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The introduction of materials with dual-functionalities, i.e., the catalytic (adsorption) features to inhibit shuttle effects at the cathode side, and the capability to facilitate homogenous Li-ion fluxes at the anode side, is a promising strategy to realize high performance lithium-sulfur batteries (LSBs). Herein, a facile and rational organic "ligand-induced" (trimesic acid (TMA)) transformation tactic is proposed, which achieves the regulation of electronic performance and d-band center of bimetallic oxides (NiFe2O4) to promote bidirectional sulfur conversion kinetics and stabilize the Li plating/striping during the charge/discharge process. The battery assembled with NiFe2O4-TMA modified separator exhibits a remarkable initial specific capacity of 1476.6 mAh·g−1 at 0.1 C, outstanding rate properties (661.1 mAh·g−1 at 8.0 C), and excellent cycling ability. The "ligand-induced" transformation tactic proposed in this work will open a whole new possibility for tuning the electronic structure and d-band center to enhance the performance of LSBs [ABSTRACT FROM AUTHOR]

Colonizing populations of alien invasive species are often unstable due to their small population size, ongoing gene flow, and ongoing adaptation to local conditions. These processes should lead to molecular signatures at the population level. However, temporal changes in genetic patterns after introduction are rarely examined. The western flower thrips, Frankliniella occidentalis (Pergande), is a globally invasive pest of vegetables and ornamental crops. Populations collected early in the invasion of China by this pest exhibited a strong population structure reflecting different invasion sources. Here, we re-examine this pattern after ten years. Over this period, genetic diversity has increased significantly, and the strong population genetic structure found in early sampling has declined. Gene flow between both geographically close and distant populations was identified. The loss of population structure likely reflects ongoing gene flow after colonization. Our results emphasize the importance of continuing to manage gene flow among invaded areas to limit the exchange of alleles that might facilitate further adaptive changes following a pest invasion. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) play important roles in the progression of hepatocellular carcinoma (HCC). However, the exact function of circ_0008934 in HCC is unknown. Our study aimed to investigate the expression characteristics of circ_0008934 in HCC and its effects on the proliferation and metastasis of HCC, and to explore the potential mechanism. In this study, circ_0008934 expression was found to be significantly upregulated in HCC tissues and cell lines by qRT-PCR. High level of circ_0008934 is closely associated with higher serum AFP (P < 0.001), larger tumor diameter (P = 0.012), microvascular invasion (P = 0.008) and poorer prognosis (P = 0.007) of HCC patients. Functionally, knockdown of circ_0008934 inhibited HCC cell proliferation, invasion and migration in vitro and vivo. Mechanically, circ_0008934 was a sponge of miR-1305 to facilitate the TMTC3 expression, and the TMTC3 expression in HCC tissues was negatively associated with the survival of HCC patients. Furthermore, rescued assays revealed that the circ_0008934 facilitated HCC proliferation, invasion and migration by regulating miR-1305/ TMTC3 signaling pathways. Overall, these results demonstrate that downregulation of circ_0008934 repress HCC growth and metastasis by upregulating miR-1305 to inhibit TMTC3, suggesting circ_0008934/ miR-1305/ TMTC3 regulatory axis may be a possible novel therapeutic target for HCC. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the effect of comprehensive therapy based on Chinese medicine (CM) patterns on self-efficacy and satisfaction with its effectiveness in patients with chronic obstructive pulmonary disease (COPD). Methods: A total of 216 patients were randomly divided into the trial group (n =108) and the control group (n=108) based on the stratified and block randomization design. Patients in the trial group were treated with conventional Western medicine combined with Bufei Jianpi Granules (补肺健脾颗粒), Bufei Yishen Granules (补肺益肾颗粒), and Yiqi Zishen Granules (益气滋肾颗粒) according to the CM patterns respectively, and patients in the control group were treated with conventional Western medicine. The COPD Self-Efficacy Scale (CSES) and the Effectiveness Satisfaction Questionnaire for COPD (ESQ-COPD) were employed in a 6-month treatment and in further 6 month follow-up visit. Results: Among the 216 patients, 191 patients (97 in the trial group and 94 in the control group) fully completed the study. After 12-month treatment and follow-up, the mean scores of the trial group all continued to increase over time, which were significantly higher than those of the control group (P <0.05), and the improvement in the following trial group domain: negative affect domain (12.13%), intense emotional arousal domain (12.21%), physical exertion domain (11.72%), weather/environmental domain (13.77%), behavioral risk domain (7.67%) and total score (10.65%). The trial group also exhibited significantly higher mean scores in the ESQ-COPD (P <0.05) and the improvement in the following domain: capacity for life and work domain (30.59%), clinical symptoms domain (53.52%), effect of therapy domain (35.95%), convenience of therapy domain (35.54%), and whole effect domain (52.47%). Conclusions: Bufei Jianpi Granules, Bufei Yishen Granules and Yiqi Zishen Granules can improve the self-efficacy and satisfaction of COPD patients. [ABSTRACT FROM AUTHOR]

