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Due to their ability to achieve higher DOA estimation accuracy and larger degrees of freedom (DOF) using a fixed number of antennas, sparse arrays, etc., nested and coprime arrays have attracted a lot of attention in relation to research into direction of arrival (DOA) estimation. However, the usage of the sparse array is based on the assumption that the signals are independent of each other, which is hard to guarantee in practice due to the complex propagation environment. To address the challenge of sparse arrays struggling to handle coherent wideband signals, we propose the following method. Firstly, we exploit the coherent signal subspace method (CSSM) to focus the wideband signals on the reference frequency and assist in the decorrelation process, which can be implemented without any pre-estimations. Then, we virtualize the covariance matrix of sparse array due to the decorrelation operation. Next, an enhanced spatial smoothing algorithm is applied to make full use of the information available in the data covariance matrix, as well as to improve the decorrelation effect, after which stage the multiple signal classification (MUSIC) algorithm is used to obtain DOA estimations. In the simulation, with reference to the root mean square error (RMSE) that varies in tandem with the signal-to-noise ratio (SNR), the algorithm achieves satisfactory results compared to other state-of-the-art algorithms, including sparse arrays using the traditional incoherent signal subspace method (ISSM), the coherent signal subspace method (CSSM), spatial smoothing algorithms, etc. Furthermore, the proposed method is also validated via real data tests, and the error value is only 0.2 degrees in real data tests, which is lower than those of the other methods in real data tests. [ABSTRACT FROM AUTHOR]

In an ultra-wideband (UWB) system, the two-dimensional (2D) multiple signal classification (MUSIC) algorithms based on high-precision 2D spectral peak search can jointly estimate the time of arrival (TOA) and angle of arrival (AOA). However, the computational complexity of 2D-MUSIC is very high, and the corresponding data model is only based on the dual antennas. To solve these problems, a low-complexity algorithm for joint AOA and TOA estimation of the multipath ultra-wideband signal is proposed. Firstly, the dual antenna sensing data model is extended to the antenna array case. Then, based on the array-sensing data model, the proposed algorithm transforms the 2D spectral peak search of 2D-MUSIC into a secondary optimization problem to extract the estimation of AOA via only 1D search. Finally, the acquired AOA estimations are brought back, and the TOA estimations are also obtained through a 1D search. Moreover, in the case of an unknown transmitted signal waveform, the proposed method can still distinguish the main path signal based on the time difference of arrival of different paths, which shows wider applications. The simulation results show that the proposed algorithm outperforms the Root-MUSIC algorithm and the estimation of signal parameters using the rotational invariance techniques (ESPRIT) algorithm, and keeps the same estimation accuracy but with greatly reduced computational complexity compared to the 2D-MUSIC algorithm. [ABSTRACT FROM AUTHOR]

