Many factors contribute to the stress of transporting broilers from the farm to the processing plant. Using a motion simulation machine, a total of 144 male broilers were employed to determine the effect of motion, vibration, and feed withdrawal during transportation on serum biochemical parameters, postmortem muscle metabolism, and meat quality of broilers. The results indicated that transportation did not affect the activity of lactate dehydrogenase, γ-glutamyl transferase, aspartate aminotransferase, creatine kinase, and glucose in the serum, glutathione peroxidase in the breast and thigh muscle, nitric oxide synthase (NOS) in the breast, and heat stress protein 70 mRNA expression level in the liver (p > 0.05). Serum triiodothyronine, thyroxine, and insulin concentration declined with 2 h transportation (p < 0.05) and recovered with 4 h transportation (p < 0.05). NOS concentration in the thigh increased with 2 h transportation (p < 0.05) and recovered with 4 h transportation (p < 0.05). Two-hour and 4 h transportation increased the activity of superoxide dismutase in both muscles. Malondialdehyde, lactic acid, and drip loss_{24 h} in both thigh and breast muscles increased, and glycogen in both muscles decreased with increasing transportation times (p < 0.05). Two-hour transportation did not influence pH_{45 min} and pH_{24 h} in the breast and thigh muscle, but these indexes decreased with 4 h transportation. This experiment supports and extends previous work that identified transportation as a major risk in relation to bird welfare and meat quality.

To screen out potential prognostic hub genes for adult patients with sepsis via RNA sequencing and construction of a microRNA–mRNA–PPI network and investigate the localization of these hub genes in peripheral blood monocytes. The peripheral blood of 33 subjects was subjected to microRNA and mRNA sequencing using high-throughput sequencing, and differentially expressed genes (DEGs) and differentially expressed microRNAs (DEMs) were identified by bioinformatics. Single-cell transcriptome sequencing (10 × Genomics) was further conducted. Among the samples from 23 adult septic patients and 10 healthy individuals, 20,391 genes and 1633 microRNAs were detected by RNA sequencing. In total, 1114 preliminary DEGs and 76 DEMs were obtained using DESeq2, and 454 DEGs were ultimately distinguished. A microRNA–mRNA–PPI network was constructed based on the DEGs and the top 20 DEMs, which included 10 upregulated and 10 downregulated microRNAs. Furthermore, the hub genes TLR5, FCGR1A, ELANE, GNLY, IL2RB and TGFBR3, which may be associated with the prognosis of sepsis, and their negatively correlated microRNAs, were analysed. The genes TLR5, FCGR1A and ELANE were mainly expressed in macrophages, and the genes GNLY, IL2RB and TGFBR3 were expressed specifically in T cells and natural killer cells. Parallel analysis of mRNAs and microRNAs in patients with sepsis was demonstrated to be feasible using RNA-seq. Potential hub genes and microRNAs that may be related to sepsis prognosis were identified, providing new prospects for sepsis treatment. However, further experiments are needed.

Hepatocellular carcinoma (HCC) is a deadly malignancy with high genetic heterogeneity. TP53 mutation and c-MET activation are frequent events in human HCCs. Here, we discovered that the simultaneous mutations in TP53 and activation of c-MET occur in ~20% of human HCCs, and these patients show a poor prognosis. Importantly, we found that concomitant deletion of Trp53 and overexpression of c-MET (c-MET/sgp53) in the mouse liver led to HCC formation in vivo. Consistent with human HCCs, RNAseq showed that c-MET/sgp53 mouse HCCs were characterized by activated c-MET and Ras/MAPK cascades and increased tumor cell proliferation. Subsequently, a stably passaged cell line derived from a c-MET/sgp53 HCC and corresponding subcutaneous xenografts were generated. Also, in silico analysis suggested that the MEK inhibitor trametinib has a higher inhibition score in TP53 null human HCC cell lines, which was validated experimentally. We consistently found that trametinib effectively inhibited the growth of c-MET/sgp53 HCC cells and xenografts, supporting the possible usefulness of this drug for treating human HCCs with TP53-null mutations. Altogether, our study demonstrates that loss of TP53 cooperates with c-MET to drive hepatocarcinogenesis in vivo. The c-MET/sgp53 mouse model and derived HCC cell lines represent novel and useful preclinical tools to study hepatocarcinogenesis in the TP53 null background.

Diarrhea in piglets is one of the most important diseases and a significant cause of death in piglets. Preliminary studies have confirmed that taurine reduces the rate and index of diarrhea in piglets induced by LPS. However, there is still a lack of relevant information on the specific target and mechanism of action of taurine. Therefore, we investigated the effects of taurine on the growth and barrier functions of the intestine, microbiota composition, and metabolite composition of piglets induced by LPS. Eighteen male weaned piglets were randomly divided into the CON group (basal diet + standard saline injection), LPS group (basal diet + LPS-intraperitoneal injection), and TAU + LPS group (basal diet + 0.3% taurine + LPS-intraperitoneal injection). The results show that taurine significantly increased the ADG and decreased the F/G (p < 0.05) compared with the group of CON. The group of TAU + LPS significantly improved colonic villous damage (p < 0.05). The expression of ZO-1, Occludin and Claudin-1 genes and proteins were markedly up-regulated (p < 0.05). Based on 16s rRNA sequencing analysis, the relative abundance of Lactobacilluscae and Firmicutes in the colon was significantly higher in the LPS + TAU group compared to the LPS group (p < 0.05). Four metabolites were significantly higher and one metabolite was significantly lower in the TAU + LPS group compared to the LPS group (p < 0.01). The above results show that LPS disrupts intestinal microorganisms and metabolites in weaned piglets and affects intestinal barrier function. Preventive addition of taurine enhances beneficial microbiota, modulates intestinal metabolites, and strengthens the intestinal mechanical barrier. Therefore, taurine can be used as a feed additive to prevent intestinal damage by regulating intestinal microorganisms and metabolites.