The anti-inflammatory and antibacterial mechanisms of bone marrow mesenchymal stem cells (MSCs) ameliorating lung injury in chronic obstructive pulmonary disease (COPD) mice induced by cigarette smoke and Haemophilus Parainfluenza (HPi) were studied. The experiment was divided into four groups in vivo: control group, COPD group, COPD+HPi group, and COPD+HPi+MSCs group. The indexes of emphysematous changes, inflammatory reaction and lung injury score, and antibacterial effects were evaluated in all groups. As compared with control group, emphysematous changes were significantly aggravated in COPD group, COPD+HPi group and COPD+HPi+MSCs group ( P<0.01), the expression of necrosis factor-kappaB (NF-κB) signal pathway and proinflammatory cytokines in bronchoalveolar lavage fluid (BALF) were increased ( P<0.01), and the phagocytic activity of alveolar macrophages was downregulated ( P<0.01). As compared with COPD group, lung injury score, inflammatory cells and proinflammatory cytokines were significantly increased in the BALF of COPD+HPi group and COPD+HPi+MSCs group ( P<0.01). As compared with COPD+HPi group, the expression of tumor necrosis factor-α stimulated protein/gene 6 (TSG-6) was increased, the NF-κB signal pathway was depressed, proinflammatory cytokine was significantly reduced, the anti-inflammatory cytokine IL-10 was increased, and lung injury score was significantly reduced in COPD+HPi+MSCs group. Meanwhile, the phagocytic activity of alveolar macrophages was significantly enhanced and bacterial counts in the lung were decreased. The results indicated cigarette smoke caused emphysematous changes in mice and the phagocytic activity of alveolar macrophages was decreased. The lung injury of acute exacerbation of COPD mice induced by cigarette smoke and HPi was alleviated through MSCs transplantation, which may be attributed to the fact that MSCs could promote macrophages into anti-inflammatory phenotype through secreting TSG-6, inhibit NF-кB signaling pathway, and reduce inflammatory response through reducing proinflammatory cytokines and promoting the expression of the anti-inflammatory cytokine. Simultaneously, MSCs could enhance phagocytic activity of macrophages and bacterial clearance. Meanwhile, we detected anti-inflammatory and antibacterial activity of macrophages regulated by MSCs in vitro. As compared with RAW264.7+HPi+CSE group, the expression of NF-кB p65, IL-1β, IL-6 and TNF-α was significantly reduced, and the phagocytic activity of macrophages was significantly increased in RAW264.7+HPi+CSE+MSCs group ( P<0.01). The result indicated the macrophages co-cultured with MSCs may inhibit NF-кB signaling pathway and promote phagocytosis by paracrine mechanism. [ABSTRACT FROM AUTHOR]

A new rhodamine B-based 'reactive' optical sensor ( 1) for Hg was synthesized. Sensor 1 shows a unique colorimetric and fluorescent 'turn-on' selectivity to Hg over 14 other metal ions with a hypersensitivity (detection limits are 27.6 nM (5.5 ppb) and 6.9 nM (1.4 ppb), respectively) in neutral buffer solution. To test its applicability in the environment, sensor 1 was applied to quantify and visualize low levels of Hg in tap water and river water samples. The results indicate sensor 1 is a highly sensitive fluorescent sensor for Hg with a detection limit of 1.7 ppb in tap water and river water. Moreover, sensor 1 is a convenient visualizing sensor for low levels of Hg (0.1 ppm) in water environment (from colorless to light pink). In addition, sensor 1 shows good potential as a fluorescent visualizing sensor for Hg in fetal bovine serum and living 293T cells. The results indicate that sensor 1 shows good potential as a highly sensitive sensor for the detection of Hg in environmental and biological samples. [ABSTRACT FROM AUTHOR]

