Pivoted Table Index for Querying Product- Property-Value Information

Abstract—The query for triple information on product– attribute (property)–value is one of the most frequent queries in e-commerce. In storing the triple (product–attribute– value) information, a vertical schema is effective for avoiding sparse data and schema evolution, while a conventional horizontal schema often shows better query performance, since the properties are queried as groups clustered by each product. Therefore, we propose two storage schemas: a vertical schema as a primary table structure for the triple information in RDBMS and a pivoted table index created from the basic vertical table as an additional index structure for accelerating query processing. The pivoted table index is beneficial to improving the performance of the frequent pattern query on the group properties associated with each product class. Index Terms—Ontology, index, RDBMS, e-commerce, pivoted table, vertical schema I

Modeling Considerations for Product Ontology

An issue in utilizing ontology in product information domain is how to make it operational. This requires considering the features to be included in a pragmatic product information database which should contain the key concepts and the relationships in the domain. Ontological modeling of product information is a starting as well as a most important point for practical deployment. It often involves problems such as the choice and representation of the proper semantic relationships, handling of product properties, and product descriptions associated with their units of measure. In this paper, we introduce an approach to those problems. We recently engaged in a project to build an operational product ontology system. The directions to problems, which are presented in this paper, were obtained from this project, and may serve a role as a reference model for similar projects in future

Vitamin C enters mouse T cells as dehydroascorbic acid in vitro and does not recapitulate in vivo vitamin C effects

Vitamin C is an essential micronutrient, which has been implicated in various biological processes, including immune response. In fact, in vivo administration of vitamin C modulates T cell proliferation and cytokine secretion. In this study, we analyzed the mechanism by which mouse T cells take up vitamin C, and whether this uptake directly affected T cell functions. T cells internalized more vitamin C when they were activated, due to enhanced glucose transporter (GLUT)-1 and GLUT-3 expression that persisted up to 48h after activation. Blocking oxidation of ascorbic acid (the reduced form of vitamin Q in the culture medium with 1,4-dithio-threitol (DTT) almost completely inhibited the enhanced vitamin C uptake. The presence of vitamin C at low concentrations during in vitro T cell activation did not affect proliferation or cytokine secretion (IFN-gamma, TNF-alpha, or IL-4) in response to PMA/ionomycin. In contrast, high concentrations (0.25-0.5mM) of vitamin C lowered cell viability, reduced thymidine uptake, and decreased cytokine secretion. In conclusion, activated T cells upregulated GLUT-1 and -3 to increase vitamin C uptake. They took up vitamin C mostly in its oxidized form, rarely in its reduced form. Application of vitamin C to T cells in vitro did not recapitulate previously reported in vivo responses to vitamin C, suggesting that in vivo, vitamin C modulates T cells indirectly through other components of the microenvironment.Maratou E, 2007, EUR J CLIN INVEST, V37, P282Mazzoni A, 2006, J IMMUNOL, V177, P3577Wintergerst ES, 2006, ANN NUTR METAB, V50, P85, DOI 10.1159/000090495PEARCE EJ, 2006, CHEM IMMUNOL ALLERGY, V90, P82Noh K, 2005, IMMUNOL LETT, V98, P63, DOI 10.1016/j.imlet.2004.10.012de Jong EC, 2005, SPRINGER SEMIN IMMUN, V26, P289, DOI 10.1007/s00281-004-0167-1Hartel C, 2004, CYTOKINE, V27, P101, DOI 10.1016/j.cyto.2004.02.004Mazzoni A, 2004, J LEUKOCYTE BIOL, V75, P721, DOI 10.1189/jlb.1003482Hosoya K, 2004, INVEST OPHTH VIS SCI, V45, P1232, DOI 10.1167/iovs.03-0505Patak P, 2004, ENDOCR RES, V30, P871, DOI 10.1081/ERC-20044126Fu YC, 2004, BLOOD CELL MOL DIS, V32, P182, DOI 10.1016/j.bcmd.2003.09.002Matsue H, 2003, J IMMUNOL, V171, P3010Nualart FJ, 2003, J BIOL CHEM, V278, P10128, DOI 10.1074/jbc.M210686200DETULLIO MC, 2002, VITAMIN C FUNCTION B, P159Maldonado-Lopez R, 2001, SEMIN IMMUNOL, V13, P275, DOI 10.1006/smim.2001.0323Baoutina A, 2001, FASEB J, V15, P1580, DOI 10.1096/fj.00-0704fjeClement MV, 2001, ANTIOXID REDOX SIGN, V3, P157Rumsey SC, 2000, J BIOL CHEM, V275, P28246Campbell JD, 1999, CELL IMMUNOL, V194, P1Tsukaguchi H, 1999, NATURE, V399, P70Verhasselt V, 1999, J IMMUNOL, V162, P2569Long KZ, 1999, PEDIATR INFECT DIS J, V18, P283Tatla S, 1999, FREE RADICAL BIO MED, V26, P14Lykkesfeldt J, 1999, METHOD ENZYMOL, V299, P83Podmore ID, 1998, NATURE, V392, P559Vera JC, 1998, BLOOD, V91, P2536Rumsey SC, 1997, J BIOL CHEM, V272, P18982Ngkeekwong FC, 1997, BIOCHEM J, V324, P225EYLAR E, 1996, P R HEALTH SCI J, V15, P21JEANNIN P, 1995, J EXP MED, V182, P1785VERA JC, 1995, J BIOL CHEM, V270, P23706VERA JC, 1994, BLOOD, V84, P1628VERA JC, 1993, NATURE, V364, P79BERGSTEN P, 1990, J BIOL CHEM, V265, P2584VANDERJAGT DJ, 1987, AM J CLIN NUTR, V46, P290KENNES B, 1983, GERONTOLOGY, V29, P305OKAMURA M, 1980, CLIN CHIM ACTA, V103, P259ANDERSON R, 1980, AM J CLIN NUTR, V33, P71Roe JH, 1943, J BIOL CHEM, V147, P399

Modulation of E-cadherin by hepatocyte growth factor induces aggressiveness of gastric carcinoma

OBJECTIVE: Hepatocyte growth factor (HGF) is well known as a scatter factor because it can disperse cells. E-cadherin is a protein that plays a main role in the establishment of cell-cell adhesion. This study focused on the role of HGF on the expression and distribution of E-cadherin. Furthermore, we found induction of aggressiveness of gastric carcinoma by modulation of E-cadherin by HGF. MATERIALS AND METHODS: Tumor tissues from 50 patients with gastric carcinoma were evaluated for the expression of HGF, its receptor c-Met, and E-cadherin. Western blot analysis and invasion assay were performed to confirm the role of HGF on the modulation of E-cadherin using human gastric cancer cell lines. RESULTS: Seventy-eight percent of the gastric carcinoma tissues showed overexpression of c-Met. E-cadherin expression was found in 86%, which could be further classified as membranous type (52%) or nonmembranous type (48%). The levels of HGF in tumor tissues increased significantly according to the tumor progression. The levels of HGF in tumors with nonmembranous type E-cadherin expression were significantly higher than those in tumors with membranous expression. A striking morphologic change from epithelial shape to fibroblastic shape was observed in SNU-16 cells after 3 days' exposure to HGF, accompanied by down-regulation of functional E-cadherin in the membrane. Treatment of the cells with HGF induced significant invasion into the matrigel. CONCLUSION: We can conclude that HGF can modulate the expression of E-cadherin in gastric carcinoma, which was accompanied by more aggressive phenotype