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During our ongoing survey of dematiaceous hyphomycetes associated with dead branches in tropical forests, eight Acrodictys isolates were collected from Hainan, China. Morphology from the cultures and phylogeny based on partial small subunit (SSU), entire internal transcribed spacer regions with intervening 5.8S (ITS), partial large subunit (LSU) of rRNA gene, partial beta-tubulin (tub2), and partial RNA polymerase II second largest subunit (rpb2) genes were employed to identify these isolates. As a result, four new species, namely Acrodictys bawanglingensis sp. nov., A. diaoluoshanensis sp. nov., A. ellisii sp. nov., and A. pigmentosa sp. nov., are introduced. Illustrations and descriptions of the four taxa are provided, along with comparisons with closely related taxa in the genus. For facilitating relative studies, an updated key to all accepted species of this genus is also compiled. [ABSTRACT FROM AUTHOR]

Background: It is reported that progestin and adipoQ receptor 4 (PAQR4) has a tumorigenic effect on human breast cancer, but the role of PAQR4 in non-small-cell lung cancer (NSCLC) is unknown. The aim of this study was to investigate the role of PAQR4 in NSCLC. Methods: Quantitative real-time PCR (qRT-PCR) and immunohistchemical (IHC) staining were used to analyze the expression of PAQR4 in HCC tissues and adjacent normal tissues. MTT, colony formation assay, flow cytometry (FCM), wound healing assays and transwell invasion assays were used to investigate the effects of PAQR4 on cell proliferation, colony formation, cell cycle, migration and invasion. Murine xenograft model assay was carried out to characterize the effects of PAQR4 knockdown on tumor growth in vivo. Results: In this study, we found that the expression of PAQR4 was significantly upregulated in the NSCLC tissues of patients compared with that in the matched non-cancerous tissues. In addition, we found that PAQR4 was also significantly up-regulated in the NSCLC cell lines compared with normal human lung epithelial cells. Besides, we found that the over-expression of PAQR4 promoted promoted proliferation, colony formation, migration and invasion of the NSCLC cells, whereas the knockdown of PAQR4 inhibited proliferation, colony formation, migration and invasion of the NSCLC cells. Furthermore, mechanistic studies showed that the CDK4-pRB-E2F1 pathway was involved in NSCLC. Conclusion: Hence, these results suggest that PAQR4 may be used as a new target in NSCLC therapy. [ABSTRACT FROM AUTHOR]

In this paper, a kind of zero valent FeNi alloy nano powder was coated on the surface of SrFe-MOF powder by a simple, efficient and pollution-free method, forming a core-shell type FeNi p @SrFe-MOF Magnetic powder (FSM). The FSM powder has a porous structure and a specific surface area of 9.16 ​m2/g. Under normal temperature and without changing the pH value of the wastewater, the FSM magnetic powder has an immediate and efficient removal effect on Congo Red (CR) dye wastewater. Furthermore, the powder has good cycling performance, with the CR removal rate remaining above 90% after five cycles. Also at room temperature and without changing the pH value of the wastewater, the FSM magnetic powder provides some immediate, efficient, and repeated use degradation of Cr(VI) wastewater. The FSM magnetic powder has good magnetic properties so that can be easily separated and recovered by magnetic field treatment, which solves the problem of efficient recovery of raw materials in wastewater treatment. FSM magnetic powder has broad application prospects for treating wastewater. In this paper, a kind of zero valent FeNi alloy nano powder was coated on the surface of SrFe-MOF powder by a simple, efficient and pollution-free method, forming a core-shell type FeNi p @SrFe-MOF Magnetic powder (FSM). Under normal temperature and without changing the pH value of the wastewater, the FSM magnetic powder has an immediate and efficient removal effect on Congo Red (CR) dye wastewater. Furthermore, the powder has good cycling performance, with the CR removal rate remaining above 90% after five cycles. Also at room temperature and without changing the pH value of the wastewater, the FSM magnetic powder provides some immediate, efficient, and repeated use degradation of Cr(VI) wastewater. The FSM magnetic powder has good magnetic properties so that can be easily separated and recovered by magnetic field treatment. [Display omitted] • FSM powder has an immediate and efficient removal effect on CR at room temperature and without changing the pH value of the wastewater. • FSM powder has some removal effect on Cr(VI) at room temperature and without changing the pH value of the wastewater. • FSM powder has good magnetic properties, which can be separated and recycled by magnetic field treatment. [ABSTRACT FROM AUTHOR]