Bone marrow mesenchymal stem cells (MSCs) transplantation could repair injury tissue, but no study confirms whether MSCs can promote the proliferation of endogenous lung stem cells to repair alveolar epithelial cells of mice with chronic obstructive pulmonary disease (COPD). This study was designed to investigate the effect of MSCs on the proliferation of endogenous lung stem cells in COPD mice to confirm the repair mechanism of MSCs. The mice were divided into control group, COPD group, and COPD+MSCs group. The following indexes were detected: HE staining of lung tissue, the mean linear intercept (MLI) and alveolar destructive index (DI), the total cell number in bronchoalveolar lavage fluid (BALF), pulmonary function, alveolar wall apoptosis index (AI) and proliferation index (PI), the number of CD45/CD31/Sca-1 cells by flow cytometry (FCM), and the number of bronchoalveolar stem cells (BASCs) in bronchoalveolar duct junction (BADJ) by immunofluorescence. As compared with control group, the number of inflammatory cells in lung tissue was increased, alveolar septa was destroyed and the emphysema-like changes were seen, and the changes of lung function were in line with COPD in COPD group; AI of alveolar wall was significantly increased and PI significantly decreased in COPD group. There was no significant difference in the number of CD45/CD31/Sca-1 cells and BASCs between control group and COPD group. As compared with COPD group, the number of inflammatory cells in BALF was decreased, the number of CD45/CD31/Sca-1 cells and BASCs was increased, AI of alveolar wall was decreased and PI was increased, and emphysema-like changes were relieved in COPD+MSCs group. These findings suggested that MSCs transplantation can relieve lung injury by promoting proliferation of endogenous lung stem cells in the cigarette smoke-induced COPD mice. [ABSTRACT FROM AUTHOR]

Two probes ( 1 and 2 ) bearing two dansyl fluorophores were synthesized and applied to the detection of mercury(ii) ions in aqueous solution. These probes exhibited a selective response to Hg2+ in a buffered solution, with high sensitivity and a unique fluorescence response signal which displayed a blue-shift effect in the fluorescence emission peak. The Hg2+ recognition mechanisms of the probes were determined by NMR spectroscopy, ESI-MS and UV-vis spectroscopy. The results showed that probe 1 and mercury(ii) ions formed an unusual 2 : 2 stoichiometric ratio complex, while probe 2 and Hg2+ formed a multidentate complex with a stoichiometric ratio of 2 : 1. [ABSTRACT FROM AUTHOR]

Airway remodeling is an important pathological feature of asthma and the basis of severe asthma. Proliferation of airway smooth muscle cells (ASMCs) is a major contributor to airway remodeling. As an important Ca channel, transient receptor potential vanilloid 1 (TRPV1) plays the key role in the cell pathological and physiological processes. This study investigated the expression and activity of TRPV1 channel, and further clarified the effect of TRPV1 channel on the ASMCs proliferation and apoptosis in order to provide the scientific basis to treat asthmatic airway remodeling in clinical practice. Immunofluorescence staining and reverse transcription polymerase chain reaction (RT-PCR) were used to detect the expression of TRPV1 in rat ASMCs. Intracellular Ca was detected using the single cell confocal fluorescence microscopy measurement loaded with Fluo-4/AM. The cell cycles were observed by flow cytometry. MTT assay and Hoechst 33258 staining were used to detect the proliferation and apoptosis of ASMCs in rats respectively. The data showed that: (1) TRPV1 channel was present in rat ASMCs. (2) TRPV1 channel agonist, capsaicin, increased the Ca influx in a concentration-dependent manner (EC=284.3±58 nmol/L). TRPV1 channel antagonist, capsazepine, inhibited Ca influx in rat ASMCs. (3) Capsaicin significantly increased the percentage of S+GM ASMCs and the absorbance of MTT assay. Capsazepine had the opposite effect. (4) Capsaicin significantly inhibited the apoptosis, whereas capsazepine had the opposite effect. These results suggest that TRPV1 is present and mediates Ca influx in rat ASMCs. TRPV1 activity stimulates proliferation of ASMCs in rats. [ABSTRACT FROM AUTHOR]

