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Summary: A graphene nanosheet‐TiO2 nanoparticle composite (L‐GNS‐TiO2) was prepared for an application as a high‐performance lithium storage device (or lithium‐ion battery anode). The composite features a well‐defined hybrid structure of GNS and homogeneously distributed anatase TiO2 nanoparticles due to nanoparticulation and modification by organic ligands (polyacrylic acid, tartaric acid, and diethylene glycol). Despite its low overall carbon content (~8.4%), the L‐GNS‐TiO2 composite‐based anode exhibited highly reversible lithiation/delithiation (Coulombic efficiency >97%), excellent capacity retention (206 (92%) and 331 (147%) mAh g−1 after 50 and 450 cycles, respectively, at 0.15 A g−1) and decent rate capability (164 mAh g−1 at 0.75 A g−1). In addition, the stable morphology/structure of the composite after lengthy cycle tests reflected its mechanical robustness and electrochemical reversibility. The excellent performance of L‐GNS‐TiO2 was attributed to the enhanced electronic conductivity, retained charge storage sites, and a short Li+ diffusion pathway enabled by the unique composite structure constructed through optimized ligand mediation. Highlights: A graphene nanosheet‐TiO2 nanoparticle composite (L‐GNS‐TiO2) was prepared for Li storage applications.L‐GNS‐TiO2 possesses a structure containing uniformly distributed anatase TiO2 nanoparticles on GNS due to optimized mediation and nanoparticulation by organic ligands.L‐GNS‐TiO2 exhibits enhanced conductivity, retains charge storage sites, and facilitates Li+ transport/charge transfer.Excellent cycle stability (>100% capacity retention, 331 mAh g−1) and Coulombic efficiency (>99%) were realized after 450 cycles at 0.15 A g−1.Decent rate capability was achieved with a high capacity (164 mAh g−1) at 0.75 A g−1. [ABSTRACT FROM AUTHOR]

Otoancorin (OTOA), encoded by OTOA, is required for the development of the tectorial membrane in the inner ear. Mutations in this gene cause nonsyndromic hearing loss (DFNB22). The molecular mechanisms underlying most DFNB22 remain poorly understood. Disruption of glycosylphosphatidylinositol (GPI) anchorage has been assumed to be the pathophysiology mandating experimental validation. From a Korean deaf family, we identified two trans OTOA variants (c.1320 + 5 G > C and p.Gln589ArgfsX55 [NM_144672.3]). The pathogenic potential of c.1320 + 5 G > C was confirmed by a minigene splicing assay. To experimentally determine the GPI anchorage, wild‐type (WT) and mutant OTOA harboring p.Gln589ArgfsX55 were expressed in HEK293T cells. The mutant OTOA with p.Gln589ArgfsX55 resulted in an uncontrolled release of OTOA into the medium in contrast with phosphatidylinositol‐specific phospholipase C‐induced controlled release of WT OTOA from the cell surface. Together, the results of this reverse translational study confirmed GPI‐anchorage of OTOA and showed that downstream sequences from the 589th amino acid are critical for GPI‐anchorage. [ABSTRACT FROM AUTHOR]

The soil-borne pathogen Phytophthora capsici causes severe destruction of Capsicum spp. Resistance in Capsicum against P. capsici is controlled by numerous minor quantitative trait loci (QTLs) and a consistent major QTL on chromosome 5. Molecular markers on Capsicum chromosome 5 have been developed to identify the predominant genetic contributor to resistance but have achieved little success. In this study, previously reported molecular markers were used to reanalyze the major QTL region on chromosome 5 (6.2 Mbp to 139.2 Mbp). Candidate resistance gene analogs (RGAs) were identified in the extended major QTL region including 14 nucleotide binding site leucine-rich repeats, 3 receptor-like kinases, and 1 receptor-like protein. Sequence comparison of the candidate RGAs was performed between two Capsicum germplasms that are resistant and susceptible, respectively, to P. capsici. 11 novel RGA-based markers were developed through high-resolution melting analysis which were closely linked to the major QTL for P. capsici resistance. Among the markers, CaNB-5480 showed the highest cosegregation rate at 86.9% and can be applied to genotyping of the germplasms that were not amenable by previous markers. With combination of three markers such as CaNB-5480, CaRP-5130 and CaNB-5330 increased genotyping accuracy for 61 Capsicum accessions. These could be useful to facilitate high-throughput germplasm screening and further characterize resistance genes against P. capsici in pepper. [ABSTRACT FROM AUTHOR]

