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After a major debt crisis occurs in a listed company, the stock prices of related enterprises may also fluctuate sharply, resulting in the spread of debt risk to more enterprises. Taking the stocks of listed companies as network nodes, we constructed a complex stock market network over three periods of time through the logarithmic return rate of stocks for the three periods of prophase, metaphase, and anaphase of the debt crisis. We studied the topological characteristics of the network and destructiveness over the three periods. Finally, the minimum spanning tree was used to construct a network and the community structure of the network. The empirical analysis took the debt crisis of the China Evergrande Company as an example to analyze the impact of its major debt crisis on the Chinese stock market. The research findings were as follows: First, the debt crisis increased the inter-industry connections within the network, that is, the correlations between enterprises in different industries was enhanced. Second, the closeness of the cross-industry connections increased the connectivity efficiency of the network, but compared with the other two periods, the debt crisis in the metaphase was less stable. Third, community research showed that in the metaphase of the debt crisis, the enterprises became the core nodes of the network. [ABSTRACT FROM AUTHOR]

A novel fowl adenovirus 4 (FAdV-4) has caused significant economic losses to the poultry industry in China since 2015. We established an easy-to-use reverse genetics system for modification of the whole right and partial left ends of the novel FAdV-4 genome, which worked through cell-free reactions of restriction digestion and Gibson assembly. Three recombinant viruses were constructed to test the assumption that species-specific viral genes of ORF4 and ORF19A might be responsible for the enhanced virulence: viral genes of ORF1, ORF1b and ORF2 were replaced with GFP to generate FAdV4-GFP, ORF4 was replaced with mCherry in FAdV4-GFP to generate FAdV4-GX4C, and ORF19A was deleted in FAdV4-GFP to generate FAdV4-CX19A. Deletion of ORF4 made FAdV4-GX4C form smaller plaques while ORF19A deletion made FAdV4-CX19A form larger ones on chicken LMH cells. Coding sequence (CDS) replacement with reporter mCherry demonstrated that ORF4 had a weak promoter. Survival analysis showed that FAdV4-CX19A-infected chicken embryos survived one more day than FAdV4-GFP- or FAdV4-GX4C-infected ones. The results illustrated that ORF4 and ORF19A were non-essential genes for FAdV-4 replication although deletion of either gene influenced virus growth. This work would help function study of genes on the right end of FAdV-4 genome and facilitate development of attenuated vaccines. [ABSTRACT FROM AUTHOR]