To meet the current requirements for absorbing materials with broadband, lower thickness, and lower density, the FeNi@C@Fe 3 O 4 magnetic powders with a density of 1.75 g/cm3 are constructed by the hydrothermal method and the liquid phase reduction method. The powders have good matching performance with air impedance in the band of 0.3 GHz ~ 18 GHz, and can consider both dielectric loss and magnetic loss-absorbing mechanisms. The loss tangent, tgδ, of the powders is 0.4–0.5. The powder coat is designed by using the interference absorption mechanism. When the thickness of the coat is 1.8 mm, the absorption peak of the coat is about − 30 dB. The coat has a maximum of effective absorption band for 12.2 GHz ~ 17.3 GHz, and the effective absorption bandwidth is 5.1 GHz. When the glass fiber/epoxy resin composite material of thickness 0.5 mm is coated on the FCFp coat of thickness 1.7 mm, the effective absorption band is further widened to 11.9 GHz ~ 17.6 GHz, and the effective absorption bandwidth reaches 5.7 GHz. The FeNi@C@Fe 3 O 4 powders have the characteristics of dielectric and magnetic loss-absorbing materials, and have the remarkable advantages of the wider effective absorption bandwidth and the lower density, which is a kind of high-efficiency absorbing material with outstanding comprehensive absorption performance. [Display omitted] [ABSTRACT FROM AUTHOR]

The fungal genus Gnomoniopsis (Gnomoniaceae, Diaporthales) has been reported all around the world and isolated from multiple plant hosts. Based on multilocus phylogenies from a combined dataset of internal transcribed spacer (ITS) region, the ribosomal RNA gene cluster, and partial regions of translation elongation factor 1 alpha (tef1) and partial beta-tubulin (tub2), in conjunction with morphological characteristics, we describe and illustrate herein four new species, including Gnomoniopsisdiaoluoshanensis sp. Nov., G. lithocarpi sp. Nov., G. mengyinensis sp. Nov. and G.yunnanensis sp. Nov. Alongside this, their similarity and dissimilarity to morphologically-allied and phylogenetically-related species are annotated and discussed. For facilitating future identification, we update the key to all species currently recognized in this genus. [ABSTRACT FROM AUTHOR]

Liquid metal extraction (LME) is considered to be one of the alternatives for green production of rare earth elements from secondary resources. It leads to shift paradigm to eco-friendly economy to reduce carbon footprint and support sustainable development. However, separation of rare earths elements (REEs) from generated magnesium (Mg)-REEs after LME process is still remained as vacant technology due to lack of databases. In this work, fundamental investigation on the mechanism and kinetics for separation of REEs from Mg-REEs alloys by vacuum distillation is proposed. Experimental parameters of the process are thermodynamically designed at 2.0 × 10−5 atm in the range of 600 °C to 900 °C for selective distillation of Mg. Mg distillation is observed with gradual phase transformation from raw materials to phases including less Mg. 99.5 % yield of REEs and 99 % of pure Mg are successfully recovered as the metallic state, respectively. Interestingly, relatively rapid separation behavior of dysprosium (Dy) than neodymium (Nd) is observed and evaluated by variation Gibbs free energy and heat of mixing enthalpy based on the unique databases from practical experiments. It is indicated that the kinetics of phase transformation shows the different distillation behavior between individual REEs through thermodynamic and experimental assessments even if REEs group shares similar chemistry properties. This investigation can provide fundamental databases for grafting vacuum distillation after LME to secure sustainability for recycling industry. [Display omitted] • The vacuum distillation process is designed to separate REEs from Mg-REEs alloys based on the thermodynamic prediction. • Depending on the REEs, unexpected separation and recovery behaviors are observed due to relative affinity of compounds. • The derived results can provide fundamental databases for grafting vacuum distillation after LME for recycling industry. [ABSTRACT FROM AUTHOR]

