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A total of 320 1-day-old broilers were randomly divided into five groups. The control group (CON) received a basal diet, while the FAP4, FAP2, and FAP1 groups were provided with the basal diet supplemented with 4%, 2%, and 1% fermented Astragalus powder, respectively. The unfermented Astragalus powder (UAP2) group was fed the basal diet supplemented with 2% UAP. Each group contained eight replicates of eight chicks each. The results revealed that the final BW and ADG in the FAP 1 and FAP2 were higher than those in the UAP2 and CON groups, while reducing F/G from day 14 to day 42. On day 42, the thymus index in the UAP and FAP groups as well as the bursa index in the FAP4 group showed significant increases compared to those in the CON group. Supplementation with 2% FAP elevated serum IgA levels in broilers on day 28 and day 42, and it also increased serum IgG levels on day 42. Furthermore, supplementation with 2% FAP elevated serum albumin (ALB) levels in broilers, while supplementation with 4% FAP increased serum (glucose) GLU levels in broilers on day 28. The serum biochemical parameters and pathological observation of the liver and kidney in the groups did not show any adverse effects on broilers' health. In addition, the serum total antioxidant capacity (T-AOC) level significantly increased in the FAP4 and FAP2 groups on day 28, and the malondialdehyde (MDA) level in both serum and liver tissue decreased in the FAP2 group on day 28 and day 42. Compared to the CON group, 2% FAP and 2% UAP supplementation reduced the relative abundance of Bacteroides and supplementation with 2% FAP increased the relative abundance of Alistipes on day 42. In conclusion, the dietary supplementation of FAP can enhance the growth performance, immune function, and antioxidant capacity and regulate microflora in broilers, of which 2% FAP is more effective. It indicates FAP exhibits significant application potential as a promising feed additive for broilers.

Strain-specific probiotics can present antioxidant activity and reduce damage caused by oxidation. Streptococcus alactolyticus strain FGM (S. alactolyticus strain FGM) isolated from the chicken cecum shows potential probiotic properties which have been previously demonstrated. However, the antioxidant properties of S. alactolyticus strain FGM remain unknown. In this view, cell-free supernatant (CFS), intact cells (IC) and intracellular extracts (CFE) of strain FGM and 3 strains of Lactobacillus (LAB) were prepared, and their scavenging capacities against DPPH, hydroxyl radicals and linoleic acid peroxidation inhibitory were compared in this study. The effects of strain FGM cell-free supernatant (FCFS) on NO production, activity of SOD and GSH-Px in RAW264.7 cells and LPS-induced RAW264.7 cells were analyzed. The metabolites in the supernatant were quantitated by N300 Quantitative Metabolome. It was shown that the physicochemical characteristics of CFS to scavenge DPPH, hydroxyl radicals, and linoleic acid peroxidation inhibitory were significantly stronger than that of IC and CFE in the strain FGM (P < 0.05), respectively 87.12% ± 1.62, 45.03% ± 1.27, 15.63% ± 1.34. FCFS had a promotional effect on RAW264.7 cells, and significantly elevated SOD and GSH-Px activities in RAW264.7 cells. 25 μL FCFS significantly promoted the proliferation of RAW264.7 cells induced by LPS, increased the activities of SOD and GSH-PX, and decreased the release of NO. Furthermore, among the differential metabolites of FCFS quantified by N300, 12 metabolites were significantly up-regulated, including lactic acid, indole lactic acid, linoleic acid, pyruvic acid etc., many of which are known with antioxidant properties. In conclusion, FCFS had good antioxidant properties and activity, which can be attributed to metabolites produced from strain FGM fermentation. It was further confirmed that S. alactolyticus strain FGM and its postbiotic have potential probiotic properties and bright application prospects in livestock and poultry breeding., (© 2024. The Author(s).)

Arsenic is a human carcinogen widely distributed in the environment, and arsenic exposure from drinking water has received widespread attention as a global public health problem. Curcumin is a natural bioactive substance with high efficiency and low toxicity extracted from turmeric, which has a variety of biological properties such as antioxidation, anti-inflammation, anticancer, and immuno-modulatory activities. Curcumin is widely used in daily life as a food additive and dietary supplement. However, its protective effects in lung injuries by chronic arsenic exposure orally remain unexplored. In this study, curcumin treatment not only significantly accelerated arsenic elimination and improved lung tissue morphology, but also decreased arsenic-generated ROS by activating Nrf2 and its down-stream antioxidants. Further, curcumin alleviated inflammatory changes in mice exposed to arsenic for 6 and 12 weeks, as manifested by lung MPO levels, total protein and cellular levels in bronchoalveolar lavage fluid (BALF), serum IL-4 levels, and MAPK/NF-κB expression in lung tissue. Notably, our study also confirmed that curcumin could promote the expression and nuclear translocation of the transcription factor EB (TFEB), as well as activate TFEB-regulated autophagy in lung tissue of arsenic-treated mice, accompanied by inhibition of the AKT-mTOR signaling pathway. Overall, our study here suggests that natural bioactive compound curcumin could alleviate arsenic-induced pulmonary oxidative stress and inflammation in vivo, which is closely related to enhanced TFEB activity and induction of the autophagic process., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Feline interferon omega (IFN-ω) has been proven to have high antiviral activity; however, its in-depth antiviral effects remain unknown. Extracellular vesicles (EVs) have been demonstrated to participate in the regulation of the immune response pathway for the body through various active substances, especially through the microRNA (miRNA) carried by them. In this study, we isolated EVs from feline peripheral blood by differential centrifugation, and further found that the content of IFN-ω in EVs increased continuously within 24 h after IFN-ω treatment, and a large number of miRNAs were significantly downregulated in EVs within 12 h after IFN-ω treatment. These significantly differentially expressed miRNAs were important for regulating changes in antiviral cytokines. This study reveals for the first time the correlation between EVs-mediated miRNA in feline peripheral blood and IFN-ω on antiviral immune response, which may provide strong data support for the development of novel antiviral nanomedicine and the research of the antiviral effects of IFN-ω.

Arsenic (As) is a prevalent and hazardous environmental toxicant associated with cancer and various health problems, which has been shown suppressive effects on dendritic cells (DCs). Autophagy is essential for the innate and adaptive immune responses of DCs, and the transcription factors TFEB and TFE3 are key regulators of autophagic and lysosomal target genes. However, the detrimental alterations of the autophagy-lysosome pathway in As-exposed DCs and the possible coordinating roles of TFEB and TFE3 in the immune dysfunction of this cell are less understood. In this paper, we found that As exposure significantly impaired lysosomal number, lysosomal acidic environment, and lysosomal membrane permeabilization, which might lead to blocked autophagic flux in cultured DCs. Furthermore, our results confirmed that TFEB or TFE3 knockdown exacerbated the disorders of lysosome and the blockade of autophagic flux in As-exposed DCs, and also enhanced the inhibitory expression of co-stimulatory molecules Cd80 and Cd83; adhesion molecule Icam1; cytokines TNF-α, IL-1β, and IL-6; chemokine receptor Ccr7; and antigen-presenting molecules MHC II and MHC I. By contrast, overexpression of TFEB or TFE3 partially alleviated the above-mentioned impairment of DCs by inorganic As exposure. In conclusion, these findings reveal a previously unappreciated inhibition of lysosome-mediated degradation and damage of lysosomal membrane integrity leading to dysregulated autophagy and impaired immune functions of DCs by arsenicals, and also suggest TFEB and TFE3 as potential therapeutic targets for ameliorating As toxicity., (© 2024. The Author(s).)

