N-methyl-N-nitrosourea (MNU) is a prevalent environmental carcinogen, which leads to tumors in various organs in animal models, while the mechanisms involved were still not fully understood. It is well known that anomalous angiogenesis is a key step in tumorigenesis and progression. In this study, we found that MNU induced abnormal angiogenesis which was accompanied by upregulation of rspo1 , p53 and vegfaa in zebrafish embryos. Moreover, it revealed that MNU-induced ectopic sprouting of blood vessels was significantly reduced in rspo1 -knockdown but not p53 -knockdown embryos, indicating that rspo1 was necessary for MNU-induced abnormal angiogenesis. Additionally, pharmaceutical activation or inhibition of Wnt/β-catenin signaling pathway using (2'Z,3'E)− 6-bromoindirubin-3'-oxime or CCT036477 significantly increased or inhibited the pro-angiogenic effect of MNU on developing zebrafish embryos, which was confirmed by the effect of proliferation and migration in MNU-treated bEnd.3 cells. These data together indicated that rspo1/Wnt/β-catenin/vegfaa axis is involved in the modulation of MNU-induced anomalous angiogenesis. • MNU induces abnormal embryonic angiogenesis in zebrafish. • MNU up-regulates rspo1/vegfaa expression in zebrafish. • MNU induces anomalous angiogenesis through regulating Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

Peanut stem rot caused by Sclerotium rolfsii is a serious soil-borne disease and poses a threat to the peanut production. The antibiotic fungicide tetramycin has a broad antifungal spectrum against multiple pathogens and possess low environmental risks. In current study, a total of 250 isolates collected from Huanghuai peanut-growing region of China (Henan, Shandong and Hebei Province) were used to establish the baseline sensitivity of S. rolfsii to tetramycin. The baseline sensitivity curve was unimodal and distributed from 0.01 to 0.36 mg/L, with a mean EC 50 (50% effective concentration) value of 0.11 ± 0.06 mg/L. Tetramycin also had strong inhibitory activity on the formation and germination of sclerotia. There was no significant correlation of S. rolfsii sensitivity to tetramycin and other commonly used SDHI (succinate dehydrogenase inhibitor), QoI (quinone outside respiration inhibitor) and DMI (demethylation inhibitor) fungicides. Moreover, tetramycin significantly increased the cell membrane permeability and reduced the oxalate acid content. Greenhouse experiments showed that tetramycin has both protective and curative efficacy against S. rolfsii , while protective efficacy was higher than curative efficacy. Anyhow, the bioactivity of tetramycin is similar (curative efficacy) or higher (protective efficacy) than the control fungicide validamycin. In terms of application method, root drench may be more suitable for tetramycin than spraying, because root drench of tetramycin obtained a higher efficacy. These results indicated that tetramycin may be a potential alternative fungicide for the efficient control of peanut stem rot. ● The baseline sensitivity of S. rolfsii to tetramycin was 0.11 ± 0.06 mg/L and ranged from 0.01 to 0.36 mg/L. ● Tetramycin had both protective and curative efficacy against S. rolfsii. ● There was no correlation of S. rolfsii sensitivity to tetramycin and other commonly used SDHI, QoI and DMI fungicides. ● Compared with spraying, tetramycin may be more suitable for root irrigation to control S. rolfsii. [ABSTRACT FROM AUTHOR]

Innate lymphoid cells (ILCs) are a newly identified heterogeneous family of innate immune cells. We conducted this study to investigate the frequency of circulating ILC subsets in various chronic kidney diseases (CKD). In DN, the proportion of total ILCs and certain ILC subgroups increased significantly. Positive correlations between proportion of total ILCs, ILC1s and body mass index, glycated hemoglobin were observed in DN. In LN, a significantly increased proportion of ILC1s was found in parallel with a reduced proportion of ILC2s. The proportions of total ILCs and ILC1s were correlated with WBC count and the level of C3. In all enrolled patients, the proportion of total ILCs and ILC1s was significantly correlated with the levels of ACR and GFR. In the present study, the proportion of circulating ILC subsets increased significantly in various types of CKD and correlated with clinico-pathological features, which suggests a possible role for ILCs in CKD. [ABSTRACT FROM AUTHOR]

An Eu(phen) 2 (NO 3) 3 complex was synthesized from a single 1,10-phenanthroline (phen) ligand; the complex possessed a special porous structure, which increased its specific surface area and resulted in a stronger ultraviolet absorption. Flexible light-emitting fibers prepared from the complex via electrospinning exhibited improved photophysical properties, and the quantum yield calculated via the Judd–Ofelt (J–O) theory was up to 55.4%. Moreover, the fluorescence lifetime of the fibers was longer than that of Eu(phen) 2 (NO 3) 3. Under irradiation with 340 ​nm UV light, stronger fluorescence quenching was observed with increasing Fe3+ concentration, highlighting the Fe3+ adsorption capabilities of the present system. Fluorescence measurements showed that the complex had high sensitivity for Fe3+ in aqueous solution. The fluorescence characteristics and porous structure of the complex not only meet the requirements of precursors for flexible high-luminescence fibers, but also have promising application potential for ion adsorption and sensing in aqueous solution. [Display omitted] • Eu(phen) 2 (NO 3) 3 with porous structure was successfully prepared. • Eu(phen) 2 (NO 3) 3 exhibited strong fluorescence emission. • Eu(phen) 2 (NO 3) 3 showed specific sensing and high sensitivity to Fe3+. • Eu(phen) 2 (NO 3) 3 /PAN-based fibers exhibited longer fluorescence lifetime. [ABSTRACT FROM AUTHOR]

