AIM: To investigate the tryptase and histamine release ability of human colon mast cells upon IgE dependent or independent activation and the potential mechanisms.METHODS: Enzymatically dispersed cells from human colo...AIM: To investigate the tryptase and histamine release ability of human colon mast cells upon IgE dependent or independent activation and the potential mechanisms.METHODS: Enzymatically dispersed cells from human colons were challenged with anti-IgE or calcium ionophore A23187, and the cell supernatants after challenge were collected. Both concentration dependent and time course studies with anti-IgE or calcium ionophore A23187 were performed. Tryptase release was determined with a sandwich ELISA procedure and histamine release was measured using a glass fibre-based fiuorometric assay.RESULTS:Both anti-IgE and calcium ionophore were able to induce dose dependent release of histamine from colon mast cells with up to approximately 60% and 25% net histamine release being achieved with 1μg/mL calcium ionophore and 10μg/mL anti-IgE, respectively. Dose dependent release of tryptase was also observed with up to approximately 19ng/mL and 21ng/mL release of tryptase being achieved with 10μg/mL anti-IgE and 1μg/mL calcium ionophore, respectively. Time course study revealed that both tryptase and histamine release from colon mast cells stimulated by anti-IgE initiated within 10 sec and reached their maximum release at 6 min following challenge. Pretreatment of cells with metabolic inhibitors abolished the actions of anti-IgE as well as calcium ionophore. Tryptase and histamine release, particularly that induced by calcium ionophore was inhibited by pretreatment of cells with pertussis toxin.CONCLUSION: Both anti-IgE and calcium ionophore are able to induce significant release of tryptase and histamine from colon mast cells, indicating that this cell type is likely to contribute to the pathogenesis of colitis and other mast cell associated intestinal diseases.展开更多
AIM:To investigate the ability of agonists of PAR-2 to stimulate release of tryptase and histamine from human colon mast cells and the potential mechanisms.METHODS:Enzymatically dispersed cells from human colons were ...AIM:To investigate the ability of agonists of PAR-2 to stimulate release of tryptase and histamine from human colon mast cells and the potential mechanisms.METHODS:Enzymatically dispersed cells from human colons were challenged with tc-LIGRLO, tc-OLRGIL, SLIGKV,VKGILS, trypsin, anti-IgE or calcium ionophore A23187,and the cell supematants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure and histamine release was measured using a glass fibrebased fluorometric assay.RESULTS: Both PAR-2 agonists tc-LIGRLO-NH2 and SLIGKVNH2 were able to induce dose dependent release of tryptase and histamine from colon mast cells. More than 2.5 fold increase in both tryptase and histamine release was provoked by 100μmol/mL tc-LIGRLO-NH2, in comparison with only 2.0 fold increase being stimulated by SLIGKV-NH2，The reverse peptides tc-OLRGIL-NH2 and VKGILS-NH2 at the concentrations tested had no effect on the release of these two mediators.The maximum tryptase release elicited by tc-LIGRLO-NH2 was similar to that induced by anti-IgE(10μg/mL) or calcium ionophore (1μg/mL), though the latter was a more potent stimulus for histamine release.Both histamine and tryptase release in response to tc-LIGRLONH2 were completed within 3 rain. Trypsin at concentrations from 1.0 to 100μg/mL was capable of provoking a dose dependent release of tryptase as well as histamine with a maximum of 16ng/mL tryptase and 14ng/mL histamine release being achieved. An approximately 80% and 70% inhibition of trypsin induced release of tryptase and histamine were observed with SBTI, respectively. Pretreatment of cells with metabolic inhibitors or pertussis toxin abolished the actions of tc-LIGRLO-NH2, SLIGKV-NH2 and trypsin.CONCLUSION: The agonists of PAR-2 and trypsin are potent secretagogues of human colon mast cells, which are likely to contribute to the development of inflammatory disorders in human gut.展开更多
AIM:To investigate the ability of protease inhibitors to modulate histamine release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophor...AIM:To investigate the ability of protease inhibitors to modulate histamine release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors, and histamine release was determined.RESULTS: IgE dependent histamine release from colon mast ceils was inhibited by up to approximately 37%, 26% and 36.8% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2 Me(ZIGPFM), N-TosyI-L-phenylalanyl-chloromethyl ketone (TPCK), and C^l-antitrypsin, respectively. Similarly, inhibitors of tryptase leupeptin, N-tosyI-L-lysine chloromethyl ketone (TLCK), lactoferrin and protamine were also able to inhibit anti-IgE induced histamine release by a maximum of some 48%,37%,40% and 34%, respectively. Preincubation of these inhibitors with cells for 20 rain before challenged with anti-IgE had small effect on the inhibitory actions of these inhibitors on colon mast cells. A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced histamine release. The significant inhibition of calcium ionophore induced histamine release was also observed with the inhibitors of tryptase and chymase examined. Apart from leupeptin and protamine, the inhibitors tested by themselves did not stimulate colon mast cells.CONCLUSION: It was demonstrated that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced histamine release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man.展开更多
