RESUMO
In this paper, a novel finite time fault tolerant control (FTC) is proposed for uncertain robot manipulators with actuator faults. First, a finite time passive FTC (PFTC) based on a robust nonsingular fast terminal sliding mode control (NFTSMC) is investigated. Be analyzed for addressing the disadvantages of the PFTC, an AFTC are then investigated by combining NFTSMC with a simple fault diagnosis scheme. In this scheme, an online fault estimation algorithm based on time delay estimation (TDE) is proposed to approximate actuator faults. The estimated fault information is used to detect, isolate, and accommodate the effect of the faults in the system. Then, a robust AFTC law is established by combining the obtained fault information and a robust NFTSMC. Finally, a high-order sliding mode (HOSM) control based on super-twisting algorithm is employed to eliminate the chattering. In comparison to the PFTC and other state-of-the-art approaches, the proposed AFTC scheme possess several advantages such as high precision, strong robustness, no singularity, less chattering, and fast finite-time convergence due to the combined NFTSMC and HOSM control, and requires no prior knowledge of the fault due to TDE-based fault estimation. Finally, simulation results are obtained to verify the effectiveness of the proposed strategy.
RESUMO
Down syndrome candidate region 1 (DSCR1) is one of more than 50 genes located in a region of chromosome 21 that has been implicated in Down syndrome. DSCR1 can be expressed as four isoforms, one of which, isoform 4 (DSCR1-4), has recently been found to be strongly induced by vascular endothelial growth factor A (VEGF-A(165)) and to provide a negative feedback loop that inhibits VEGF-A(165)-induced endothelial cell proliferation in vitro and angiogenesis in vivo. We report here that another DSCR1 isoform, DSCR1-1L, is also up-regulated by VEGF-A(165) in cultured endothelial cells and is strongly expressed in several types of pathologic angiogenesis in vivo. In contrast to DSCR1-4, the overexpression of DSCR1-1L induced the proliferation and activation of the transcription factor NFAT in cultured endothelial cells and promoted angiogenesis in Matrigel assays in vivo, even in the absence of VEGF-A. Similarly, small interfering RNAs specific for DSCR1-1L and DSCR1-4 had opposing inhibitory and stimulatory effects, respectively, on these same functions. DSCR1-4 is thought to inhibit angiogenesis by inactivating calcineurin, thereby preventing activation and nuclear translocation of NFAT, a key transcription factor. In contrast, DSCR1-1L, regulated by a different promoter than DSCR1-4, activates NFAT and its proangiogenic activity is inhibited by cyclosporin, an inhibitor of calcineurin. In sum, DSCR1-1L, unlike DSCR1-4, potently activates angiogenesis and could be an attractive target for antiangiogenesis therapy.