Fluoride is capable of inducing developmental neurotoxicity, yet its mechanisms remain elusive. We aimed to explore the possible role and mechanism of autophagic flux blockage caused by abnormal lysosomal pH in fluoride-induced developmental neurotoxicity, focusing on the role of V-ATPase in regulating the neuronal lysosomal pH. Using Sprague-Dawley rats exposed to sodium fluoride (NaF) from gestation through delivery until the neonatal offspring reached six months of age as an in vivo model. The results showed that NaF impaired the cognitive abilities of the offspring rats. In addition, NaF reduced V-ATPase expression, diminished lysosomal degradation capacity and blocked autophagic flux, and increased apoptosis in the hippocampus of offspring. Consistently, these results were validated in SH-SY5Y cells incubated with NaF. Moreover, NaF increased the SH-SY5Y lysosomal pH. Mechanistically, V-ATPase B2 overexpression and ATP effectively restored V-ATPase expression, reducing NaF-induced lysosomal alkalinization while increasing lysosomal degradation capacity. Notably, those above pharmacological and molecular interventions diminished NaF-induced apoptosis by restoring autophagic flux. Collectively, the present findings suggested that NaF impairs the lysosomal pH raised by V-ATPase. This leads to reduced lysosomal degradation capacity and triggers autophagic flux blockage and apoptosis, thus contributing to neuronal death. Therefore, V-ATPase might be a promising indicator of developmental fluoride neurotoxicity. [Display omitted] • NaF exposure caused developmental neurotoxicity. • NaF-induced neuronal apoptosis results from autophagic flux blockage. • Raised lysosomal pH disrupting lysosomal degradation caused autophagic flux blockage. • V-ATPase is a crucial factor regulating neuronal lysosomal pH. • Upregulation of V-ATPase alleviate NaF-induced developmental neurotoxicity. [ABSTRACT FROM AUTHOR]

We investigated the phytoremediation potential of Elodea nuttallii to remove rare earth metals from contaminated water. The laboratory experiments were designed to assess the responses induced by lanthanum (5–20 mg L −1 ) in E. nuttallii over a period of 7 days. The results showed that most La (approximately 85%) was associated with the cell wall. The addition of La to the culture medium reduced the concentration of K, Ca, Cu, Mg, and Mn. However, O 2 ·− levels increased with a concomitant increase in the malondialdehyde (MDA) concentration as the La concentration increased, which indicated that the cells were under oxidative stress. Significant reductions in the levels of chlorophyll (Chl) a , b , and carotenoids (Car) were observed in a concentration-dependent manner. However, the levels of reduced glutathione (GSH), total non-protein thiols (TNP-SH) and phytochelatins (PCs) increased for all La concentrations. The results suggested that La was toxic to E. nuttallii because it induced oxidative stress and disturbed mineral uptake. However, E. nuttallii was able to combat La induced damage via an immobilization mechanism, which involved the cell wall and the activation of non-enzymatic antioxidant. [ABSTRACT FROM AUTHOR]

The association between prenatal exposure to the metal mixture and allergic diseases is poorly understood. We aimed to explore the individual effect and the combined effect of prenatal exposure to vanadium (V), chromium (Cr), nickel (Ni), arsenic (As), cadmium (Cd), thallium (Tl), and lead (Pb) on early childhood allergic diseases based on a birth cohort study that included 628 mother-infant pairs. Metals were measured in maternal urine samples collected in the first, second, and third trimesters. Children were prospectively followed up at age 4 years to collect information on allergic rhinitis, wheeze, and eczema status. By applying logistic regression models, weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR), the different statistical analyses revealed urinary metals were only associated with early childhood allergic rhinitis. The averaged prenatal As exposure was significantly associated with an increased OR for allergic rhinitis in both single-metal (OR = 2.04, 95% CI: 1.35, 3.07) and multiple-metal logistic regression models (OR = 1.78, 95% CI: 1.15, 2.78). The WQS index of mixed metal exposure was positively associated with allergic rhinitis (OR = 1.66, 95% CI: 1.26, 2.19), and As and Tl had the largest weights in the WQS index (weighted 0.51 and 0.29, respectively). The BKMR analysis also showed the overall effect of the metal mixture was significantly associated with allergic rhinitis when all the metals were at their 55th percentile or above, compared to their 50th percentile. The effect of As and Tl on the risk of allergic rhinitis was significant when all of the other metals were fixed at the specific percentiles. Our findings suggest that prenatal co-exposure to higher levels of the seven metals increases the risk of allergic rhinitis in children, and As and Tl may contribute most to the combined risk. • The effects of prenatal exposure to multiple metals on childhood allergic disease were investigated. • Prenatal metal mixture exposure was only associated with childhood allergic rhinitis. • Arsenic and thallium contributed most to the overall risk of childhood allergic rhinitis. [ABSTRACT FROM AUTHOR]

Insect defensins are effector components of the innate defense system. Defensins, which are widely distributed among insects, are a type of small cysteine-rich plant antimicrobial peptides with broad-spectrum antimicrobial activity. Here, the cDNAs of the black soldier fly, Hermetia illucens (L.), encoding six defensins, designated herein as Hidefensin1-1, 2, 3, 4, 5, 6. Moreover, Hidefensin1-1, 2, and 5 were identified for the first time by genome-targeted analysis. These Hidefensins were found to mainly adopt α-helix and β-sheet conformation homology as modeled by PRABI, Swiss-Model and ProFunc server. Six conserved cysteine residues that contribute to three disulfide bonds formed the spacing pattern "C-X 12 -C-X 3 -C-X 9 -C-X 5 -C-X-C", which play a vital role in the molecular stability of Hidefensins. Phylogenetic analysis revealed that the homology of five Hidefensins (except Hidefensin4) was about 59%–92% compared with other insect defensins, indicating that they are novel antimicrobial peptides genes in black soldier fly. Furthermore, the Hidefensin1-1 was expressed in the Escherichia coli strain BL21(DE3) as a fusion protein with thioredoxin. Results showed that the purified TRX-Hidefensin1-1 exerted strong inhibitory effects against the Gram-positive bacteria Staphylococcus aureus and the Gram-negative bacteria Escherichia coli. The inhibitory efficacy of TRX-Hidefensin1-1 against Gram-positive bacteria was better than that against Gram-negative bacteria. These results indicated that Hidefensin1-1 has potent antimicrobial activities against test pathogens. • Three novel antimicrobial peptide defensin genes from Hermetia illucens (L.) has been identified. • The CSαβ motif of Hidefensin1-1 is important to antimicrobial activity. • The peptide shows significant antimicrobial activity against pathogenic Gram-positive and Gram-negative bacteria. [ABSTRACT FROM AUTHOR]