Distributed array manifold perturbation, which includes synchronization errors, amplitude-phase errors, and path attenuation, has seriously degraded the accuracy of existing direct position determination (DPD) methods. In this paper, a DPD method under unknown multi-perturbation with moving distributed coprime arrays is advocated for. Firstly, by means of array position interchange, the integrated signals received from distributed arrays can be fused, which contributes to multi-position fusion. Subsequently, by resorting to the orthogonality between the noise subspace and steering vector received via distributed arrays, a quadratic optimization problem is constructed. Finally, we realize multi-parameter decoupling and achieve localization regardless of unknown perturbations. The superiority of the advocated method is substantiated from simulation examples. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2009.08.038 Byline: Rui Yue (1), Jiuhong Kang (1)(2), Cong Zhao (1), Wenxiang Hu (1), Yawei Tang (1), Xiaosong Liu (1), Gang Pei (1)(2) Keywords: DEVBIO; DNA; PROTEINS Abstract: [beta]-Arrestin1 is a multifunctional protein critically involved in signal transduction. Recently, it is also identified as a nuclear transcriptional regulator, but the underlying mechanisms and physiological significance remain to be explored. Here, we identified [beta]-arrestin1 as an evolutionarily conserved protein essential for zebrafish development. Zebrafish embryos depleted of [beta]-arrestin1 displayed severe posterior defects and especially failed to undergo hematopoiesis. In addition, the expression of cdx4, a critical regulator of embryonic blood formation, and its downstream hox genes were downregulated by depletion of [beta]-arrestin1, while injection of cdx4, hoxa9a or hoxb4a mRNA rescued the hematopoietic defects. Further mechanistic studies revealed that [beta]-arrestin1 bound to and sequestered the polycomb group (PcG) recruiter YY1, and relieved PcG-mediated repression of cdx4-hox pathway, thus regulating hematopoietic lineage specification. Taken together, this study demonstrated a critical role of [beta]-arrestin1 during zebrafish primitive hematopoiesis, as well as an important regulator of PcG proteins and cdx4-hox pathway. Author Affiliation: (1) Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences; Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China (2) School of Life Science and Technology, Tongji University, 200092, Shanghai, China Article History: Received 15 January 2009; Revised 4 May 2009; Accepted 21 August 2009 Article Note: (miscellaneous) Published: October 29, 2009

Iguratimod (IGU) is a novel disease modified anti-rheumatic drug, which has been found to act directly on B cells for inhibiting the production of antibodies in rheumatoid arthritis (RA) patients. Follicular helper T (Tfh) cells, a key T cell subsets in supporting B cell differentiation and antibody production, have been shown to play critical roles in RA. However, whether IGU can inhibit RA Tfh cells which further restrains B cell function remains unclear. Here, we aimed to explore the roles of IGU in regulating RA circulating Tfh (cTfh) cell function and investigate the potential mechanism associated with cell glucose metabolism. In our study, we found that IGU could act on RA-CD4+ T cells to reduce T cell-dependent antibody production. IGU decreased the percentage of RA cTfh cells and the expression of Tfh cell-related molecules and cytokines which were involved in B cell functions. Importantly, our data showed that IGU significantly restrained the cTfh cell function by inhibiting glucose metabolism, which relied on Hif1α-HK2 axis. In summary, we clarified a new target and mechanism of IGU by restraining RA cTfh cell function via inhibiting Hif1α-HK2-glucose metabolism axis. Our study demonstrates the potential application of IGU in the treatment of diseases related to abnormal metabolism and function of Tfh cells. [ABSTRACT FROM AUTHOR]

Peripheral helper T cells (Tph), characterized by PD‐1+CXCR5‐CD4+ phenotypes cells, played critical roles in inflamed tissues. Yet, to date, no researches were developed for lung adenocarcinoma (LADC) that was associated with worse outcome, advanced invasion and chronic inflammation in lung cancer cases. Accordingly, we aimed to investigate the impact of Tph cell subsets on the disease progress in peripheral blood and tumour tissue of patients with LADC. The percentages of Tph cell subsets in peripheral blood and tumour tissues obtained from 35 LADC and 10 healthy controls were examined by flow cytometry. In addition, invasion and tumour node metastasis (TNM) stage were also determined by Spearman's correlation test to assess their association with Tph cell subset. Furthermore, the effects of tumour microenvironment on Tph were investigated. The present results revealed that the percentage of Tph cells significantly increased in PBMC compared with healthy controls. In addition, similar results were observed in tumour tissues of LADC patients when compared to tumour‐adjacent control tissue. In addition, Tph cells were highly activated, appearing as ICOS increased, and associated with LADC invasion, compared with healthy controls. Notably, tumour environment could prefer Tph cells to promote tumour malignancy. Tph cells were observed in PBMC and tumour tissues from patients with LADC and highly associated with LADC invasion. Altogether, the present study indicates that elevated Tph cells could primarily be used as a potential therapeutic target in LADC patients. [ABSTRACT FROM AUTHOR]

