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A keloid is a classic fibrotic skin disease characterized by excessive deposition of extracellular matrix (ECM). Osteomodulin (OMD) is a heterologous protein that is a part of osteoadherin and plays a role in modulating ECM deposition. In this study, we investigated the effects of OMD on ECM synthesis and the tumor‐like phenotype of keloid fibroblasts. We enrolled 10 patients with keloids and 10 age‐ and sex‐matched healthy individuals, whose keloid or normal skin tissues were collected during surgery. Real‐time quantitative polymerase chain reaction (qRT‐PCR), western blotting, and immunohistochemical staining were performed to analyze OMD expression in skin tissues. Cell transfection, CCK‐8 assay, EdU staining, Transwell assay, qRT‐PCR, western blotting, and immunofluorescence were performed to study the effects of OMD on primary keloid‐derived fibroblasts (KFs). OMD exhibited greater expression in human keloid specimens than in normal skin tissues. Consistently, higher expression of OMD was observed in KFs, compared to that in normal fibroblasts. Silencing OMD expression in transforming growth factor (TGF)‐β1‐treated KFs inhibited cell proliferation and migration, as well as collagen and fibronectin expression; however, overexpression of OMD had the opposite effect. p38 mitogen‐activated protein kinase (MAPK) was activated in keloid tissues but not in normal skin. OMD was positively correlated with p38 MAPK activation. Adding SB203580, p38 MAPK inhibitor, significantly reversed the effects of OMD on the regulation of KF phenotype. The high expression of OMD may contribute to hyperproliferation of KFs, their migration, and excess ECM synthesis in KFs via regulation of the p38 MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Objectives. To explore the effect and mechanism of miR-34a on the proliferation, migration, and invasion of keloid fibroblasts (KFB). Methods. Isolate and culture KFB and normal skin fibroblast (NFB), detect the mRNA expression levels of miR-34a and integrin β5 (SATB1) in KFB and NFB by RT-qPCR, and detect SATB1 by western blot. The level of protein expression, MTT method, Transwell method, RT-qPCR, and western blot were used to detect the effects of overexpression of miR-34a or inhibition of SATB1 expression on the proliferation, migration, and invasion of KFB cells and the expression of related proteins. The dual luciferase reporter gene test verifies the targeting relationship between miR-34a and SATB1. Results. Compared with NFB, the expression of miR-34a was downregulated in KFB and the mRNA and protein expression levels of SATB1 were upregulated. Overexpression of miR-34a or inhibition of SATB1 expression inhibited the proliferation, migration, and invasion of KFB. miR-34a can negatively regulate the expression of SATB1, and overexpression of SATB1 reverses the effects of overexpression of miR-34a on the proliferation, migration, and invasion of KFB. Conclusions. miR-34a inhibits the proliferation, migration, and invasion of keloid fibroblasts by downregulating the expression of SATB1. [ABSTRACT FROM AUTHOR]

An N-doped graphene aerogel (NGA) is used as a reactive container for growing MnO2 nanoparticles via a soaking–hydrothermal strategy. MnO2 nanoparticles pile up on the surface of reduced graphene oxide sheets with crosslinked structures serving as electrical conductors. Importantly, the NGA generates extra capacitance during the electrochemical process, which accomplishes a satisfactory compensation in the physical–chemical properties of MnO2. As a cathodic electrode for Zn-ion batteries, the MnO2/NGA exhibits a specific capacity of 275.8 mA h g−1 and pre-eminent cycling stability with a retention of 93.6% at 3 A g−1 after 1000 cycles. Meanwhile, the proposed electrode also shows a relatively high specific capacitance of 341 F g−1 for a supercapacitor in 1 M Na2SO4. Meanwhile, the long-term cycling stability shows only a slight decrease by 5.1% of the initial capacitance after 5000 continuous cycles at 3 A g−1, which indicates its superior electrochemical stability. Additionally, the assembled asymmetric supercapacitor also shows good electrochemical performance. This work highlights the extensive function of an N-doped graphene aerogel as a promising substrate for enhancing the electrochemical performance of MnO2, which opens the gate for wide potential applications of graphene aerogel composites emphasizing their complementary effects. [ABSTRACT FROM AUTHOR]