AIM: TOtryptasepotentialinvestigate the ability of histamine to modulate release from human colon mast cells and the mechanisms.METHODS: Enzymatically dispersed cells from human colons were challenged with histamine, ...AIM: TOtryptasepotentialinvestigate the ability of histamine to modulate release from human colon mast cells and the mechanisms.METHODS: Enzymatically dispersed cells from human colons were challenged with histamine, anti-IgE or calcium ionophore A23187 (CI), and the cell supernatants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure.RESULTS:Histamine at concentrations from 1ng/mL was able to induce a “bell” shape dose related release of tryptase from colon mast cells. The maximum release of tryptase was approximately 3.5 fold more than spontaneous release. As little as 10ng/ml histamine showed a similar potency to 10μg/mL anti-IgE in induction of tryptase release. Histamine induced release of tryptase initiated at 10s when histamine (100ng/mL) was added to cells, gradually increased thereafter, and completed at 5 rain.Both pertussis toxin or metabolic inhibitors were able to inhibit histamine induced tryptase release. When histamine and anti-IgE were added to colon mast cells at the same time, the quantity of tryptase released was similar to that induced by anti-IgE alone.The similar results were observed with CI. However, when various concentrations of histamine were incubated with cells for 20min before adding anti-IgE or CI, the quantity of tryptase released was similar to that was induced by histamine alone.CONCLUSION:Histamine is a potent activator of human colon mast cells, which represents a novel and pivotal selfamplification mechanism of mast cell degranulation.展开更多
AIM: To investigate the ability of protease inhibitors to modulate tryptase release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophor...AIM: To investigate the ability of protease inhibitors to modulate tryptase release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors,and tryptase release was determined.RESULTS:IgE dependent tryptase release from colon mast cells was inhibited by up to approximately 37%, 40% and 36.6% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2Me (ZIGPFM), N-tosyI-L-phenylalanyl-chloromethyl ketone (TPCK), and α1-antitrypsin, respectively. Similarly, the inhibitors of tryptase leupeptin, N-tosyI-L-lysine chloromethyl ketone (TLCK) and lactoferrin were also able to inhibit anti-IgE induced tryptase release by a maximum of 39.4%,47.6% and 36.6%, respectively. The inhibitory actions of chymase inhibitors, but not tryptase inhibitors on colon mast cells were enhanced by preincubation of them with cells for 20min before challenged with anti-IgE. At a concentration of 10μg/mL, protamine was able to inhibit anti-IgE and calcium ionophore induced tryptase release. However, at 100μg/mL, protamine elevated tryptase levels in supematants.A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced tryptase release. The significant inhibition of calcium ionophore induced tryptase release was also observed with the inhibitors of tryptase and chymase examined. The inhibitors tested by themselves did not stimulate tryptase release from colon mast cells.CONCLUSION:It was demonstrated for the first time that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced tryptase release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man.展开更多
According to traditional phenomenological fatigue methodology and moderncontinuum damage mechanics theory, dual fatigue cumulative damage rules to predict fatigue damageformation and propagation lives of the notched c...According to traditional phenomenological fatigue methodology and moderncontinuum damage mechanics theory, dual fatigue cumulative damage rules to predict fatigue damageformation and propagation lives of the notched composite laminates are presented. A 3-dimensionaldamage constitutive equation of anisotropic composites is also established. Damage strain energyrelease rate is interpreted as a driving force of the fatigue delamination damage propagation. A newdamage evolution equation and a damage propagation σ_a-σ_m-N~* surface (stress amplitude-meanstress-life surface) are derived. Hence, using the method above, the fatigue life of compositecomponents can be predicted. Finally, theoretically predicted results are compared with experimentaldata. It is found that the deviation of theoretic prediction from experimental results is about22%.展开更多
Abstract Spatial soliton solutions of a class of generalized nonlinear Schrdinger equations in N space are discussed analytically and numerically. This achieved using a traveling wave method to formulate one soli...Abstract Spatial soliton solutions of a class of generalized nonlinear Schrdinger equations in N space are discussed analytically and numerically. This achieved using a traveling wave method to formulate one soliton solution and the P R method is employed to the numerical solutions and the interactions between the solitons for the generalized nonlinear systems in 2 space. The results presented show that the soliton phenomena are characteristics associated with the nonlinearities of the dynamical systems.展开更多
