716 research outputs found

    Recognizing Customer Knowledge Level towards Products for Recommendation in Electronic Commerce

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    A powerful online recommendation system in Electronic Commerce (EC) must know its targeted customers well and employ effective marketing strategies. Market research is a very important way to know the customers well. For high-tech products with great variety such as computers, cellular phones, and digital cameras, customers’ knowledge level towards products may have a decisive influence on their purchase decision. While many online recommendation systems focus on utilizing data mining techniques in user profile and transaction data, this paper presents a method for recognizing customer knowledge level as a preprocess for more effective online recommendation in EC. The method consists of two Back Propagation Networks (BPN) and predicts based on customer characteristics and online navigation behaviors. A simple simulated digital camera EC store case study was conducted and the good preliminary result implies the good potential of the proposed method

    Molecular Detection of Circulating Tumor Cells With Multiple mRNA Markers by Genechip for Colorectal Cancer Early Diagnosis and Prognosis Prediction

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    Early detection is the hallmark of successful cancer treatment. Evidence is accumulating that primary cancers begin shedding neoplastic cells into the circulation at an early stage. To date, many different methodologies have been used for the detection of circulating tumor cells (CTCs) with variable sensitivity and specificity. In many studies, including patients with different clinical stages of colorectal cancer, the detection of CTCs in early and/or metastatic colorectal cancer has been shown to correlate with unfavorable clinical outcome. However, a high-sensitivity and high-throughput method for the detection of CTCs is currently lacking. Here, we introduce a high-sensitivity genechip analysis method from a colorimetric membrane array to a weighted enzymatic chip array in order to detect the CTC-related multiple mRNA markers derived from colorectal cancer patients as a convenient and practical tool for early diagnosis and prognosis prediction

    Macrophage-derived macrophage migration inhibitory factor mediates renal injury in anti-glomerular basement membrane glomerulonephritis

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    Macrophages are a rich source of macrophage migration inhibitory factor (MIF). It is well established that macrophages and MIF play a pathogenic role in anti-glomerular basement membrane crescentic glomerulonephritis (anti-GBM CGN). However, whether macrophages mediate anti-GBM CGN via MIF-dependent mechanism remains unexplored, which was investigated in this study by specifically deleting MIF from macrophages in MIFf/f−lysM−cre mice. We found that compared to anti-GBM CGN induced in MIFf/f control mice, conditional ablation of MIF in macrophages significantly suppressed anti-GBM CGN by inhibiting glomerular crescent formation and reducing serum creatinine and proteinuria while improving creatine clearance. Mechanistically, selective MIF depletion in macrophages largely inhibited renal macrophage and T cell recruitment, promoted the polarization of macrophage from M1 towards M2 via the CD74/NF-κB/p38MAPK-dependent mechanism. Unexpectedly, selective depletion of macrophage MIF also significantly promoted Treg while inhibiting Th1 and Th17 immune responses. In summary, MIF produced by macrophages plays a pathogenic role in anti-GBM CGN. Targeting macrophage-derived MIF may represent a novel and promising therapeutic approach for the treatment of immune-mediated kidney diseases

    THE PREDICTION OF FATIGUE-RELATED MUSCLE ADAPTATION IN DIFFERENT WORKLOAD DURING CYCLING ROWING EXERCISE

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    The purpose of this study was to identify the fatigue-related muscles during the different percentage of the maximal workload. Seven subjects were recruited and, firstly, performed the maximal workload test for 3 minutes. After 24 hours, the different workload tests (60%, 70% and 80% of the maximal workload) were used to reveal the fatigue-related muscle. The result showed that the biceps and triceps had the extreme contribution at the minor and greater workload. However, the neuromuscular fatigue threshold (NFT) is to predict the possibly fatigue muscle condition during the entire exercise. And the most contribution of the EMG expression didn’t stand for the greater value of the EMG number

    Enhancement of polar phases in PVDF by forming PVDF/SiC nanowire composite

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    Different contents of silicon carbide (SiC) nanowires were mixed with Poly(vinylidene fluoride) (PVDF) to facilitate the polar phase crystallization. It was shown that the annealing temperature and SiC content affected on the phase and crystalline structures of PVDF/SiC samples. Furthermore, the addition of SiC nanowire enhanced the transformation of non-polar α phase to polar phases and increased the relative fraction of β phase in PVDF. Due to the nucleating agent mechanism of SiC nanowires, the ion-dipole interaction between the negatively charged surface of SiC nanowires and the positive CH2 groups in PVDF facilitated the formation of polar phases in PVDF

    Disruption of Smad4 impairs TGF-β/Smad3 and Smad7 transcriptional regulation during renal inflammation and fibrosis in vivo and in vitro

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    The mechanism by which TGF-β regulates renal inflammation and fibrosis is largely unclear; however, it is well accepted that its biological effects are mediated through Smad2 and Smad3 phosphorylation. Following activation, these Smads form heteromeric complex with Smad4 and translocate into the nucleus to bind and regulate the expression of target genes. Here we studied the roles of Smad4 to regulate TGF-β signaling in a mouse model of unilateral ureteral obstruction using conditional Smad4 knockout mice and in isolated Smad4 mutant macrophages and fibroblasts. Disruption of Smad4 significantly enhanced renal inflammation as evidenced by a greater CD45+ leukocyte and F4/80+ macrophage infiltration and upregulation of IL-1β, TNF-α, MCP-1, and ICAM-1 in the obstructed kidney and in IL-1β-stimulated macrophages. In contrast, deletion of Smad4 inhibited renal fibrosis and TGF-β1-induced collagen I expression by fibroblasts. Further studies showed that the loss of Smad4 repressed Smad7 transcription, leading to a loss of functional protein. This, in turn, inhibited IκBα expression but enhanced NF-κB activation, thereby promoting renal inflammation. Interestingly, deletion of Smad4 influenced Smad3-mediated promoter activities and the binding of Smad3 to the COL1A2 promoter, but not Smad3 phosphorylation and nuclear translocation, thereby inhibiting the fibrotic response. Thus, Smad4 may be a key regulator for the diverse roles of TGF-β1 in inflammation and fibrogenesis by interacting with Smad7 and Smad3 to influence their transcriptional activities in renal inflammation and fibrosis
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