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In order to improve the control capability of distributed photovoltaic support, a distributed photovoltaic support consumption method based on energy storage configuration mode and random events is proposed. A networked and constrained parameter analysis model for distributed photovoltaic power supply control was constructed. Based on the direct flexible mode of optical storage, an AC/DC voltage level control model for distributed solar power supply control was constructed. In the operation mode of DC hybrid distribution network, the demand response tracking identification method was used to analyze the uncertain characteristic parameters of distributed solar power supply load, and combined with the planned energy storage capacity parameters, the distributed solar power supply load and photovoltaic output were estimated. By configuring the optimal energy storage capacity, adjusting the power distribution of the microgrid, and integrating the analysis of uncertain factors and random events in the energy storage configuration mode, the design of distributed photovoltaic support consumption has been achieved. The experimental results show that the distributed photovoltaic absorption control using this method has lower load requirements, can effectively reduce the exchange power of the interconnection line, and improve the configuration scale, system reliability, and economy of the photovoltaic energy storage system.

This study proposes a multi-consensus formation control algorithm by artificial potential field (APF) method based on velocity threshold. The algorithm improves the multi-consensus technique. This algorithm can split a group of agents into multiple agent groups. Note that the algorithm can easily complete the queue transformation as long as the entire proxy group is connected initially and no specific edges need to be removed. Furthermore, collision avoidance and maintenance of existing communication connectivity should be considered during the movement of all agents. Therefore, we design a new swarm motion potential function. The stability of multi-consensus formation control has proven to be effective in avoiding collisions, maintaining connectivity, and generating formations. The final numerical simulation results show the role of the controller we designed.

In this paper, we propose a method that removes raindrops with light field image using image inpainting. We first use the depth map generated from light field image to detect raindrop regions which are then expressed as a binary mask. The original image with raindrops is improved by refocusing on the far regions and filtering by a high-pass filter. With the binary mask and the enhanced image, image inpainting is then utilized to eliminate raindrops from the original image. We compare pre-trained models of several deep learning based image inpainting methods. A light field raindrop dataset is released to verify our method. Image quality analysis is performed to evaluate the proposed image restoration method. The recovered images are further applied to object detection and visual localization tasks.

For the problem of hypersonic target interception, a novel midcourse guidance method with terminal-angle constraint is proposed. Referring to the air-breathing and the boost-gliding hypersonic targets, flight characteristics and difficulties of interception are analyzed, respectively. The requirements of midcourse guidance for interceptors are provided additionally. The kinematics model of adversaries is established concerning line-of-sight coupling in longitudinal and lateral planes. Suboptimal guidance law with terminal-angle constraint, specifically the final line-of-sight angle or impact angle, is presented by means of model predictive static programming. The trajectory is optimized and the load factor would finally converge after penalizing control sequence and output deviations. The realization of terminal angle is firstly verified with a constant speed target. A full interception scenario is further simulated focusing on a typical boost-gliding target, which flies along a skipping trajectory. Results show the success of providing handover conditions for intercepting hypersonic targets.

Hypersonic technology plays an important role in prompt global strike. Because the flight dynamics of a hypersonic vehicle is nonlinear, uncertain, and highly coupled, the controller design is challenging, especially to design its guidance and control law during the attack of a maneuvering target. In this paper, the sliding mode control (SMC) method is used to develop the guidance law from which the desired flight path angle is derived. With the desired information as control command, the adaptive neural control in discrete time is investigated ingeniously for the longitudinal dynamics of the hypersonic missile. The proposed guidance and control laws are validated by simulation of a hypersonic missile against a maneuvering target. It is demonstrated that the scheme has good robustness and high accuracy to attack a maneuvering target in the presence of external disturbance and missile model uncertainty.

Dysregulation of miRNAs is well associated with the development of non-small cell lung cancer (NSCLC). It is imperative that dysregulation of miRNAs by cigarette smoke will affect the expression of their targets, either leading to the activation of oncoproteins or suppression of tumor suppressor proteins. In this study, we have carried out miRNA sequencing and SILAC-based proteomics analysis of H358 cells chronically exposed to cigarette smoke condensate. miRNA sequencing resulted in the identification of 208 miRNAs, of which 6 miRNAs were found to be significantly dysregulated (fold change ≥ 4, p-value ≤ 0.05) in H358-smoke exposed cells. Proteomic analysis of the smoke exposed cells compared to the parental cells resulted in the quantification of 2,396 proteins, of which 681 proteins were found to be differentially expressed (fold change ≥ 2). Gene ontology based analysis of target proteins revealed enrichment of proteins involved in biological processes driving metabolism and a decrease in expression of proteins associated with immune response in the cells exposed to cigarette smoke. Pathway analysis using Ingenuity Pathway Analysis (IPA) revealed activation of ERK/MAPK and integrin signaling and repression of RhoGDI signaling in H358 smoke exposed cells. We also identified 5 novel miRNA in H358 smoke exposed cells using unassigned reads of small RNA-Seq dataset. In summary, this study indicates that chronic exposure to cigarette smoke leads to widespread dysregulation of miRNAs and their targets, resulting in signaling aberrations in NSCLC. The miRNAs and their targets identified in the study need to be further investigated to explore their role as potential targets and/or molecular markers in NSCLC especially in smokers.