Abstract Background CD8+ T cells participate in airway hyperresponsiveness (AHR) and allergic pulmonary inflammation that are characteristics of asthma. CXCL10 by binding to CXCR3 expressed preferentially on activated CD8+ T cells, attracts T cells homing to the lung. We studied the contribution and limitation of CXCR3 to AHR and airway inflammation induced by ovalbumin (OVA) using CXCR3 knockout (KO) mice. Methods Mice were sensitized and challenged with OVA. Lung histopathological changes, AHR, cellular composition and levels of inflammatory mediators in bronchoalveolar lavage (BAL) fluid, and lungs at mRNA and protein levels, were compared between CXCR3 KO mice and wild type (WT) mice. Results Compared with the WT controls, CXCR3 KO mice showed less OVA-induced infiltration of inflammatory cells around airways and vessels, and less mucus production. CXCR3 KO mice failed to develop significant AHR. They also demonstrated significantly fewer CD8+ T and CD4+ T cells in BAL fluid, lower levels of TNFα and IL-4 in lung tissue measured by real-time RT-PCR and in BAL fluid by ELISA, with significant elevation of IFNγ mRNA and protein expression levels. Conclusions We conclude that CXCR3 is crucial for AHR and airway inflammation by promoting recruitment of more CD8+ T cells, as well as CD4+ T cells, and initiating release of proinflammatory mediators following OVA sensitization and challenge. CXCR3 may represent a novel therapeutic target for asthma.

Chemokine C-X-C motif receptor 3 (CXCR3) is a chemokine receptor that is mainly expressed by activated T lymphocytes. T cells play important roles in allergic pulmonary inflammation, which is a hallmark of asthma and elicits the localized accumulation of activated T cells in the lung. In China, a marked increase in the incidence rate of chronic allergic pulmonary inflammation has made it a major public health threat. In the present study, we investigated the role of CXCR3 and its ligands in airway inflammation induced by house dust mite protein (HDMP) in a CXCR3 knockout (CXCR3KO) asthma mouse model. Pathological manifestations in the lung, cell counts and bronchoalveolar lavage fluid (BALF) classifications were studied using hematoxylin and eosin (H&E) staining. The levels of IL-4 and IFN-γ in the BALF and splenocyte supernatants were measured using ELISA. CD4+ and CD8+ T cells in the lung and spleen were analyzed by flow cytometry. RT-PCR was applied to measure the mRNA transcript levels of monokines induced by IFN-γ(CXCL9) and IFN-γ inducible protein 10(CXCL10). The total cell counts, eosinophil counts, and IL-4 levels in the BALF and cultured splenocyte supernatants were significantly increased, while the levels of IFN-γ were reduced in the HDMP groups(P<0.01). Changes in the total cell counts, eosinophil counts, and lymphocyte counts, as well as the total protein levels in the BALF, the levels of IL-4 in splenocyte supernatants, and the pathological manifestations in the lung, were all greater in CXCR3KO mice than in C57BL/6 wild-type mice. Furthermore, the expression levels of CXCL9 and CXCL10 mRNA transcripts in the lungs of CXCR3KO mice were lower than those in C57BL/6 wild-type mice (P<0.05). CXCR3 and its ligands (i.e., CXCL9 and CXCL10) may play anti-inflammatory roles in this animal model. Promoting the expression of CXCR3 and its ligands may represent a novel therapeutic approach for preventing and curing asthma. [ABSTRACT FROM AUTHOR]