The closed-loop stability issue of finite-precision realizations was investigated for digital control-lers implemented in block-floating-point format. The controller coefficient perturbation was analyzed resultingfrom...The closed-loop stability issue of finite-precision realizations was investigated for digital control-lers implemented in block-floating-point format. The controller coefficient perturbation was analyzed resultingfrom using finite word length (FWL) block-floating-point representation scheme. A block-floating-point FWL closed-loop stability measure was derived which considers both the dynamic range and precision. To facilitate the design of optimal finite-precision controller realizations, a computationally tractable block-floating-point FWL closed-loop stability measure was then introduced and the method of computing the value of this measure for a given controller realization was developed. The optimal controller realization is defined as the solution that maximizes the corresponding measure, and a numerical optimization approach was adopted to solve the resulting optimal realization problem. A numerical example was used to illustrate the design procedure and to compare the optimal controller realization with the initial realization.展开更多
The need to provide efficient public transport services in urban areas has led to the implementation of bus priority measures in many congested cities. Much interest has recently centred on priority at signal controll...The need to provide efficient public transport services in urban areas has led to the implementation of bus priority measures in many congested cities. Much interest has recently centred on priority at signal controlled junctions, including the concept of pre-signals, where traffic signals are installed at or near the end of a with-flow bus lane to provide buses with priority access to the downstream junction. Although a number of pre-signals have now been installed in the UK, particularly in London, there has been very little published research into the analysis of benefits and disbenefits to both buses and non-priority vehicles at pre-signalised intersections.This paper addresses these points through the development of analytical procedures which allow pre-implementation evaluation of specific categories of pre-signals.展开更多
Soliton solutions of a class of generalized nonlinear evolution equations are discussed analytically and numerically. This is done by using a travelling wave method to formulate one soliton solution and the finite di...Soliton solutions of a class of generalized nonlinear evolution equations are discussed analytically and numerically. This is done by using a travelling wave method to formulate one soliton solution and the finite difference method to the numerical solutions and the interactions between the solitons for the generalized nonlinear Schrdinger equations. The characteristic behavior of the nonlinearity admitted in the system has been investigated and the soliton states of the system in the limit when α→0 and α→∞ have been studied. The results presented show that the soliton phenomenon is characteristics associated with the nonlinearities of the dynamical systems.展开更多
基金Supported by the National Natural Science Foundation of China,No.30140023,and the Li Ka Shing Foundation,Hong Kong,China,No.C0200001
文摘AIM: To investigate the tryptase and histamine release ability of human colon mast cells upon IgE dependent or independent activation and the potential mechanisms.METHODS: Enzymatically dispersed cells from human colons were challenged with anti-IgE or calcium ionophore A23187, and the cell supernatants after challenge were collected. Both concentration dependent and time course studies with anti-IgE or calcium ionophore A23187 were performed. Tryptase release was determined with a sandwich ELISA procedure and histamine release was measured using a glass fibre-based fiuorometric assay.RESULTS:Both anti-IgE and calcium ionophore were able to induce dose dependent release of histamine from colon mast cells with up to approximately 60% and 25% net histamine release being achieved with 1μg/mL calcium ionophore and 10μg/mL anti-IgE, respectively. Dose dependent release of tryptase was also observed with up to approximately 19ng/mL and 21ng/mL release of tryptase being achieved with 10μg/mL anti-IgE and 1μg/mL calcium ionophore, respectively. Time course study revealed that both tryptase and histamine release from colon mast cells stimulated by anti-IgE initiated within 10 sec and reached their maximum release at 6 min following challenge. Pretreatment of cells with metabolic inhibitors abolished the actions of anti-IgE as well as calcium ionophore. Tryptase and histamine release, particularly that induced by calcium ionophore was inhibited by pretreatment of cells with pertussis toxin.CONCLUSION: Both anti-IgE and calcium ionophore are able to induce significant release of tryptase and histamine from colon mast cells, indicating that this cell type is likely to contribute to the pathogenesis of colitis and other mast cell associated intestinal diseases.