NLRC5, the largest member of the Nod‐like receptor (NLR) family, has been reported to play a pivotal role in regulating inflammatory responses. Recent evidence suggests that NLRC5 participates in Toll‐like receptor (TLR) signaling pathways and negatively modulates nuclear factor‐κB (NF‐κB) activation. In this study, we investigated the interaction between NLRC5 and TLR2 in the NF‐κB inflammatory signaling pathway and the involvement of NLRC5 in TLR2‐mediated allergic airway inflammation. We knocked down TLR2 and NLRC5, respectively in the RAW264.7 macrophage cell line by small interfering RNA (siRNA) and then stimulated the knockdown cells with lipoteichoic acid (LTA). In comparison with the negative siRNA group, the level of NLRC5 expression was lower in the TLR2 siRNA group, with a reduction in the NF‐κB‐related inflammatory response. Conversely, in the NLRC5 knockdown cells, after LTA‐treated the level of TLR2 expression did not change but the expression levels of both NF‐κB pp65 and NLRP3 increased remarkably. Thus, we hypothesize that NLRC5 participates in the LTA‐induced inflammatory signaling pathway and regulates the inflammation via TLR2/NF‐κB. Similarly, in subsequent in vivo experiments, we demonstrated that the expression level of NLRC5 was significantly increased in the ovalbumin‐induced allergic airway inflammation. However, this effect disappeared in TLR2‐deficient (TLR2 −/−) mice and was accompanied by reduced levels of NF‐κB expression and airway inflammation. In conclusion, NLRC5 negatively regulates LTA‐induced inflammatory response via a TLR2/NF‐κB pathway in macrophages and also participates in TLR2‐mediated allergic airway inflammation. [ABSTRACT FROM AUTHOR]

Severe hemorrhagic shock and resuscitation (HS/R) can lead to lung injury, resulting in respiratory insufficiency. We investigated whether treatment with Alda-1, an ALDH2 activator, decreased lung injury induced by severe HS/R in a rat model. Male Sprague-Dawley rats were randomized into three groups, hemorrhagic shock + placebo, hemorrhagic shock + Alda-1, and sham. All animals were heparinized, and then 50% of the total calculated blood volume was collected over 60 minutes. After 40 minutes of hemorrhagic shock, animals were reinfused with the shed blood over 40 minutes and then observed for an additional 2 hours. Concentrations of 4-HNE, TNF-α, IL-6, and ALDH2 activity were detected; lung injury and lung wet-to-dry weight ratios were assessed. Expression of occludin and ZO-1 proteins in lung tissues was also determined. At 2 hours after resuscitation, lung injury was significantly reduced and the wet-to-dry weight ratio was notably decreased in the Alda-1 group compared with placebo (P<0.05). Alda-1 treatment also significantly increased the activity of ALDH2 and decreased the levels of toxic 4-HNE (P<0.05). In the Alda-1 group, IL-6 and TNF-α were dramatically decreased compared with placebo-treated animals (P<0.05). Expression of occludin and ZO-1 proteins was significantly decreased in the placebo group compared with the Alda-1 group (P<0.05). Thus, in a rat model of severe HS/R, treatment with Alda-1 increased the activity of ALDH2, significantly accelerated the clearance of reactive aldehydes, and concomitantly alleviated lung injury through improvement of pulmonary epithelial barrier integrity resulting in decreased alveolar epithelial tissue permeability, lung edema, and diffuse infiltration of inflammatory cells. [ABSTRACT FROM AUTHOR]

Galectin-1 (Gal-1) has immunomodulatory activities in various allergic inflammatory disorders, but its potential anti-inflammatory properties on allergic airway diseases have not been confirmed. We explored the pharmacological effects of Gal-1 on the progression of allergic airway inflammation and investigated the underlying mechanism. Female C57BL/6 mice were sensitized on day 0 and challenged with ovalbumin (OVA) on days 14-17 to establish an allergic airway inflammation model. In the challenge phase, a subset of mice was treated intraperitoneally with recombinant Gal-1 (rGal-1) or dexamethasone (Dex). We found that rGal-1 inhibited pulmonary inflammatory cell recruitment, mucus secretion, bronchoalveolar lavage fluid (BALF) inflammatory cell infiltration, and cytokine production. The treatment also suppressed the infiltration of eosinophils into the allergic lung as indicated by decreased expression levels of eotaxin and eosinophil peroxidase (EPX). However, only the expression levels of IL-25, neither IL-33 nor TSLP, were significantly decreased in the lung by rGal-1 treatment. These immunomodulatory effects in the allergic lung were correlated with the activation of extracellular signal-regulated kinase (ERK) signaling pathway and downregulation of endogenous Gal-1. In addition, rGal-1 reduced the plasma concentrations of anti-OVA immunoglobulin E (IgE) and IL-17. Our findings suggest that rGal-1 is an effective therapy for allergic airway inflammation in a murine model and may be a potential pharmacological target for allergic airway inflammatory diseases. [ABSTRACT FROM AUTHOR]

