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An application method for working ship crossing safely is proposed to determine how to make navigation scheme at a certain time. This method makes it possible for decision makers to make reasonable judgments at different times. In this paper, the position relationship between working ship and navigation vessel in waterway is analysed by considering the ship size, hydrological conditions of waterway, ship arrival model and ship navigation trajectory. Using genetic algorithm, the operation scheme of keeping a safe distance between the working ship and the vessel in the channel is solved by taking the speed and direction of the working ship as genetic factors. By analysing the crossing scheme at each starting time in a given time range, the optimal crossing scheme with the farthest distance between the working ship and the vessels in the channel is obtained. According to the measured data, the simulation is carried out with MATLAB to verify the model of working ship crossing channel. The results show that it is safe and reliable to choose the navigation scheme proposed in this paper, which has strong application value.

This study aimed to investigate the antitumor effect and the underlying molecular mechanism of eriodictyol on ovarian cancer cells. CaoV3 and A2780 were exposed to eriodictyol at different concentrations of 0−800 μM. Cell apoptosis and viability were determined by TdT‐mediated dUTP Nick‐End Labeling (TUNEL) assay and Cell Counting Kit‐8 (CCK‐8) assay, respectively. Mitochondrial membrane potential was evaluated by flow cytometers with a JC‐1 detection kit. Fe2+ content was evaluated using an iron assay kit. The section of tumor tissues was observed using hematoxylin‐eosin (H&E) staining and nuclear factor erythroid 2‐related factor 2 (Nrf2) expression was detected by immunohistochemistry (IHC) staining. Eriodictyol suppressed cell viability and induced cell apoptosis of CaoV3 and A2780 cells. Half maximal inhibitory concentration (IC50) value of CaoV3 at 24 and 48 h was (229.74 ± 5.13) μM and (38.44 ± 4.68) μM, and IC50 value of A2780 at 24 and 48 h was (248.32 ± 2.54) μM and (64.28 ± 3.19) μM. Fe2+ content and reactive oxygen species production were increased and protein levels of SLC7A11 and GPX4 were decreased by eriodictyol. Besides, eriodictyol reduced the ratio of JC‐1 fluorescence ratio, glutathione and malondialdehyde contents but elevated Cytochrome C level. Nrf2 phosphorylation were obviously downregulated by eriodictyol. Finally, eriodictyol suppressed tumor growth, aggravated mitochondrial dysfunction and downregulated Nrf2 expression in tumor tissue in mice. Eriodictyol regulated ferroptosis, mitochondrial dysfunction and cell viability via Nrf2/HO‐1/NQO1 signaling pathway in ovarian cancer. [ABSTRACT FROM AUTHOR]

Vocalizations that signal predation risk such as alarm calls provide crucial information for the survival of group-living individuals. However, alarm calling may attract the predator's attention and, to avoid this cost, animals can opt for alternative strategies to indicate danger, such as 'adaptive silence', which is the cessation of vocalizations. We investigate here whether abrupt contact call cessation would provoke alarm responses, or would reinforce the signal given by an alarm call. In an aviary setting, we conducted playback experiments with a group-living passerine, the Swinhoe's white-eye, Zosterops simplex. We found that birds did not respond to a sudden call cessation, nor did they have a stronger response to alarm calls followed by silence than to alarm calls followed by contact calls. Confirming previous work investigating contact call rate, it appears that in this species contact calls encode information about social factors but not environmental conditions. [ABSTRACT FROM AUTHOR]

The present study aimed to identify the genes directly or indirectly correlated with the amplification of MYCN in neuroblastoma (NB). Microarray data (GSE53371) were downloaded from Gene Expression Omnibus, and included 10 NB cell lines with MYCN amplification and 10 NB cell lines with normal MYCN copy numbers. Differentially expressed genes (DEGs) were identified using the Linear Models for Microarray Data package, and a false discovery rate of <0.05 and |log2FC (fold change)|>1 were selected as cut‑off criteria. Hierarchical clustering analysis and Gene Ontology analysis were respectively performed for the DEGs using the Pheatmap package in R language and The Database for Annotation, Visualization and Integrated Discovery. A protein‑protein interaction network (PPI) was constructed for the DEGs using the Search Tool for the Retrieval of Interacting Genes database. Pathway analysis was performed for the DEGs in the PPI network using the WEB‑based GEne SeT AnaLysis Toolkit. The correlation between MYCN and the key gene associated with MYCN was determined using Pearson's correlation coefficient. In total, 137 downregulated and 35 upregulated DEGs were identified. Functional enrichment analysis indicated that KCNMB4 was involved in the regulation of action potential in neuron term, and the FOS, GLI3 and GLI1 genes were involved in the extracellular matrix‑receptor interaction pathway. The PPI network and correlation analysis revealed that the expression of SOX2 was directly correlated with the expression of MYCN, and the correlation coefficient of SOX2 and MYCN was ‑0.83. Therefore, SOX2, KCNMB4, FOS, GLI3 and GLI1 may be involved in the pathogenesis of NB, with the expression of SOX2 downregulating the expression of MYCN.