Based on the bijective mapping between cyclostationary features and the cyclic delays in orthogonal frequency division multiplexing (OFDM) systems, cyclostationary signatures can be used for signal representation in statistical spectrum domain. However, the conventional detection method for this kind of statistical signals is hindered by huge computational complexity. In this letter, we propose a novel detection method for such statistical signals with cyclostationarity, which only extract local features on the cyclic autocorrelation function (CAF) coordinate plane. Analytical and simulation results show that the proposed method achieves significant performance gain over the conventional detection method under practical scenarios, even with the reduced computational complexity. [ABSTRACT FROM PUBLISHER]

The energy consumption in radio access network is expected to increase significantly as the network expends to fulfill the explosively growing data traffics. However, when evaluating the energy saving mechanisms, the impact on other performance metrics such as spectral efficiency, should also be taken into account. In this paper, based on the multiple component carrier (CC) feature specified in Long Term Evolution-Advanced (LTE-A) systems, an energy-efficient coordinated scheduling mechanism is proposed to reduce the energy consumption in cellular networks by dynamically switching off CCs and base stations (BS) according to load variations, with special attention on the switching off order and BS transmit power adjustment to maintain service continuity of downlink users. Both the energy and spectral efficiency of the system under the proposed scheduling mechanism are analyzed. Simulation results show that when data traffics are below a quarter of the system capacity, with the proposed scheme more than half of the network power consumption can be saved, while the requirements for user data rate, service continuity, network coverage and spectral efficiency are guaranteed. [ABSTRACT FROM PUBLISHER]

Background: CD8+ T cells participate in airway hyperresponsiveness (AHR) and allergic pulmonary inflammation that are characteristics of asthma. CXCL10 by binding to CXCR3 expressed preferentially on activated CD8+ T cells, attracts T cells homing to the lung. We studied the contribution and limitation of CXCR3 to AHR and airway inflammation induced by ovalbumin (OVA) using CXCR3 knockout (KO) mice.Methods: Mice were sensitized and challenged with OVA. Lung histopathological changes, AHR, cellular composition and levels of inflammatory mediators in bronchoalveolar lavage (BAL) fluid, and lungs at mRNA and protein levels, were compared between CXCR3 KO mice and wild type (WT) mice.Results: Compared with the WT controls, CXCR3 KO mice showed less OVA-induced infiltration of inflammatory cells around airways and vessels, and less mucus production. CXCR3 KO mice failed to develop significant AHR. They also demonstrated significantly fewer CD8+ T and CD4+ T cells in BAL fluid, lower levels of TNFα and IL-4 in lung tissue measured by real-time RT-PCR and in BAL fluid by ELISA, with significant elevation of IFNγ mRNA and protein expression levels.Conclusions: We conclude that CXCR3 is crucial for AHR and airway inflammation by promoting recruitment of more CD8+ T cells, as well as CD4+ T cells, and initiating release of proinflammatory mediators following OVA sensitization and challenge. CXCR3 may represent a novel therapeutic target for asthma. [ABSTRACT FROM AUTHOR]

The paper presents a novel strategy for the fabrication of sandwich-like N, S co-doped graphene aerogels using π-π and H-bonding interactions between 2, 5-Dimercapto-1, 3, 4-thiadiazole (DMTD) and GO via hydrothermal method. The synergistic effect between N and S atoms plays key role to improve the supercapacitor performance of the fabricated graphene aerogel material. • π-conjugated DMTD molecules are used as dopant precursors and pillared agents for the fabrication of NSGA. • NSGA delivers a high gravimetric specific capacitance of 321 F g−1 at a current density of 1 A g−1. • The π-conjugated and H-bonding interactions improve the accessible surface area of NSGA. • The synergistic effect of N andS and enhancement of surface area are the main reason in promoting the SC performance. Rational constructing carbon electrode materials with heteroatoms (eg. N, S, B, F) and high surface area is essencial to the appealing performance of supercapacitor (SC). Here we present a novel fabrication strategy for sandwich-like N, S co-doped three-dimensional (3D) porous graphene aerogels (NSGAs) via one-pot hydrothermal method for high performance SCs materials. The unique advantage of the proposed synthesis strategy is the applications of 2, 5-Dimercapto-1, 3, 4-thiadiazole (DMTD) as bifunctional pillared agents and efficient dopant precursors. The planar DMTD molecules have shown strong supramolecular π-π and H-bonding interactions with graphene oxide (GO), thus avoiding the restacking of graphene sheets and enhancing the doping efficiency and amount of S atoms, which are beneficial to the SC performance of NSGA. The synthesized NSGA samples exhibit the atomic content of S up to 2.39 at.% with surface area at 366.0 m2 g−1, and display a maximum energy density of 10.52 W h kg−1 for assembled symmetric supercapacitor. The relatively high tandem device performance with a remarkable current response, even at 2000 mV s−1, reaches the top level for graphene-based SC system. The proposed simple fabrication strategy and attracting performance of NSGA material shed light on the potential practical applications of graphene-based material as SCs, and the observed structure-function relations also provides physical-chemical insight into the function principle of heteroatom doped graphene in SCs. [ABSTRACT FROM AUTHOR]

