Design and Implementation of a Web Usage Mining Model Based On Upgrowth and Preflxspan

Web Usage Mining (WUM) integrates the techniques of two popular research fields - Data Mining and the Internet. By analyzing the potential rules hidden in web logs, WUM helps personalize the delivery of web content and improve web design, customer satisfaction and user navigation through pre-fetching and caching. This paper introduces two prevalent data mining algorithms - FPgrowth and PrefixSpan into WUM and they are applied in a real business case. Maximum Forward Path (MFP) is also used in the web usage mining model during sequential pattern mining along with PrefixSpan so as to reduce the interference of false visit caused by browser cache and raise the accuracy of mining frequent traversal paths. Detailed analysis and application on the corresponding results are discussed

Design and Implementation of a Web Usage Mining Model Wang, Yang & Zeng Design and Implementation of a Web Usage Mining Model Based On

Web Usage Mining (WUM) integrates the techniques of two popular research fields- Data Mining and the Internet. By analyzing the potential rules hidden in web logs, WUM helps personalize the delivery of web content and improve web design, customer satisfaction and user navigation through pre-fetching and caching. This paper introduces two prevalent data mining algorithms- FPgrowth and PrefixSpan into WUM and they are applied in a real business case. Maximum Forward Path (MFP) is also used in the web usage mining model during sequential pattern mining along with PrefixSpan so as to reduce the interference of “false visit ” caused by browser cache and raise the accuracy of mining frequent traversal paths. Detailed analysis and application on the corresponding results are discussed

Glycerol kinase 5 confers gefitinib resistance through SREBP1/SCD1 signaling pathway

Abstract Background Drug resistance is common in cancer chemotherapy. This study investigates the role of Glycerol kinase 5 (GK5) in mediating gefitinib resistance in NSCLC. Methods The exosomal mRNA of GK5 was detected using a tethered cationic lipoplex nanoparticle (TCLN) biochip. Real-time PCR and Western blot were used to examine the expression of GK5 mRNA and protein in gefitinib-sensitive and -resistant human lung adenocarcinoma cells. The cell counting kit-8, EdU assay, flow cytometry, and JC-1 dye were used to measure cell proliferation, cell cycle, and the mitochondrial membrane potential. Results We found that the exosomal mRNA of GK5 in the plasma of patients with gefitinib-resistant adenocarcinoma was significantly higher compared with that of gefitinib-sensitive patients. The mRNA and protein levels of GK5 were significantly upregulated in gefitinib-resistant human lung adenocarcinoma PC9R and H1975 cells compared with gefitinib-sensitive PC9 cells. Silencing GK5 in PC9R cells induced mitochondrial damage, caspase activation, cell cycle arrest, and apoptosis via SREBP1/SCD1 signaling pathway. Conclusions We demonstrated that GK5 confers gefitinib resistance in lung cancer by inhibiting apoptosis and cell cycle arrest. GK5 could be a novel therapeutic target for treatment of NSCLC with resistance to EGFR tyrosine kinase inhibitors

Potential toxicity of quercetin: The repression of mitochondrial copy number via decreased POLG expression and excessive TFAM expression in irradiated murine bone marrow

The cytotoxicity of quercetin is not well understood. Using an ICR murine model, we unexpectedly found that mice exposed to 7 Gy total body irradiation (TBI) exhibited general in vivo toxicity after receiving quercetin (100 mg/kg PO), whereas this result was not observed in mice that received TBI only. In order to understand the involvement of alterations in mitochondrial biogenesis, we used a real-time qPCR to analyze the mitochondrial DNA copy number (mtDNAcn) by amplifying the MTRNR1 (12S rRNA) gene in murine bone marrow. We also utilized reverse transcription qPCR to determine the mRNA amounts transcribed from the polymerase gamma (POLG), POLG2, and mammalian mitochondrial transcription factor A (TFAM) genes in the tissue. In the mice exposed to TBI combined with quercetin, we found: (1) the radiation-induced increase of mtDNAcn was inhibited with a concurrent significant decrease in POLG expression; (2) TFAM expression was significantly increased; and (3) the expression of POLG2 was not influenced by the treatments. These data suggest that the overall toxicity was in part associated with the decrease in mtDNAcn, an effect apparently caused by the inhibition of POLG expression and overexpression of TFAM; unaltered POLG2 expression did not seem to contribute to toxicity