A challenge faced by protection and planning engineers is the development and validation of accurate wind turbine generator(WTG)models to study the impact of increasing wind integration on system protection.Thispaper ...A challenge faced by protection and planning engineers is the development and validation of accurate wind turbine generator(WTG)models to study the impact of increasing wind integration on system protection.Thispaper is on the experimental validation of a generic electromagnetic transient-type(EMT-type)model of aggregated WTGs or wind parks suitable for transient studies.The phasor domain equivalent of the generic model,suitable for protection tools based on steady-state solvers,is also considered.The model has been validated using two sets of actual relay records for the fault response of two wind parks consisting of Type-III WTGs and connected to115 kV and 230 kV transmission systems.The objective is to show that the generic model can reproduce the actual fault response in simulations,and protection engineers can obtain accurate models of wind parks using fault records.A distinctive characteristic of a WTG is its substantially different negative sequence fault current contribution compared to a synchronous generator.The paper shows that the generic model provides enough options to reproduce the negative sequence behavior and hence is suitable for fault studies involving negative sequence-based protection.展开更多
The G551D-CFTR mutation causing cystic fibrosis(CF) results from a missense mutation at codon 551(G551D) in the gene encoding of the cystic fibrosis transmembrane conductance regulator(CFTR). The G551D mutation in CFT...The G551D-CFTR mutation causing cystic fibrosis(CF) results from a missense mutation at codon 551(G551D) in the gene encoding of the cystic fibrosis transmembrane conductance regulator(CFTR). The G551D mutation in CFTR results in a reduced functional channel but G551D-CFTR is appropriately inserted in the apical membrane. In previous studies we discovered a class of high-affinity bicyclooctane(BCO) G551D-CFTR activators(G551D_ BCOs) with K_d down to 1 μmol/L. In this study, we analyzed the pharmacological activation of G551D-CFTR by the G551D_ BCOs by means of short circuit current analysis and cell-based fluorescence quenching assay. The G551D_ BCOs-induced G551D-CFTR activation is cAMP-dependent and is less sensitive to thiazolidinone CFTR inhibitor CFTRinh-172. These data suggest that (1) the phosphorylation of G551D-CFTR by protein kinase A is required for the activation by G551D_ BCOs; (2) G551D_ BCOs and CFTRinh-172 may act at the same site on the G551D-CFTR molecule.展开更多
文摘A challenge faced by protection and planning engineers is the development and validation of accurate wind turbine generator(WTG)models to study the impact of increasing wind integration on system protection.Thispaper is on the experimental validation of a generic electromagnetic transient-type(EMT-type)model of aggregated WTGs or wind parks suitable for transient studies.The phasor domain equivalent of the generic model,suitable for protection tools based on steady-state solvers,is also considered.The model has been validated using two sets of actual relay records for the fault response of two wind parks consisting of Type-III WTGs and connected to115 kV and 230 kV transmission systems.The objective is to show that the generic model can reproduce the actual fault response in simulations,and protection engineers can obtain accurate models of wind parks using fault records.A distinctive characteristic of a WTG is its substantially different negative sequence fault current contribution compared to a synchronous generator.The paper shows that the generic model provides enough options to reproduce the negative sequence behavior and hence is suitable for fault studies involving negative sequence-based protection.
文摘The G551D-CFTR mutation causing cystic fibrosis(CF) results from a missense mutation at codon 551(G551D) in the gene encoding of the cystic fibrosis transmembrane conductance regulator(CFTR). The G551D mutation in CFTR results in a reduced functional channel but G551D-CFTR is appropriately inserted in the apical membrane. In previous studies we discovered a class of high-affinity bicyclooctane(BCO) G551D-CFTR activators(G551D_ BCOs) with K_d down to 1 μmol/L. In this study, we analyzed the pharmacological activation of G551D-CFTR by the G551D_ BCOs by means of short circuit current analysis and cell-based fluorescence quenching assay. The G551D_ BCOs-induced G551D-CFTR activation is cAMP-dependent and is less sensitive to thiazolidinone CFTR inhibitor CFTRinh-172. These data suggest that (1) the phosphorylation of G551D-CFTR by protein kinase A is required for the activation by G551D_ BCOs; (2) G551D_ BCOs and CFTRinh-172 may act at the same site on the G551D-CFTR molecule.