This article reports on a study which investigated the positional cloning of the pleiotropic quantitative trait loci (QTL) Ghd7.1 in rice. It is noted that Ghd7.1 greatly delays rice heading and enhances grain productivity. Researchers concluded that the isolation of Ghd7.1 provided an opportunity to breed high-yield varieties with improved adaptive flexibility for special farming regions.

Highlights: [•] We developed a set of chromosome segment substitution lines of an elite hybrid. [•] All the identified 15 QTLs showed partial dominance on plant height in the CSSL-F2 population. [•] Significant digenic interactions between main QTLs were detected to control plant height. [•] Directional dominance could well explain the midparent heterosis for plant height in an elite rice hybrid. [•] Dominance together with epistasis could explain the better parent heterosis. [ABSTRACT FROM AUTHOR]

Aims: Growing evidence has suggested that lncRNAs play a regulatory role in tumorigenesis. Dysregulation of a newly identified lncRNA (LINC00847) has been involved in several tumors. Nevertheless, the expression and roles of lncRNAs in skin melanoma remain unclear. Therefore, we attempted to investigate the expressions and roles of lncRNAs in this study., Materials and Methods: Expression levels of LINC00847 were quantified in tissue samples from the TCGA database and clinically recruited participants. LINC00847 was inhibited in cells by transfecting with si-LINC00847 or si-NC. Expressions of LINC00847 and miR-133a-3p were determined using RT-qPCR, and the TGFBR1 level was determined using Western blotting. Targeting sites of LINC00847 with miR-133a-3p and miR-133a-3p with TGFBR1 were predicted by bioinformatic tools and proved by dual-luciferase reporter system and RNA immunoprecipitation. Cell proliferation, invasion, and migration abilities were assessed using CCK8, cell colony formation, cell wound scratch, and transwell assay, respectively., Results: In both TCGA and clinical cohorts, the expression of LINC00847 was abnormally upregulated in skin melanoma tissues than that of benign nevus. Besides, LINC00847 expression increased more markedly in A375 and SK-MEL-28 cells than in normal epidermal melanocytes (HEMa-LP cells). LINC00847 knockdown remarkably restrained skin melanoma cell proliferation, metastasis, and wound healing rate. Furthermore, miR-133a-3p/TGFBR1 was the downstream target for LINC00847. LINC00847 negatively regulated miR-133a-3p expression in skin melanoma cells. Both miR-133a-3p inhibitors and TGFBR1 vector transfection reversed the effect of LINC00847 silence in skin melanoma cells., Conclusion: LINC00847 was highly expressed in skin melanoma, and its overexpression accelerated the malignant tumor behavior of skin melanoma cells. The miR-133a-3p /TGFBR1 axis was involved in the roles of LINC00847 in skin melanoma., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Sphingolipid metabolism plays important roles in maintaining cell growth and signal transduction. However, this pathway has not been investigated in keloid, a disease characterized by the excessive proliferation of fibroblasts., Methods: Based on the expression profiles of three datasets, the differentially expressed genes (DEGs) were explored between keloid fibroblasts and normal