Decision-making Method for Control of A-SMGCS Taxiway Centre Line Lights

Abstract-For automatic decision-making on the control command of A-SMGCS (Advance Surface Movement Guidance and Control System) taxiway centre line lights in line segment, Petri net based approach is proposed. Firstly, the dynamic operation model for taxiway line segment is established based on Petri net, and the corresponding marking control regulation is defined. And then, the controller synthesis for the operation model is fulfilled based on the local incidence matrix approach and it can prevent the model from evolving into forbidden states. Furthermore, the control command decision-making method and corresponding algorithm are provided based on the state of transition. Finally, an example on the decisionmaking of control command for taxiway centre line lights demonstrates the effectiveness of this approach

The miR-31/FIH1 pathway involved in TGFβ-induced liver fibrosis

Abstract MicroRNAs (miRNAs) are small, non-coding RNAs that regulate various biological processes, including liver fibrosis. Hepatic stellate cells (HSC) play a central role in the pathogenesis of liver fibrosis. By microarray profiling and real-time PCR, we noted that micorRNA-31 (miR-31) expression was significantly increased during activation of HSC from rat, mouse and human respectively. We found miR-31 was particularly upregulated in HSC but not in Hepatocyte during fibrogenesis. Thus, we hypothesized that miR-31 may mediate liver fibrosis. In our study, we observed that reduction of miR-31 expression significantly inhibited HSC activation while overexpression of its expression obviously promoted HSC activation. Moreover, overexpression of miR-31 promoted HSC migration while inhibition of miR-31 had an opposite effect. The biological function of miR-31 during HSC activation might be through targeting FIH1, a suppressor of hypoxia-inducible factor (HIF-1), as knockdown of FIH1 by short hairpin RNA (shRNA) could mimic the effects of miR-31. In addition, we found that only TGFβ, a pivotal regulator in liver fibrosis, remarkably increased miR-31 expression in HSC. And that the effects of TGFβ upon HSCs can be partially counteracted by inhibition of miR-31. Additionally, ChIP experiments and Luciferase reporter assay demonstrated that Smad3, a major TGF--downstream transcription factor, stimulated the transcription activity of miR-31 by binding directly to the promoter of miR-31. In conclusion, miR-31/FIH1 pathway associates with liver fibrosis, perhaps by participating TGFβ/Smad3 signaling in HSC. A c c e p t e d M a n u s c r i p