A reputation mechanism is introduced in P2P- based Semantic Web to solve the problem of lacking trust. It enables Semantic Web to utilize reputation information based on semantic similarity of peers in the network. Th...A reputation mechanism is introduced in P2P- based Semantic Web to solve the problem of lacking trust. It enables Semantic Web to utilize reputation information based on semantic similarity of peers in the network. This approach is evaluated in a simulation of a content sharing system and the experiments show that the system with reputation mechanism outperforms the system without it.展开更多
A kind of trust mechanism-based task scheduling model was presented. Referring to the trust relationship models of social persons, trust relationship is built among Grid nodes, and the trustworthiness of nodes is eval...A kind of trust mechanism-based task scheduling model was presented. Referring to the trust relationship models of social persons, trust relationship is built among Grid nodes, and the trustworthiness of nodes is evaluated by utilizing the Bayes method. Integrating the trustworthiness of nodes into a Dynamic Level Scheduling （DLS） algorithm, the Trust-Dynamic Level Scheduling （Trust-DLS） algorithm is proposed. Theoretical analysis and simulations prove that the Trust-DLS algorithm can efficiently meet the requirement of Grid tasks in trust, sacrificing fewer time costs, and assuring the execution of tasks in a security way in Grid environment.展开更多
Leukotriene B4(LTB4)synthesis is enhanced in the colonic mucosa in patients with inflammatory bowel disease(IBD).BLT1,a highaffinity receptor for LTB4,exhibits no effect on the progression of dextran sodium sulfate(DS...Leukotriene B4(LTB4)synthesis is enhanced in the colonic mucosa in patients with inflammatory bowel disease(IBD).BLT1,a highaffinity receptor for LTB4,exhibits no effect on the progression of dextran sodium sulfate(DSS)-induced colitis,which mostly relies on innate immunity.Here,we reported that BLT1 regulates trinitrobenzene sulfonic acid(TNBS)-induced colitis,which reflects CD4+T-cell-dependent adaptive immune mechanisms of IBD.We found that BLT1 signaling enhanced the progression of colitis through controlling the production of proinflammatory cytokines by dendritic cells(DCs)and modulating the differentiation of Th1 and Th17.BLT1−/−mice displayed an alleviated severity of TNBS-induced colitis with reduced body weight loss and infiltrating cells in the lamina propria.BLT1 deficiency in DCs led to reduced production of proinflammatory cytokines,including IL-6,TNF-α,and IL-12,and these results were further confirmed via treatment with a BLT1 antagonist.The impaired cytokine production by BLT1−/−DCs subsequently led to reduced Th1 and Th17 differentiation both in vitro and in vivo.We further performed a conditional DC reconstitution experiment to assess whether BLT1 in DCs plays a major role in regulating the pathogenesis of TNBS-induced colitis,and the results indicate that BLT1 deficiency in DCs also significantly reduces disease severity.The mechanistic study demonstrated that BLT1-regulated proinflammatory cytokine production through the Gαiβγsubunit-phospholipase Cβ(PLCβ)-PKC pathway.Notably,we found that treatment with the BLT1 antagonist also reduced the production of proinflammatory cytokines by human peripheral blood DCs.Our findings reveal the critical role of BLT1 in regulating adaptive immunity and TNBS-induced colitis,which further supports BLT1 as a potential drug target for adaptive immunity-mediated IBD.展开更多
基金Supported by the National Natural Science Foun-dation of China (60173026) the Ministry of Education Key Project(105071) Foundation of E-Institute of Shanghai HighInstitutions(200301)
文摘A reputation mechanism is introduced in P2P- based Semantic Web to solve the problem of lacking trust. It enables Semantic Web to utilize reputation information based on semantic similarity of peers in the network. This approach is evaluated in a simulation of a content sharing system and the experiments show that the system with reputation mechanism outperforms the system without it.
基金This work is supported by the 863 High-Tcch Project （No. 2004AA104340）, the National Natural Science Foundation of China （No. 60173026） and SEC E-Institute： Shanghai High Institutions Grid （No. 200301-1）.
基金the National Natural Science Foundation of China (Grant No. 60673157)the Ministry of Education Key Project (Grant No. 105071)SEC E-Institute: Shanghai High Institutions Grid (Grant No. 200301)
文摘A kind of trust mechanism-based task scheduling model was presented. Referring to the trust relationship models of social persons, trust relationship is built among Grid nodes, and the trustworthiness of nodes is evaluated by utilizing the Bayes method. Integrating the trustworthiness of nodes into a Dynamic Level Scheduling （DLS） algorithm, the Trust-Dynamic Level Scheduling （Trust-DLS） algorithm is proposed. Theoretical analysis and simulations prove that the Trust-DLS algorithm can efficiently meet the requirement of Grid tasks in trust, sacrificing fewer time costs, and assuring the execution of tasks in a security way in Grid environment.
基金This work was supported by grants from the Ministry of Science and Technology of China(2014CB541903)the National Natural Science Foundation of China(31171348 and 31371414)the Fundamental Research Funds for the Central Universities.
文摘Leukotriene B4(LTB4)synthesis is enhanced in the colonic mucosa in patients with inflammatory bowel disease(IBD).BLT1,a highaffinity receptor for LTB4,exhibits no effect on the progression of dextran sodium sulfate(DSS)-induced colitis,which mostly relies on innate immunity.Here,we reported that BLT1 regulates trinitrobenzene sulfonic acid(TNBS)-induced colitis,which reflects CD4+T-cell-dependent adaptive immune mechanisms of IBD.We found that BLT1 signaling enhanced the progression of colitis through controlling the production of proinflammatory cytokines by dendritic cells(DCs)and modulating the differentiation of Th1 and Th17.BLT1−/−mice displayed an alleviated severity of TNBS-induced colitis with reduced body weight loss and infiltrating cells in the lamina propria.BLT1 deficiency in DCs led to reduced production of proinflammatory cytokines,including IL-6,TNF-α,and IL-12,and these results were further confirmed via treatment with a BLT1 antagonist.The impaired cytokine production by BLT1−/−DCs subsequently led to reduced Th1 and Th17 differentiation both in vitro and in vivo.We further performed a conditional DC reconstitution experiment to assess whether BLT1 in DCs plays a major role in regulating the pathogenesis of TNBS-induced colitis,and the results indicate that BLT1 deficiency in DCs also significantly reduces disease severity.The mechanistic study demonstrated that BLT1-regulated proinflammatory cytokine production through the Gαiβγsubunit-phospholipase Cβ(PLCβ)-PKC pathway.Notably,we found that treatment with the BLT1 antagonist also reduced the production of proinflammatory cytokines by human peripheral blood DCs.Our findings reveal the critical role of BLT1 in regulating adaptive immunity and TNBS-induced colitis,which further supports BLT1 as a potential drug target for adaptive immunity-mediated IBD.