Fluoride is capable of inducing developmental neurotoxicity, but the mechanisms involved remain unclear. We aimed to explore the role of autophagosome-lysosome fusion in developmental fluoride neurotoxicity, particularly focusing on the interaction between ATG14 and the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex. We developed in vivo models of Sprague–Dawley rats exposed to sodium fluoride (NaF) from the pregnancy of parental rats until the offspring were two months old and in vitro models of NaF and/or Ad-ATG14-treated SH-SY5Y cells. We assessed neurobehavioral changes in offspring and further investigated the effects of NaF exposure on autophagic flux, apoptosis, autophagosome-lysosome fusion, and the interaction between ATG14 and the SNARE complex. NaF exposure impaired offspring learning and memory capabilities and induced the accumulation of autophagosomes and autophagic flux blockage and apoptosis, as indicated by increased LC3-II, p62, and cleaved-caspase-3 expression in vivo and in vitro. In addition, NaF treatment downregulated the protein expression of ATG14 and the SNARE complex and induced autophagosome-lysosome fusion blockage as evidenced by decreased ATG14, STX17, SNAP29, and VAMP8 expression and diminished colocalization of autophagosomes and lysosomes in vivo and in vitro. Furthermore, ATG14 upregulation enhanced the interaction of ATG14 and the SNARE complex to facilitate autophagosome-lysosome fusion, thereby restoring autophagic flux and alleviating NaF-induced apoptosis. In conclusion, NaF exhibited developmental neurotoxicity by restraining the interaction of ATG14 with the SNARE complex and hindering autophagosome-lysosome fusion, thereby participating in the occurrence and development of fluoride neurotoxicity. Notably, ATG14 upregulation protects against developmental fluoride neurotoxicity, and ATG14 may serve as a promising biomarker for further epidemiological investigation. [Display omitted] • NaF induced autophagosome-lysosome fusion blockage. • NaF weakened the interaction of ATG14 and SNARE complex. • ATG14 regulates the SNARE complex in NaF-induced developmental neurotoxicity. • ATG14 upregulation restored autophagosome-lysosome fusion and autophagic flux. • ATG14 upregulation protects against developmental fluoride neurotoxicity. [ABSTRACT FROM AUTHOR]

• Multi-element analysis combined with chemometric techniques was used to classify three Codonopsis Radix varieties. • The content of twenty-two elemens in 147 samples from three R. Codonopsis varieties was analyzed. • Twenty-two elements with significant differences could clearly distinguish three R. Codonopsis varieties. • The correct classification rate of linear discriminant analysis was 98.6 %. • Environment with less AAP and lower RH was more conducive for cultivation of high-quality R. Codonopsis. The feasibility of using chemometric techniques associated with multi-element analysis for the classification of three varieties of Codonopsis Radix samples was investigated, and the correlation between environmental factors and metal element content was further explored. It was found that R. Codonopsis was a good source of potassium (average content of 9420 μg/g), magnesium (average content of 1590 μg/g), calcium (average content of 388 μg/g) and iron (average content of 333 μg/g). The statistical analysis results indicated that twenty-two elements content (K, Ca, Mg, Fe, Se, Na, Zn, V, Cu, Cr, Mn, Ni, Co, Sr, Pb, Cd, As, Hg, Al, Ba, Tl and U) were significantly different among three R. Codonopsis varieties, hence it was possible to discriminate R. Codonopsis according to their varieties by LDA (correct classification rate of 98.6 % and cross-validation rate of 95.9 %). In addition, the correlation analysis results indicated that the relative humidity showed significantly negative correlation with essential elemental content such as K, Mg, Ca and Se (correlation coefficients ranged from -0.321 to -0.564, p < 0.05); the annual average precipitation exhibited significantly positive correlation with toxic elemental elements such as As, Cd, Pb and Hg (correlation coefficients ranged from 0.266 to 0.897, p < 0.05). [ABSTRACT FROM AUTHOR]

Based on a medical record or questionnaire survey approach, previous epidemiological studies have investigated associations between maternal antibiotic exposure during pregnancy and childhood allergic diseases. However, biomonitoring studies on the prenatal low-dose antibiotic exposure, mainly from the environment and contaminated food, and in relation to children allergic diseases, are missing. This research aimed to examine the associations between prenatal low-dose antibiotic exposure measured at multiple time points and children current allergic diseases at 4 years of age. The current study including 2453 mother-child pairs was based on the Ma'anshan Birth Cohort study. Selected 41 antibiotics and their two metabolites, which including human antibiotics (HAs), preferred as human antibiotics (PHAs), veterinary antibiotics (VAs) and preferred as veterinary antibiotics (PVAs), in urine samples from 2453 pregnant women were biomonitored through liquid chromatography-triple quadrupole tandem mass spectrometry. Information on children current allergic diseases were collected via validated questionnaires. Generalized estimating equation were used to explore the associations between the repeated measurements of maternal urinary antibiotic over three trimesters and current allergic diseases in children. The detection rates of nine individual antibiotics in the three trimester during pregnancy are greater than 10%, and the 90th percentile concentration of the detected antibiotics ranges from 0.07 to 22.34 µg/g, and the 95th percentile concentration ranges from 0.17 to 59.57 µg/g. Among the participants, each one-unit concentration increment of sulfamethazine (adjusted OR=1.28, 95% CI: 1.10, 1.49, P - FDR =0.014) in the first trimester and ciprofloxacin (adjusted OR=1.17, 95% CI: 1.07, 1.28, P - FDR =0.008) in the second trimester were associated with an increased risk of current eczema in children. In the third trimester, each one-unit concentration increment of oxytetracycline (adjusted OR=1.90, 95% CI: 1.30, 2.78, P - FDR =0.014) was associated with an increased risk of current asthma in children. Gender-stratified analyses demonstrated that no gender differences were observed in the associations between prenatal antibiotic exposure and current allergic diseases in children. Maternal exposure to certain specific VAs or PVAs (sulfamethazine, ciprofloxacin and oxytetracycline) in different trimesters was associated with an increased risk of current asthma and current eczema in 4-year-old children. No gender differences were found in these associations. Further studies are warranted to confirm our findings and explore the potential mechanisms. [Display omitted] • Pregnant women were commonly exposed to low-dose antibiotics during pregnancy. • Sulfamethazine exposure (1st trimester) increases the risk of eczema in children. • Ciprofloxacin exposure (2nd trimester) elevates the risk of eczema in children. • Oxytetracycline exposure (3nd trimester) increases the risk of asthma in children. • No gender differences were found in these associations. [ABSTRACT FROM AUTHOR]