基金Supported by the National Natural Science Foundation of China,No.30140023,and the Li Ka Shing Foundation,Hong Kong,China,No.C0200001
文摘AIM:To investigate the ability of agonists of PAR-2 to stimulate release of tryptase and histamine from human colon mast cells and the potential mechanisms.METHODS:Enzymatically dispersed cells from human colons were challenged with tc-LIGRLO, tc-OLRGIL, SLIGKV,VKGILS, trypsin, anti-IgE or calcium ionophore A23187,and the cell supematants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure and histamine release was measured using a glass fibrebased fluorometric assay.RESULTS: Both PAR-2 agonists tc-LIGRLO-NH2 and SLIGKVNH2 were able to induce dose dependent release of tryptase and histamine from colon mast cells. More than 2.5 fold increase in both tryptase and histamine release was provoked by 100μmol/mL tc-LIGRLO-NH2, in comparison with only 2.0 fold increase being stimulated by SLIGKV-NH2，The reverse peptides tc-OLRGIL-NH2 and VKGILS-NH2 at the concentrations tested had no effect on the release of these two mediators.The maximum tryptase release elicited by tc-LIGRLO-NH2 was similar to that induced by anti-IgE(10μg/mL) or calcium ionophore (1μg/mL), though the latter was a more potent stimulus for histamine release.Both histamine and tryptase release in response to tc-LIGRLONH2 were completed within 3 rain. Trypsin at concentrations from 1.0 to 100μg/mL was capable of provoking a dose dependent release of tryptase as well as histamine with a maximum of 16ng/mL tryptase and 14ng/mL histamine release being achieved. An approximately 80% and 70% inhibition of trypsin induced release of tryptase and histamine were observed with SBTI, respectively. Pretreatment of cells with metabolic inhibitors or pertussis toxin abolished the actions of tc-LIGRLO-NH2, SLIGKV-NH2 and trypsin.CONCLUSION: The agonists of PAR-2 and trypsin are potent secretagogues of human colon mast cells, which are likely to contribute to the development of inflammatory disorders in human gut.
基金Supported by the National Natural Science Foundation of China,No.30140023,and the Li Ka Shing Foundation,Hong Kong,China,No.C0200001
文摘AIM:To investigate the ability of protease inhibitors to modulate histamine release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors, and histamine release was determined.RESULTS: IgE dependent histamine release from colon mast ceils was inhibited by up to approximately 37%, 26% and 36.8% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2 Me(ZIGPFM), N-TosyI-L-phenylalanyl-chloromethyl ketone (TPCK), and C^l-antitrypsin, respectively. Similarly, inhibitors of tryptase leupeptin, N-tosyI-L-lysine chloromethyl ketone (TLCK), lactoferrin and protamine were also able to inhibit anti-IgE induced histamine release by a maximum of some 48%,37%,40% and 34%, respectively. Preincubation of these inhibitors with cells for 20 rain before challenged with anti-IgE had small effect on the inhibitory actions of these inhibitors on colon mast cells. A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced histamine release. The significant inhibition of calcium ionophore induced histamine release was also observed with the inhibitors of tryptase and chymase examined. Apart from leupeptin and protamine, the inhibitors tested by themselves did not stimulate colon mast cells.CONCLUSION: It was demonstrated that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced histamine release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man.
基金Supported by the National Natural science Foundation of China,No.30140023,and the Li Ka Shing Foundation,Hong Kong,China,No.C0200001
文摘AIM: TOtryptasepotentialinvestigate the ability of histamine to modulate release from human colon mast cells and the mechanisms.METHODS: Enzymatically dispersed cells from human colons were challenged with histamine, anti-IgE or calcium ionophore A23187 (CI), and the cell supernatants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure.RESULTS:Histamine at concentrations from 1ng/mL was able to induce a “bell” shape dose related release of tryptase from colon mast cells. The maximum release of tryptase was approximately 3.5 fold more than spontaneous release. As little as 10ng/ml histamine showed a similar potency to 10μg/mL anti-IgE in induction of tryptase release. Histamine induced release of tryptase initiated at 10s when histamine (100ng/mL) was added to cells, gradually increased thereafter, and completed at 5 rain.Both pertussis toxin or metabolic inhibitors were able to inhibit histamine induced tryptase release. When histamine and anti-IgE were added to colon mast cells at the same time, the quantity of tryptase released was similar to that induced by anti-IgE alone.The similar results were observed with CI. However, when various concentrations of histamine were incubated with cells for 20min before adding anti-IgE or CI, the quantity of tryptase released was similar to that was induced by histamine alone.CONCLUSION:Histamine is a potent activator of human colon mast cells, which represents a novel and pivotal selfamplification mechanism of mast cell degranulation.
