2 research outputs found

    A Service Composition Approach Based on Pre-joined Service Network in Graph Database

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    We solve the service composition problem with plugin semantic matching in a graph database. We present a Prejoined Service Network (PJSN) approach which firstly constructs and stores a service composition network with all services and compositions in a graph database. Then, this approach fetches a satisfying solution by converting the composition request into Cypher and querying the graph database. We evaluate the performance of the proposed PJSN approach by conducting experiments and comparing with that of the Pre-joined Semantic Indexing Graph (PJSIG) method. The experiment results show that compared with the PJSIG method, the proposed approach can always find a solution and lead to higher user’s satisfaction

    Gain-of-Function Mutation of KIT Ligand on Melanin Synthesis Causes Familial Progressive Hyperpigmentation

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    Familial progressive hyperpigmentation (FPH) is an autosomal-dominantly inherited disorder characterized by hyperpigmented patches in the skin, present in early infancy and increasing in size and number with age. The genetic basis for FPH remains unknown. In this study, a six-generation Chinese family with FPH was subjected to a genome-wide scan for linkage analysis. Two-point linkage analysis mapped the locus for FPH at chromosome 12q21.31-q23.1, with a maximum two-point LOD score of 4.35 (Ø = 0.00) at D12S81. Haplotype analysis confined the locus within an interval of 9.09 cM, flanked by the markers D12S1667 and D12S2081. Mutation profiling of positional candidate genes detected a heterozygous transversion (c. 107A→G) in exon 2 of the KIT ligand (KITLG) gene, predicted to result in the substitution of a serine residue for an asparagine residue at codon 36 (p.N→S). This mutant “G” allele cosegregated perfectly with affected, but not with unaffected, members of the FPH family. Function analysis of the soluble form of sKITLG revealed that mutant sKITLGN36S increased the content of the melanin by 109% compared with the wild-type sKITLG in human A375 melanoma cells. Consistent with this result, the tyrosinase activity was significantly increased by mutant sKITLGN36S compared to wild-type control. To our knowledge, these data provided the first genetic evidence that the FPH disease is caused by the KITLGN36S mutation, which has a gain-of-function effect on the melanin synthesis and opens a new avenue for exploration of the genetic mechanism of FPH
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