Jianhui Wang

Earthquake is a kind of natural disaster, which will have a great impact on the building structure. In the vibration control field of building structures, the timeliness of system stability is extremely important. In traditional control methods, the timeliness is not paid enough attention for systems with uncertain seismic waves. For setting this problem, fuzzy adaptive compensation control for uncertain building structural systems by sliding-mode technology is proposed. It is combined with fuzzy adaptive control and sliding-mode control to ensure that the system can be stable with satisfied timeliness. Also, saturation function is used to ensure the feasible physical implementation of the control system. Compared with the traditional LQR control, the simulation results showed that the proposed method can make the system reach a stable state with rapid convergence performance and has a feasible physical implementation.

Aiming at suppressing harmful effect for building structure by surface motion, semiactive nonsmooth control algorithm with Deep Learning is proposed. By finite-time stable theory, the building structure closed-loop system’s stability is discussed under the proposed control algorithm. It is found that the building structure closed-loop system is stable. Then the proposed control algorithm is applied on controlling the building structural vibration. The seismic action is chosen as El Centro seismic wave. Dynamic characteristics have comparative analysis between semiactive nonsmooth control and passive control in two simulation examples. They demonstrate that the designed control algorithm has great robustness and anti-interference. The proposed control algorithm is more effective than passive control in suppressing structural vibration.

The human cationic antimicrobial protein LL-37 is a multifunctional host defense peptide with a wide range of immunomodulatory activities. Previous work has shown that LL-37 exerts both pro- and anti-inflammatory effects. The role of mitochondria in the skin inflammatory effects of LL-37 has not been well studied. Therefore, our aim was to investigate the immunomodulatory effect of LL-37 in HaCaT cells and to delineate the underlying mechanisms related to mitochondrial function. Immunohistochemistry results from tissue microarrays showed strong cytoplasmic LL-37 staining in inflammatory cells in chronic dermatic inflammation. Using exogenous LL-37 stimulation and LL-37 knockdown and overexpression, LL-37 was demonstrated to dramatically reduce the mRNA levels and protein secretion of inflammatory cytokines including IL-6, IL-8, IL-1α and tumor necrosis factor-α, which are induced by lipopolysaccharides. The anti-inflammatory effects of LL-37 are dependent upon its ability to increase mitochondrial biogenesis and to maintain mitochondrial homeostasis. Furthermore, we observed that LL-37 enhances the LPS-induced phosphorylation of extracellular signal-regulated kinase and mammalian target of rapamycin. The mTOR inhibitor rapamycin can neutralize the protective effects of LL-37 on mitochondria. In conclusion, these results suggest that high LL-37 expression levels correlate with chronic skin inflammation; mitochondrial dysfunction occurs in HaCaT cells during inflammation; and LL-37 attenuates inflammatory impairment by stimulating mitochondrial biogenesis and protecting mitochondrial function, which are dependent upon mTOR signaling. These findings provide new insights into targeting mitochondria with LL-37 to prevent skin inflammatory reactions. © 2014 Elsevier Ltd.