基金Supported by the National Natural Science Foundation of China,No.30140023,and the Li Ka Shing Foundation,Hong Kong,China,No.C0200001
文摘AIM: To investigate the ability of protease inhibitors to modulate tryptase release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors,and tryptase release was determined.RESULTS:IgE dependent tryptase release from colon mast cells was inhibited by up to approximately 37%, 40% and 36.6% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2Me (ZIGPFM), N-tosyI-L-phenylalanyl-chloromethyl ketone (TPCK), and α1-antitrypsin, respectively. Similarly, the inhibitors of tryptase leupeptin, N-tosyI-L-lysine chloromethyl ketone (TLCK) and lactoferrin were also able to inhibit anti-IgE induced tryptase release by a maximum of 39.4%,47.6% and 36.6%, respectively. The inhibitory actions of chymase inhibitors, but not tryptase inhibitors on colon mast cells were enhanced by preincubation of them with cells for 20min before challenged with anti-IgE. At a concentration of 10μg/mL, protamine was able to inhibit anti-IgE and calcium ionophore induced tryptase release. However, at 100μg/mL, protamine elevated tryptase levels in supematants.A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced tryptase release. The significant inhibition of calcium ionophore induced tryptase release was also observed with the inhibitors of tryptase and chymase examined. The inhibitors tested by themselves did not stimulate tryptase release from colon mast cells.CONCLUSION:It was demonstrated for the first time that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced tryptase release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man.
基金This project is supported by National Natural Science Foundation of China (No.50005003)Aeronautic Science Foundation of China (No.0lA5l0l1)
文摘According to traditional phenomenological fatigue methodology and moderncontinuum damage mechanics theory, dual fatigue cumulative damage rules to predict fatigue damageformation and propagation lives of the notched composite laminates are presented. A 3-dimensionaldamage constitutive equation of anisotropic composites is also established. Damage strain energyrelease rate is interpreted as a driving force of the fatigue delamination damage propagation. A newdamage evolution equation and a damage propagation σ_a-σ_m-N~* surface (stress amplitude-meanstress-life surface) are derived. Hence, using the method above, the fatigue life of compositecomponents can be predicted. Finally, theoretically predicted results are compared with experimentaldata. It is found that the deviation of theoretic prediction from experimental results is about22%.
文摘Abstract Spatial soliton solutions of a class of generalized nonlinear Schrdinger equations in N space are discussed analytically and numerically. This achieved using a traveling wave method to formulate one soliton solution and the P R method is employed to the numerical solutions and the interactions between the solitons for the generalized nonlinear systems in 2 space. The results presented show that the soliton phenomena are characteristics associated with the nonlinearities of the dynamical systems.
文摘The closed-loop stability issue of finite-precision realizations was investigated for digital control-lers implemented in block-floating-point format. The controller coefficient perturbation was analyzed resultingfrom using finite word length (FWL) block-floating-point representation scheme. A block-floating-point FWL closed-loop stability measure was derived which considers both the dynamic range and precision. To facilitate the design of optimal finite-precision controller realizations, a computationally tractable block-floating-point FWL closed-loop stability measure was then introduced and the method of computing the value of this measure for a given controller realization was developed. The optimal controller realization is defined as the solution that maximizes the corresponding measure, and a numerical optimization approach was adopted to solve the resulting optimal realization problem. A numerical example was used to illustrate the design procedure and to compare the optimal controller realization with the initial realization.
文摘The need to provide efficient public transport services in urban areas has led to the implementation of bus priority measures in many congested cities. Much interest has recently centred on priority at signal controlled junctions, including the concept of pre-signals, where traffic signals are installed at or near the end of a with-flow bus lane to provide buses with priority access to the downstream junction. Although a number of pre-signals have now been installed in the UK, particularly in London, there has been very little published research into the analysis of benefits and disbenefits to both buses and non-priority vehicles at pre-signalised intersections.This paper addresses these points through the development of analytical procedures which allow pre-implementation evaluation of specific categories of pre-signals.
文摘Soliton solutions of a class of generalized nonlinear evolution equations are discussed analytically and numerically. This is done by using a travelling wave method to formulate one soliton solution and the finite difference method to the numerical solutions and the interactions between the solitons for the generalized nonlinear Schrdinger equations. The characteristic behavior of the nonlinearity admitted in the system has been investigated and the soliton states of the system in the limit when α→0 and α→∞ have been studied. The results presented show that the soliton phenomenon is characteristics associated with the nonlinearities of the dynamical systems.