B cell dysfunction and inflammatory cytokine over‐production participate in the pathogenesis of rheumatoid arthritis (RA). Here we compared peripheral B cell homeostasis and immune functions between RA patients and healthy controls (HC) and explored vital signaling pathways involved in altered RA B cells. We found that RA patients showed significantly decreased frequencies of peripheral CD19+CD27+CD24high regulatory B (Breg) cells but increased frequencies of CD19+CD27+CD38high plasmablasts and CD19+CD138+ plasma cells, and higher levels of serum immunoglobulin (Ig)M and IgG. Compared to HC peripheral B cells, RA peripheral B cells had more increased proliferation and higher expression of activation markers. Importantly, our results showed that RA peripheral B cells displayed the mTOR signaling pathway to be more activated, and inhibition of mTOR could restore RA B cell homeostasis and functions. RA serum‐treated B cells exhibited more increased expressions of mTOR, which could be restored with the addition of anti‐interleukin (IL)‐27 neutralizing antibody. Serum IL‐27 levels were significantly increased in RA patients and positively correlated with disease activity, the frequencies of plasma cells and the levels of autoantibodies. In vitro, IL‐27 notably promoted immune dysfunction of RA B cells, which were inhibited by anti‐IL‐27 neutralizing antibody. Also, the mTOR pathway was more activated in IL‐27‐treated RA B cells, and mTOR inhibition apparently reversed abnormalities of RA B cells mediated by IL‐27. These results suggest that increased serum IL‐27 levels could promote peripheral B cell dysfunction in RA patients via activating the mTOR signaling pathway. Thus, IL‐27 may play a pro‐pathogenic role in the development of RA, and antagonizing IL‐27 could be a novel therapy strategy for RA. [ABSTRACT FROM AUTHOR]

Mycobacterium tuberculosis (Mtb) can subvert host immune responses and survive in macrophages. Specific Mtb antigens play a critical role in this process. Rv1987, a secretory protein encoded by the gene rv1987 in the region of difference‐2 (RD2) of the Mtb genome, is specifically expressed in pathogenic mycobacteria. Our previous work proved that Rv1987 induced a Th2 response in mice and enhanced mycobacterial survival in mouse lungs, but its effect on macrophages, the most important effector immune cell involved in killing Mtb, remains unclear. In this study, we used an M. smegmatis strain overexpressing Rv1987 protein to infect alveolar macrophages and the macrophage cell line RAW264.7 and analyzed the effect of Rv1987 protein on macrophage polarization. Rv1987 induced M2 polarization in macrophages both in vivo and in vitro. The bactericidal ability of these M2 polarized macrophages decreased remarkably, which resulted in the increased survival of bacteria in macrophages. Proteomics, RT‐qPCR and western blotting results revealed that the PI3K/Akt1/mTOR signaling pathway was activated in Rv1987‐induced M2 macrophages. Meanwhile, the SHIP molecule, a negative regulator of the PI3K/Akt1/mTOR signaling pathway, was significantly downregulated. These results suggest that Rv1987 plays an important role in modulating the host immune response and could be established as a potential drug target. [ABSTRACT FROM AUTHOR]