Abstract Although autophagy and phagocytosis are involved in the regulation of host inflammatory response to bacterial infection in macrophages, the underlying mechanisms have not been completely elucidated. In the present study, we found that infecting RAW264.7 macrophages with Staphylococcus aureus (S. aureus) activated multiple signaling pathways including phosphatidylinositide 3-kinase (PI3K)/protein kinase B (Akt), nuclear factor-κB (NF-κB), and Rac1, as well as triggered autophagy. LY294002, a specific PI3K activity inhibitor, significantly decreased autophagy and phagocytosis of macrophages upon S. aureus infection. Similarly, knockdown of Beclin1 by specific siRNA significantly inhibited autophagy and phagocytosis of S. aureus -infected macrophages. Additionally, we showed that although administration of Beclin1 siRNA had no effects on phosphorylation of Akt (p-Akt), inhibition of PI3K activity by LY294002 significantly decreased the expression of Beclin1, suggesting that Beclin1 is a downstream molecular of PI3K. Furthermore, inhibition of autophagy significantly increased the production of NF-κB-dependent TNFα/IL-1β in S. aureus -infected macrophages. Collectively, these findings demonstrated, for the first time, that the PI3K/Akt-Beclin1 signaling pathway positively regulates phagocytosis and negatively mediates NF-κB-dependent inflammation in S. aureus -infected macrophages. Highlights • S. aureus activates multiple signaling pathways and triggers autophagy in RAW264.7 cells. • Inhibition of PI3K activity decreases autophagy and phagocytosis of S. aureus -infected RAW264.7 cells. • Knockdown of Beclin1 reduces the phagocytosis of S. aureus -infected RAW264.7 cells. • Inhibition of autophagy increases the production of NF-κB dependent TNF-α/IL-1β in S. aureus -infected RAW264.7 cells. [ABSTRACT FROM AUTHOR]

Unresolved inflammation underpins the pathogenesis of allergic airway diseases, such as asthma. Ketamine, accepted as a promising therapy for resistant asthma, has been demonstrated to attenuate allergic airway inflammation. However, the anti-inflammatory mechanism by ketamine in this setting is largely unknown. We aimed to investigate whether autophagy was involved in the protective effect of ketamine on allergic airway inflammation. Female C57BL/6 mice were sensitized to ovalbumin (OVA) and treated with ketamine at 25, 50, or 100 mg/kg prior to OVA challenge. In this model, the pulmonary morphological findings and airway inflammation were significantly inhibited at 50 mg/kg but not at 25 or 100 mg/kg. Moreover, 50 mg/kg ketamine abrogated the increased concentrations of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) of allergic mice, as well as activated the expression of phosphorylated mammalian target of rapamycin (p-MTOR) and inhibited autophagy in allergic mice. To confirm whether the effect of 50 mg/kg ketamine on asthma was mediated by inhibiting autophagy, rapamycin was administered to mice sensitized to OVA and exposed to 50 mg/kg ketamine. All of the effect of 50 mg/kg ketamine was reversed by rapamycin treatment, including increased p-MTOR and decreased autophagy. Taken together, the present study demonstrates that 50 mg/kg ketamine inhibits allergic airway inflammation by suppressed autophagy, and this effect is mediated by the activation of MTOR in the lungs of allergic mice. [ABSTRACT FROM AUTHOR]