fibroblasts. Metabolism-related genes were obtained from a previous study. Then, enrichment analysis and protein-protein interaction (PPI) network analysis were performed for genes. Differences in metabolism-related pathways between keloid fibroblasts and normal fibroblasts were analyzed by the gene set variation analysis (GSVA). Quantitative PCR was used to confirm the expression of key genes in keloid fibroblast., Results: A total of 42 up-regulated co-DEGs and 77 down-regulated co-DEGs were revealed based on three datasets, and were involved in extracellular matrix structural constituent, collagencontaining extracellular matrix and sphingolipid metabolism pathway. A total of 15 metabolism- DEGs were screened, including serine palmitoyltransferase long chain base subunit (SPTLC) 3, UDP-glucose ceramide glucosyltransferase (UGCG) and sphingomyelin synthase 2 (SGMS2). All these three genes were enriched in the sphingolipid pathway. GSVA showed that the biosynthesis of glycosphingolipids (GSLs) in keloid fibroblasts was lower than that in normal fibroblasts. Quantitative PCR suggested SPTLC3, UGCG and SGMS2 were regulated in keloid fibroblasts., Conclusion: Sphingolipids metabolism pathway might take part in the disease progression of keloid by regulating keloid fibroblasts. SPTLC3, UGCG and SGMS2 might be key targets to investigate the underlying mechanism., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: As a tumor suppressor or oncogenic gene, abnormal expression of RUNX family transcription factor 3 (RUNX3) has been reported in various cancers., Introduction: This study aimed to investigate the role of RUNX3 in melanoma., Methods: The expression level of RUNX3 in melanoma tissues was analyzed by immunohistochemistry and the Oncomine database. Based on microarray datasets GSE3189 and GSE7553, differentially expressed genes (DEGs) in melanoma samples were screened, followed by functional enrichment analysis. Gene Set Enrichment Analysis (GSEA) was performed for RUNX3. DEGs that co-expressed with RUNX3 were analyzed, and the transcription factors (TFs) of RUNX3 and its co-expressed genes were predicted. The protein-protein interactions (PPIs) for RUNX3 were analyzed utilizing the GeneMANIA database. MicroRNAs (miRNAs) that could target RUNX3 expression, were predicted., Results: RUNX3 expression was significantly up-regulated in melanoma tissues. GSEA showed that RUNX3 expression was positively correlated with melanogenesis and melanoma pathways. Eleven DEGs showed significant co-expression with RUNX3 in melanoma, for example, TLE4 was negatively co-expressed with RUNX3. RUNX3 was identified as a TF that regulated the expression of both itself and its co-expressed genes. PPI analysis showed that 20 protein-encoding genes interacted with RUNX3, among which 9 genes were differentially expressed in melanoma, such as CBFB and SMAD3. These genes were significantly enriched in transcriptional regulation by RUNX3, RUNX3 regulates BCL2L11 (BIM) transcription, regulation of I-kappaB kinase/NFkappaB signaling, and signaling by NOTCH. A total of 31 miRNAs could target RUNX3, such as miR-326, miR-330-5p, and miR-373-3p., Conclusion: RUNX3 expression was up-regulated in melanoma and was implicated in the development of melanoma., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

