1,486 research outputs found

    Urban Regional Social Community Detection Using Location Based Social Network Big Data

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    In this paper, we propose a methodology of applying location based social network (LBSN) Big Data to detect urban regional social communities (URSCs) and analyze their activation levels. For this, we first construct a social spatial network (SSN) based on the LBSN Big Data of a city. Then, by applying a modularity optimization algorithm to the SSN constructed, where modularity is a measure to check the strength of clustered networks, we detect the boundaries of the URSCs. The activation level of each detected URSC is further analyzed based on a diversity index, i.e., Shannon entropy. For experiments, we apply the proposed methodology to the city of Seoul where the LBSN Big Data is collected from Foursquare social networks. Through the experimental results, we observe that the detected URSCs match well with the URSCs known by the Seoul citizen from which we can confirm the effectiveness of our proposed methodology in detecting USRCs and analyzing their activation levels

    Molecular characterization and expression pattern of a novel Keratin-associated protein 11.1 gene in the Liaoning cashmere goat ()

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    Objective An experiment was conducted to determine the relationship between the KAP11.1 and the regulation wool fineness. Methods In previous work, we constructed a skin cDNA library and isolated a full-length cDNA clone termed KAP11.1. On this basis, we conducted a series of bioinformatics analysis. Tissue distribution of KAP11.1 mRNA was performed using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis. The expression of KAP11.1 mRNA in primary and secondary hair follicles was performed using real-time PCR (real-time polymerase chain reaction) analysis. The expression location of KAP11.1 mRNA in primary and secondary hair follicles was performed using in situ hybridization. Results Bioinformatics analysis showed that KAP11.1 gene encodes a putative 158 amino acid protein that exhibited a high content of cysteine, serine, threonine, and valine and has a pubertal mammary gland) structural domain. Secondary structure prediction revealed a high proportion of random coils (76.73%). Semi-quantitative RT-PCR showed that KAP11.1 gene was expressed in heart, skin, and liver, but not expressed in spleen, lung and kidney. Real time PCR results showed that the expression of KAP11.1 has a higher expression in catagen than in anagen in the primary hair follicles. However, in the secondary hair follicles, KAP11.1 has a significantly higher expression in anagen than in catagen. Moreover, KAP11.1 gene has a strong expression in inner root sheath, hair matrix, and a lower expression in hair bulb. Conclusion We conclude that KAP11.1 gene may play an important role in regulating the fiber diameter

    Disease-Associated Mutations Prevent GPR56-Collagen III Interaction

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    GPR56 is a member of the adhesion G protein-coupled receptor (GPCR) family. Mutations in GPR56 cause a devastating human brain malformation called bilateral frontoparietal polymicrogyria (BFPP). Using the N-terminal fragment of GPR56 (GPR56N) as a probe, we have recently demonstrated that collagen III is the ligand of GPR56 in the developing brain. In this report, we discover a new functional domain in GPR56N, the ligand binding domain. This domain contains four disease-associated mutations and two N-glycosylation sites. Our study reveals that although glycosylation is not required for ligand binding, each of the four disease-associated mutations completely abolish the ligand binding ability of GPR56. Our data indicates that these four single missense mutations cause BFPP mostly by abolishing the ability of GPR56 to bind to its ligand, collagen III, in addition to affecting GPR56 protein surface expression as previously shown

    Density dependence across multiple life stages in a temperate old-growth forest of northeast China

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    Recent studies on species coexistence suggest that density dependence is an important mechanism regulating plant populations. However, there have been few studies of density dependence conducted for more than one life-history stage or that control for habitat heterogeneity, which may influence spatial patterns of survival and mask density dependence. We explored the prevalence of density dependence across multiple life stages, and the effects of controlling for habitat heterogeneity, in a temperate forest in northeast China. We used generalized linear mixed-effects models to test for density-dependent mortality of seedlings and spatial point pattern analysis to detect density dependence for sapling-to-juvenile transitions. Conspecific neighbors had a negative effect on survival of plants in both life stages. At the seedling stage, we found a negative effect of conspecific seedling neighbors on survival when analyzing all species combined. However, in species-level analyses, only 2 of 11 focal species were negatively impacted by conspecific neighbors, indicating wide variation among species in the strength of density dependence. Controlling for habitat heterogeneity did not alter our findings of density dependence at the seedling stage. For the sapling-to-juvenile transition stage, 11 of 15 focal species showed patterns of local scale (<10 m) conspecific thinning, consistent with negative density dependence. The results varied depending on whether we controlled for habitat heterogeneity, indicating that a failure to account for habitat heterogeneity can obscure patterns of density dependence. We conclude that density dependence may promote tree species coexistence by acting across multiple life-history stages in this temperate forest. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00442-012-2481-y) contains supplementary material, which is available to authorized users