Background and Aims Vitamin E (tocochromanol) is a lipid-soluble antioxidant and an essential nutrient for human health. Among cereal crops, barley (Hordeum vulgare) contains a high level of vitamin E, which includes both tocopherols and tocotrienols. Although the vitamin E biosynthetic pathway has been characterized in dicots, such as Arabidopsis , which only accumulate tocopherols, knowledge regarding vitamin E biosynthesis in monocots is limited because of the lack of functional mutants. This study aimed to obtain gene knockout mutants to elucidate the genetic control of vitamin E composition in barley. Methods Targeted knockout mutations of HvHPT and HvHGGT in barley were created with CRISPR/Cas9-enabled genome editing. High-performance liquid chromatography (HPLC) was performed to analyse the content of tocochromanol isomers in transgene-free homozygous Hvhpt and Hvhggt mutants. Key Results Mutagenesis efficiency among T0 regenerated plantlets was 50–65 % as a result of two simultaneously expressed guide RNAs targeting each gene; most of the mutations were stably inherited by the next generation. The transgene-free homozygous mutants of Hvhpt and Hvhggt exhibited decreased grain size and weight, and the HvHGGT mutation led to a shrunken phenotype and significantly lower total starch content in grains. HPLC analysis revealed that targeted mutation of HvHPT significantly reduced the content of both tocopherols and tocotrienols, whereas mutations in HvHGGT completely blocked tocotrienol biosynthesis in barley grains. Transient overexpression of an HvHPT homologue in tobacco leaves significantly increased the production of γ- and δ-tocopherols, which may partly explain why targeted mutation of HvHPT in barley grains did not eliminate tocopherol production. Conclusions Our results functionally validated that HvHGGT is the only committed gene for the production of tocotrienols, whereas HvHPT is partly responsible for tocopherol biosynthesis in barley. [ABSTRACT FROM AUTHOR]

Hull‐less barley (HLB), especially waxy HLB, contains many physiologically active ingredients; however, its poor processing performance and end‐product quality are unfavorable. In this study, 80% waxy or normal HLB wholegrain flour (WGF) and 20% wheat flour were used for baking bread. The farinograph and pasting properties of composite powders, and the nutritional value, textural properties, and in vitro hydrolysis of resultant breads were evaluated. The addition of a high proportion of HLB WGFs significantly increased the nutritional value of breads, especially the β‐glucan contents of waxy HLB breads. The addition of HLB WGFs and a suitable amount of wheat gluten led to a lower degree of softening of HLB bread flours but improved its farinograph characteristics, such as higher water absorption rate, development time, stability time, and farinograph quality number. Although the sensory profiles of HLB breads were considerably lower than those of wheat bread, they still received a good overall acceptability from a panel of sensory evaluators. HLB breads, particularly the waxy types, exhibited higher hardness, gumminess, chewiness, and lower specific volume, glycemic index and equilibrium concentration in starch hydrolysis. After baking, the starch crystallinity of dough changed from A to V type, and the relative crystallinity decreased. Overall, waxy HLB breads had more nutritional value than normal HLB breads. Higher β‐glucan and total dietary fiber content in HLB might have a positive effect on the nutritional value of the resultant breads. However, high β‐glucan and total dietary fiber was also accompanied by a negative effect on the sensory quality and processing performance of the end product. Practical Application: The composite flour with 80 g hull‐less barley wholegrain flour, 20 g wheat flour, and 30 g wheat gluten can be substituted in breadmaking. Compared to wheat bread, hull‐less barley bread exhibited different but acceptable sensory properties and had more nutritional value, particularly the waxy one. Therefore, a high proportion of hull‐less barley could be recommended for bread production. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is the major autoimmune destructive disease of joints with a complicated pathogenesis. The contribution of tumor necrosis factor‐like ligand 1A (TL1A) in RA pathogenesis, especially on fibroblast‐like synoviocytes (FLS), has been suggested clinically. The present study investigated the role of TL1A in mitochondrial dysfunction, induced oxidative stress in mitochondria, apoptosis resistance and the inflammatory response in FLS obtained from RA patients (RA‐FLS). RA‐FLS were incubated with TL1A and tumor necrosis factor receptor 2 (TNFR2) antagonist. Respiratory function, mitochondrial membrane potential and respiration associated genes of mitochondria were measured in both TL1A stimulated and non‐stimulated RA‐FLS. Additionally, the effects of TL1A on reactive oxygen species (ROS) production in mitochondria, apoptosis and the inflammatory response in RA‐FLS were also assessed. The role of TL1A in association between ROS generation, especially mitochondrial type and the inflammatory response, was evaluated by measuring inflammation‐related cytokines and signaling pathways using ROS inhibitors, diphenyleneiodonium chloride and Mito‐TEMPO (Sigma‐Aldrich, Miamisburg, OH, USA). We found that TL1A induced mitochondrial dysfunction by weakening mitochondrial respiration and membrane potential, which was blocked by a TNFR2 antagonist. Increased ROS synthesis in impaired mitochondria was observed with MitoSOX (Invitrogen, CA, USA) immunofluorescence staining in TL1A‐stimulated RA‐FLS but inhibited by a TNFR2 antagonist. TL1A influenced apoptosis resistance and inflammatory mediators via TNFR2. Inhibition of mitochondria‐derived ROS compromised the production of inflammatory factors in TL1A‐stimulated RA‐FLS, suggesting that mitochondrial dysfunction mediated by the TL1A/TNFR2 axis might amplify the inflammatory response via regulation of mitochondria‐derived ROS generation. Collectively, our results reveal that TL1A might be involved in making FLS more aggressive in RA pathogenesis via cell respiration interruption. [ABSTRACT FROM AUTHOR]

