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Using 448.1 × 106 ψ(3686) decays collected with the BESIII detector at the BEPCII e+e− storage rings, the branching fractions and angular distributions of the decays χcJ → Ξ−Ξ¯¯¯¯+ and Ξ0Ξ¯¯¯¯0 (J = 0, 1, 2) are measured based on a partial-reconstruction technique. The decays χc1 → Ξ0Ξ¯¯¯¯0 and χc2 → Ξ0Ξ¯¯¯¯0 are observed for the first time with statistical significances of 7σ and 15σ, respectively. The results of this analysis are in good agreement with previous measurements and have significantly improved precision.
Using a data sample of e+e− collision data corresponding to an integrated luminosity of 2.93 fb−1 collected with the BESIII detector at a center-of-mass energy of s=3.773GeV, we search for the singly Cabibbo-suppressed decays D0→π0π0π0, π0π0η, π0ηη and ηηη using the double tag method. The absolute branching fractions are measured to be B(D0→π0π0π0)=(2.0±0.4±0.3)×10−4, B(D0→π0π0η)=(3.8±1.1±0.7)×10−4 and B(D0→π0ηη)=(7.3±1.6±1.5)×10−4 with the statistical significances of 4.8σ, 3.8σ and 5.5σ, respectively, where the first uncertainties are statistical and the second ones systematic. No significant signal of D0→ηηη is found, and the upper limit on its decay branching fraction is set to be B(D0→ηηη)<1.3×10−4 at the 90% confidence level.
The specimens which form the basis of the following notes and descriptions were received by the writer from Mr. Ch'i Ho, Asistant Entomologist of Fan Memorial Institute of Biology, who collected thern either in Peiping or Eastern Tomb (40.2 N, 117.0 E), Hopei Province. They belong to nineteen species and are included in fifteen genera. Two of the species are believed to be new to science.
Background: Gan–Dou–Fu–Mu decoction (GDFMD) improves liver fibrosis in experimental and clinical studies including those on toxic mouse model of Wilson disease (Model). However, the mechanisms underlying the effect of GDFMD have not been characterized. Herein, we deciphered the potential therapeutic targets of GDFMD using transcriptome analysis.
Methods: We constructed a tx-j Wilson disease (WD) mouse model, and assessed the effect of GDFMD on the liver of model mice by hematoxylin and eosin, Masson, and immunohistochemical staining. Subsequently, we identified differentially expressed genes (DEGs) that were upregulated in the Model (Model vs. control) and those that were downregulated upon GDFMD treatment (compared to the Model) using RNA-sequencing (RNA-Seq). Biological functions and signaling pathways in which the DEGs were involved were determined by gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses. A protein–protein interaction (PPI) network was constructed using the STRING database, and the modules were identified using MCODE plugin with the Cytoscape software. Several genes identified in the RNA-Seq analysis were validated by real-time quantitative PCR. Results: Total of 2124 DEGs were screened through the Model vs. control and Model vs. GDFMD comparisons, and dozens of GO and KEGG pathway terms modulated by GDFMD were identified. Dozens of pathways involved in metabolism (including metabolic processes for organic acids, carboxylic acids, monocarboxylic acids, lipids, fatty acids, cellular lipids, steroids, alcohols, eicosanoids, long-chain fatty acids), immune and inflammatory response (such as complement and coagulation cascades, cytokine–cytokine receptor interaction, inflammatory mediator regulation of TRP channels, antigen processing and presentation, T-cell receptor signaling pathway), liver fibrosis (such as ECM-receptor interactions), and cell death (PI3K-Akt signaling pathway, apoptosis, TGF-beta signaling pathway, etc.) were identified as potential targets of GDFMD in the Model. Some hub genes and four modules were identified in the PPI network. The results of real-time quantitative PCR analysis were consistent with those of RNA-Seq analysis. Conclusions: We performed gene expression profiling of GDFMD-treated WD model mice using RNA-Seq analysis and found the genes, pathways, and processes effected by the treatment. Our study provides a theoretical basis to prevent liver fibrosis resulting from WD using GDFMD.