Abstract: An ultrasensitive chemiluminescence (CL) method for determination of melamine at picogram level was reported in a flow system. It was found that melamine can accelerate the electrons transferring rate of excited 3-aminophthalate with notable enhanced CL intensity of luminol-hydrogen peroxide reaction. The increased CL intensity was proportional to the concentration of melamine in the range from 2.5 to 250pgmL−1 (R 2 =0.9953), with a detection limit of 0.9pgmL−1 (3σ) and the relative standard deviations lower than 5.0%. The proposed method was successfully applied to determine the melamine in liquid milk, yogurt, human urine and serum samples with the recovery of 98–105%, 93–105%, 98–105%, 97–109%, respectively. [Copyright &y& Elsevier]

Abstract: Objectives. : To study the role of arsenic trioxide (As2O3) in regulating peritoneal invasive activity of ovarian carcinoma cells in vitro and in vivo. Methods. : The effects of As2O3 on human ovarian cancer cell lines (3AO, SW626 and HO-8910PM) migration, invasion and adhesion with tumor cells and human peritoneal mesothelial cells (HPMC) were observed by means of cell migration test, cell invasion test and cell adhesion test. The effects of As2O3 on MMP-2, MMP-9, TIMP-1 and TIMP-2 gene expressions and protein expressions of tumor cells were determined by RT-PCR and ELISA, respectively. In animal experiments, ovarian tumor cells were implanted into abdominal cavity of nude mice and then the nude mice were treated by intraperitoneal injection of different doses As2O3. The foci on the surface of peritoneum were counted. Results. : As2O3 inhibited tumor cells migration, invasion and adhesion with HPMC in a dose-dependent manner, while the same treatment enhanced tumor cell–tumor cell interactions. As2O3 inhibited mRNA and protein expressions of MMP-2, MMP-9 and TIMP-2 of tumor cells. In contrast, As2O3 increased mRNA and protein expressions of TIMP-1. As2O3 could reduce tumor cells peritoneal metastasis in nude mice. Conclusion. : As2O3 inhibits in vitro and in vivo peritoneal invasive activity of ovarian carcinoma cells in a dose-dependent manner. Its anti-invasive activity may be the results of reduced cell motility, inhibited attachment of tumor cells to HPMC and enhanced tumor cell–tumor cell interaction, as well as down-regulation of MMP-2 and MMP-9 levels and up-regulation of TIMP-1 level. [Copyright &y& Elsevier]

In mammals, β-catenin participates in innate immune process through interaction with NF-κB signaling pathway. However, its role in teleost immune processes remains largely unknown. We aimed to clarify the function of β-catenin in the natural defense mechanism of Qi river crucian carp (Carassius auratus). β-catenin exhibited a ubiquitous expression pattern in adult fish, as indicated by real-time PCR analysis. Following lipopolysaccharide (LPS), Polyinosinic-polycytidylic acid (polyI: C) and Aeromonas hydrophila (A. hydrophila) challenges, β-catenin increased in gill, intestine, liver and kidney, indicating that β-catenin likely plays a pivotal role in the immune response against pathogen infiltration. Inhibition of the β-catenin pathway using FH535, an inhibitor of Wnt/β-catenin pathway, resulting in pathological damage of the gill, intestine, liver and kidney, significant decrease of innate immune factors (C3 , defb3 , LYZ-C , INF-γ), upregulation of inflammatory factors (NF-κB , TNF-α , IL-1 , IL-8), and downregulation of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) activities, increase of Malondialdehyde (MDA) content. Following A. hydrophila invasion, the mortality rate in the FH535 treatment group exceeded that of the control group. In addition, the diversity of intestinal microflora decreased and the community structure was uneven after FH535 treatment. In summary, our findings strongly suggest that β-catenin plays a vital role in combating pathogen invasion and regulating intestinal flora in Qi river crucian carp. • β-catenin were upregulated in different tissues after pathogen challenge.. • Inhibition of β-catenin led to pathological damage of tissues.. • Inhibition of β-catenin resulted in low immune defense capacity. • Inhibition of β-catenin destroyed intestinal flora structure. [ABSTRACT FROM AUTHOR]