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Bronchial asthma is a common chronic airway inflammatory disease. Asthma is associated with high mortality, especially in the elderly patients. Repeated exacerbations cause disease progression. Therefore, identifying the onset of acute elderly asthma as soon as possible and giving the effective treatment is crucial to improve the prognosis. This study was to investigate the significance of fractional exhaled nitric oxide (FeNO) combined with serum procalcitonin (PCT) and C-reactive protein (CRP) in the evaluation of elderly asthma. A total of 120 elderly patients with an acute attack of asthma from July, 2010 to May, 2012 were studied. On presentation, FeNO, serum PCT and CRP concentrations were measured and sputum culture was also performed. The elderly patients were re-evaluated when they had returned to their stable clinical state. The elderly patients were classified into two groups: positive bacterial culture group (A) and negative bacterial culture group (B). The results showed that: (1) In patients with an acute exacerbation of asthma, 48 (40%) patients had positive sputum bacterial culture and 72 (60%) had negative sputum bacterial culture. (2) The levels of FeNO in patients with acute exacerbation of asthma were significantly higher than in those with no acute exacerbation state (63.8±24.6 vs. 19±6.5 ppb, P<0.05). There was no significant difference in FeNO between group A and group B ( P>0.05). (3) The levels of PCT and CRP in group A patients with an acute exacerbation of asthma were significantly higher ( P<0.05) than in group B (for PCT: 27.46±9.32 vs. 7.85±3.52 ng/mL; for CRP: 51.25±11.46 vs. 17.11±5.87 mg/L, respectively). When they had returned to stable clinical state, the levels of PCT and CRP in group A were decreased significantly ( P<0.05), and those in group B had no significant change ( P>0.05) when compared with the exacerbation group. There were no significant differences in the levels of PCT and CRP between the two groups in non-acute exacerbation state ( P>0.05). These results suggest that the increase in FeNO indicates the acute exacerbation of asthma, and the elevation of serum PCT and CRP levels may be associated with bacterial infection. [ABSTRACT FROM AUTHOR]

To investigate the relationship between the proliferation of sensitized human airway smooth muscle cells (HASMCs) and the expression of extracellular signal regulated kinase (ERK) and the effect of Shenmai Injection (参麦注射液, SMI) on HASMCs. The HASMCs cultured in vitro were divided into three groups: (1) control group; (2) sensitized group: containing 10% asthmatic serum; (3) SMI group: further divided into three different concentration subgroups interferred with 10 μL/mL, 50 μL/mL, and 100 μL/mL SMI, respectively. The proliferation of HASMCs was detected using MTT method, the expression of proliferating cell nucleus antigen (PCNA) in HASMCs was detected using immunocytochemical staining, and the expression of phosphoration-ERK1/2 (p-ERK1/2) protein was detected using Western-blot. After passive sensitization,: the optical density value (A A490 value) of HASMCs was significantly increased from 0.366±0.086 to 0.839± 0.168 ( P<0.05). In addition, the expression of PCNA was significantly increased from 28.7%±5.9% in the control group to 69.8%±7.5% in the sensitized group ( P<0.05). At the same time, the expression of p-ERK1/2 in passively sensitized HASMCs was significantly increased compared with the control group (all P<0.05). After application of 10 μL/mL, 50 μL/mL, and 100 μL/mL SMI to the cultured media of passively sensitized group, the A570 value was significantly decreased from 0.839±0.168 to 0.612±0.100, 0.412±0.092, and 0.339±0.077, respectively ( P<0.05). Moreover, the expression of PCNA was significantly decreased from 69.8%±7.5% to 57.8%±6.2%, 40.7%±5.4%, and 26.1%±5.2%, respectively. At the same time, the expression of p-ERK1/2 in each SMI group was significantly decreased compared with the sensitized group (all P<0.05). ERK signal transduction pathway may be involved in the airway remodeling in asthma. The expression of ERK can be inhibited by SMI in a dose-dependent manner, thus preventing the proliferation of HASMCs. [ABSTRACT FROM AUTHOR]

Fusarium species are among the most important phytopathogenic and toxigenic fungi. To understand the molecular underpinnings of pathogenicity in the genus Fusarium, we compared the genomes of three phenotypically diverse species: Fusarium graminearum, Fusarium verticillioides and Fusarium oxysporum f. sp. lycopersici. Our analysis revealed lineage-specific (LS) genomic regions in F. oxysporum that include four entire chromosomes and account for more than one-quarter of the genome. LS regions are rich in transposons and genes with distinct evolutionary profiles but related to pathogenicity, indicative of horizontal acquisition. Experimentally, we demonstrate the transfer of two LS chromosomes between strains of F. oxysporum, converting a non-pathogenic strain into a pathogen. Transfer of LS chromosomes between otherwise genetically isolated strains explains the polyphyletic origin of host specificity and the emergence of new pathogenic lineages in F. oxysporum. These findings put the evolution of fungal pathogenicity into a new perspective. [ABSTRACT FROM AUTHOR]

Regardless of the initial injury, the long-term consequence for the patient depends upon the ensuing balance of profibrotic vs reparative modulators activated. The glomerulus has some capacity for repair. Even when sclerosis has developed with accumulation of extracellular matrix, this lesion may be remodeled, with a change in balance between profibrotic and antifibrotic and collagen synthesis vs proteolytic mediators. We will focus here on the interplay between mediators of fibrosis and reparative mechanisms and potential regression of fibrosis. Based on the clinical efficacy of interventions that inhibit angiotensin, we will focus on factors related to the renin–angiotensin system. [ABSTRACT FROM AUTHOR]