The major histocompatibility complexes of vertebrates play a key role in the immune response. Antigen-presenting cells are loaded on MHC I molecules, which mainly present endogenous antigens; when MHC I presents exogenous antigens, this is called cross-presentation. The discovery of cross-presentation provides an important theoretical basis for the study of exogenous antigens. Cross-presentation is a complex process in which MHC I molecules present antigens to the cell surface to activate CD8 + T lymphocytes. The process of cross-representation includes many components, and this article briefly outlines the origins and development of MHC molecules, gene structures, functions, and their classical presentation pathways. The cross-presentation pathways of MHC I molecules, the cell lines that support cross-presentation, and the mechanisms of MHC I molecular transporting are all reviewed. After more than 40 years of research, the specific mechanism of cross-presentation is still unclear. In this paper, we summarize cross-presentation and anticipate the research and development prospects for cross-presentation.

The aim of this study was to investigate the inhibitory effects of Cordyceps militaris solid medium extract (CME) and cordycepin (COR) on LTA-induced inflammation in MH-S cells and their mechanisms of action. In this study, the establishment of an LTA-induced MH-S inflammation model was determined, the CCK-8 method was used to determine the safe concentration range for a drug for COR and CME, the optimal concentration of COR and CME to exert anti-inflammatory effects was further selected, and the expression of inflammatory factors of TNF-α, IL-1β, IL-18, and IL-6 was detected using ELISA. The relative expression of TNF-α, IL-1β, IL-18, IL-6, IL-10, TLR2 and MyD88 mRNA was detected using RT-PCR, and the IL-1β, IL-18, TLR2, MyD88, NF-κB p-p65, NLRP3, pro-caspase-1, Caspase-1 and ASC protein expression in the cells were detected using Western blot; immunofluorescence assay detected the expression of Caspase-1 in MH-S cells. The results revealed that both CME and COR inhibited the levels of IL-1β, IL-18, IL-6, and TNF-α in the supernatants of LTA-induced MH-S cells and the mRNA expression levels of IL-1β, IL-18, IL-6, TNF-α, TLR2 and MyD88, down-regulated the LTA-induced IL-1β, IL-18, TLR2 in MH-S cells, MyD88, NF-κB p-p65/p65, NLRP3, ASC, pro-caspase-1, and caspase-1 protein expression levels, and inhibited LTA-induced caspase-1 activation in MH-S cells. In conclusion, CME can play a therapeutic role in LTA-induced inflammation in MH-S cells via TLR2/NF-κB/NLRP3, and may serve as a potential drug for bacterial pneumonia caused by Gram-positive bacteria.

Achromobacter marplatensis strain YKS2 isolated from the yak rumen has the feature of producing cellulose. This study aims to analyze the genome and safety of strain YKS2 in vivo, considering its future research and application prospects. The genome of strain YKS2 was sequenced and used for genomic in silico studies. The administration of strain YKS2 in three doses was carried out on mice for 3 days of oral and 7 days of clinical observation tests. The BW, FI, organ indices, gut microbiota, and histological appearances of organs and intestines, along with hematological parameters and serum biochemistry, were measured in mice. The chromosome size of strain YKS2 was 6,588,568 bp, with a GC content of 65.27%. The 6058 coding sequences of strain YKS2 without plasmid were predicted and annotated and have multiple functions. The mice in all groups were alive, with good mental states and functional activities. Compared with the control group, there was no significant difference in the three dose groups on BW, FI, hematological parameters (WBC, LYM, etc.), and serum biochemistry (ALB, ALT, etc.). No abnormalities were observed in the main visceral organs, intestinal tissue, and V/C value in groups. However, the IEL number of duodenum and gut microbiota diversity (Shannon's index) in the high-dose group was significantly higher than in the control group (p < 0.05). Besides, the low dose of strain YKS2 also significantly affected the bacterial abundance of Firmicutes, Actinobacteria, and desulphurizing Bacteroidetes at the phylum level. There was no significant effect at genus levels in groups. In conclusion, the study revealed the genome and potential functional genes of strain YKS2, which is beneficial to understanding the features of the A. marplatensis strain and proved strain YKS2 to be without acute toxicity to mice. However, a long-term feeding toxicity experiment in vivo should be performed to further ensure its potential application value strain in the animal industry., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

For opening a way to synthesize novel metal-free catalysts and clarifying the photodegradation performance difference of photoactive species (such as ·O 2 - , h + ), a series of metal-free photocatalysts have been synthesized by using different existing forms of the same materials (boron carbon nitride (BCN) and boron carbon nitride-citric acid quantum dot (BCQD)) as precursors via calcinating their mixture at 350 °C. BCQD has good fluorescence and up-conversion fluorescence performance. BCN/BCQD-350 has the highest removal efficiency (90%, including adsorption 60% and photodegradation 30%) for tetracycline (TC) among all samples under visible light irradiation. TC adsorption by BCN/BCQD-350 conforms to pseudo-second-order kinetic and Langmuir isotherm models. TC photodegradation by BCN/BCQD-350 conforms to type II heterojunction mechanism. Photoactive species capture experiments suggest that·O 2 - makes a higher contribution for TC photodegradation, followed by h + , ·OH, 1 O 2 and e - . From LC-MS results, TC photodegradation is initiated by the dehydration step. TC dehydration activated by ·O 2 - has the lowest barrier (43.4 kcal/mol) than that (50.1 kcal/mol) activated by h + , that (64.8 kcal/mol) without the activation by photoactive species. TC removal rate of BCN/BCQD-350 (0.01563 min -1 ) is higher than that of g-C 3 N 4 , P25 (TiO 2 ), BNPA, BCNPA, etc. Furthermore, BCN/BCQD-350 can also photodegrade TC under infrared light irradiation (λ > 800 nm)., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Cerebral venous sinus thrombosis (CVST) has become a rare but potentially life-threatening condition in perinatal women. Early and rapid identification of CVST in pregnant women is a challenge for frontline clinical workers. In this study, 40 perinatal patients with CVST in our hospital were included in the five-year period, and 120 normal perinatal pregnant women in the obstetrics and gynecology department of our hospital were randomly enrolled in the five-year period as the control group, including 60 cases in pregnancy and puerperium. 5 mL of fasting venous blood was collected from puerperal CVST patients in the acute phase of onset (within 72 h of onset) and the recovery phase (fourth week of treatment). In the control group, 5 mL of fasting venous blood was collected. Coagulation factors X, XI, and XII, plasma D-Dimer were analyzed and compared. Coagulation factors X, XI, and XII in plasma of CVST patients were significantly increased compared with controls. Plasma coagulation factors X, XI, and XII and their combined detection (Union Model = 0.056 * FX: C + 0.046 * FXI: C + 0.081 * FXII: C) have diagnostic values for perinatal CVST. Plasma coagulation factors X, XI, and XII were significantly positively correlated with plasma D-dimer levels in perinatal CVST patients. Plasma coagulation factors X, XI, and XII have diagnostic values for perinatal CVST.

