Successive spin-flop transitions of a Neel-type antiferromagnet Li2MnO3 single crystal with a honeycomb lattice

We have carried out high magnetic field studies of single-crystalline Li2MnO3, a honeycomb lattice antiferromagnet. Its magnetic phase diagram was mapped out using magnetization measurements at applied fields up to 35 T. Our results show that it undergoes two successive meta-magnetic transitions around 9 T fields applied perpendicular to the ab plane (along the c* axis). These phase transitions are completely absent in the magnetization measured with the field applied along the ab plane. In order to understand this magnetic phase diagram, we developed a mean-field model starting from the correct Neel-type magnetic structure, consistent with our single crystal neutron diffraction data at zero field. Our model calculations succeeded in explaining the two meta-magnetic transitions that arise when Li2MnO3 enters two different spin-flop phases from the zero field Neel phase.open1187Nsciescopu

Thermoelectric power measurements of wide band gap semiconducting nanowires

We investigated the temperature-dependent thermoelectric power (TEP) of individual wide band gap ZnO and GaN semiconducting nanowires by fabricating the devices with good Ohmic contacts. In the temperature range of 10-300 K, the measured TEP of both nanowires was linearly dependent on temperature, indicating the degenerate doping nature of these nanowires. The room temperature TEP value of ZnO nanowires was as high as -400 mu V/K while an order of magnitude smaller TEP value was observed in GaN. The negative sign of TEP values shows that electrons are the majority carriers in these wide band gap nanowires. More importantly, in comparison with gate-dependent transport measurements of the nanowire field effect transistors, analysis of temperature-dependent TEP measurements provides a reliable way of estimating the majority carrier concentration of nanowires, where conventional Hall effect measurements cannot be used.open116075sciescopu

Agrobacterium-mediated genetic transformation of Miscanthus sinensis

Miscanthus species are tall perennial rhizomatous grasses with C4 photosynthesis originating from East Asia, and they are considered as important bioenergy crops for biomass production. In this study, Agrobacterium-mediated transformation system for M. sinensis was developed using embryogenic calli derived from mature seeds. In order to establish a stable system, optimum conditions to obtain highly regenerable and transformation-competent embryogenic calli were investigated, and embryogenic calli were efficiently induced with callus induction medium containing 3 mg L-1 2,4-dichlorophenoxyacetic acid and 25 mM l-proline, at pH 5.7 with an induction temperature of 28 A degrees C. In addition, the embryogenic callus induction and regeneration potentials were compared between seven M. sinensis germplasms collected from several sites in Korea, which revealed that the germplasm SNU-M-045 had superior embryogenic callus induction and regeneration potentials. With this germplasm, the genetic transformation of M. sinensis was performed using Agrobacterium tumefaciens EHA105 carrying pCAMBIA1300 with a green fluorescence protein gene as a reporter. After putative transgenic plants were obtained, the genomic integration of transgenes was confirmed by genomic PCR, transgene expression was validated by Northern blot analysis, and the number of transgene integration was confirmed by DNA gel blot analysis. Furthermore, the Agrobacterium-mediated transformation of M. sinensis was also performed with pCAMBIA3301 which contains an herbicide resistance gene (BAR), and we obtained transgenic M. sinensis plants whose herbicide resistance was confirmed by spraying with BASTA(A (R)). Therefore, we have established a stable Agrobacterium-mediated transformation system for M. sinensis, and also successfully produced herbicide-resistant Miscanthus plants by introducing BAR gene via the established method.X111210Ysciescopu

Distributed Deep Learning at the Edge: A Novel Proactive and Cooperative Caching Framework for Mobile Edge Networks

© 2012 IEEE. We propose two novel proactive cooperative caching approaches using deep learning (DL) to predict users' content demand in a mobile edge caching network. In the first approach, a content server (CS) takes responsibilities to collect information from all mobile edge nodes (MENs) in the network and then performs the proposed DL algorithm to predict the content demand for the whole network. However, such a centralized approach may disclose the private information because MENs have to share their local users' data with the CS. Thus, in the second approach, we propose a novel distributed deep learning (DDL)-based framework. The DDL allows MENs in the network to collaborate and exchange information to reduce the error of content demand prediction without revealing the private information of mobile users. Through simulation results, we show that our proposed approaches can enhance the accuracy by reducing the root mean squared error (RMSE) up to 33.7% and reduce the service delay by 47.4% compared with other machine learning algorithms

PIKfyve, a class III lipid kinase, is required for TLR-induced type I IFN production via modulation of ATF3

Type I IFN plays a key role in antiviral responses. It also has been shown that deregulation of type I IFN expression following abnormal activation of TLRs contributes to the pathogenesis of systemic lupus erythematosus. In this study, we find that PIKfyve, a class III lipid kinase, is required for endolysosomal TLR-induced expression of type I IFN in mouse and human cells. PIKfyve binds to phosphatidylinositol 3-phosphate and synthesizes phosphatidylinositol 3,5-bisphosphate, and plays a critical role in endolysosomal trafficking. However, PIKfyve modulates type I IFN production via mechanisms independent of receptor and ligand trafficking in endolysosomes. Instead, pharmacological or genetic inactivation of PIKfyve rapidly induces expression of the transcription repressor ATF3, which is necessary and sufficient for suppression of type I IFN expression by bin'ding to its promoter and blocking its transcription. Thus, we have uncovered a novel phosphoinositide-mediated regulatory mechanism that controls TLR-mediated induction of type I IFN, which may provide a new therapeutic indication for the PIKfyve inhibitor.X111313Ysciescopu