The sensitivity of only a few tumors to anti-epidermal growth factor receptor EGFR tyrosine kinase inhibitors (TKIs) can be explained by the presence of EGFR tyrosine kinase (TK) domain mutations. In addition, such mutations were rarely found in tumor types other than lung, such as pancreatic and head and neck cancer. In this study we sought to elucidate mechanisms of resistance to EGFR-targeted therapies in tumors that do not harbor TK sensitizing mutations in order to identify markers capable of guiding the decision to incorporate these drugs into chemotherapeutic regimens. Here we show that EGFR activity was markedly decreased during the evolution of resistance to the EGFR tyrosine kinase inhibitor (TKI) erlotinib, with a concomitant increase of mitogen-inducible gene 6 (Mig6), a negative regulator of EGFR through the upregulation of the PI3K-AKT pathway. EGFR activity, which was more accurately predicted by the ratio of Mig6/EGFR, highly correlated with erlotinib sensitivity in panels of cancer cell lines of different tissue origins. Blinded testing and analysis in a prospectively followed cohort of lung cancer patients treated with gefitinib alone demonstrated higher response rates and a marked increased in progression free survival for patients with a low Mig6/EGFR ratio (approximately 100 days, P = 0.01).

The human cysteine dioxygenase 1 (CDO1) gene is a non-heme structured, iron-containing metalloenzyme involved in the conversion of cysteine to cysteine sulfinate, and plays a key role in taurine biosynthesis. In our search for novel methylated gene promoters, we have analyzed differential RNA expression profiles of colorectal cancer (CRC) cell lines with or without treatment of 5-aza-2'-deoxycytidine. Among the genes identified, the CDO1 promoter was found to be differentially methylated in primary CRC tissues with high frequency compared to normal colon tissues. In addition, a statistically significant difference in the frequency of CDO1 promoter methylation was observed between primary normal and tumor tissues derived from breast, esophagus, lung, bladder and stomach. Downregulation of CDO1 mRNA and protein levels were observed in cancer cell lines and tumors derived from these tissue types. Expression of CDO1 was tightly controlled by promoter methylation, suggesting that promoter methylation and silencing of CDO1 may be a common event in human carcinogenesis. Moreover, forced expression of full-length CDO1 in human cancer cells markedly decreased the tumor cell growth in an in vitro cell culture and/or an in vivo mouse model, whereas knockdown of CDO1 increased cell growth in culture. Our data implicate CDO1 as a novel tumor suppressor gene and a potentially valuable molecular marker for human cancer.

BACKGROUND: The major established etiologic risk factor for bladder cancer is cigarette smoking and one of the major antineoplastic agents used for the treatment of advanced bladder cancer is cisplatin. A number of reports have suggested that cancer patients who smoke while receiving treatment have lower rates of response and decreased efficacy of cancer therapies. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we investigated the effect of cigarette smoke condensate (CSC) vapor on cisplatin toxicity in urothelial cell lines SV-HUC-1 and SCaBER cells. We showed that chronic exposure to CSC vapor induced cisplatin resistance in both cell lines. In addition, we found that the expression of mitochondrial-resident protein adenylate kinase-3 (AK3) is decreased by CSC vapor. We further observed that chronic CSC vapor-exposed cells displayed decreased cellular sensitivity to cisplatin, decreased mitochondrial membrane potential (ΔΨm) and increased basal cellular ROS levels compared to unexposed cells. Re-expression of AK3 in CSC vapor-exposed cells restored cellular sensitivity to cisplatin. Finally, CSC vapor increased the growth of the tumors and also curtail the response of tumor cells to cisplatin chemotherapy in vivo. CONCLUSIONS/SIGNIFICANCE: The current study provides evidence that chronic CSC vapor exposure affects AK3 expression and renders the cells resistant to cisplatin.

Aerobic glycolysis and mitochondrial dysfunction are common features of aggressive cancer growth. We observed promoter methylation and loss of expression in neurofilament heavy polypeptide (NEFH) in a significant proportion of primary esophageal squamous cell carcinoma (ESCC) samples that were of a high tumor grade and advanced stage. RNA interference-mediated knockdown of NEFH accelerated ESCC cell growth in culture and increased tumorigenicity in vivo, whereas forced expression of NEFH significantly inhibited cell growth and colony formation. Loss of NEFH caused up-regulation of pyruvate kinase-M2 type and down-regulation of pyruvate dehydrogenase, via activation of the Akt/beta-catenin pathway, resulting in enhanced aerobic glycolysis and mitochondrial dysfunction. The acceleration of glycolysis and mitochondrial dysfunction in NEFH-knockdown cells was suppressed in the absence of beta-catenin expression, and was decreased by the treatment of 2-Deoxyglucose, a glycolytic inhibitor, or API-2, an Akt inhibitor. Loss of NEFH activates the Akt/beta-catenin pathway and increases glycolysis and mitochondrial dysfunction. Cancer cells with methylated NEFH can be targeted for destruction with specific inhibitors of deregulated downstream pathways.