Background: Our colleagues have demonstrated an impressive therapeutic role of sevoflurane in a murine allergic airway inflammation model, but the mechanisms underlying this effect remain undefined. In this study, we tried to investigate the effect of sevoflurane on the resolution of allergic airway inflammation and to assess whether NLRP3 or the NLRP3 inflammasome is involved in this process.Methods: Female (C57BL/6) mice were sensitized and challenged with ovalbumin (OVA). Then, some of the mice received MCC950 (10 mg/kg; i.p.) or 3% sevoflurane. Total and differential inflammatory cell numbers, proinflammatory cytokines in bronchoalveolar lavage fluid (BALF), the peribronchial inflammation density, and mucus production were evaluated. In addition, we analysed the protein levels of NLRP3, the apoptosis-associated speck-like protein containing the caspase activation and recruitment domain (ASC), pro-caspase-1, and caspase-1 in the lung tissue.Results: We found that OVA-induced inflammatory cell recruitment to peribronchial regions, goblet cell hyperplasia, the serum levels of IgE, inflammatory cells, and the Th2 cytokine secretion in BALF was potently suppressed by sevoflurane with an efficacy comparable with that suppressed by MCC950 treatment. Furthermore, sevoflurane, similar to MCC950, clearly inhibited the OVA-induced activity of NLRP3 in the lungs. In addition, we found that OVA challenge failed to increase the expression of ASC, pro-caspase-1, and caspase-1 in the lungs and the levels of IL-18 and IL-1β in BALF.Conclusion: Taken together, our data showed that sevoflurane ameliorated allergic airway inflammation by inhibiting Th2 responses and NLRP3 expression. The NLRP3 independent of inflammasomes participated in the pathogenesis of allergic asthma in this model. [ABSTRACT FROM AUTHOR]

Nebulized lidocaine has been suggested to be beneficial in asthma therapy, but the underlying mechanisms are little known. We aimed to investigate whether Toll-like receptor (TLR) 2 was involved in the protective effect of lidocaine on allergic airway inflammation. Female C57BL/6 mice were sensitized and challenged with ovalbumin (OVA). Meanwhile, some of the mice were treated with TLR2 agonist (Pam3CSK4, 100 μg) intraperitoneally in combination with OVA on day 0. Just after allergen provocation, mice were treated with inhaled lidocaine or vehicle for 30 min. In this model, we found that lidocaine markedly attenuated OVA-evoked airway inflammation, leukocyte recruitment and mucus production. Moreover, lidocaine abrogated the increased concentrations of T cytokines and TNF-α in bronchoalveolar lavage fluid (BALF) of allergic mice, as well as reducing the expression of phosphorylated nuclear factor (P-NF)-κBp65 and the NOD-like receptor pyridine containing 3 (NLRP3), which are important for the production of pro-inflammatory cytokines. In addition, our study showed that lidocaine dramatically decreased OVA-induced increased expression of TLR2 in the lung tissues. Furthermore, activation of TLR2 aggravated OVA-challenged airway inflammation, meanwhile, it also elevated OVA-induced expression of P-NF-κBp65 and NLRP3 in the lungs. However, lidocaine effectively inhibited airway inflammation and counteracted the expression of P-NF-κBp65 and NLRP3 in allergic mice pretreated with Pam3CSK4. Taken together, the present study demonstrated that lidocaine prevented allergic airway inflammation via TLR2 in an OVA-induced murine allergic airway inflammation model. TLR2/NF-κB/NLRP3 pathway may serve as a promising therapeutic strategy for allergic airway inflammation. [ABSTRACT FROM AUTHOR]

The challenge of detecting research topics in a specific research field has attracted attention from researchers in the bibliometrics community. In this study, to solve two problems of clustering papers, i.e., the influence of different distributions of citation links and involved textual features on similarity computation, the authors propose a hybrid self-optimized clustering model to detect research topics by extending the hybrid clustering model to identify “core documents”. First, the Amsler network, consisting of bibliographic coupling and co-citation links, is created to calculate the citation-based similarity based on the cosine angle of papers. Second, the cosine similarity is also used to compute the text-based similarity, which consists of the textual statistical and topological features. Then, the cosine angle of the linear combination of citation- and text-based similarity is considered as the hybrid similarity. Finally, the Louvain method is applied to cluster papers, and the terms based on term frequency are used to label clusters. To test the performance of the proposed model, a dataset related to the data envelopment analysis field is used for comparison and analysis of clustering results. Based on the benchmark built, different clustering methods with different citation links or textual features are compared according to evaluation measures. The results show that the proposed model can obtain reasonable and effective clustering results, and the research topics of data envelopment analysis field are also analyzed based on the proposed model. As different features are considered in the proposed model compared with previous hybrid clustering models, the proposed clustering model can provide inspiration for further studies on topic identification by other researchers. [ABSTRACT FROM AUTHOR]