As industry is the world's leading carbon emitter, promoting industrial carbon reduction is of key significance to carbon peak and carbon neutrality. Using a data-driven method, based on the collection and processing of relevant data from statistical yearbooks and others, we analyze the efficiency and amount of carbon emission of each industrial sector after processing multi-dimensional data by the improved IPCC EF method of calculating carbon emissions. In addition, we adopt the LMDI decomposition method for data modeling to measure the contribution of energy efficiency, industrial structure, GDP per capita, and population size to carbon emission changes, to identify targets for industrial carbon reduction, and to propose a targeted optimization path for carbon emission. We show how the method is implemented by taking the statistics of Anhui Province from 2010 to 2019 as an example and advises on an optimization path for carbon emission in Anhui Province. This study is of both theoretical and practical significance as it provides theoretical and methodological support for the low-carbon development of the regional industry, and provides a reference for other countries and regions to explore the path of low-carbon and environment-friendly green transformation and upgrading., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Herein, the photodegradation performances difference of rice straw biochar-derived dissolved black carbon (DBC) for Tetracycline and Methylene Blue under visible light irradiation have been investigated. Tetracycline is easier degraded (degradation rate: 68%), followed by Methylene Blue (degradation rate: 14%). Singlet oxygen ( 1 O 2 ), superoxide radicals (O 2 - ), holes (h + ) and triplet DBC ( 3 DBC*) are all make contribution for Tetracycline degradation by DBC, whereas just singlet oxygen ( 1 O 2 ), superoxide radicals (O 2 - ) and 3 DBC* are involved in the MB degradation by DBC. Singlet oxygen ( 1 O 2 ) maybe from the fulvic acid-like structure of DBC, while band structure of DBC can explain why superoxide radicals (O 2 - ) and holes (h + ) can be formed, whereas hydroxyl radicals (OH) cannot be formed. The oxidation-reduction potential results of Tetracycline and Methylene Blue suggests that Tetracycline is easier to be oxidized than Methylene Blue as well as Methylene Blue is easier to be reduced than Tetracycline. Furthermore, experimental and theoretical results support that DBC has good interaction with Tetracycline, but the interaction between DBC and Methylene Blue is very weak. This likely explain why holes (h + ) is not detected for Methylene Blue degradation by DBC since Methylene Blue has not too much chance to meet holes (h + ). TC photodegradation intermediates are less toxic than Tetracycline based on QSAR method. Two possible photodegradation path of Tetracycline by DBC are proposed according to HPLC-MS results., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Numerous studies on arsenic-induced hepatonephric toxicity including cancer have been reported. Given that chronic inflammatory response and immune imbalance are associated with oncogenesis, we investigated whether arsenic could influence the hepatic and nephritic expression of inflammatory factors and the differentiation of T cells. Mice were exposed to NaAsO 2 (0, 25, and 50 mg/L) for 1 and 3 months. Our data showed the destruction of the structure and inflammatory infiltration in the liver. The arsenic markedly increased the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The myeloperoxidase (MPO) activities increased in the liver at 25 and 50 mg/L arsenic for 3 months as well as in the kidney at both 1 and 3 months. An increased expression of inflammatory indicators (IL-1 β , IL-12, and TNF- α ) at 25 and 50 mg/L arsenic for 1 and 3 months in the liver and kidney, as well as IL-1 β in the liver for 3 months and in the kidney at 50 mg/L for 1 and 3 months were demonstrated in our experiments. Besides, a definite tendency toward Th1/Th17 cytokines in the liver while Th2/Th17 cytokines in kidney was also observed by arsenic. Moreover, arsenic enhanced the expression of MAPK/Nrf2/NF- κ B signaling molecules. In conclusion, the results of the study suggested that arsenic induces continuous immune-inflammatory responses in the liver and kidney., Competing Interests: The authors declare that there are no conflicts of interest., (Copyright © 2022 Xiaoxu Duan et al.)

African swine fever (ASF) has brought excellent barriers to swine production in China and the world. Studies have shown that extracellular vesicles mediate the RNA and protein spread of pathogenic microorganisms and RNA and proteins. After infection by pathogenic microorganisms causes significant differences in the proteins contained within extracellular vesicles. Based on the above studies, the extracellular vesicles were extracted from ASF virus (ASFV)-infected swine plasma. And qPCR, western blot, and confocal experiment were carried out. The research shows that extracted extracellular vesicles significantly promote the replication of ASFV in susceptible and non-susceptible cells Proteomics analysis of the extracellular vesicle proteins revealed that ASFV infection could cause significant differences in the protein profile. This study demonstrates that extracellular vesicles play a critical role in ASFV replication and transmission and cause significant differences in the protein profile encapsulated in extracellular vesicles., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Xu, Shi, Liu, Shen, Yang, Zhang, Chen, Zhao, Yang, Hao, Cui, Yuan, Liu, Zhang and Zheng.)

Chronic arsenic exposure has been associated with various toxic effects, especially to the organs of liver and kidney. As a plant polyphenol, curcumin is the most vital bioactive ingredient of turmeric and has a wide range of pharmacological activities. In the present study, we investigated the potential roles of curcumin against arsenic-induced liver and kidney dysfunctions in mice. Curcumin treatment (200 mg/kg) not only decreased the deposition of arsenic in liver and kidney, but also relieved the hepatic and nephritic biochemical indexes (Glutamic oxaloacetic transaminase [AST], Alanine aminotransferase [ALT], albumin, and creatinine) altered by arsenic at doses of 10 and 25 mg/L via drinking water. What's more, curcumin exerted influences on the activities of myeloperoxidase and on the secretion of inflammatory cytokines in liver and kidney tissues. In addition, the levels of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) phosphorylation were declining while NRF2-signaling targets were increasing in mice liver and kidney by curcumin administration. In conclusion, our results here suggest that curcumin could exert both anti-inflammatory and antioxidant functions on arsenic-induced hepatic and kidney injury by inhibiting MAPKs/NF-κB and activating Nrf2 pathways cooperatively., (© 2021 Wiley Periodicals LLC.)

[This corrects the article .]., (Copyright © 2021 Hao, Shen, Wei, Yan, Zhang, Xu, Zhang, Hou, Cao, Jin, Zhang, Zheng and Liu.)

