A vertical and floor line-based monocular SLAM system for corridor environments

In this paper, we propose a vertical and floor line-based monocular simultaneous localization and mapping (SLAM) system which utilizes vertical lines, floor lines, and vanishing points as sensory input to perform robust SLAM in corridor environments. By combining three map feature types, our design can help a robot to perform accurate pose estimation, repeatable loop closure, and to construct a more expressive environmental map. As a primitive element of a geometric structure, a line segment has one additional dimension compared to a point feature, thereby allowing the use of line segments to easily represent a geometric structure using a smaller number of features. This system presents map features on a 2D ground space: the vertical line as a projection point, the floor line as the original line, and the vanishing point as a directional vector. Although the vertical line, floor line, and vanishing point use different parameterization and initialization methods, their measurement models are integrated into a unified extended Kalman filter (EKF) framework. Experimental results show that our system can be deployed in a structured indoor environment as a suitable SLAM solution.     

Effect of hydrogen on the impedance of passivating oxide films formed on aluminium in sodium nitrate solution

A.c. impedance has been determined at room temperature on hydrogen-free and hydrogen-charged passivating oxide films on aluminium in 0.05m Na₂SO₄ solution. Analysis of the impedance data enabled a clear distinction between the capacitance and inductance of the hydrogen-free oxide film and those of the hydrogen-charged oxide film to be made. The changes in capacitance and inductance by hydrogen-charging into the oxide films are discussed in relation to the compositional change from -Al₂O₃ to hydrated alumina.     

Biocompatibility of surface treated pure titanium and titanium alloy by<Emphasis Type="Italic">in vivo</Emphasis> and<Emphasis Type="Italic">in vitro</Emphasis> test

In the present study, commercial pure Ti and Ti-6Al-4V alloy specimens with and without alkali and heat treatments were implanted in the abdominal connective tissue of mice. Conventional stainless steel 316L was also implanted for comparison. After three months, their biocompatibility was evaluated byin vitro andin vivo experiments. Surface structural changes of specimens due to the alkali treatment and soaking in Hank’s solution were analyzed by XRD, SEM, XPS and AES. An apatite layer, which accelerates the connection with bone, was formed more easily on the alkali treated specimens than the non-treated specimens. The number of macrophages, which is known to increase as the inflammatory reaction proceeds, was much lower for the alkali and heat treated specimens than for the others. The average thickness of the fibrous capsule formed around the implant was much thinner for the alkali and heat treated specimens than for the others.     

Apoptotic Effects of Anthocyanins from Vitis coignetiae Pulliat Are Enhanced by Augmented Enhancer of the Rudimentary Homolog (ERH) in Human Gastric Carcinoma MKN28 Cells

Evidence suggests that augmented expression of a certain gene can influence the efficacy of targeted and conventional chemotherapies. Here, we tested whether the high expression of enhancer of the rudimentary homolog (ERH), which serves as a prognostic factor in some cancers, can influence the efficacy of anthocyanins isolated from fruits of Vitis coignetiae Pulliat, Meoru in Korea (AIMs) on human gastric cancer cells. The anticancer efficacy of AIMs was augmented in ERH-transfected MKN28 cells (E-MKN28 cells). Molecularly, ERH augmented AIM-induced caspase-dependent apoptosis by activating caspase-3 and -9. The ERH-augmented apoptotic effect was related to mitochondrial depolarization and inhibition of antiapoptotic proteins, XIAP, and Bcl-2. In addition, reactive oxygen species (ROS) generation was augmented in AIMs-treated E-MKN28 cells compared to AIMs-treated naïve MKN28 cells. In conclusion, ERH augmented AIM-induced caspase-dependent mitochondrial-related apoptosis in MKN28 cells. A decrease in expression of Bcl-2 and subsequent excessive ROS generation would be the mechanism for ERH-augmented mitochondrial-related apoptosis in AIMs-treated MKN28 cells. A decrease in expression of XIAP would be another mechanism for ERH-augmented caspase-dependent apoptosis in AIMs-treated MKN28 cells.     

Potential Antitumor Effects of 6-Gingerol in p53-Dependent Mitochondrial Apoptosis and Inhibition of Tumor Sphere Formation in Breast Cancer Cells

Hormone-specific anticancer drugs for breast cancer treatment can cause serious side effects. Thus, treatment with natural compounds has been considered a better approach as this minimizes side effects and has multiple targets. 6-Gingerol is an active polyphenol in ginger with various modalities, including anticancer activity, although its mechanism of action remains unknown. Increases in the level of reactive oxygen species (ROS) can lead to DNA damage and the induction of DNA damage response (DDR) mechanism, leading to cell cycle arrest apoptosis and tumorsphere suppression. Epidermal growth factor receptor (EGFR) promotes tumor growth by stimulating signaling of downstream targets that in turn activates tumor protein 53 (p53) to promote apoptosis. Here we assessed the effect of 6-gingerol treatment on MDA-MB-231 and MCF-7 breast cancer cell lines. 6-Gingerol induced cellular and mitochondrial ROS that elevated DDR through ataxia-telangiectasia mutated and p53 activation. 6-Gingerol also induced G0/G1 cell cycle arrest and mitochondrial apoptosis by mediating the BAX/BCL-2 ratio and release of cytochrome c. It also exhibited a suppression ability of tumorsphere formation in breast cancer cells. EGFR/Src/STAT3 signaling was also determined to be responsible for p53 activation and that 6-gingerol induced p53-dependent intrinsic apoptosis in breast cancer cells. Therefore, 6-gingerol may be used as a candidate drug against hormone-dependent breast cancer cells.