TLR9 regulates adipose tissue inflammation and obesity-related metabolic disorders

ObjectiveRecent studies have revealed a link between Toll-like receptor (TLR) signaling and the adipose tissue inflammation associated with obesity. Although TLR9 is known to play an important role in inflammation and innate immunity, its role in mediating adipose tissue inflammation has not yet been investigated. Thus, the objective of this study was to determine the role of TLR9 in regulating immune cells in visceral adipose tissue and maintaining the metabolic homeostasis. MethodsWild-type and TLR9-deficient mice were fed with a high-fat diet, and the body weight gain, glucose tolerance, insulin sensitivity, and adipose tissue inflammation were examined. ResultsTLR9-deficient mice gained significantly more weight and body fat under a high-fat diet than wild-type mice and exhibited more severe glucose intolerance and insulin resistance. We also found a dramatic increase of M1 macrophages as well as T(H)1 cells in the adipose tissue of TLR9-deficient mice compared to wild-type mice. Furthermore, the levels of various proinflammatory cytokines and chemokines were higher in TLR9-deficient mice. ConclusionsTLR9 signaling is involved in regulating adipose tissue inflammation and controlling obesity and the metabolic syndrome.1174Ysciescopu

Low energy intensity production of fuel-grade bio-butanol enabled by membrane-based extraction

Widespread use of biofuels is inhibited by the significant energy burden of recovering fuel products from aqueous fermentation systems. Here, we describe a membrane-based extraction (perstraction) system for the recovery of fuel-grade biobutanol from fermentation broths which can extract n-butanol with high purity (>99.5%) while using less than 25% of the energy of current technology options. This is achieved by combining a spray-coated thin-film composite membrane with 2-ethyl-1-hexanol as an extractant. The membrane successfully protects the micro-organisms from the extractant, which, although ideal in other respects, is a metabolic inhibitor. In contrast to water, the extractant does not form a heterogeneous azeotrope with n-butanol, and the overall energy consumption of for n-butanol production is 3.9 MJ kg−1, substantially less than other recovery processes (17.0–29.4 MJ kg−1). By (a) extracting n-butanol from the fermentation broth without a phase change, (b) breaking the heterogeneous azeotrope relationship (less energy consumption for distillation), and (c) utilizing a small volume ratio of extractant : fermentation broth (1 : 100, v/v), the need for high energy intensity processes such as pervaporation, gas stripping or liquid–liquid extraction is avoided. The application of this perstraction system to continuous production of a range of higher alcohols is explored and shown to be highly favourable

Mechanism of Cisplatin-Induced Cytotoxicity Is Correlated to Impaired Metabolism Due to Mitochondrial ROS Generation

The chemotherapeutic use of cisplatin is limited by its severe side effects. In this study, by conducting different omics data analyses, we demonstrated that cisplatin induces cell death in a proximal tubular cell line by suppressing glycolysis-and tricarboxylic acid (TCA)/mitochondria-related genes. Furthermore, analysis of the urine from cisplatin-treated rats revealed the lower expression levels of enzymes involved in glycolysis, TCA cycle, and genes related to mitochondrial stability and confirmed the cisplatin-related metabolic abnormalities. Additionally, an increase in the level of p53, which directly inhibits glycolysis, has been observed. Inhibition of p53 restored glycolysis and significantly reduced the rate of cell death at 24 h and 48 h due to p53 inhibition. The foremost reason of cisplatin-related cytotoxicity has been correlated to the generation of mitochondrial reactive oxygen species (ROS) that influence multiple pathways. Abnormalities in these pathways resulted in the collapse of mitochondrial energy production, which in turn sensitized the cells to death. The quenching of ROS led to the amelioration of the affected pathways. Considering these observations, it can be concluded that there is a significant correlation between cisplatin and metabolic dysfunctions involving mROS as the major player.116224Ysciescopu

Extracellular Vesicles Derived from Gram-Negative Bacteria, such as Escherichia coli, Induce Emphysema Mainly via IL-17A-Mediated Neutrophilic Inflammation

Recent evidence indicates that Gram-negative bacteria-derived extracellular vesicles (EVs) in indoor dust can evoke neutrophilic pulmonary inflammation, which is a key pathology of chronic obstructive pulmonary disease (COPD). Escherichia coli is a ubiquitous bacterium present in indoor dust and secretes nanometer-sized vesicles into the extracellular milieu. In the current study, we evaluated the role of E. coli-derived EVs on the development of COPD, such as emphysema. E. coli EVs were prepared by sequential ultrafiltration and ultracentrifugation. COPD phenotypes and immune responses were evaluated in C57BL/6 wild-type (WT), IFN-gamma-deficient, or IL-17A-deficient mice after airway exposure to E. coli EVs. The present study showed that indoor dust from a bed mattress harbors E. coli EVs. Airway exposure to E. coli EVs increased the production of proinflammatory cytokines, such as TNF-alpha and IL-6. In addition, the repeated inhalation of E. coli EVs for 4 wk induced neutrophilic inflammation and emphysema, which are associated with enhanced elastase activity. Emphysema and elastase activity enhanced by E. coli EVs were reversed by the absence of IFN-gamma or IL-17A genes. In addition, during the early period, lung inflammation is dependent on IL-17A and TNF-alpha, but not on IFN-gamma, and also on TLR4. Moreover, the production of IFN-gamma is eliminated by the absence of IL-17A, whereas IL-17A production is not abolished by IFN-gamma absence. Taken together, the present data suggest that E. coli-derived EVs induce IL-17A-dependent neutrophilic inflammation and thereby emphysema, possibly via upregulation of elastase activity.X111613Ysciescopu