Electric vehicles (EVs) are recognized as one of the effective measures to realize sustainable transport. Therefore, many countries have issued related policy initiatives and measures to promote EVs. However, consumer's cognition and acceptance of EVs is not ideal, which affects the early diffusion speed of EVs on the market. This research attempts to explore how consumer's driving experience affects EVs adoption intention from the perspective of consumer's emotional response (satisfaction and trust) by using stimulus-organism-response framework. Based on the analysis of 692 sample data collected through questionnaire survey, we found that consumer's driving experience has a significant and positive impact on EVs adoption intention. Meanwhile, driving experience also significantly and positively affects consumer's satisfaction while has no significant effect on trust. Furthermore, satisfaction has a significantly positive effect on trust, and satisfaction and trust are both significantly and positively associated with EVs adoption intention. The results further uncovered that satisfaction not only plays a mediating role between driving experience and adoption intention but also plays a multiple mediating role between driving experience and adoption intention together with trust. On this basis, relevant recommendations have been made to promote the development of EVs from the perspective of government and enterprise.

Tumor progression locus 2 (TPL2) is a serine/threonine kinase that belongs to the mitogen-activated protein 3 kinase (MAP3K) family, and it plays an important role in pathogen infection. The trimer complex of TPL2, p105, and ABIN2 is essential for maintenance of TPL2 steady-state levels and host cell response to pathogens. Foot-and-mouth disease virus (FMDV) is a positive-strand RNA virus of the family Picornaviridae that encodes proteins capable of antagonizing host immune responses to achieve infection. The VP1 protein of FMDV is a multifunctional protein that can bind host cells and induce an immune response as well as cell apoptosis. However, the role and mechanisms of TPL2 in FMDV infection remain unknown. Here, we determined that FMDV infection could inhibit TPL2, p105, and ABIN2 at the transcription and protein levels, while VP1 could only inhibit TPL2, p105 and ABIN2 at protein level. TPL2 inhibited the replication of FMDV in vivo and in vitro , the 268 to 283 amino-acid region in the TPL2 kinase domain was essential for interaction with VP1. Moreover, VP1 promoted K48-linked polyubiquitination of TPL2 and degraded TPL2 by the proteasome pathway. However, VP1-induced degradation of p105 and ABIN2 was independent of proteasome, autophagy, lysosome, and caspase-dependent pathways. Further studies showed that VP1 destroyed the stability of the TPL2-p105-ABIN2 complex. Taken together, these results revealed that VP1 antagonized TPL2-meditated antivirus activity by degrading TPL2 and destroying its complex. These findings may contribute to understand FMDV-host interactions and improve development of a novel vaccine to prevent FMDV infection. Importance Virus-host interactions are critical for virus infection. This study was the first to demonstrate the antiviral effect of host TPL2 during FMDV replication by increasing production of interferons and antiviral cytokines. Both FMDV and VP1 protein can reduce host TPL2, ABIN2 and p105 to destroy TPL2-p105-ABIN2 trimer complex. VP1 interacted with TPL2 and degrade TPL2 via proteasome pathway to repress TPL2-mediated antivirus activity. This study provided new insights into FMDV immune evasion mechanisms, elucidating new informations regarding FMDV counteraction of host antivirus activity., (Copyright © 2020 Zhang et al.)

Arsenic is a ubiquitous metalloid element present in both inorganic and organic forms in the environment. The liver is considered to be a primary organ of arsenic biotransformation and methylation, as well as the main target of arsenic toxicity. Studies have confirmed that Chang human hepatocytes have an efficient arsenic methylating capacity. Our previous studies have proven that arsenite activates nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in hepatocytes. This study aimed to explore the activation of the Nrf2 pathway upon treatment of arsenic in various forms, including inorganic and organic arsenic. Our results showed that inorganic arsenic-both As 2 O 3 and Na 2 HAsO 4 significantly induced the expression of Nrf2 protein and mRNA, enhanced the transcription activity of Nrf2, and induced the expression of downstream target genes. These results confirmed the inorganic arsenic-induced Nrf2 pathway activation in hepatocytes. Although all arsenic chemicals used in the study induced Nrf2 protein accumulation, the organic arsenic C 2 H 7 AsO 2 did not affect the expression of Nrf2 downstream genes which were elevated by inorganic arsenic exposures. Through qRT-PCR and Nrf2 luciferase reporter assays, we further confirmed that C 2 H 7 AsO 2 neither increased Nrf2 mRNA level nor activated the Nrf2 transcription activity. Mechanistically, our results confirmed inorganic arsenic-induced both the nuclear import of Nrf2 and export of Bach1 (BTB and CNC homology 1), which is an Nrf2 transcriptional repressor, while organic arsenic only induced Nrf2 translocation. The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Foot-and-mouth disease (FMD) is a severe, highly contagious viral disease of cloven-hoofed animals. In order to establish an infection, the FMD virus (FMDV) needs to counteract host antiviral responses. Tumor progression locus 2 (TPL2), a mitogen-activated protein kinase, can regulate innate and adaptive immunity; however, its exact mechanisms underlying TPL2-mediated regulation of the pathogenesis of FMDV infection remain unknown. In this study, we confirmed that TPL2 could inhibit FMDV replication in vitro and in vivo . The virus replication increased in Tpl2 -deficient suckling mice in association with reduced expression of interferon-stimulated genes interferon-α (IFN-α) and myxovirus resistance (MX2) and significantly reduced expression of C-X-C motif chemokine ligand 10 (CXCL10), interferon regulatory factor 3 (IRF3), and IRF7, while the phosphorylation of IRF3 was not detected. Moreover, the interactions between TPL2 and VP1 were also confirmed. The overexpression of TPL2 promoted IRF3-mediated dose-dependent activation of the IFN-β signaling pathway in association with interactions between IRF3 and TPL2. VP1 also inhibited phosphorylation of TPL2 at Thr290, while Thr290 resulted as the key functional site associated with the TPL2-mediated antiviral response. Taken together, this study indicated that FMDV capsid protein VP1 antagonizes TPL2-mediated activation of the IRF3/IFN-β signaling pathway for immune escape and facilitated virus replication., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer LP declared a shared affiliation, with no collaboration, with the authors to the handling editor at the time of review., (Copyright © 2021 Hao, Shen, Wei, Yan, Zhang, Xu, Zhang, Hou, Cao, Jin, Zhang, Zheng and Liu.)

Foot-and-mouth disease (FMD) is a highly contagious infection caused by foot-and-mouth disease virus (FMDV). Exosomes are extracellular vesicles that mediate antiviral immune responses in host cells and could be used by pathogens to evade host cell immune responses. Whether FMDV affects exosome secretion or whether exosomes derived from FMDV-infected cells mediate host cell antiviral immune responses is not yet clarified. In this study, the exosomes were identified and extracted from FMDV-infected PK-15 cells, and it was found that FMDV inhibits exosome secretion. Further investigation revealed that FMDV suppresses exosomes by degrading Rab27a via the autophagy-lysosome pathway. Also, microRNA (miRNA) differential analysis was performed in exosomes, which revealed that miRNA-136 was highly differentially expressed in exosomes and may be the key miRNA that inhibits the proliferation of FMDV. In summary, these results showed that host cells take advantage of exosomes to mediate their antiviral immune response, while FMDV evades exosome-mediated immune responses by degrading the exosome molecular switch, Rab27a., (Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.)

