Yuxiang Zhao

This trial aimed to investigate the influence of graded replacing fish meal (D1: 0.00%, D2: 27.27%, and D3: 54.55%) with mixed protein ingredients (i.e., chicken meal, krill meal, fermented soybean meal, and soy protein concentrate) on the growth performance, muscle nutritional composition, blood biochemical indices, gut bacterial community, and transcriptome of Chinese perch. Two hundred seventy Chinese perch were divided into three groups (90 per group) and the diet lasted for 56 days. Results showed that the weight gain rate and specific growth rate were significantly lower, and the feed conversion ratio was significantly higher in the D3 group than in fish fed D1 ( ), with no significant differences between the D1 and D2 groups ( ). The muscle crude protein content was highest in the D2 group, and the crude fat content was significantly different in the order: D3 > D1 > D2 ( ). The levels of serum triglycerides (TG) and low-density lipoprotein cholesterol in the D2 group were significantly lower than those in the D1 group ( ), but there was no significant difference compared to the D3 group ( ). The microbial community structure changed significantly. Mycoplasma showed the highest abundance in the D1 and D2 groups ( ), and Cetobacterium peaked in D2 group, and significantly higher than that in D1 group ( ). Network analysis and cohesion index calculation showed that both network complexity and cohesion peaked in D2 group, and Cetobacterium was highly correlated with the cohesion index ( ). Further, muscle transcriptome analysis results showed that compared with the control group, differentially expressed genes were clustered (Q < 0.05) in the arginine and proline metabolism pathways in D2 group. Fish in D3 group significantly (Q < 0.05) affected genes involved in KEGG pathways of ribosome, circadian rhythm, thermogenesis, insulin signaling pathway, fatty acid degradation, oxidative phosphorylation, and apoptosis. In conclusion, under the experimental conditions, the replacement of 27.27% of fish meal by the compound protein did not have a negative impact on the growth performance of Chinese perch and could improve muscle quality, lipid metabolism, and the interaction of intestinal microbiota.

Polycyclic aromatic hydrocarbons (PAHs) are organic pollutants widely present in industrial sites. Microbial degradation is an effective method of removing PAHs. The identification of microorganisms that have important ecological functions at the site is of great significance for PAH removal. We collected soil samples at three depths in the range of 0–100 cm at 70-day intervals at the coking site and explored the degradation of PAHs. We combined molecular ecology networking, metagenomics, and genome assembly to search for microorganisms that persist, dominate, and affect the microbial community construction in the degradation process and analyzed their adaptation strategies. The results showed that 15.78 mg/kg of PAHs naturally decayed, and 13.33 mg/kg of PAHs migrated from 30–100 cm to 0–30 cm in the soil. Sphingomonas, which occupied a niche advantage, was both the core and keystone microorganism, and its spatial distribution pattern and temporal change dynamics were consistent with those of PAHs. We assembled the genome of Sphingomonas sp., revealing its multiple potential for degrading PAHs and other pollutants. Additionally, flagellar assembly and bacterial chemotaxis genes ranked high in the assembled genome of Sphingomonas sp., which might help it obtain a competitive advantage in the soil. The findings underscored the strategy of Sphingomonas to maintain dominance, enriched the understanding of PAH-degrading microorganisms in site soil, and provided references for the remediation of PAHs.

N6-methyladenosine (m6A) is a common transcriptomic modification in cancer. Recently, it has been found to be involved in the regulation of non-small cell lung cancer (NSCLC) formation and metastasis. Interleukin 37 (IL-37) plays a crucial protective role in lung cancer. In our previous studies, we found that IL-37 is a potential novel tumor suppressor by inhibiting IL-6 expression to suppress STAT3 activation and decreasing epithelial-to-mesenchymal transition. Moreover, we found that treatment of IL-37 in lung cancer cells induced widespread and dynamic RNA m6A methylation. The effects of RNA m6A methylation of IL-37 treatment require further study. However, the functions of RNA m6A methylation of IL-37 treatment still await elucidation. Using MeRIP-seq and RNA-seq, we uncovered a unique m6A methylation profile in the treatment of IL-37 on the A549 cell line. We also showed the expression of m6A writers METTL3, METTL14, and WTAP and erasers ALKBH5 and FTO in A549 cells and lung cancer tissues after the treatment of IL-37. This study showed that IL-37 could lead to changes in m6A methylation level and related molecule expression level in A546 cells and may downregulate the proliferation by inhibiting Wnt5a/5b pathway in A549 cells. We conclude that IL-37 suppresses tumor growth through regulation of RNA m6A methylation in lung cancer cells.