Experimental and epidemiological studies have linked antibiotics use to gut dysbiosis-mediated risk of chronic metabolic diseases. However, whether adiposity is linked to antibiotic exposure in elderly remains inadequately understood. To investigate the association between internal exposure of antibiotics and adiposity in elderly by using a biomonitoring method. We included 990 participants (≥ 60 years) from the baseline survey of the Cohort of Elderly Health and Environment Controllable Factors in Lu'an city, China, from June to September 2016. Forty-five antibiotics and two metabolites in urine were monitored through liquid chromatography-electrospray tandem mass spectrometry (HPLC-MS/MS). Creatinine-corrected urinary concentrations were used to assess antibiotic exposure levels. Body mass index (BMI), waist circumference (WC) and body fat percentage (BFP) were used as indicators of adiposity. Multiple linear regression and binary logistic regression analyses were used to analyze the association of antibiotic concentrations with obesity-related indices. Subsequently, a gender-stratified analysis was performed. Of the included elderly, 50.7% were defined as having overweight/ obesity, 59.8% as having central preobesity/obesity, and 37.5% as having slightly high/high BFP. Linear regression analysis revealed that a 1-unit increase in the logarithmic transformation of norfloxacin concentrations was related with an increase of 0.29 kg/m2 (95% CI: 0.02–0.04), 0.99 cm (95% CI：0.24–1.75), and 0.69% (95% CI：0.21–1.17) in BMI, WC, and BFP, respectively. Compared with the control group, exposure to doxycycline (tertile 2: odds ratio, 2.06 [95% CI: 1.12–3.76]) and norfloxacin (tertile 2: 2.13 [1.05–4.29]; tertile 3: 2.07 [1.03–4.17]) had BMI-based overweight/obesity risk. Additionally, ciprofloxacin (tertile 2: 2.06 [1.12–3.76]), norfloxacin (tertile 3: 2.95 [1.34–6.49]), and florfenicol (tertile 3: 1.84 [1.07–3.14]) were related to WC-based central preobesity/obesity risk. Norfloxacin (tertile 3: 2.54 [1.23–5.24]) was positively associated with a slightly high/high BFP risk. Gender-stratified analysis demonstrated an increased adiposity risk in women compared with men. Our research provided an evidence that exposure to specific types of antibiotics (tetracyclines and fluoroquinolones) probably from the food chain contributed to obesity in elderly. Prospective cohort studies with larger sample size are warrented to explore the causation. • The elderly were widely exposed to antibiotics from various sources. • Some veterinary antibiotics were associated with adiposity risk in the elderly. • The significant associations differed by gender, and mainly existed in women. [ABSTRACT FROM AUTHOR]

Sn–Se based layer crystals, including both SnSe and SnSe 2 , are promising thermoelectric materials with intrinsic ultra-low thermal conductivity due to strong anharmonicity of phonon spectrum and special bonding circumstances. In contrast to the rigid growth condition, high cost, and poor mechanical property of single crystals, Sn–Se based polycrystalline samples prepared by spark plasma sintering (SPS) or hot-pressing are more friendly for industrial scale-up. Also, it is possible to take advantage of the anisotropic transport characteristics of the Sn–Se based compounds by introducing texture in polycrystalline samples. To investigate the influences of texture and off-stoichiometry on the thermoelectric property, Sn-rich millimeter-scale SnSe crystal sheets were used as precursor in SPS. Three types of polycrystalline samples with different composition, phase structure, and texture strength were obtained. The formation mechanism and their influences on the thermoelectric properties were studied and correlated. For comparison, Se-rich millimeter-scale SnSe 2 crystals were also prepared and sintered by SPS to achieve polycrystalline samples. The phase evolution, texture, thermoelectric properties and its difference and similarity with SnSe were also analyzed. By using millimeter-scale Sn-rich SnSe and Se-rich SnSe 2 crystal sheets as precursors, Sn–Se based polycrystalline samples were prepared by SPS, and the formation mechanism and the influences of composition, phase structure, and texture strength on the thermoelectric properties were studied and correlated. Image 1 • By using SnSe and SnSe 2 crystal sheets as precursors, Sn-Se based polycrystalline samples were prepared by SPS. • Formation mechanism and influences of composition, phase structure on the thermoelectric properties were studied. • The phase evolution, thermoelectric properties for SnSe 2 and its difference and similarity with SnSe were analyzed. [ABSTRACT FROM AUTHOR]

The widespread existence of microplastics in wastewater has caused great concern. As the exposure time of microplastics in the environment increases, the microplastic leaching solution (i.e.,chemical additives) may be released into the environment causing toxic effects. In this study, the effect of polystyrene (PS) microplastics on the anaerobic digestion system was investigated. The results showed that the exposure to 80 nm and 5 μm polystyrene microplastics with the concentrations of 0.2 g/L or lower did not significantly affect the cumulative methane production (P ≥ 0.05). On the other hand, 80 nm and 5 μm PS microplastic level of 0.25 g/L led to a decrease in methane production by 19.3% (P = 2 × 10−5) and 17.9% (P = 4 × 10−5), respectively. The 80 nm PS nanoplastics therefore had slightly higher inhibition capacity on methane production than 5 μm PS microplastics. The pH of all groups remained stable at 6.7–7.5. Volatile fatty acids (VFAs) concentration and ammonium-nitrogen concentration had no obvious relationship to PS micro and nanoplastics addition. Further investigation showed that PS micro and nanoplastics concentration of 0.25 g/L or higher could inhibit acidification and methanation stage of anaerobic digestion. However, the main negative influence of PS micro and nanoplastics on methane production was due to the severe inhibition on the methanization stage. • Impacts of micro and nanoplastics on anaerobic digestion system were investigated. • 80 nm polystyrene reduced CH 4 -production by 19.3%, while 5 μm polystyrene decreased by 17.9% during anaerobic digestion. • Inhibitory effects of nanoplastics on anaerobic digestion process were slightly more significant than that of microplastics. • Microplastics (80 nm and 5 μm) with a concentration of 0.25 g/L inhibit acidification and methanation of anaerobic digestion. [ABSTRACT FROM AUTHOR]