Foot-and-mouth disease virus (FMDV) causes a highly contagious vesicular disease in cloven-hoofed livestock that results in severe consequences for international trade, posing a great economic threat to agriculture. The FMDV infection antagonizes the host immune responses via different signaling pathways to achieve immune escape. Strategies to escape the cell immune system are key to effective infection and pathogenesis. This review is focused on summarizing the recent advances to understand how the proteins encoded by FMDV antagonize the host innate and adaptive immune responses.

Arsenic is a toxic metalloid, which also compromises immunity and causes various immunological disorders. Exposure to arsenic exerts the immunosuppressive properties of dendritic cells (DCs). Autophagy is a self-renewal process of cells, which degrades damaged macromolecules and organelles through the lysosomal pathway. Thus, herein, we attempt to clarify the impacts of autophagy and the autophagy-lysosome pathway on arsenic-exposed DCs. Bone marrow-derived dendritic cells (BMDCs) were exposed to different concentrations of arsenic (0.25, 0.5 and 1 μM) with or without LPS stimulation. Initially, we observed that arsenic induced autophagosome accumulation, significantly enhanced the LC3 II and p62 expressions and down-regulated the p-mTOR protein levels. We also determined that arsenic-induced autophagy occurred via an mTOR pathway. The results further revealed that arsenic inhibited autophagic flux in LPS-stimulated BMDCs using the autophagy inhibitor chloroquine (CQ). Meanwhile, arsenic significantly decreased the number of lysosomes, protein expression of lysosomal-specific markers LAMP1 and LAMP2, and the protein levels of lysosomal cysteine cathepsins (CTSD and CTSL). Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion. In summary, our results support the idea that arsenic induces autophagy through an mTOR-dependent pathway in cultured BMDCs. Meanwhile, arsenic weakens the process of autophagic flux, which may be partially due to lysosomal dysfunction. Furthermore, we also suggest that TFEB can positively act on the autophagy-lysosome pathway and influence the expression of immunocytokines in DCs.

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Background: Arsenic exposure has become a matter of worldwide concern, which is associated with immune-related diseases. However, little is known about its effect on inflammatory immune-related homeostasis. The purpose of our study was to understand the potential tuning of above responses exerted by chronic arsenic exposure., Methods: Kunming mice were treated with 25 and 50 mg/L sodium arsenite for 1, 3 and 12 months via drinking water. At different endpoints of arsenic exposure, all animals and the whole spleen of the mice were weighed. The total arsenic levels of spleen were determined by the HPLC-HG-AFS method. Splenic NF-κB, MAPK and NRF2 protein levels by treatment of 25 mg/L NaAsO 2 for 1, 3 and 12 months and 25 mg/L and 50 mg/L NaAsO 2 for 12 months were assessed by western blot. Total RNA of spleen was isolated and relative mRNA levels of Foxp3 , Il - 10 , Tnf - α , Il - 6 , Ifn - γ , Il - 1β and Il - 12 were measured by real-time PCR., Results: Our results shown that NF-κB were continuously activated with treatment of 25 mg/L arsenic from 1, 3 to 12 months and 50 mg/L arsenic for 12 months. The transcription factor Foxp3 increased at 1 month but decreased at 3 and 12 months no matter 25 or 50 mg/L arsenic exposure. However, cytokine Il - 10 always showed increased trend in mice treated with 25 or 50 mg/L arsenic for 1, 3 and 12 months. The transcriptional profiles of Tnf - α , Il - 1β , Il - 6 , Ifn - γ and Il - 12 revealed transient elevation at 1 and 3 months but shown significant decrease at 12 months on the whole. In addition, the sustained activation of inflammatory MAPK and anti-oxidative Nrf2 signaling pathways were observed in mice exposed to arsenic for 1, 3 and 12 months., Conclusion: In summary, our experiment in vivo suggested chronic arsenic exposure induces the time-dependent modulation of the inflammation and immunosuppression in spleen, which may be related to the activation of Tregs induced by MAPK/NF-κB as well as the increased transcription level of Foxp3 and Il - 10 ., Competing Interests: Competing interestsThe authors declare that they have no competing interests., (© The Author(s) 2020.)

Seneca Valley virus (SVV) is a non-encapsulated single-stranded positive-strand RNA virus whose transmission routes have not yet been fully elucidated. Exosomes have been implicated in the intercellular transport of a variety of materials, such as proteins, RNA, and liposomes. However, whether exosomes can mediate SVV intercellular transmission remains unknown. In this study, we extracted exosomes from SVV-infected IBRS-2 cells to investigate intercellular transmission. Our results suggest that the intercellular transmission of SVV is mediated by exosomes. The results of co-localization and RT-qPCR studies showed that exosomes harbor SVV and enable the virus to proliferate in both susceptible and non-susceptible cells. Furthermore, the replication of SVV was inhibited when IBRS-2 cells were treated with interfering RNA Rab27a and exosome inhibitor GW4869. Finally, neutralization experiments were performed to further verify whether the virus was encapsulated by the exosomes that mediated transmission between cells. It was found that exosome-mediated intercellular transmission was not blocked by SVV-specific neutralizing antibodies. This study reveals a new transmission route of SVV and provides clear evidence regarding the pathogenesis of SVV, information which can also be useful for identifying therapeutic interventions.

Influenza viruses are responsible for severe respiratory tract infections of individuals and may cause pandemics with a high risk of mortality and morbidity. Although vaccination is a primary means for prevention of influenza virus infections, poor vaccine performance or inadequate immune responses limits the efficacy of current vaccines and raises question regarding whether a better correlates of protection procedures should be performed. Here, we want to evaluate whether mixed polysaccharides (MPs) derived from shiitake mushroom, poriacocos, ginger, and dried tangerine peel could promote the immune response of inactivated influenza vaccine. Firstly, MPs were given to mice each day and for a total of 30 days, during which two immunizations were performed on mice on days 14 and 21. The results showed that serum total IgG and IgG2a levels were increased in MPs-treated mice on day 30. Following A/WSN/33 (H1N1) virus challenge, we found that MPs pretreatment in mice could increase mice weight gain and attenuate their clinical symptoms. Additional protective factors were also observed including prevention of excessive lung inflammation, promotion of CD19 + and CD278 + cell proportions in lung, elimination of virus in lung, and elevation of IFN-γ levels in serum. The current study demonstrate that MPs from shiitake mushroom, poriacocos, ginger, and dried tangerine peel could promote the immune efficacy and alleviate lung inflammation in mice with vaccines against H1N1 virus infection by activating both humoral and cellular immunity., Competing Interests: Declaration of Competing Interest The authors declare that there are no conflicts of interest., (Copyright © 2020 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Electric vehicles (EVs) are known to be effective in reducing dependence on fossil fuels, in turn reducing the emission of greenhouse gas and other pollutants. To promote EVs, considerable efforts and measures have been taken. However, the public's awareness and acceptance of EVs are still low, which has affected the diffusion of EVs in the market. Based on the stimulus-organism-response (SOR) framework, this research aims to explore how consumers' EV driving experience (S) affects their emotions and cognitions regarding EVs (O: perceived relative advantage, perceived ease of use, and perceived risk of EVs) and then activates their intentions to adopt EVs (R). Based on survey data from 692 respondents, the results suggested that consumers' EV driving experience has a significantly positive effect on perceived relative advantage and perceived ease of use, and then perceived relative advantage and perceived ease of use positively affect consumers' intentions to adopt EVs. The EV driving experience negatively affects perceived risk, and perceived risk is also negatively associated with EV adoption intentions. Furthermore, consumers' EV driving experience also has a significant direct effect on EV adoption intentions. Based on the research results, relevant recommendations and suggestions have been proposed to promote EVs from the government and enterprise perspectives.

