Regularized Denoising Masked Visual Pretraining for Robust Embodied PointGoal Navigation.

Embodied PointGoal navigation is a fundamental task for embodied agents. Recent works have shown that the performance of the embodied navigation agent degrades significantly in the presence of visual corruption, including Spatter, Speckle Noise, and Defocus Blur, showing the weak robustness of the agent. To improve the robustness of embodied navigation agents to various visual corruptions, we propose a navigation framework called Regularized Denoising Masked AutoEncoders Navigation (RDMAE-Nav). In a nutshell, RDMAE-Nav mainly consists of two modules: a visual module and a policy module. In the visual module, a self-supervised pretraining method, dubbed Regularized Denoising Masked AutoEncoders (RDMAE), is designed to enable the Vision Transformers (ViT)-based visual encoder to learn robust representations. The bidirectional Kullback-Leibler divergence is introduced in RDMAE as the regularization term for a denoising masked modeling task. Specifically, RDMAE mitigates the gap between clean and noisy image representations by minimizing the bidirectional Kullback-Leibler divergence. Then, the visual encoder is pretrained by RDMAE. In contrast to existing works, RDMAE-Nav applies denoising masked visual pretraining for PointGoal navigation to improve robustness to various visual corruptions. Finally, the pretrained visual encoder with frozen weights is applied to extract robust visual representations for policy learning in the RDMAE-Nav. Extensive experiments show that RDMAE-Nav performs competitively compared with state of the arts (SOTAs) on various visual corruptions. In detail, RDMAE-Nav performs the absolute improvement: 28.2% in SR and 23.68% in SPL under Spatter; 2.28% in SR and 6.41% in SPL under Speckle Noise; and 9.46% in SR and 9.55% in SPL under Defocus Blur.

TO901317 inhibits the development of hepatocellular carcinoma by LXRα/Glut1 decreasing glycometabolism.

This study was conducted to observe the effect and possible mechanism of TO901317 in vivo and in vitro to provide a new basis for the targeted therapy of hepatocellular carcinoma (HCC). The expressions of liver X receptor (LXR)-α, glucose transporter (Glut)-1, proliferating cell nuclear antigen (PCNA), and matrix metalloproteinase (MMP)-9 were analyzed from HCC public database (NCBI PubMed database). The result showed that LXRα was downregulated, whereas Glut1, PCNA, and MMP9 were upregulated in human HCC compared with normal liver. Furthermore, LXRα mRNA was negatively correlated with Glut1 mRNA. At the same time, HCC cells were cultivated in vitro and axillary injected in nude mice to establish the xenograft model. The xenograft in the TO901317-treated group was slower and smaller than the control group. The protein expression of LXRα, Glut1, and MMP9 could be detected by Western blot and glucose level. As a result, TO901317 could inhibit the cell proliferation of HCC in a dose-dependent manner by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. With the increase of TO901317 concentration, the cellular glucose concentration and ATP level were gradually decreased. Western blot results showed TO901317 could upregulate LXRα expression but downregulate MMP9 and Glut1 expression. Transwell and wound-healing analysis confirmed that, by increasing the concentration of TO901317, the cell invasion and migration were both decreased. LXRα small-interfering RNA (siRNA) could relieve the suppression effect of TO901317 on the cell invasion and migration and the expression of LXRα, Glut1, and MMP9. The glucose concentration was also raised. TO901317 could repress the progress of HCC cells by reducing the glucose concentration, upregulating LXRα expression, but downregulating the expression of Glut1 and MMP9. NEW & NOTEWORTHY This subject confirmed that TO901317, a specific liver X receptor agonist, could inhibit the progression of liver cancer through upregulating liver X receptor-α, downregulating the expression of glucose transporter-1 and matrix metalloproteinase-9, and decreasing the glucose content in SMMC-7721 and HepG2 cells.

ATP-binding cassette transporter A1: A promising therapy target for prostate cancer.

ATP-binding cassette transporter A1 (ABCA1) has been found to mediate the transfer of cellular cholesterol across the plasma membrane to apolipoprotein A-I (apoA-I), and is essential for the synthesis of high-density lipoprotein. Mutations of the ABCA1 gene may induce Tangier disease and familial hypoalphalipoproteinemia; they may also lead to loss of cellular cholesterol homeostasis in prostate cancer, and increased intracellular cholesterol levels are frequently found in prostate cancer cells. Recent studies have demonstrated that ABCA1 may exert anticancer effects through cellular cholesterol efflux, which has been attracting increasing attention in association with prostate cancer. The aim of the present review was to focus on the current views on prostate cancer progression and the various functions of ABCA1, in order to provide new therapeutic targets for prostate cancer.