Search

Cyber-Physical Energy Systems (CPESs) integrate cyber and hardware components to ensure a reliable and safe physical power production and supply. Renewable Energy Sources (RESs) add uncertainty to energy demand that can be dealt with flexible operation (e.g., load-following) of CPES; at the same time, scenarios that could result in severe consequences due to both component stochastic failures and aging of the cyber system of CPES (commonly overlooked) must be accounted for Operation & Maintenance (O&M) planning. In this paper, we make use of Deep Reinforcement Learning (DRL) to search for the optimal O&M strategy that, not only considers the actual system hardware components health conditions and their Remaining Useful Life (RUL), but also the possible accident scenarios caused by the failures and the aging of the hardware and the cyber components, respectively. The novelty of the work lies in embedding the cyber aging model into the CPES model of production planning and failure process; this model is used to help the RL agent, trained with Proximal Policy Optimization (PPO) and Imitation Learning (IL), finding the proper rejuvenation timing for the cyber system accounting for the uncertainty of the cyber system aging process. An application is provided, with regards to the Advanced Lead-cooled Fast Reactor European Demonstrator (ALFRED).

Tumor cell-endothelial adhesion is one of the key steps in tumor cell haematogenous dissemination in metastasis and was previously shown to be mediated by interaction of galectin-3 with the transmembrane mucin protein MUC1. In this study, the effect of exogenous as well as endogenous galectin-3 on adhesion of two cell lines (low MUC1-expressing human prostate cancer PC-3M cells and non-small-cell lung cancer A549 cells) to monolayer of umbilical vein endothelial cells (HUVECs) was investigated. We found that suppression of endogenous galectin-3 expression reduced tumor cell adhesion to HUVECs and also decreased cell invasion and migration. Exogenous galectin-3 promoted tumor cell adhesion to HUVECs by entering cells. Both exogenous and endogenous galectin-3 upregulated the expression of β-catenin and increased β-catenin nuclear accumulation, and subsequently upregulated the expression of N-cadherin and CD44. We deduced that both exogenous as well as endogenous galectin-3 promoted low MUC1-expressing cancer cell adhesion to HUVECs by increasing the expression of N-cadherin and CD44 via an increase of nuclear β-catenin accumulation. These results were confirmed further by using a β-catenin/TCF transcriptional activity inhibitor, N-cadherin or CD44 siRNAs. Taken together, our results suggest a new molecular mechanism of galectin-3-mediated cell adhesion in cancer metastasis. Tumor cell-endothelial adhesion is one of the key steps for invasion and metastasis. The authors show that Gal-3 promotes cancer cell adhesion to vascular endothelial cells by increasing the expression of N-cadherin and CD44 via an increase of β-catenin nuclear accumulation. This new molecular mechanism of Gal-3-mediated cell adhesion may aid in the development of new strategies to prevent metastasis.

Tumor cell-endothelial adhesion is one of the key steps in tumor cell haematogenous dissemination in metastasis and was previously shown to be mediated by interaction of galectin-3 with the transmembrane mucin protein MUC1. In this study, the effect of exogenous as well as endogenous galectin-3 on adhesion of two cell lines (low MUC1-expressing human prostate cancer PC-3M cells and non-small-cell lung cancer A549 cells) to monolayer of umbilical vein endothelial cells (HUVECs) was investigated. We found that suppression of endogenous galectin-3 expression reduced tumor cell adhesion to HUVECs and also decreased cell invasion and migration. Exogenous galectin-3 promoted tumor cell adhesion to HUVECs by entering cells. Both exogenous and endogenous galectin-3 upregulated the expression of β-catenin and increased β-catenin nuclear accumulation, and subsequently upregulated the expression of N-cadherin and CD44. We deduced that both exogenous as well as endogenous galectin-3 promoted low MUC1-expressing cancer cell adhesion to HUVECs by increasing the expression of N-cadherin and CD44 via an increase of nuclear β-catenin accumulation. These results were confirmed further by using a β-catenin/TCF transcriptional activity inhibitor, N-cadherin or CD44 siRNAs. Taken together, our results suggest a new molecular mechanism of galectin-3-mediated cell adhesion in cancer metastasis.

Availability is the embodiment of the combat effectiveness of the equipment, of which the level determines the ability of the equipment to perform tasks to a certain extent. In this paper, an evaluation method of availability of naval gun weapon systems based on Palm's theorem is developed. This evaluation method, based on maintenance strategy, takes into consideration factors that make the system unavailable, such as repair, backorders, etc.