Adenylate cyclases (ACs), play a critical role in the conversion of adenosine triphosphate (ATP) into the second messenger cyclic adenosine monophosphate (cAMP). Studies have indicated that adenylyl cyclase type 2 (AC2) is potential drug target for many diseases, however, up to now, there is no AC2-selective agonist reported. In this research, docking-based virtual screening with the combination of cell-based biological assays have been performed for discovering novel potent and selective AC2 agonists. Virtual screening disclosed a novel hit compound 8 as an AC2 agonist with EC 50 value of 8.10 μM on recombinant human hAC2 + HEK293 cells. The SAR (structure activity relationship) based on the derivatives of compound 8 was further explored on recombinant AC2 cells and compound 73 was found to be the most active agonist with the EC 50 of 90 nM, which is 160-fold more potent than the reported agonist Forskolin and could selectively activate AC2 to inhibit the expression of Interleukin-6. The discovery of a new class of AC2-selective agonists would provide a novel chemical probe to study the physiological function of AC2., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Adenylyl cyclases (ACs), which are responsible for catalyzing the conversion of adenosine triphosphate (ATP) into the second messenger cyclic adenosine monophosphate (cAMP), play a critical role in cell signal transduction. In this study, a combined approach involving docking-based virtual screening, with the combination of homology modeling followed by an in-vitro, and cell-based biological assay have been performed for discovering a class of novel potent and selective isoform adenylyl cyclase type 8 (AC8) agonist. The computer-aided virtual screening was used to identify fourteen virtual cluster compounds as potential hits which were further subjected to rigorous bioassays. A novel hit compound VHC-7 (ethyl 3-(2,4-dichlorobenzyl)-2-oxoindoline-3-carboxylate) was identified as a highly potent selective AC8 agonist with EC 50 value of 0.1052 ± 0.038 µM. Remarkably, the molecule herein reported can be explored further to discover greater number of hit compounds with better pharmacokinetic properties as well as to serve as a promising novel hit agonist of AC8 for the treatment of various central nervous system disorders and its associated diseases., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Exosomes are small membrane-enclosed vesicles that participate in intercellular communication between cells. Numerous evidences suggested that exosomes derived from virus-infected cells can mediate virus transmission or/and regulate immune response. Foot-and-mouth disease virus (FMDV) is the prototype member of the Aphthovirus genus of the Picornaviridae family. It can cause highly infectious disease of cloven-hoofed livestock and significantly increase public awareness. However, the role of exosomes in the transmission of FMDV has still remained unknown. In this study, full length of FMDV genomic RNA and partial viral proteins were identified in purified exosomes isolated from FMDV-infected PK-15 cells with qRT-PCR and /MS. Exosomes from FMDV-infected cells were capable of transmitting infection to naive PK-15 cells and suckling mice. Furthermore, exosome-mediated infection cannot be fully blocked by FMDV-specific neutralizing antibodies. This finding highlights that FMDV transmission by exosomes as a potential immune evasion mechanism., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Canine distemper virus (CDV) is an infectious agent that can cause canine distemper (CD), a lethal disease. Immunization is an effective method to control the infection; however, some cases of failed immunization are observed in animal hospitals every year. Therefore, in this study, we conducted phylogenetic analysis of the H gene of isolated CDVs. We first constructed a modified MDCK cell line, which constitutively expressed signaling lymphocyte activation molecule (SLAM), a specific receptor for CDV. The modified cell line was more suitable for propagation of CDV than the original MDCK cell line. Next, 9 CDVs were successfully isolated from 20 dogs with suspected CD-associated diseases. Of these CDV isolates, three were from vaccinated dogs. The analysis indicated that the H gene sequences of these 9 viruses were highly similar. The present study further supported the finding that the majority of CDV in China belonged to the genotype Asia-1, which was different from vaccine strains (America-1 and America-2). Although the clinical application of the vaccine suggested that it is effective against CDV infection, it remains an open question whether a novel vaccine based on the genotype of the Asia-1 strain would be more suitable for protection of dogs against Asia-1 CDVs infection.

Cancer is the leading cause of human death which seriously threatens human life. The antimalarial drug artemisinin and its derivatives have been discovered with considerable anticancer properties. Simultaneously, a variety of target-selective artemisinin-related compounds with high efficiency have been discovered. Many researches indicated that artemisinin-related compounds have cytotoxic effects against a variety of cancer cells through pleiotropic effects, including inhibiting the proliferation of tumor cells, promoting apoptosis, inducing cell cycle arrest, disrupting cancer invasion and metastasis, preventing angiogenesis, mediating the tumor-related signaling pathways, and regulating tumor microenvironment. More importantly, artemisinins demonstrated minor side effects to normal cells and manifested the ability to overcome multidrug-resistance which is widely observed in cancer patients. Therefore, we concentrated on the new advances and development of artemisinin and its derivatives as potential antitumor agents in recent 5 years. It is our hope that this review could be helpful for further exploration of novel artemisinin-related antitumor agents.

Due to its excellent biological and mechanical properties, silk fibroin has been intensively explored for tissue engineering and regenerative medicine applications. However, lack of translational evidence has hampered its clinical application for tissue repair. Here a silk fibroin film is developed and its translational potential is investigated for skin repair by performing comprehensive preclinical and clinical studies to fully evaluate its safety and effectiveness. The silk fibroin film fabricated using all green chemistry approaches demonstrates remarkable characteristics, including transmittance, fluid handling capacity, moisture vapor permeability, waterproofness, bacterial barrier properties, and biocompatibility. In vivo rabbit full-thickness skin defect study shows that the silk fibroin film effectively reduces the average wound healing time with better skin regeneration compared with the commercial wound dressings. Subsequent assessment in porcine model confirms its long-term safety and effectiveness for full-thickness skin defects. Finally, a randomized single-blind parallel controlled clinical trial with 71 patients shows that the silk fibroin film significantly reduces the time to wound healing and incidence of adverse events compared to commercial dressing. Therefore, the study provides systematic preclinical and clinical evidence that the silk fibroin film promotes wound healing thereby establishing a foundation towards its application for skin repair and regeneration in the clinic., (© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Hyperactivity of acetylcholinesterase (AChE) in the brain is the immediate cause of Alzheimer's disease (AD), which is one of the most prevalent fatal diseases afflicting numerous older people. In this research, an in silico study was carried out to find potential AChE inhibitors from a large chemical library. With clustering and lots of comprehensive analysis, some molecules were screened using in vitro bioassays. The IC 50 values against AChE ranged from 33.620 to 101.570 μM, while the inhibition ratios at 50 μM ranged from 11.37% to 77.35%. The binding mode between the inhibitor and the binding sites of AChE was studied. Four residues (Tyr133, Tyr124, Ser203 and Trp86) were suggested to be crucial because they can form hydrogen bonds with the ligand. Therefore, ZYQ1 and its derivatives might represent a promising starting point for the development of highly potent lead compounds for the treatment of AD.