Non-small cell lung cancer (NSCLC) constitutes the majority of all lung-cancer cases. Aquaporin 5 (AQP5) may be involved in NSCLC by promoting lung-cancer initiation and progression. The present study aimed to determine the role of AQP5 in migration and angiogenesis using NSCLC cells and HUVECs. AQPs 1, 3, 4, 5, 8 and 9 were screened in the NSCLC cell line H1299, and the present results showed that AQP5 mRNA was upregulated compared with the other AQP genes. At the protein level, AQP5 was significantly increased in H1299 cells compared with 16HBE cells. AQP5 knockdown in H1299 cells significantly decreased cell migration compared with untransfected cells, as demonstrated by both Transwell and wound closure assays. The present study further investigated H1299 ability to promote HUVEC vascularisation. The supernatants of both transfected and untransfected H1299 cells were used as conditioned medium for HUVECs, and tube formation was measured. The supernatant of AQP5-downregulated cells exhibited significantly low tube formation potential compared with untransfected cells. Similarly, vascular endothelial growth factor was significantly increased in control cells (si-NC) compared with cells transfected with small interfering RNA targeting AQP5. The present study found that AQP5 downregulation significantly decreased the phosphorylation level of epidermal growth factor receptor and the activity of the ERK1/2 pathway. In summary, the present study suggested that AQP5 influenced migration and angiogenesis in NSCLCs in vitro and may potentially exhibit similar in vivo effects. [ABSTRACT FROM AUTHOR]

Waxy barley referred to as low‐amylose or amylose‐free has special advantages in nutrition composition and food processing. Waxy gene encoding granule–bound starch synthase I (GBSSI) is responsible for amylose synthesis in barley. The G3935‐to‐T in Waxy gene has been previously found in amylose–free barley. In this study, G3935‐to‐T was proved to co‐segregate with the waxy phenotype of barley, but has no obvious effect on GBSSI catalytic activity and starch chain length distribution. However, recombinant inbred lines with G3935‐to‐T in Waxy gene are of significant modification in starch granules morphology and pasting properties, increase of grain β‐glucan content, and decrease of thousand kernel weight along with lower kernel width. A polymerase chain reaction with confronting two–pair primers marker was developed for economic and efficient screening of G3935‐to‐T. This study provides the basis for cultivar improvement of waxy barley then fully developing its potential value and utility in food processing. [ABSTRACT FROM AUTHOR]