A taxonomic study on twenty-nine species of jumping spiders from South China is presented. Twenty new species are diagnosed and described: Heliophanoides proszynskii Wang, Mi & Peng sp. nov. (♂♀), Myrmage lii Wang, Mi & Peng sp. nov. (♂♀), Myrmarachne hamata Wang, Mi & Peng sp. nov. (♂), M. xingrenensis Wang, Mi & Peng sp. nov. (♂♀), M. yinae Wang, Mi & Peng sp. nov. (♂♀), Phintella fodingensis Wang, Mi & Peng sp. nov. (♂♀), P. jiugongensis Wang, Mi & Peng sp. nov. (♂♀), P. liae Wang, Mi & Peng sp. nov. (♂), P. liui Wang, Mi & Peng sp. nov. (♂♀), P. subpanda Wang, Mi & Peng sp. nov. (♂♀), P. wandae Wang, Mi & Peng sp. nov. (♂♀), Ptocasius dian Wang, Mi & Peng sp. nov. (♂♀), P. subhubeiensis Wang, Mi & Peng sp. nov. (♂♀), Rhene elongata Wang, Mi & Peng sp. nov. (♂♀), Stertinius donglinsiensis Wang, Mi & Peng sp. nov. (♂♀), S. logunovi Wang, Mi & Peng sp. nov. (♂), Synagelides fanjingensis Wang, Mi & Peng sp. nov. (♂♀), Thyene xingrenensis Wang, Mi & Peng sp. nov. (♂♀), Toxeus fodingensis Wang, Mi & Peng sp. nov. (♂♀), and Yaginumaella zabkai Wang, Mi & Peng sp. nov. (♂♀). The genus Heliophanoides Prószyński, 1992 is redefined and two new combinations, transferred from the genus Phintella Strand, 1906, are proposed: H. tengchongensis (Lei & Peng 2013) comb. nov., and H. longlingensis (Lei & Peng 2013) comb. nov. The unknown sexes of the following six species are described for the first time: Phintella fanjingshan Li, Wang, Zhang & Chen, 2019, P. panda Huang, Wang & Peng, 2015, P. pygmaea (Wesołowska, 1981), P. sancha Cao & Li, 2016, P. wulingensis Huang, Wang & Peng, 2015, and Rhene yunnanensis (Peng & Xie, 1995). Brettus anchorum Wanless, 1979 and Phintella aequipeiformis Żabka, 1985 are newly recorded from China. Icius indicus (Simon, 1901) comb. nov. (transferred from Phintella) is re-described. Phintella levii Huang, Wang & Peng, 2015 is assigned to be a synonym of P. arcuata Huang, Wang & Peng, 2015. Thyene zhangi (Peng, Yin, Yan & Kim, 1998) comb. nov. is transferred from Plexippoides Prószyński, 1984, and T. bilaguncula (Xie & Peng, 1995) comb. nov. is transferred from Ptocasius Simon, 1885. Diagnostic illustrations of the twenty-nine species and the distributional maps of the studied specimens are provided.
A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets
(2018)
NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCRB6C14R strain. Ly5.1C14R NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46C14R in 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1C14R mice had normal number of NK cells, they showed an increased number of early maturation stage NK cells. CD49a+ILC1s were also increased but these cells lacked the expression of TRAIL. ILC3s that expressed NKp46 were not detectable and were not apparent when examined by T-bet expression. Thus, the C14R mutation reveals that NKp46 is important for NK cell and ILC differentiation, maturation and function.
Molecular cause and functional impact of altered synaptic lipid signaling due to a prg‐1 gene SNP
(2015)
Loss of plasticity-related gene 1 (PRG-1), which regulates synaptic phospholipid signaling, leads to hyperexcitability via increased glutamate release altering excitation/inhibition (E/I) balance in cortical networks. A recently reported SNP in prg-1 (R345T/mutPRG-1) affects ~5 million European and US citizens in a monoallelic variant. Our studies show that this mutation leads to a loss-of-PRG-1 function at the synapse due to its inability to control lysophosphatidic acid (LPA) levels via a cellular uptake mechanism which appears to depend on proper glycosylation altered by this SNP. PRG-1(+/-) mice, which are animal correlates of human PRG-1(+/mut) carriers, showed an altered cortical network function and stress-related behavioral changes indicating altered resilience against psychiatric disorders. These could be reversed by modulation of phospholipid signaling via pharmacological inhibition of the LPA-synthesizing molecule autotaxin. In line, EEG recordings in a human population-based cohort revealed an E/I balance shift in monoallelic mutPRG-1 carriers and an impaired sensory gating, which is regarded as an endophenotype of stress-related mental disorders. Intervention into bioactive lipid signaling is thus a promising strategy to interfere with glutamate-dependent symptoms in psychiatric diseases.