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In this study, the stability of cow’s milk with fat replacement by soybean oil bodies (SOB) was investigated under different environmental conditions. Moreover, the effect of replacing milk fat with SOB or anhydrous milk fat (AMF) on the stability of milk stability and yogurt quality was evaluated. The results showed that the particle sizes of milk with fat replacement and raw milk were larger at pH 2.0 and 4.0 than at other pH values. The particle size of SOB milk was significantly higher than those of AMF milk and raw milk at pH 2.0–10.0 (P < 0.05). At NaCl concentrations ranging from 0 to 500 mmol/L except for 200 mmol/L, significantly higher particle sizes were observed for SOB milk than AMF milk (P < 0.05). However, all three milks were stable without droplet aggregation. Under different heat treatments, they were very stable. After 6 h of fermentation, SOB milk reached the ideal pH (about 4.5) of yogurt, while a longer fermentation period was required for AMF milk and raw milk. The viscosity of fermented SOB milk was significantly higher than those of fermented AMF and raw milk (P < 0.05), but they had similar good sensory and texture properties. This study can provide a reference for the application of soybean oil bodies as a substitute for milk fat in dairy product processing.

Postharvest deterioration is among the major challenges for the fruit industry. Regulation of the fruit softening rate is an effective strategy for extending shelf-life and reducing the economic losses due postharvest deterioration. The tomato myoinositol monophosphatase 3 gene SlIMP3, which showed highest expression level in fruit, was expressed and purified. SlIMP3 demonstrated high affinity with the L-Gal 1-P and D-Ins 3-P, and acted as a bifunctional enzyme in the biosynthesis of AsA and myoinositol. Overexpression of SlIMP3 not only improved AsA and myoinositol content, but also increased cell wall thickness, improved fruit firmness, delayed fruit softening, decreased water loss, and extended shelf-life. Overexpression of SlIMP3 also increased uronic acid, rhamnose, xylose, mannose, and galactose content in cell wall of fruit. Treating fruit with myoinositol obtained similar fruit phenotypes of SlIMP3-overexpressed fruit, with increased cell wall thickness and delayed fruit softening. Meanwhile, overexpression of SlIMP3 conferred tomato fruit tolerance to Botrytis cinerea. The function of SlIMP3 in cell wall biogenesis and fruit softening were also verified using another tomato species, Ailsa Craig (AC). Overexpression of SlDHAR in fruit increased AsA content, but did not affect the cell wall thickness or fruit firmness and softening. The results support a critical role for SlIMP3 in AsA biosynthesis and cell wall biogenesis, and provide a new method of delaying tomato fruit softening, and insight into the link between AsA and cell wall metabolism.

Objective: Several clinical studies have shown an association between polycystic ovary syndrome (PCOS) and asthma; however, the molecular link between these conditions remains unclear. In this study, we conducted a reanalysis and repurposing of existing databases in order to depict the common key genes, related signaling pathways, and similarity of the immune microenvironment between PCOS and asthma. Methods: PCOS and asthma data sets were downloaded, and common signal pathways were identified by using gene set enrichment analysis. Identified common susceptibility genes were explored by intersecting the weighted gene coexpression network analysis module genes for both diseases. Then, we performed protein–protein interaction, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes analyses of the common susceptibility genes. Finally, we analyzed the immune environment of PCOS and asthma. Results: We identified five hub genes, namely, MMP9, CDC42, CD44, CD19, and BCL2L1, and uncovered that these five hub genes showed a tendency to be upregulated in both PCOS and asthma and possessed good diagnostic ability. In addition, we revealed that both PCOS and asthma were significantly enriched in the FcεRI‐mediated signaling pathway. Moreover, we found that both PCOS and asthma exhibited infiltration of similar types of immune cells, such as monocytes, suggesting that the two diseases have similar pathological features. Conclusion: PCOS and asthma share common causative genes with a similar immune environment. Taken together, we uncovered previously unsuspected traits for comprehensive diagnosis and treatment of PCOS and asthma in the future. Synopsis: Polycystic ovary syndrome and asthma share common characteristic genes and related signaling pathways and have a similar immune microenvironment. [ABSTRACT FROM AUTHOR]