The soil-borne pathogen Phytophthora capsici causes severe destruction of Capsicum spp. Resistance in Capsicum against P. capsici is controlled by numerous minor quantitative trait loci (QTLs) and a consistent major QTL on chromosome 5. Molecular markers on Capsicum chromosome 5 have been developed to identify the predominant genetic contributor to resistance but have achieved little success. In this study, previously reported molecular markers were used to reanalyze the major QTL region on chromosome 5 (6.2 Mbp to 139.2 Mbp). Candidate resistance gene analogs (RGAs) were identified in the extended major QTL region including 14 nucleotide binding site leucine-rich repeats, 3 receptor-like kinases, and 1 receptor-like protein. Sequence comparison of the candidate RGAs was performed between two Capsicum germplasms that are resistant and susceptible, respectively, to P. capsici. 11 novel RGA-based markers were developed through high-resolution melting analysis which were closely linked to the major QTL for P. capsici resistance. Among the markers, CaNB-5480 showed the highest cosegregation rate at 86.9% and can be applied to genotyping of the germplasms that were not amenable by previous markers. With combination of three markers such as CaNB-5480, CaRP-5130 and CaNB-5330 increased genotyping accuracy for 61 Capsicum accessions. These could be useful to facilitate high-throughput germplasm screening and further characterize resistance genes against P. capsici in pepper. [ABSTRACT FROM AUTHOR]

Eosinophil cationic protein (ECP), a cytotoxic protein contained in eosinophils granules, can contribute to various inflammatory responses. Although Helicobacter pylori infection increases infiltration of eosinophils, the mechanisms of eosinophil degranulation by H. pylori infection are largely unknown. The goal of this study was to investigate the role of H. pylori outer membrane vesicles (OMVs) in modulating eosinophil degranulation. We found that eosinophils treated with H. pylori OMVs released significantly more ECP compared with untreated controls. In addition, eosinophils cocultured with OMV-preexposed primary gastric epithelial cells exhibited significantly increased ECP release. Similarly, eosinophils cocultured with culture supernatant (CM) from primary gastric epithelial cells exposed to OMVs (OMV-CM) released significantly higher amounts of ECP compared with eosinophils cocultured with CM from unexposed control cells. Furthermore, OMVs and OMV-CM both induced the upregulation of ICAM-1 on gastric epithelial cells and β2 integrin CD11b on eosinophils. In addition, both transduction of ICAM-1 shRNA into gastric epithelial cells and treatment with neutralizing mAbs to CD18 significantly decreased OMV-mediated or OMV-CM-mediated release of ECP. These results suggest that the eosinophil degranulation response to H. pylori OMVs occurs via a mechanism that is dependent on both β2 integrin CD11/CD18 and ICAM-1. [ABSTRACT FROM AUTHOR]

Natural killer dendritic cells (NKDCs) possess potent anti-tumor activity, but the cellular effect of NKDC interactions with other innate immune cells is unclear. In this study, we demonstrate that the interaction of NKDCs and natural killer T (NKT) cells is required for the anti-tumor immune responses that are elicited by ¿ -galactosylceramide ( ¿ -GC) in mice. The rapid and strong expression of interferon- ¿ by NKDCs after ¿ -GC stimulation was dependent on NKT cells. Various NK and DC molecular markers and cytotoxic molecules were up-regulated following ¿ -GC administration. This up-regulation could improve NKDC presentation of tumor antigens and increase cytotoxicity against tumor cells. NKDCs were required for the stimulation of DCs, NK cells, and NKT cells. The strong anti-tumor immune responses elicited by ¿ -GC may be due to the down-regulation of regulatory T cells. Furthermore, the depletion of NKDCs dampened the tumor clearance mediated by ¿ -GC-stimulated NKT cells in vivo. Taken together, these results indicate that complex interactions of innate immune cells might be required to achieve optimal anti-tumor immune responses during the early stages of tumorigenesis. [ABSTRACT FROM AUTHOR]