Mer receptor tyrosine kinase (MerTK) expressed in macrophages is essential for phagocytosis of apoptotic cells. Here, we investigate whether MerTK is involved in the phagocytosis of Staphylococcus aureus ( S. aureus) and regulation of staphylococcal lipoteichoic acid (LTA)-induced inflammatory response in macrophages. We found that stimulating RAW264.7 macrophages with S. aureus activated multiple signaling pathways including toll-like receptor 2 (TLR2), scavenger receptor A (SR-A), and MerTK. Meanwhile, S. aureus stimulation also induced activation of proteins focal adhesion kinase (FAK) and Rac1, which are related to phagocytosis. Pretreatment with a specific Mer-blocking antibody significantly inhibited S. aureus-induced phosphorylation of MerTK, while it had no effect on S. aureus-induced activation of FAK and Rac1. Moreover, by confocal laser microscope, we observed that the antibody blockade of MerTK had little impact on the phagocytosis of S. aureus by RAW264.7 macrophages. Additionally, pretreatment with this antibody further promoted LTA-induced phosphorylation of nuclear factor κB (NF-κB) p65 subunit and production of pro-inflammatory cytokines, such as TNF-α, IL-6, IL-1β, and macrophage inflammatory protein-2 (MIP-2). Collectively, these results suggest that MerTK does not play an essential role in the phagocytosis of S. aureus but attenuates inflammation induced by staphylococcal LTA through blocking NF-κB activation. [ABSTRACT FROM AUTHOR]

Industry consumes approximately half of the total worldwide energy usage. With the increasingly rising energy costs in recent years, it is critically important to consider one of the most widely used energies, electricity, during the production planning process. We propose a new mathematical model that can determine efficient scheduling to minimize the makespan and electricity consumption cost (ECC) for the flexible job shop scheduling problem (FJSSP) under a time-of-use (TOU) policy. In addition to the traditional two subtasks in FJSSP, a new subtask called speed selection, which represents the selection of variable operating speeds, is added. Then, a modified biogeography-based optimization (MBBO) algorithm combined with variable neighborhood search (VNS) is proposed to solve the biobjective problem. Experiments are performed to verify the effectiveness of the proposed MBBO algorithm for obtaining an improved scheduling solution compared to the basic biogeography-based optimization (BBO) algorithm, genetic algorithm (GA), and harmony search (HS). [ABSTRACT FROM AUTHOR]

Toll-like receptors (TLRs) are innate pattern recognition receptors that play a critical role in allergic inflammation, yet their contribution to autophagy in asthma remains poorly defined. Here, we investigate the role of Toll-like receptor 2 (TLR2) in phosphoinositide 3-kinases/protein kinase B (PI3K/Akt) pathway-mediated autophagy in ovalbumin-induced airway inflammation in mice. Wild-type (WT) and TLR2-knockout (TLR2) C57BL/6 mice were ovalbumin-sensitized and ovalbumin-challenged. In ovalbumin-challenged WT mice, enhanced expression of TLR2 in lung tissue, remarkable inflammatory cell infiltrates, goblet cell hyperplasia, and increased mucus production were observed. The number of inflammatory cells and interleukin-13 (IL-13) levels increased, while interferon-gamma (IFN-γ) levels decreased in bronchoalveolar lavage fluid. Expression of PI3K, phospho-Akt, Beclin-1 and LC3-II was enhanced significantly. These changes were mitigated dose-dependently in 3-methyl adenine-treated mice. In contrast, similar but weaker changes were found in ovalbumin-challenged TLR2 mice, and the changes were not significantly attenuated by 3-methyl adenine treatment. These results indicate that TLR2 confers a pivotal role in allergic airway inflammation via regulating the PI3K/Akt signaling pathway-related autophagy in mice. [ABSTRACT FROM AUTHOR]

