Objective. This study investigated the nature of shared transcriptomic alterations in PBMs from periodontitis and atherosclerosis to unravel molecular mechanisms underpinning their association. Methods. Gene expression data from PBMs from patients with periodontitis and those with atherosclerosis were each downloaded from the GEO database. Differentially expressed genes (DEGs) in periodontitis and atherosclerosis were identified through differential gene expression analysis. The disease-related known genes related to periodontitis and atherosclerosis each were downloaded from the DisGeNET database. A Venn diagram was constructed to identify crosstalk genes from four categories: DEGs expressed in periodontitis, periodontitis-related known genes, DEGs expressed in atherosclerosis, and atherosclerosis-related known genes. A weighted gene coexpression network analysis (WGCNA) was performed to identify significant coexpression modules, and then, coexpressed gene interaction networks belonging to each significant module were constructed to identify the core crosstalk genes. Results. Functional enrichment analysis of significant modules obtained by WGCNA analysis showed that several pathways might play the critical crosstalk role in linking both diseases, including bacterial invasion of epithelial cells, platelet activation, and Mitogen-Activated Protein Kinases (MAPK) signaling. By constructing the gene interaction network of significant modules, the core crosstalk genes in each module were identified and included: for GSE23746 dataset, RASGRP2 in the blue module and VAMP7 and SNX3 in the green module, as well as HMGB1 and SUMO1 in the turquoise module were identified; for GSE61490 dataset, SEC61G, PSMB2, SELPLG, and FIBP in the turquoise module were identified. Conclusion. Exploration of available transcriptomic datasets revealed core crosstalk genes (RASGRP2, VAMP7, SNX3, HMGB1, SUMO1, SEC61G, PSMB2, SELPLG, and FIBP) and significant pathways (bacterial invasion of epithelial cells, platelet activation, and MAPK signaling) as top candidate molecular linkage mechanisms between atherosclerosis and periodontitis.

This study was conducted to evaluate the effects of dietary supplementation with Glycyrrhiza polysaccharide (GCP) on growth performance, serum biochemistry, immunity, and egg laying in female quail. 300 1-day-old female quail were sorted into four dietary treatments with five replicate cages of 15 birds each. The basic diet in the four treatment groups was supplemented with 0, 500, 1000 and 1500 mg/kg GCP, and the experiment continued for 80 days. Results showed that dietary supplementation with GCP significantly (p < 0.05) increased average daily gain in a dose-dependent fashion, and decreased (p < 0.05) the feed-to-gain ratio and mortality. The relative weights of the thymus and bursa of Fabricius increased (p < 0.05) linearly with increasing dose of GCP from 0 to 1500 mg/kg on day 20. GCP birds showed higher serum levels of protein, glucose, immunoglobulin A and immunoglobulin M, but lower serum triglycerides (p < 0.05) on day 50. GCP increased (p < 0.05) average laying rate and average egg weight linearly from days 60 to 80, whereas feed to egg ratio was decreased (p < 0.05). Taken together, these results revealed that GCP could improve growth performance, serum biochemistry, immunity, and egg laying in female quail. Therefore, GCP may be a potential replacement for antibiotic growth promoters in poultry.

Fatty liver hemorrhage syndrome (FLHS) in chickens is characterized by steatosis and bleeding in the liver, which has caused huge losses to the poultry industry. This study aimed to use primary cultured broiler hepatocytes to establish a steatosis model to explore the optimal conditions for inducing steatosis by incubating the cells with a fat emulsion. Primary hepatocytes were isolated from an AA broiler by a modified two-step in situ perfusion method. Hepatocytes were divided into an untreated control group and a fat emulsion group that was incubated with 2.5, 5, 10, or 20% fat emulsion for different times to determine the optimal conditions for inducing steatosis of primary hepatocytes. Incubation of the cells with 10% fat emulsion resulted in cell viability at 48 h of 67%, which was higher than the control group and met the requirements of the model. In the second experiment, steatosis was induced by incubating hepatocytes with 10% fat emulsion for 48 h. In consequence, the apoptosis rate decreased (p > 0.05) and the concentration of ALT (p < 0.001), AST (p < 0.01), and TG (p < 0.05) increased significantly; the expression level of SREBP-1c (p < 0.05) increased, and the expression levels of PPARα (p < 0.001), CPT1 (p < 0.001), and CPT2 (p < 0.05) were lower in the fat emulsion group than in the control group. In conclusion, the induction condition was selected as 10% fat emulsion incubation for 48 h, and we successfully established a fatty liver degeneration model for broilers.