CD4+CXCR5+ICOS+ T cells, known as Tfh (T Follicular helper) cells, are required for antibody production. Abnormal production and differentiation of Tfh cells are involved in many autoimmune diseases, including rheumatoid arthritis (RA). Leptin has the property of modulating immune system. Here, we explored the effect of leptin on CD4+CXCR5+ICOS+ T cells production in RA patients. Serum leptin levels were measured by enzyme-linked immunosorbent assay (ELISA). Peripheral blood mononuclear cells (PBMC) stimulated with CD3/CD28 were cultured in the presence and absence of leptin and with or without anti-IL-6 receptor (anti-IL-6R), anti-IL-21R, and anti-IL-12R antibody respectively. IL-6, IL-21, and IL-12 levels were determined by ELISA. Bcl-6 was detected by reverse transcription-polymerase chain reaction. STAT1, pSTAT1, STAT3, and pSTAT3 were examined by western blot. We found that leptin levels were higher in RA patients than healthy controls. Leptin-stimulated RA PBMC upregulated CD4+CXCR5+ICOS+ T cells, along with increased IL-6, IL-21, and IL-12.CD4+CXCR5+ICOS+ T cells, Bcl-6 mRNA expression, pSTAT1, and pSTAT3 obviously declined when anti-IL-6R antibody was added into leptin-treated RA PBMC, which suggested that leptin upregulated RA CD4+CXCR5+ICOS+ T cells via increased IL-6 by activation of STAT1 and STAT3. We presented an innovative mechanism on how leptin participated in RA pathogenesis. [ABSTRACT FROM AUTHOR]

IL-34 is a pleiotropic cytokine, which is a key regulator of monocytes/macrophages and might participate in the pathogenesis of RA. In this study, we aimed to explore the effect of IL-34 on the monocyte-like cell line THP-1 and the quantitative variation of Th17 cells in THP-1 and RA CD4T cells coculture system. CD4T cells were purified from RA PBMC using immunomagnetic beads. THP-1 were cultured with RA CD4T cells. The frequency of Th17 cells was determined by FACS. Fluorscence indensity and expression of ROS were detected by FACS and cell staining, respectively. The expression of IL-6, IL-23, IL-21, TNF-α and IL-1β in the coculture supernatants were detected by ELISA. We found that CSF-1R was constitutively expressed on peripheral monocytes as well as THP-1, but not on the T/B cells. IL-34-CSF-1R binding could activate THP-1 to secret IL-6. IL-34 could up-regulate the numbers of Th17 cells in coculture system, which was possibly via the production of IL-6. We further observed ROS levels were increased in the coculture system. The percentage of Th17 cells was reduced when ROS production was inhibited by NAC, a specific inhibitor of ROS production. In addition, TNFRII antagonist but not IL-1βR antagonist could restrict the production of ROS, expression of IL-6 and generation of Th17 cells. In conclusion, IL-34-stimulated THP-1 can produce higher levels of ROS, which promoted IL-6 secretion and up-regulated Th17 cells. Our study suggests a novel mechanistic insight into how the interaction of IL-34-stimulated monocytes and CD4T cells participates in the RA pathogenesis. [ABSTRACT FROM AUTHOR]

Cold injury often results in a drastic reduction in the yields of hulless barley, however, the genome-wide transcriptome changes in response to cold stress have not been intensively studied in hulless barley. Using mRNA sequencing, we compared the transcriptome profiles of two hulless barley genotypes (cv. H8 and T148: cold tolerant and susceptible genotypes, respectively) under cold acclimation and freezing treatments, which aim to identify genes that specifically respond to chilly conditions. Under cold acclimation and freezing treatments, the total number of differentially expressed genes (DEGs) in H8 is much higher than that in T148. In addition, the number of cold acclimation induced DEGs is higher than the number of DEGs induced by freezing in both cultivars. Based on gene ontology enrichment analysis and the construction of gene regulatory interaction networks, a group of genes that may contribute to the distinct cold tolerance between the two hulless barley genotypes were identified. This study provides a valuable source that can benefit for future cold tolerance improvement in barley and other crops. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a chronic autoimmune disease which is characterized by synovial inflammation and cartilage damage for which causes articular dysfunction. Activation of fibroblast-like synoviocytes (FLS) is a critical step that promotes disease progression. In this study, we aimed to explore the effect of interleukin-34 (IL-34) on RA FLS as a proinflammatory factor and IL-34-stimulated FLS on the production of Th17. We found that serum IL-34 levels were increased compared to those of the healthy controls and had positive correlations with C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), and anticyclic citrullinated peptide (CCP) antibody accordingly. CSF-1R was also highly expressed on RA FLS. The interaction of IL-34 and CSF-1R promoted a dramatic production of IL-6 by FLS through JNK/P38/NF-κB signaling pathway. Further, the IL-34-stimulated IL-6 secretion by RA FLS was found to upregulate the number of Th17. The treatment of IL-6R antagonist could attenuate the production of Th17 mediated by IL-34-stimulated RA FLS. Our results suggest that the increased IL-34 levels were closely related to the disease activity of RA. Additionally, the overexpression of IL-6 in the IL-34-stimulated FLS promoted the generation of Th17. Therefore, IL-34 was supposed to be involved in the pathogenesis of RA. The inhibition of IL-34 might provide a novel target for therapies of RA. [ABSTRACT FROM AUTHOR]