Aims Glucocorticoids are the most effective anti-inflammatory agent in treating pulmonary diseases typically accompanied by hypoxia. Our previous study has demonstrated that glucocorticoid receptor α (GRα) expression is reduced in hypoxia but the underlying mechanism remains elusive. In this study we aim to identify the signaling pathway involved in hypoxia-induced down-regulation of GRα, and whether hypoxia affects nuclear translocation of GRα. Main methods Female C57BL/6 mice were sensitized with saline or ovalbumin (OVA) as the in vivo model. Mice were divided into control and OVA groups, and their lung histology and the expression of hypoxia inducible factor (HIF-1) and GRα were examined. A549 cells were exposed to chemical hypoxia as the in vitro model, where mitogen-activated protein kinases (MAPKs) were inhibited specifically by SB203580. Next, under normal or hypoxic conditions, the expression of GRα, MAPKs and HIF-1 signal protein were determined by Western blot analysis, and GRα translocation were observed through live-cell imaging. Key findings In OVA challenged mice the expression of GRα was down-regulated whereas HIF-1 was up-regulated. Hypoxia caused a time-dependent decrease of GRα expression, and activated multiple signaling pathways including MAPKs and HIF-1. Moreover, GRα expression increased with MAPK inhibition. Interestingly, only MAPK inhibitor SB203580, but not JNK inhibitor SP600125 or ERK inhibitor U0126 improved the expression of GRα under hypoxic condition. GRα nuclear translocation was also significantly inhibited by hypoxia. Significance Hypoxia down-regulated the expression of GRα through p38 signaling pathway, as well as inhibited GRα nuclear translocation significantly. [ABSTRACT FROM AUTHOR]

• A glucan (18.3 kDa) from purple sweet potato is composed of →4)Glc p (1→ glycosyls. • It branches at O -2, O -3, and O -6 positions with α- d -Glc p (1→ residue as side chain. • Its particle size is concentrated at 230 nm and has no triple-helix conformation. • Its height and width rangs from 1.0 to 6.1 nm and 65 to 210 nm, respectively. • Its maximum ring diameter and chain length is ∼800 nm and ∼7.0 μm, respectively. A novel glucan PSPP-1 (18.3 kDa) was purified from the foot tuber of purple sweet potato Ipomoea Batatas (L.) Lam. Its backbone was composed of →4)-α- d -Glc p (1→ glycosyl, and branching at the O -2, O -3, and O -6 positions with α- d -Glc p (1→ residues. X-ray diffraction experiment showed that PSPP-1 existed as an amorphous form. Its microstructure was detected via scanning electron microscopy. Its particle size was mainly concentrated at 230 nm in water. Congo red and circular dichroism experiments showed there was no triple-helix conformation. Atomic force microscopy data suggested that its height and width ranged from 1.0 to 6.1 nm and 65 to 210 nm, respectively; its maximum ring diameter and chain length was ∼800 nm and ∼7.0 μm, respectively. Furthermore, it exhibited inhibitory activities on HepG2, LOVO, and MCF-7 cells. Collectively, our data are useful for understanding the structural characteristics of sweet potato polysaccharides, and their application in foods and pharmaceutical areas. [ABSTRACT FROM AUTHOR]

Numerous studies indicate that toll-like receptor 2 (TLR2) led to divergent effects in asthma. The occurrence of autophagy in asthma pathogenesis is still incompletely understood. Here, we aimed to investigate the role of TLR2 and the underlying mechanisms in allergic airway inflammation and autophagy activation. C57BL/6 and TLR2 knockout (TLR2−/−) mice were subjected to an ovalbumin (OVA)-immunized allergic airway model, and were treated with SP600125. Differential cell counts in bronchoalveolar lavage fluid were determined by Wright's staining. Histological analysis of airway inflammation was determined by haematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining. The levels of OVA-specific immunoglobulin E (IgE), tumor necrosis factor α (TNF-α) and interleukin 10 (IL-10) were detected by enzyme-linked immunosorbent assay (ELISA). Proteins expression in lung tissues was detected by western blot, expression of TLR2 was further observed by immunofluorescence. Autophagy activation was determined by western blot and transmission electron microscopy (TEM). TLR2 expression was increased upon OVA challenge, and TLR2 deficiency was associated with decreased allergic airway inflammation. Meanwhile, TLR2 deficiency weakened autophagy activation. Moreover, inhibition of c-Jun N-terminal kinase (JNK) by SP600125 also suppressed OVA-induced allergic airway inflammation and autophagy activation. Interestingly, treating TLR2−/− mice with SP600125 showed similar OVA-induced allergic airway inflammation and autophagy activation compared to that in vehicle-treated TLR2−/− mice. TLR2 might contribute to the maintenance of allergic airway inflammation through JNK signaling pathway accompanying with autophagy activation. These findings may provide a novel signal target for prevention of allergic airway inflammation. [ABSTRACT FROM AUTHOR]