SnSe 2 compound, closely related to the well-known SnSe thermoelectric material, is a layered compound displaying strong anisotropic transport properties and intrinsically low lattice thermal conductivity. SnSe 2 is dimorphic, which has a well-defined hexagonal structure (JCPDS #01-089-3197, S-3197) and an unidentified structure described by JCPDS #00-038-1055. In this study, Br-doped SnSe 2 with both entangled phases were prepared by a melting and hot-pressing route. The evolution of phase structure with temperature was recorded by two cycles of DSC measurement and XRD. A complex, partly kinetically controlled phase transition between two structures was observed. SnSe 2 is stable only with coexistence of the two phases. By substituting Se with Br, both carrier concentration and Hall mobility are improved, along with the enhanced stability of the hexagonal structure S-3197. Meanwhile, an abnormal high thermal conductivity was discovered in Br-doped polycrystalline samples compared with both pristine SnSe 2 single crystal and non-doped polycrystalline samples, which is contradicted to the thumb of law that the "perfect" single crystal free of boundary scattering should possess a maximum lattice thermal conductivity, and that the doped samples should have a lower lattice thermal conductivity due to the point defect scattering aroused by dopant. The results suggest that intrinsic defects within grains, such as interstitial atoms, vacancies, and antisite defects, have much stronger scattering effects on phonons, than the grain boundaries and point defects introduced by dopants in polycrystalline samples, as shown in well-studied SnSe compound. The doping of Br in SnSe 2 not only increases the carrier concentration and carrier mobility at the same time, but also plays an important role in determining the phase structure. Image 1 [ABSTRACT FROM AUTHOR]

In this study, magnetic deep eutectic solvent-dispersive liquid-liquid microextraction combined with high-performance liquid chromatography method was developed for the extraction and determination of succinate dehydrogenase inhibitors in water, juice, wine, and vinegar. A new green magnetic deep eutectic solvent was synthesized using quaternary phosphorus salt, metal chloride, and fatty acid. The special self-dispersion magnetic deep eutectic solvent achieved rapid extraction without auxiliary dispersion and separation via neodymium magnets without centrifugation, avoiding the use of toxic disperser solvents and disperser instruments and reducing the separation time. The recovery of succinate dehydrogenase inhibitors under optimal extraction conditions was 76.5–97.8 %, and the limit of detection was 0.0011–0.0029 mg L−1. The method could be a fast, simple, green, and reliable alternative for the analysis of succinate dehydrogenase inhibitors. The self-dispersion magnetic deep eutectic solvent can facilitate the development of dispersive liquid-liquid microextraction methods of other pesticides in food samples. • The developed MDES-DLLME-HPLC method can be used for SDHIs detection. • Novel green hydrophobic MDESs can be synthesized by heating. • MDESs can self-disperse without assisted disperser solvent and equipment. • Magnetic separation can be achieved without magnetism strengthening. • MDESs are hydrophobic and suitable for aqueous samples. [ABSTRACT FROM AUTHOR]

Extensive antibiotic exposure in the general population has been documented by bio-monitoring, but data regarding antibiotic burden across three generations in families living in the same household are lacking. We investigated the distribution of antibiotics and the potential health risk among the three generations by selecting 691 participants from 256 households in Fuyang city, China. A total of 45 antibiotics and two metabolites were screened in urine samples through liquid chromatography electrospray tandem mass spectrometry. In total, 34 antibiotics were found in the samples with an overall detection frequency of 92.0%, and the detection frequencies of individual antibiotic ranged from 0.3% to 28.7%. Specifically, the concentrations of seven antibiotics (azithromycin, amoxicillin, oxytetracycline, levofloxacin, norfloxacin, trimethoprim and sulfamethoxazole) were extremely high (i.e., above 10, 000 ng/mL). The detection rates of tetracyclines were significantly different among the three generations, with parents having the highest detection rate. Penicillin V, chlortetracycline, doxycycline, enrofloxacin, and ciprofloxacin showed a higher detection frequency in parents, whereas tetracycline, danofloxacin, and ofloxacin were more likely to be found in grandparents. The proportions of the sum of the daily exposure dose of VAs and PVAs more than 1 μg/kg/d in children, parents, and grandparents were 31.6%, 39.5%, and 26.5%, respectively. A hazard index (HI) greater than 1 was observed in 14.7% children, which was less than the 23.6% in parents and slightly higher than the 11.8% in grandparents. Ciprofloxacin was the biggest contributor to HI among the three generations. Collectively, these findings indicate that households are widely exposed to various antibiotics in Fuyang city, where parents had the highest health risk associated with the disturbance of gut microbiota. Image 1 • Thirty-four antibiotics detected in urines of three generations living together. • The overall detection frequency (>90%) of antibiotics in each generation. • A higher detection frequency of antibiotics preferred for veterinary use in parents. • The HI greater than 1 in 23.6% of parents, much higher than the other generations. • Ciprofloxacin with the biggest contributor to the HI among the three generations. [ABSTRACT FROM AUTHOR]

[Display omitted] Pelargonic acid vanillylamide (PAVA), a capsaicin-type dacryagogue agent utilized for counter-terrorism and riot control, possesses a low stimulus threshold. This characteristic can lead to environmental contamination following its application and may easily result in secondary stimulation to personnel. Cobalt-doped Ti 3 C 2 -MXene nanosheets (Co 3 O 4 /Ti 3 C 2 @C) were synthesized for the purpose of activating peracetic acid (PAA) and degrading PAVA. A carbon layer was coated on the surface of Ti 3 C 2 -MXene nanosheets to address the challenge of poor oxygen resistance in MXenes, thus preventing a significant decline in surface reactivity. The BET surface area of Co 3 O 4 /Ti 3 C 2 @C was expanded to 149.6 m2/g, significantly exceeding that of Ti 3 C 2 (13.0 m2/g) and Co 3 O 4 (56.4 m2/g). With 0.5 mg/mL of Co 3 O 4 /Ti 3 C 2 @C and 0.35 mM of PAA, 100 mg/L of PAVA was completely degraded within 60 min. The augmented BET surface area and the presence of more active sites confer remarkable PAA activation and catalytic degradation properties toward PAVA. Parameters such as initial pH, PAVA concentration, catalyst dosage, and PAA concentration on PAVA degradation were systematically assessed. Furthermore, the reusability and stability of the nanocomposite were substantiated through recycling tests. Radical quenching experiments and electron paramagnetic resonance analysis demonstrated the acetylperoxy radical (CH 3 CO 3 ) as the primary species responsible for PAVA degradation. This research serves as an illustration of the utilization of MXene and transition metal activated PAA in wastewater treatment. [ABSTRACT FROM AUTHOR]