Ustilago maydis is a ubiquitous pathogen of maize and a well-established model organism for the study of plant–microbe interactions. This basidiomycete fungus does not use aggressive virulence strategies to kill its host. U. maydis belongs to the group of biotrophic parasites (the smuts) that depend on living tissue for proliferation and development. Here we report the genome sequence for a member of this economically important group of biotrophic fungi. The 20.5-million-base U. maydis genome assembly contains 6,902 predicted protein-encoding genes and lacks pathogenicity signatures found in the genomes of aggressive pathogenic fungi, for example a battery of cell-wall-degrading enzymes. However, we detected unexpected genomic features responsible for the pathogenicity of this organism. Specifically, we found 12 clusters of genes encoding small secreted proteins with unknown function. A significant fraction of these genes exists in small gene families. Expression analysis showed that most of the genes contained in these clusters are regulated together and induced in infected tissue. Deletion of individual clusters altered the virulence of U. maydis in five cases, ranging from a complete lack of symptoms to hypervirulence. Despite years of research into the mechanism of pathogenicity in U. maydis, no ‘true’ virulence factors had been previously identified. Thus, the discovery of the secreted protein gene clusters and the functional demonstration of their decisive role in the infection process illuminate previously unknown mechanisms of pathogenicity operating in biotrophic fungi. Genomic analysis is, similarly, likely to open up new avenues for the discovery of virulence determinants in other pathogens. [ABSTRACT FROM AUTHOR]

The aspergilli comprise a diverse group of filamentous fungi spanning over 200 million years of evolution. Here we report the genome sequence of the model organism Aspergillus nidulans, and a comparative study with Aspergillus fumigatus, a serious human pathogen, and Aspergillus oryzae, used in the production of sake, miso and soy sauce. Our analysis of genome structure provided a quantitative evaluation of forces driving long-term eukaryotic genome evolution. It also led to an experimentally validated model of mating-type locus evolution, suggesting the potential for sexual reproduction in A. fumigatus and A. oryzae. Our analysis of sequence conservation revealed over 5,000 non-coding regions actively conserved across all three species. Within these regions, we identified potential functional elements including a previously uncharacterized TPP riboswitch and motifs suggesting regulation in filamentous fungi by Puf family genes. We further obtained comparative and experimental evidence indicating widespread translational regulation by upstream open reading frames. These results enhance our understanding of these widely studied fungi as well as provide new insight into eukaryotic genome evolution and gene regulation. [ABSTRACT FROM AUTHOR]

Neurospora crassa is a central organism in the history of twentieth-century genetics, biochemistry and molecular biology. Here, we report a high-quality draft sequence of the N. crassa genome. The approximately 40-megabase genome encodes about 10,000 protein-coding genes-more than twice as many as in the fission yeast Schizosaccharomyces pombe and only about 25% fewer than in the fruitfly Drosophila melanogaster. Analysis of the gene set yields insights into unexpected aspects of Neurospora biology including the identification of genes potentially associated with red light photobiology, genes implicated in secondary metabolism, and important differences in Ca2+ signalling as compared with plants and animals. Neurospora possesses the widest array of genome defence mechanisms known for any eukaryotic organism, including a process unique to fungi called repeat-induced point mutation (RIP). Genome analysis suggests that RIP has had a profound impact on genome evolution, greatly slowing the creation of new genes through genomic duplication and resulting in a genome with an unusually low proportion of closely related genes. [ABSTRACT FROM AUTHOR]

Transmembrane p24 trafficking protein 3(TMED3) is a metastatic suppressor in colon cancer, but its function in the progression of hepatocellular carcinoma (HCC) is unknown. Here, we report that TMED3 was up-regulated in HCC and portal vein tumor thrombus. TMED3 up-regulation in HCC was significantly correlated with aggressive characteristics and predicted poor prognosis in HCC patients. TMED3 overexpression in HCC cell lines promoted cell migration and invasion. In contrast, TMED3 knockdown suppressed HCC metastasis both in vitro and in vivo. Gene microarray analysis revealed decreased IL-11 expression in TMED3-knockdown cells. We propose that TMED3 promotes HCC metastasis through IL-11/STAT3 signaling. Taken together, these findings demonstrate that TMED3 promotes HCC metastasis and is a potential prognostic biomarker in HCC. [ABSTRACT FROM AUTHOR]