An N-doped graphene aerogel (NGA) is used as a reactive container for growing MnO2 nanoparticles via a soaking-hydrothermal strategy. MnO2 nanoparticles pile up on the surface of reduced graphene oxide sheets with crosslinked structures serving as electrical conductors. Importantly, the NGA generates extra capacitance during the electrochemical process, which accomplishes a satisfactory compensation in the physical-chemical properties of MnO2. As a cathodic electrode for Zn-ion batteries, the MnO2/NGA exhibits a specific capacity of 275.8 mA h g-1 and pre-eminent cycling stability with a retention of 93.6% at 3 A g-1 after 1000 cycles. Meanwhile, the proposed electrode also shows a relatively high specific capacitance of 341 F g-1 for a supercapacitor in 1 M Na2SO4. Meanwhile, the long-term cycling stability shows only a slight decrease by 5.1% of the initial capacitance after 5000 continuous cycles at 3 A g-1, which indicates its superior electrochemical stability. Additionally, the assembled asymmetric supercapacitor also shows good electrochemical performance. This work highlights the extensive function of an N-doped graphene aerogel as a promising substrate for enhancing the electrochemical performance of MnO2, which opens the gate for wide potential applications of graphene aerogel composites emphasizing their complementary effects.

Purpose: To investigate whether FGFR1 gene amplification is associated with clinicopathologic characteristics and its potential impact on survival in patients with resected esophageal squamous cell carcinoma (ESCC)., Methods: Five hundred fifty-six ESCC patients undergoing curative resection of ESCC were retrospectively studied. FGFR1 gene copy number was determined in microarrayed tumor samples using fluorescent in situ hybridization (FISH) analysis. FGFR1 gene amplification status was prespecified as copy number ≥ 6 or FGFR1/CEN 8 ratio ≥ 2.2. FGFR1 expression was evaluated by immunohistochemistry. Overall survival (OS) and disease-free survival (DFS) were analyzed using the Kaplan-Meier method followed by the log rank test. Correlation with survival was examined using multivariate Cox regression., Results: FGFR1 amplification was identified in 67 (12.1%) patients; these patients had significantly shorter OS (50.0 vs 32.0 months; log rank; P <0.001) as well as shorter DFS (47.0 vs 28.0 months; log rank; P <0.001) than those without FGFR1 amplification. Under a Cox proportional hazard model, FGFR1 amplification was associated with significantly shorter OS (adjusted hazard ratio [AHR]=1.61; 95% CI, 1.10-2.43, P =0.004) and DFS (AHR=1.72; 95%CI, 1.15-2.48; P <0.001). Moreover, cases with high intratumoral FGFR1 expression showed significantly shorter OS and DFS than those with low FGFR1 expression. The frequency of FGFR1 amplification was significantly higher in heavy drinkers than in moderate and light drinkers., Conclusion: FGFR1 amplification is an independent adverse prognostic factor in surgically resected ESCC. FGFR1 may be a promising therapeutic target in patients with ESCC., Competing Interests: CONFLICTS OF INTEREST The authors declare that they have no potential conflicts of interest.

Background: CD8+ T cells participate in airway hyperresponsiveness (AHR) and allergic pulmonary inflammation that are characteristics of asthma. CXCL10 by binding to CXCR3 expressed preferentially on activated CD8+ T cells, attracts T cells homing to the lung. We studied the contribution and limitation of CXCR3 to AHR and airway inflammation induced by ovalbumin (OVA) using CXCR3 knockout (KO) mice., Methods: Mice were sensitized and challenged with OVA. Lung histopathological changes, AHR, cellular composition and levels of inflammatory mediators in bronchoalveolar lavage (BAL) fluid, and lungs at mRNA and protein levels, were compared between CXCR3 KO mice and wild type (WT) mice., Results: Compared with the WT controls, CXCR3 KO mice showed less OVA-induced infiltration of inflammatory cells around airways and vessels, and less mucus production. CXCR3 KO mice failed to develop significant AHR. They also demonstrated significantly fewer CD8+ T and CD4+ T cells in BAL fluid, lower levels of TNFα and IL-4 in lung tissue measured by real-time RT-PCR and in BAL fluid by ELISA, with significant elevation of IFNγ mRNA and protein expression levels., Conclusions: We conclude that CXCR3 is crucial for AHR and airway inflammation by promoting recruitment of more CD8+ T cells, as well as CD4+ T cells, and initiating release of proinflammatory mediators following OVA sensitization and challenge. CXCR3 may represent a novel therapeutic target for asthma.