[Display omitted] Solar-driven interfacial evaporation materials based on nanocomposite hydrogels have emerged for seawater desalination. Nevertheless, the issue of mechanical degradation derived from the swelling behavior of hydrogel is often seriously underestimated, which strongly hinders the practical application for long-term solar vapor generation, especially in high-salinity brine. Herein, a novel CNT@Gel-nacre with enhanced capillary pumping design has been proposed and fabricated for tough and durable solar-driven evaporator through uniformly doping carbon nanotubes (CNTs) into the tough gel-nacre. Particularly, the salting out process gives rise to volume shrinkage and phase separation of polymer chains, endowing the nanocomposite hydrogel with significantly enhanced mechanical properties while simultaneously rendering more compact microchannels for water transportation, boosting the capillary pumping. Based on this unique design, the gel-nacre nanocomposite exhibits outstanding mechanical performances (13.41 MPa strength, 55.60 MJ m−3 toughness), especially mechanical durability in high salinity brine for long-term service. Furthermore, excellent water evaporation rate of 1.31 kg m-2h−1 and conversion efficiency of 93.5% in 3.5 wt% sodium chloride solution, as well as stable cycling without salt accumulation can be achieved. This work demonstrates an effective strategy for achieving solar-driven evaporator with superior mechanical properties and durability even in brine environment, showing huge potentials in long-term seawater desalination. [ABSTRACT FROM AUTHOR]

Toxin-antitoxin (TA) systems play critical roles in the environment adaptation of bacteria. Allosteric coupling between the N-terminal DNA-binding domain and the C-terminal toxin-binding domain of antitoxins contributes to conditional cooperativity in the functioning of type II TA. Herein, using circular dichroism (CD), nuclear magnetic resonance (NMR), X-ray crystallography, and size exclusion chromatography (SEC), the structure and DNA binding of CopA SO , a newly identified type II antitoxin in Shewanella oneidensis , were investigated. Our data show that CopA SO is a typical RHH antitoxin with an ordered N-terminal domain and a disordered C-terminal domain, and furthermore indicate that the C-terminal domain facilitates DNA binding of the N-terminal domain, which in turn induces the C-terminal domain to fold and associate. Image 1 • The structure and DNA binding of type Ⅱ antitoxin CopA SO were characterized. • X-ray crystallography study on CopA SO -N shows a typical RHH fold. • Biophysical investigation indicates allosteric effects of CopA SO -N on CopA SO -C. • DNA binding of CopA SO -N appears to induce CopA SO -C to fold and self-associate. [ABSTRACT FROM AUTHOR]

The ubiquity of wireless electronic-device connectivity has seen microwaves emerge as one of the fastest growing forms of electromagnetic exposure. A growing evidence-base refutes the claim that wireless technologies pose no risk to human health at current safety levels designed to limit thermal (heating) effects. The potential impact of non-thermal effects of microwave exposure, especially in electrically-excitable tissues (e.g., heart), remains controversial. We exposed human embryonic stem-cell derived cardiomyocytes (CM), under baseline and beta-adrenergic receptor (β-AR)-stimulated conditions, to microwaves at 2.4 GHz, a frequency used extensively in wireless communication (e.g., 4G, Bluetooth™ and WiFi). To control for any effect of sample heating, experiments were done in CM subjected to matched rates of direct heating or CM maintained at 37 °C. Detailed profiling of the temporal and amplitude features of Ca2+ signalling in CM under these experimental conditions was reconciled with the extent and spatial clustering of apoptosis. The data show that exposure of CM to 2.4 GHz EMF eliminated the normal Ca2+ signalling response to β-AR stimulation and provoked spatially-clustered apoptosis. This is first evidence that non-thermal effects of 2.4 GHz microwaves might have profound effects on human CM function, responsiveness to activation, and survival. • Microwaves at 2.4 GHz are fundamental to today's wireless communication (e.g., 4G, WiFi). • The non-thermal effects of 2.4 GHz microwaves on biological systems are controversial. • 2.4 GHz microwaves eliminated the response of human heart cells to β-AR stimulation. • Microwave-disrupted calcium signalling promoted spatially-clustered apoptosis. • The destructive effects of 2.4 GHz microwaves were mediated by non-thermal mechanisms. [ABSTRACT FROM AUTHOR]

Our previous study has shown that AT406, a first-in-class small molecular antagonist of IAPs (inhibitor of apoptosis proteins), inhibits pancreatic cancer cell proliferation in vitro and in vivo . The aim of this research is to increase AT406's sensitivity by adding short-chain C6 ceramide. We show that co-treatment of C6 ceramide dramatically potentiated AT406-induced caspase/apoptosis activation and cytotoxicity in established (Panc-1 and Mia-PaCa-2 lines) and primary human pancreatic cancer cells. Reversely, caspase inhibitors largely attenuated C6 ceramide plus AT406-induced above cancer cell death. Molecularly, C6 ceramide downregulated Bcl-2 to increase AT406's sensitivity in pancreatic cancer cells. Intriguingly, C6 ceramide-mediated AT406 sensitization was nullified with Bcl-2 shRNA knockdown or pretreatment of the Bcl-2 inhibitor ABT-737. In vivo , liposomal C6 ceramide plus AT406 co-administration dramatically inhibited Panc-1 xenograft tumor growth in severe combined immunodeficient (SCID) mice. The combined anti-tumor activity was significantly more potent than either single treatment. Expressions of IAPs (cIAP1/XIAP) and Bcl-2 were downregulated in Panc-1 xenografts with the co-administration. Together, we demonstrate that C6 ceramide sensitizes AT406-mediated anti-pancreatic cancer cell activity possibly via downregulating Bcl-2. [ABSTRACT FROM AUTHOR]

