A non-linear multi-rigid-body system dynamic modelling is developed for the automated clutch system in power transmission during clutch engagements, especially at sharp vehicle start-up, sudden engine flame-out, low driving speed and clutch plate overwearing. In order to guarantee an ideal dynamic performance of the clutch engagement, an adaptive optimal controller is designed by considering throttle angle, engine speed, gear ratio, vehicle acceleration and road condition. A non-linear model reference adaptive controller is utilized to prevent the engine from flame-out or fly-off effectively and the minimum value principle is also introduced to achieve an optimal dynamic performance of the non-linear system compromised in friction plate wear and vehicle drive quality. The optimal trajectory of the clutch engagement can be described in the form of explicit and analytical expressions and characterized by a deterministic and accurate control strategy instead of indeterministic and soft control techniques which need thousands of experiments. For validation of the controller, test work is carried out for the automated clutch engagements in a commercial car with a traditional mechanical transmission, a hydraulic actuator, a group of sensors and a portable computer system. It is shown through experiments that dynamic behaviours of the clutch engagement operated by the adaptive optimal control are more effective and efficient than those by a fuzzy PID control.

Given their hovering ability, static lift airships, such as airships and balloons, are proposed as stratospheric platforms flying at a high altitude of 20 km. The shape of the envelope has a major influence on the lift and drag efficiency of an airship. Furthermore, the efficiency of a conventional actuator, such as an aerodynamic control surface for stratospheric platforms, is decreased by the low-atmospheric density and flight speed. Thus, a new type of effector configuration must be proposed. A new multivectored thrust airship called flat peach is proposed in this paper. The name is attributed to the shape of the airship, which resembles a flat peach that is a cross between a ball and a water droplet. Thus, this airship has a smaller drag coefficient than the spherical airship and higher lift efficiency than a conventional airship. A control allocation strategy among the multivectored thrusters is proposed, and a composite control structure is designed for the airship to realize accurate position control and to decrease energy consumption.

Background:Jumonji domain-containing protein 2B (JMJD2B), directly targeted by hypoxia-inducible factor 1α, maintains the histone methylation balance important for the transcriptional activation of many oncogenes. Jumonji domain-containing protein 2B has been implicated in colorectal cancer (CRC) progression; however, the mechanism remains unclear.Methods:Immunofluorescence and western blotting detected phosphorylated histone H2AX, characteristic of double-strand breaks, and comet assay was used to investigate DNA damage, in CRC cells after JMJD2B small interfering RNA (siRNA) transfection. We assessed the resulting in vitro responses, that is, cell cycle progression, apoptosis, and senescence coupled with JMJD2B silencing-induced DNA damage, studying the regulatory role of signal transducers and activators of transcription 3 (STAT3). The JMJD2B silencing anti-cancer effect was determined using an in vivo CRC xenograft model.Results:Jumonji domain-containing protein 2B knockdown induced DNA damage via ataxia telangiectasia-mutated (ATM) and ATM and Rad3-related pathway activation, resulting in cell cycle arrest, apoptosis, and senescence in both normoxia and hypoxia. Signal transducers and activators of transcription 3 suppression by JMJD2B silencing enhanced DNA damage. Intratumoural injection of JMJD2B siRNA suppressed tumour growth in vivo and activated the DNA damage response (DDR).Conclusions:Jumonji domain-containing protein 2B has an essential role in cancer cell survival and tumour growth via DDR mediation, which STAT3 partially regulates, suggesting that JMJD2B is a potential anti-cancer target.

Our previous study suggested that DJ-1 has a critical role in initiating an inflammatory response, but its role in the liver progenitor cell (LPC) expansion, a process highly dependent on the inflammatory niche, remains elusive. The objective of this study is to determine the role of DJ-1 in LPC expansion. The correlation of DJ-1 expression with LPC markers was examined in the liver of patients with hepatitis B or hepatitis C virus (HBV and HCV, respectively) infection, primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), nonalcoholic fatty liver disease (NAFLD), cirrhosis or hepatocellular carcinoma (HCC), respectively. The role of DJ-1 in LPC expansion and the formation of LPC-associated fibrosis and inflammation was examined in a 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet-induced liver injury murine model. We also determined the ability of hepatic stellate cells (HSCs) in recruiting macrophages in DJ-1 knockout (KO) mice. The expression levels of DJ-1 were upregulated in the liver of HBV, HCV, PBC and PSC patients and DDC-fed mice. Additionally, DJ-1 expression was positively correlated with LPC proliferation in patients with liver injury and mice with DDC exposure. DJ-1 has no direct effect on LPC proliferation. Reduced activation of HSCs and collagen deposition were observed in DJ-1 KO mice. Furthermore, infiltrated CD11b+Gr-1low macrophages and pro-inflammatory factors (IL-6, TNF-α) were attenuated in DJ-1 KO mice. Mechanistically, we found that HSCs isolated from DJ-1 KO mice had decreased secretion of macrophage-mobilizing chemokines, such as CCL2 and CX3CL1, resulting in impaired macrophage infiltration. DJ-1 positively correlates with LPC expansion during liver injury. DJ-1 deficiency negatively regulates LPC proliferation by impairing the formation of LPC-associated fibrosis and inflammatory niches.