    Cashmere growth control in Liaoning cashmere goat by ovarian carcinoma immunoreactive antigen-like protein 2 and decorin genes

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    Objective The study investigated the biological functions and mechanisms for controlling cashmere growth of Liaoning cashmere goat by ovarian carcinoma immunoreactive antigen-like protein 2 (OCIAD2) and decorin (DCN) genes. Methods cDNA library of Liaoning cashmere goat was constructed in early stages. OCIAD2 and DCN genes related to cashmere growth were identified by homology analysis comparison. The expression location of OCIAD2 and DCN genes in primary and secondary hair follicles (SF) was performed using in situ hybridization. The expression of OCIAD2 and DCN genes in primary and SF was performed using real-time polymerase chain reaction (PCR). Results In situ hybridization revealed that OCIAD2 and DCN were expressed in the inner root sheath of Liaoning cashmere goat hair follicles. Real-time quantitative PCR showed that these genes were highly expressed in SF during anagen, while these genes were highly expressed in primary hair follicle in catagen phase. Melatonin (MT) inhibited the expression of OCIAD2 and promoted the expression of DCN. Insulin-like growth factors-1 (IGF-1) inhibited the expression of OCIAD2 and DCN, while fibroblast growth factors 5 (FGF5) promoted the expression of these genes. MT and IGF-1 promoted OCIAD2 synergistically, while MT and FGF5 inhibited the genes simultaneously. MT+IGF-1/MT+FGF5 inhibited DCN gene. RNAi technology showed that OCIAD2 expression was promoted, while that of DCN was inhibited. Conclusion Activation of bone morphogenetic protein (BMP) signaling pathway up-regulated OCIAD2 expression and stimulated SF to control cell proliferation. DCN gene affected hair follicle morphogenesis and periodic changes by promoting transforming growth factor-β (TGF-β) and BMP signaling pathways. OCIAD2 and DCN genes have opposite effects on TGF-β signaling pathway and inhibit each other to affect the hair growth

    (1E)-6-Meth­oxy-3,4-dihydro­naphthalen-1(2H)-one oxime

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    In the crystal structure of the title compound, C11H13NO2, the mol­ecules are paired into centrosymmetric dimers via inter­molecular O—H⋯N hydrogen bonds

    Protective Mechanism of KIOM-4 in Streptozotocin-Induced Pancreatic β-Cells Damage Is Involved in the Inhibition of Endoplasmic Reticulum Stress

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    Endoplasmic reticulum stress-mediated apoptosis plays an important role in the destruction of pancreatic β-cells and contributes to the development of type 1 diabetes. The present study examined the effect of KIOM-4, a mixture of four plant extracts, on streptozotocin- (STZ-) induced endoplasmic reticulum (ER) stress in rat pancreatic β-cells (RINm5F). KIOM-4 was found to inhibit STZ-induced apoptotic cell death, confirmed by formation of apoptotic bodies and DNA fragmentation. STZ was found to induce the characteristics of ER stress; mitochondrial Ca2+ overloading, enhanced ER staining, release of glucose-regulated protein 78 (GRP78), phosphorylation of RNA-dependent protein kinase (PKR) like ER kinase (PERK) and eukaryotic initiation factor-2α (eIF-2α), cleavage of activating transcription factor 6 (ATF6) and caspase 12, and upregulation of CCAAT/enhancer-binding protein-homologous protein (CHOP). However, KIOM-4 attenuated these changes induced by STZ. Furthermore, KIOM-4 suppressed apoptosis induced by STZ in CHOP downregulated cells using CHOP siRNA. These results suggest that KIOM-4 exhibits protective effects in STZ-induced pancreatic β-cell damage, by interrupting the ER stress-mediated pathway
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