In this work we describe the establishment of mesenchymal stem cells (MSCs) derived from embryonic stem cells (ESCs) and the role of bFGF in adipocyte differentiation. The totipotency of ESCs and MSCs was assessed by immunofluorescence staining and RT-PCR of totipotency factors. MSCs were successfully used to induce osteoblasts, chondrocytes and adipocytes. MSCs that differentiated into adipocytes were stimulated with and without bFGF. The OD/DNA (optical density/content of total DNA) and expression levels of the specific adipocyte genes PPARγ2 (peroxisome proliferator activated receptor γ2) and C/EBPs were higher in bFGF cells. Embryonic bodies had a higher adipocyte level compared with cells cultured in plates. These findings indicate that bFGF promotes adipocyte differentiation. MSCs may be useful cells for seeding in tissue engineering and have enormous therapeutic potential for adipose tissue engineering.

Polyvinylpyrrolidone-iodine (Povidone-iodine, PVP-I) is widely used as an antiseptic agent for lavation during joint surgery; however, the biological effects of PVP-I on cells from joint tissue are unknown. This study examined the biocompatibility and biological effects of PVP-I on cells from joint tissue, with the aim of optimizing cell-scaffold based joint repair. Cells from joint tissue, including cartilage derived progenitor cells (CPC), subchondral bone derived osteoblast and bone marrow derived mesenchymal stem cells (BM-MSC) were isolated. The concentration-dependent effects of PVP-I on cell proliferation, migration and differentiation were evaluated. Additionally, the efficacy and mechanism of a PVP-I loaded bilayer collagen scaffold for osteochondral defect repair was investigated in a rabbit model. A micromolar concentration of PVP-I was found not to affect cell proliferation, CPC migration or extracellular matrix production. Interestingly, micromolar concentrations of PVP-I promote osteogenic differentiation of BM-MSC, as evidenced by up-regulation of RUNX2 and Osteocalcin gene expression, as well as increased mineralization on the three-dimensional scaffold. PVP-I treatment of collagen scaffolds significantly increased fibronectin binding onto the scaffold surface and collagen type I protein synthesis of cultured BM-MSC. Implantation of PVP-I treated collagen scaffolds into rabbit osteochondral defect significantly enhanced subchondral bone regeneration at 6 weeks post-surgery compared with the scaffold alone (subchondral bone histological score of 8.80±1.64 vs. 3.8±2.19, p<0.05). The biocompatibility and pro-osteogenic activity of PVP-I on the cells from joint tissue and the enhanced subchondral bone formation in PVP-I treated scaffolds would thus indicate the potential of PVP-I for osteochondral defect repair., (Copyright © 2013 Acta Materialia Inc. All rights reserved.)

The repair of osteochondral defects can be enhanced with scaffolds but is often accompanied with undesirable terminal differentiation of bone marrow-derived mesenchymal stem cells (BMSCs). Parathyroid hormone-related protein (PTHrP) has been shown to inhibit aberrant differentiation, but administration at inappropriate time points would have adverse effects on chondrogenesis. This study aims to develop an effective tissue engineering strategy by combining PTHrP and collagen-silk scaffold for osteochondral defect repair. The underlying mechanisms of the synergistic effect of combining PTHrP administration with collagen-silk scaffold implantation for rabbit knee joint osteochondral defect repair were investigated. In vitro studies showed that PTHrP treatment significantly reduced Alizarin Red staining and expression of terminal differentiation-related markers. This is achieved in part through blocking activation of the canonical Wnt/β-catenin signaling pathway. For the in vivo repair study, intra-articular injection of PTHrP was carried out at three different time windows (4-6, 7-9 and 10-12 weeks) together with implantation of a bi-layer collagen-silk scaffold. Defects treated with PTHrP at the 4-6 weeks time window exhibited better regeneration (reconstitution of cartilage and subchondral bone) with minimal terminal differentiation (hypertrophy, ossification and matrix degradation), as well as enhanced chondrogenesis (cell shape, Col2 and GAG accumulation) compared with treatment at other time windows. Furthermore, the timing of PTHrP administration also influenced PTHrP receptor expression, thus affecting the treatment outcome. Our results demonstrated that intra-articular injection of PTHrP at 4-6 weeks post-injury together with collagen-silk scaffold implantation is an effective strategy for inhibiting terminal differentiation and enhancing chondrogenesis, thus improving cartilage repair and regeneration in a rabbit model., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

An optimal scaffold is crucial for osteochondral regeneration. Collagen and electrospun nanofibers have been demonstrated to facilitate cartilage and bone regeneration, respectively. However, the effect of combining collagen and electrospun nanofibers on osteochondral regeneration has yet to be evaluated. Here, we report that the combination of collagen and electrospun poly-l-lactic acid nanofibers synergistically promotes osteochondral regeneration. We first fabricated bi-layer microporous scaffold with collagen and electrospun poly-l-lactic acid nanofibers (COL-nanofiber). Mesenchymal stem cells were cultured on the bi-layer scaffold and their adhesion, proliferation and differentiation were examined. Moreover, osteochondral defects were created in rabbits and implanted with COL-nanofiber scaffold. Cartilage and subchondral bone regeneration were evaluated at 6 and 12weeks after surgery. Compared with COL scaffold, cells on COL-nanofiber scaffold exhibited more robust osteogenic differentiation, indicated by higher expression levels of OCN and runx2 genes as well as the accumulation of calcium nodules. Furthermore, implantation of COL-nanofiber scaffold seeded with cells induced more rapid subchondral bone emergence, and better cartilage formation, which led to better functional repair of osteochondral defects as manifested by histological staining, biomechanical test and micro-computed tomography data. Our study underscores the potential of using the bi-layer microporous COL-nanofiber scaffold for the treatment of deep osteochondral defects., (Copyright © 2013 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.)