Background: Hulless barley is attracting increasing attention due to its unique nutritional value and potential health benefits. However, the molecular biology of the barley grain development and nutrient storage are not well understood. Furthermore, the genetic potential of hulless barley has not been fully tapped for breeding. Methodology/Principal Findings: In the present study, we investigated the transcriptome features during hulless barley grain development. Using Illumina paired-end RNA-Sequencing, we generated two data sets of the developing grain transcriptomes from two hulless barley landraces. A total of 13.1 and 12.9 million paired-end reads with lengths of 90 bp were generated from the two varieties and were assembled to 48,863 and 45,788 unigenes, respectively. A combined dataset of 46,485 All-Unigenes were generated from two transcriptomes with an average length of 542 bp, and 36,278 among were annotated with gene descriptions, conserved protein domains or gene ontology terms. Furthermore, sequences and expression levels of genes related to the biosynthesis of storage reserve compounds (starch, protein, and β-glucan) were analyzed, and their temporal and spatial patterns were deduced from the transcriptome data of cultivated barley Morex. Conclusions/Significance: We established a sequences and functional annotation integrated database and examined the expression profiles of the developing grains of Tibetan hulless barley. The characterization of genes encoding storage proteins and enzymes of starch synthesis and (1–3;1–4)-β-D-glucan synthesis provided an overview of changes in gene expression associated with grain nutrition and health properties. Furthermore, the characterization of these genes provides a gene reservoir, which helps in quality improvement of hulless barley. [ABSTRACT FROM AUTHOR]

A wireless implantable sensor network system (WISNS) is designed for in vivo monitoring physiological signals of a population of animals. WISNS can simultaneously monitor more than 15 animals, communicating three kinds of analog information among sensor nodes. Analog signals are transmitted to relay node at 800-KHz carrier by AM. Relay nodes digitalize and package them into messages, and then forward to the Wireless sensor network by Nordic RF technology (NWSN). Smaller overall dimensions (<2 cm ^3), lower power regulation, and dedicated packaging make the system suitable and compatible for implantable devices. The implantable sensor node, protocol stack of NWSN, and performance of the system are evaluated and optimized with ECG monitoring test of rats. Compared with those commercially available sensor nodes, our implantable one is leading in the weight and volume miniaturization, and our WISNS solution shows huge potential in achieving the compatibility of different animals. [ABSTRACT FROM PUBLISHER]

Tibetan barley (Hordeum vulgare L., qingke) is the principal cereal cultivated on the Tibetan Plateau for at least 3,500 years, but its origin and domestication remain unclear. Here, based on deep-coverage whole-genome and published exome-capture resequencing data for a total of 437 accessions, we show that contemporary qingke is derived from eastern domesticated barley and it is introduced to southern Tibet most likely via north Pakistan, India, and Nepal between 4,500 and 3,500 years ago. The low genetic diversity of qingke suggests Tibet can be excluded as a center of origin or domestication for barley. The rapid decrease in genetic diversity from eastern domesticated barley to qingke can be explained by a founder effect from 4,500 to 2,000 years ago. The haplotypes of the five key domestication genes of barley support a feral or hybridization origin for Tibetan weedy barley and reject the hypothesis of native Tibetan wild barley. The origin of Tibetan barley (qingke) has been a controversial issue for many years. Here, the authors conduct population genomics study to support that qingke is derived from eastern domesticated barley instead of Tibetan wild barley and suggest southern Tibetan Plateau as its introduction route. [ABSTRACT FROM AUTHOR]