A novel GCRV strain isolated from healthy grass carp was named as grass carp reovirus - HH196 (GCRV-HH196), and its infection mechanism remains unclear. In this study, the grass carp ovary cell line (GCO cells) was used to investigate the cell death involved in GCRV-HH196 infection. The results showed that DNA damage, cells volume reduction and cytoplasm shrinkage happened during GCRV-HH196 infection. The mRNA expression levels of pro-apoptotic genes were up-regulated during infection. Two initiators of apoptosis, caspase 8 and caspase 9, and the executioner of apoptosis, caspase 3, were all significantly activated in GCRV-HH196-infected cells. Flow cytometry analysis showed that the number of apoptotic cells in infected cells was significantly higher than that in control cells as the infection progress. Meanwhile, autophagy was also involved in the regulation of GCRV - HH196 infection. We observed that LC3 puncta existed in cytoplasm in GCRV-HH196-infected cells. Furthermore, the protein level of LC3-Ⅱ and Beclin-1 increased, while that of p-Akt decreased in GCRV-HH196-infected cells. These results demonstrated that GCRV-HH196 may regulate apoptosis and autophagy for the virus proliferation and spread, which set a foundation for further research on the interaction between GCRV-HH196 and host. • Grass carp reovirus-HH196 (GCRV-HH196) infection leads to typical apoptosis GCO cells. • Caspases were activated during GCRV-HH196-induced apoptosis. • Pro-apoptotic genes levels up-regulated during GCRV-HH196-induced apoptosis. • LC3 protein shifted from diffuse distribution to punctate pattern in cytoplasmic upon infection. • The protein level of LC3-Ⅱ and Beclin-1 increased, while that of p-Akt decreased during infection. [ABSTRACT FROM AUTHOR]

The anharmonicity of the lattice vibrations caused by 5s2 lone-pair electrons at Sb site has been considered to be the main reason for the low thermal conductivity of the compounds such as Cu 3 SbSe 3 , Cu 3 SbS 3 and Cu 12 Sb 4 S 13. In this study, by substituting Sb with Ni/Co without 5s2 lone-pair electrons, the cubic Cu 3 Sb 1- x (Ni/Co) x S 3 compounds were successfully synthesized by SPS and the effect of lone-pair electrons was further studied. The results demonstrate that both of the alloying effect and the change of valence bond environment of the Sb site caused by doping have a great influence on phonon transport. In addition, the increase of thermal conductivity caused by the latter is much greater than the inhibition of thermal conductivity by the former, which indicates the vital effect of the 5s2 lone-pair electrons on the decrease of thermal conductivity. When x = 0.05, the figure-of-merit zT values of the Ni and Co doped samples reach the maximum of 0.94 and 0.85 ​at 623 ​K, respectively, which are much higher than those of the undoped sample and the Fe doped samples, showing the potential of the Ni and Co doped compounds as high performance thermoelectric materials. The cubic Cu 3 Sb 1- x (Ni/Co) x S 3 compounds were synthesized by SPS and the effect of lone-pair electrons was studied. When x = 0.05, the zT values of the Ni and Co doped samples reach the maximum of 0.94 and 0.85 ​at 623 ​K, respectively. [Display omitted] • The increase of thermal conductivity caused by doping is much greater than the inhibition by alloying effect. • Fe/Co/Ni doping is beneficial to promote the formation of cubic phase of 3-1-3 compounds. • zT values of Ni and Co doped samples reach the maximum of 0.94 and 0.85 ​at 623 ​K, respectively. [ABSTRACT FROM AUTHOR]

Gastroenteritis is a commonly diagnosed disease which sometimes may lead to hospitalization of the patients due to complications such as sepsis and dehydration. In the present study protective effect of AQU-019 against Salmonella enterica (S.enterica) induced gastroenteritis in rat model was investigated. Treatment of S.enterica infected rats with AQU-019 prevented intestinal tissue damage effectively in dose-dependent manner. The characteristic pathological features induced by S.enterica infection in rat intestines included, edema development, submucosal infiltration of leukocytes and cell necrosis. AQU-019 treatment at 1.25, 2.5, 5 and 10 mg/kg doses led to a significant (p < 0.05) reduction in MPO activity in the intestinal tissues of S.enterica infected rats. AQU-019 treatment effectively reversed S.enterica infection mediated reduction in ZO-1 and occludin expression in rat intestines. Urine volume of the AQU-019 treated rats increased significantly (p < 0.05) from day 2 to day 7 compared to the S.enterica infected group. Urine pH didn't showed any change in S.enterica infected rats on treatment with AQU-019 on day 1 to day 7. The bacterial numbers showed a significant (p < 0.05) decrease in S.enterica infected rat feces, urinary bladder and urethra on treatment with AQU-019. In summary, AQU-019 prevents intestinal epithelial damage and inhibits infiltration of neutrophils in S.enterica infected rats. Tight junction related protein expression was also regulated in S.enterica infected rats by AQU-019 treatment. Therefore, AQU-019 may be developed as a potent candidate for treatment of bacterial infection induced gastroenteritis. • Treatment of S.enterica infected rats with AQU-019 prevented intestinal tissue damage. • AQU-019 treatment led to a significant (p < 0.05) reduction in MPO activity in the intestinal tissues of S.enterica infected rats. • AQU-019 treatment effectively reversed S.enterica infection mediated reduction in ZO-1 and occludin expression in rat intestines. • Urine volume of the AQU-019 treated rats increased significantly (p < 0.05) from day 2 to day 7 compared to the S.enterica infected group. • The bacterial numbers showed a significant (p < 0.05) decrease in S.enterica infected rat feces, urinary bladder and urethra on treatment with AQU-019. [ABSTRACT FROM AUTHOR]