In bone tissue engineering, a combination of biomimetic nanofibrous scaffolds with renewable stem cells has recently emerged as a new strategy for promoting bone regeneration. We have previously developed a biomimetic nanocomposite nanofibrous scaffold of hydroxyapatite/chitosan (nHAp/CTS) [1]. However, the mechanism behind the supportive function of the scaffolds has not yet been adequately explored. Here, we evaluated the effect of nHAp/CTS seeded with bone marrow mesenchymal stem cells (BMSCs) on bone regeneration and examined the underlying mechanism in vitro and in vivo. The scaffolds of nHAp/CTS induced higher proliferation of BMSCs than membranous hydroxyapatite/chitosan (mHAp/CTS) and electrospun nanofibrous chitosan (nCTS) did. Interestingly, regardless the nanfibrous effect, nHAp/CTS and mHAp/CTS supported the spindle-shaped morphology, in contrast to the spherical shape of BMSCs on nCTS, indicating that HAp supports cell adhesion. Furthermore, the levels of the mRNA for Smad1, BMP-2/4, Runx2, ALP, collagen I, integrin subunits together with myosins were significantly up-regulated on nHAp/CTS whereas these genes were expressed at markedly low levels on mHAp/CTS and nCTS even in osteogenic medium. In addition, the critical proteins pSmad1/5/8 in BMP pathway showed clear nuclear localization and osteocalcin were significantly elevated on nHAp/CTS than mHAp/CTS (P < 0.01) and nCTS (P < 0.01). Similarly, the cells exhibited higher ALP activity on nHAp/CTS than mHAp/CTS (P < 0.01) and nCTS (P < 0.05). Therefore, the findings indicated the activating of intergrin-BMP/Smad signaling pathway of BMSCs on nHAp/CTS. Finally, in vivo, nHAp/CTS/BMSCs had a superior ability of bone reconstruction than other groups for cranial bone defects. In conclusion, our results demonstrated that nHAp/CTS scaffold promotes bone regeneration by supporting the adhesion, proliferation and activating integrin-BMP/Smad signaling pathway of BMSCs both in vitro and in vivo., (Crown Copyright © 2013. Published by Elsevier Ltd. All rights reserved.)

We report that self-assembled gold (Au) nanopyramid arrays can greatly enhance the photocurrent of narrow bandgap organic solar cells using their plasmonic near-field effect. The plasmonic enhanced power conversion efficiency exhibited up to 200% increase under the AM 1.5 solar illumination.

Plasmonic graphene is fabricated using thermally assisted self-assembly of silver nanoparticles on graphene. The localized surface-plasmonic effect is demonstrated with the resonance frequency shifting from 446 to 495 nm when the lateral dimension of the Ag nanoparticles increases from about 50 to 150 nm. Finite-difference time-domain simulations are employed to confirm the experimentally observed light-scattering enhancement in the solar spectrum in plasmonic graphene and the decrease of both the plasmonic resonance frequency and amplitude with increasing graphene thickness. In addition, plasmonic graphene shows much-improved electrical conductance by a factor of 2-4 as compared to the original graphene, making the plasmonic graphene a promising advanced transparent conductor with enhanced light scattering for thin-film optoelectronic devices., (Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Transparent conductors (TCs) are an important component of optoelectronic devices and nanoscale engineering of TCs is important for optimization of the device performance through improved light trapping. In this work, patterned periodic arrays of nanopillars and nanolines of pitch size of ~700 nm were created on fluorine-doped tin oxide (FTO) using nanoimprint lithography and reactive ion etching using environmentally friendly gases. The patterned FTO exhibits enhanced light trapping as compared to the unpatterned FTO, which agrees well with simulations based on Finite-Difference Time-Domain method for up to a distance of 4 μm. Dye sensitized solar cells (DSSCs) fabricated on the patterned FTO exhibited improved performance (fill factor and power conversion efficiency), which can be attributed to enhanced light absorption in the range 400-650 nm. Further, electrochemical impedance measurements revealed lower recombination resistance for the patterned FTO/TiO(2) electrode compared to the unpatterned FTO electrode/TiO(2) electrode as a result of better light capturing properties of patterned FTO. The direct fabrication of nanopatterns on TCs developed in the present study is expected to be a viable scheme for achieving improved performance in many other optoelectronic devices., (© 2012 American Chemical Society)

We demonstrate a new, nonlinear optical effect of electric currents. First, a steady current is generated by applying a voltage on a doped GaAs crystal. We demonstrate that this current induces second-harmonic generation of a probe laser pulse. Second, we optically inject a transient current in an undoped GaAs crystal by using a pair of ultrafast laser pulses and demonstrate that it induces the same second-harmonic generation. In both cases, the induced second-order nonlinear susceptibility is proportional to the current density. This effect can be used for nondestructive, noninvasive, and ultrafast imaging of currents. These advantages are illustrated by the real-time observations of a coherent plasma oscillation and spatial resolution of current distribution in a device. This new effect also provides a mechanism for electrical control of the optical response of materials.

The nucleation and evolution of InN nanowires in a self-catalyzed growth process have been investigated to probe the microscopic growth mechanism of the self-catalysis and a model is proposed for high pressure growth window at ~760 Torr. In the initial stage of the growth, amorphous InNx microparticles of cone shape in liquid phase form with assistance of an InNx wetting layer on the substrate. InN crystallites form inside the cone and serve as the seeds for one-dimensional growth along the favorable [0001] orientation, resulting in single-crystalline InN nanowire bundles protruding out from the cones. An amorphous InNx sheath around the faucet tip serves as the interface between growing InN nanowires and the incoming vapors of indium and nitrogen and supports continuous growth of InN nanowires in a similar way to the oxide sheath in the oxide-assisted growth of other semiconductor nanowires. Other InN 1D nanostructures, such as belts and tubes, can be obtained by varying the InN crystallites nucleation and initiation process.

This study tested the hypothesis that a controlled water deficit during grain filling of wheat (Triticum aestivum) could accelerate grain-filling rate through regulating the key enzymes involved in Suc-to-starch pathway in the grains. Two high lodging-resistant wheat cultivars were field grown. Well-watered and water-deficit (WD) treatments were imposed from 9 DPA until maturity. The WD promoted the reallocation of prefixed 14C from the stems to grains, shortened the grain-filling period, and increased grain-filling rate or starch accumulation rate (SAR) in the grains. Activities of Suc synthase (SuSase), soluble starch synthase (SSS), and starch branching enzyme (SBE) in the grains were substantially enhanced by WD and positively correlated with the SAR. ADP Glc pyrophosphorylase activity was also enhanced in WD grains initially and correlated with SAR with a smaller coefficient. Activities of granule-bound starch synthase and soluble and insoluble acid invertase in the grains were less affected by WD. Abscisic acid (ABA) content in the grains was remarkably enhanced by WD and very significantly correlated with activities of SuSase, SSS, and SBE. Application of ABA on well-watered plants showed similar results as those by WD. Spraying with fluridone, an ABA synthesis inhibitor, had the opposite effect. The results suggest that increased grain-filling rate is mainly attributed to the enhanced sink activity by regulating key enzymes involved in Suc-to-starch conversion, especially SuSase, SSS, and SBE, in wheat grains when subjected to a mild water deficit during grain filling, and ABA plays a vital role in the regulation of this process.