60 research outputs found

    Defining Urban Boundaries by Characteristic Scales

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    Defining an objective boundary for a city is a difficult problem, which remains to be solved by an effective method. Recent years, new methods for identifying urban boundary have been developed by means of spatial search techniques (e.g. CCA). However, the new algorithms are involved with another problem, that is, how to determine the characteristic radius of spatial search. This paper proposes new approaches to looking for the most advisable spatial searching radius for determining urban boundary. We found that the relationships between the spatial searching radius and the corresponding number of clusters take on an exponential function. In the exponential model, the scale parameter just represents the characteristic length that we can use to define the most objective urban boundary objectively. Two sets of China's cities are employed to test this method, and the results lend support to the judgment that the characteristic parameter can well serve for the spatial searching radius. The research may be revealing for making urban spatial analysis in methodology and implementing identification of urban boundaries in practice.Comment: 26 pages, 5 figures, 7 table

    A new transgenic reporter line reveals Wnt-dependent Snai2 re-expression and cranial neural crest differentiation in Xenopus

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    During vertebrate embryogenesis, the cranial neural crest (CNC) forms at the neural plate border and subsequently migrates and differentiates into many types of cells. The transcription factor Snai2, which is induced by canonical Wnt signaling to be expressed in the early CNC, is pivotal for CNC induction and migration in Xenopus. However, snai2 expression is silenced during CNC migration, and its roles at later developmental stages remain unclear. We generated a transgenic X. tropicalis line that expresses enhanced green fluorescent protein (eGFP) driven by the snai2 promoter/enhancer, and observed eGFP expression not only in the pre-migratory and migrating CNC, but also the differentiating CNC. This transgenic line can be used directly to detect deficiencies in CNC development at various stages, including subtle perturbation of CNC differentiation. In situ hybridization and immunohistochemistry confirm that Snai2 is re-expressed in the differentiating CNC. Using a separate transgenic Wnt reporter line, we show that canonical Wnt signaling is also active in the differentiating CNC. Blocking Wnt signaling shortly after CNC migration causes reduced snai2 expression and impaired differentiation of CNC-derived head cartilage structures. These results suggest that Wnt signaling is required for snai2 re-expression and CNC differentiation

    Xenopus Reduced Folate Carrier Regulates Neural Crest Development Epigenetically

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    Folic acid deficiency during pregnancy causes birth neurocristopathic malformations resulting from aberrant development of neural crest cells. The Reduced folate carrier (RFC) is a membrane-bound receptor for facilitating transfer of reduced folate into the cells. RFC knockout mice are embryonic lethal and develop multiple malformations, including neurocristopathies. Here we show that XRFC is specifically expressed in neural crest tissues in Xenopus embryos and knockdown of XRFC by specific morpholino results in severe neurocristopathies. Inhibition of RFC blocked the expression of a series of neural crest marker genes while overexpression of RFC or injection of 5-methyltetrahydrofolate expanded the neural crest territories. In animal cap assays, knockdown of RFC dramatically reduced the mono- and trimethyl-Histone3-K4 levels and co-injection of the lysine methyltransferase hMLL1 largely rescued the XRFC morpholino phenotype. Our data revealed that the RFC mediated folate metabolic pathway likely potentiates neural crest gene expression through epigenetic modifications

    A proton nuclear magnetic resonance-based metabonomics study of metabolic profiling in immunoglobulin a nephropathy

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    OBJECTIVES: Immunoglobulin A nephropathy is the most common cause of chronic renal failure among primary glomerulonephritis patients. The ability to diagnose immunoglobulin A nephropathy remains poor. However, renal biopsy is an inconvenient, invasive, and painful examination, and no reliable biomarkers have been developed for use in routine patient evaluations. The aims of the present study were to identify immunoglobulin A nephropathy patients, to identify useful biomarkers of immunoglobulin A nephropathy and to establish a human immunoglobulin A nephropathy metabolic profile. METHODS: Serum samples were collected from immunoglobulin A nephropathy patients who were not using immunosuppressants. A pilot study was undertaken to determine disease-specific metabolite biomarker profiles in three groups: healthy controls (N = 23), low-risk patients in whom immunoglobulin A nephropathy was confirmed as grades I-II by renal biopsy (N = 23), and high-risk patients with nephropathies of grades IV-V (N = 12). Serum samples were analyzed using proton nuclear magnetic resonance spectroscopy and by applying multivariate pattern recognition analysis for disease classification. RESULTS: Compared with the healthy controls, both the low-risk and high-risk patients had higher levels of phenylalanine, myo-Inositol, lactate, L6 lipids ( = CH-CH2-CH = O), L5 lipids (-CH2-C = O), and L3 lipids (-CH2-CH2-C = O) as well as lower levels of β -glucose, α-glucose, valine, tyrosine, phosphocholine, lysine, isoleucine, glycerolphosphocholine, glycine, glutamine, glutamate, alanine, acetate, 3-hydroxybutyrate, and 1-methylhistidine. CONCLUSIONS: These metabolites investigated in this study may serve as potential biomarkers of immunoglobulin A nephropathy. Point scoring of pattern recognition analysis was able to distinguish immunoglobulin A nephropathy patients from healthy controls. However, there were no obvious differences between the low-risk and high-risk groups in our research. These results offer new, sensitive and specific, noninvasive approaches that may be of great benefit to immunoglobulin A nephropathy patients by enabling earlier diagnosis

    A new Transgenic Reporter Line Reveals Wnt-dependent Snai2 Re-expression and Cranial Neural Crest Differentiation in Xenopus

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    During vertebrate embryogenesis, the cranial neural crest (CNC) forms at the neural plate border and subsequently migrates and diferentiates into many types of cells. The transcription factor Snai2, which is induced by canonical Wnt signaling to be expressed in the early CNC, is pivotal for CNC induction and migration in Xenopus. However, snai2 expression is silenced during CNC migration, and its roles at later developmental stages remain unclear. We generated a transgenic X. tropicalis line that expresses enhanced green fuorescent protein (eGFP) driven by the snai2 promoter/enhancer, and observed eGFP expression not only in the pre-migratory and migrating CNC, but also the diferentiating CNC. This transgenic line can be used directly to detect defciencies in CNC development at various stages, including subtle perturbation of CNC diferentiation. In situ hybridization and immunohistochemistry confrm that Snai2 is re-expressed in the diferentiating CNC. Using a separate transgenic Wnt reporter line, we show that canonical Wnt signaling is also active in the diferentiating CNC. Blocking Wnt signaling shortly after CNC migration causes reduced snai2 expression and impaired diferentiation of CNC-derived head cartilage structures. These results suggest that Wnt signaling is required for snai2 reexpression and CNC diferentiation

    Capillary hemangiomas with hemorrhage in cervicothoracic intramedullary, a case report

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    A 48-year-old male patient had presented with worsening pain at extremities and body. The MRI showed an inhomogeneously enhancing lesion at C5-T1. During the surgical evacuation through a midline myelotomy, a frozen section could not find any tumor cells or vascular malformations. Immunohistochemically, the diagnosis of capillary hemangiomas was confirmed. Keywords: Capillary hemangiomas, Intramedullary hemorrhage, Intramedullary tumor, Vascular malformatio
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