• Leptin-activated DCs promote the proliferation of PBMC and up-regulates the percentage of Th17 cells. • DCs activation by leptin depends on glycolysis. • Leptin enhances HK2 expression on DCs via STAT3 pathway. Leptin is over-secreted in many autoimmune diseases, which can promote dendritic cells (DCs) maturation and up-regulate the expression of inflammatory cytokines, but the underlying mechanisms are not fully elucidated. Considering the major role of leptin in maintaining energy balance and the significant role of glycolysis in DCs activation, our study aims to investigate whether leptin promotes the activation of DCs via glycolysis and its underlying mechanisms. We demonstrated that leptin promoted the activation of DCs, including up-regulating the expression of co-stimulatory molecules and inflammatory cytokines, enhancing the proliferation and T helper 17 (Th17) cell ratio in peripheral blood mononuclear cells (PBMC) co-cultured with leptin-stimulated DCs. Leptin also enhanced DCs glycolysis with increased glucose consumption, lactate production, and the expression of hexokinase 2 (HK2). In addition, the activation of DCs stimulated by leptin could be inhibited by the glycolysis inhibitor 2-deoxy- d -glucose (2-DG). To explore the signaling pathways involved in leptin-induced HK2 expression, we observed that the inhibitors of STAT3 (NSC74859) could repress the enhancement of HK2 triggered by leptin stimulation. Therefore, our results indicated that leptin promoted glycolytic metabolism to induce DCs activation via STAT3-HK2 pathway. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstracts Ethnopharmacological relevance Cryptotanshinone, a natural compound isolated from the roots of Salvia miltiorrhiza Bge. (Danshen), is a commonly used traditional Chinese medicine to treat high blood pressure in some countries. It has been shown that Cryptotanshinone induces cancer cells apoptosis and impairs cell migration and invasion. However, the antiproliferation and chemosensitization effects of Cryptotanshinone on ovarian cancer and the underlying mechanism are not fully elucidated. Aim of study In this study, we evaluated the inhibitory effect of Cryptotanshinone on ovarian cancer cells and explored the underlying molecular mechanism. Additionally, the chemosensitization potential of Cryptotanshinone was evaluated in combination with cisplatin. Materials and methods MTT assay was used for cell viability assessment of ovarian cancer A2780 cells treated with Cryptotanshinone and/ or cisplatin. Flow cytometry was used for apoptosis analysis. Wound healing and transwell assays were used for migratory and invasive potential assessment of Cryptotanshinone-treated ovarian cancer cells. Western blot was used to investigate proteins involved in the mechanisms for metastasis and apoptosis. γH2AX immunocytochemistry was used to detect DNA damage in A2780 cells exposed to Cryptotanshinone and/or cisplatin. Results Cryptotanshinone significantly induced ovarian cancer A2780 cells apoptosis by activating caspase cascade. Additionally, wound healing and transwell assays revealed that Cryptotanshinone could suppress migration and invasion of ovarian cancer cells and dramatically inhibited MMP-2 and MMP-9 expression. Furthermore, Cryptotanshinone could sensitize A2780 cells to cisplatin treatment in a dose-dependent manner. Conclusion Our data confirmed the anti-tumor effect of Cryptotanshinone on ovarian cancer cells and provided new findings that Cryptotanshinone could sensitize ovarian cancer cells to chemotherapy. [ABSTRACT FROM AUTHOR]