Search

Liver cirrhosis remains a significant global public health concern, with liver transplantation standing as the foremost effective treatment currently available. Therefore, investigating the pathogenesis of liver cirrhosis and developing novel therapies is imperative. Mitochondrial dysfunction stands out as a pivotal factor in its development. This study aimed to elucidate the relationship between mitochondria dysfunction and liver cirrhosis using bioinformatic methods to unveil its pathogenesis. Initially, we identified 460 co-expressed differential genes (co-DEGs) from the GSE14323 and GSE25097 datasets, alongside their combined datasets. Functional analysis revealed that these co-DEGs were associated with inflammatory cytokines and cirrhosis-related signaling pathways. Utilizing weighted gene co-expression network analysis (WCGNA), we screened module genes, intersecting them with co-DEGs and oxidative stress-related mitochondrial genes. Two algorithms (least absolute shrinkage and selection operator (LASSO) regression and SVE-RFE) were then employed to further analyze the intersecting genes. Finally, COX7A1 and IFI27 emerged as identifying genes for liver cirrhosis, validated through a receiver operating characteristic (ROC) curve analysis and related experiments. Additionally, immune infiltration highlighted a strong correlation between macrophages and cirrhosis, with the identifying genes (COX7A1 and IFI27) being significantly associated with macrophages. In conclusion, our findings underscore the critical role of oxidative stress-related mitochondrial genes (COX7A1 and IFI27) in liver cirrhosis development, highlighting their association with macrophage infiltration. This study provides novel insights into understanding the pathogenesis of liver cirrhosis. [ABSTRACT FROM AUTHOR]

Microbial contamination is one of the most common food safety issues that lead to food spoilage and foodborne illness, which readily affects the health of the masses as well as gives rise to huge economic losses. In this study, Channa argus was used as a source of antimicrobial agent that was then analyzed by untargeted metabolomics for its antibacterial mechanism against Staphylococcus aureus. The results indicated that the skin mucus extract of C. argus had great inhibitory action on the growth of S. aureus, and the morphology of S. aureus cells treated with the skin mucus extract exhibited severe morphological damage under scanning electron microscopy. In addition, metabolomics analysis revealed that skin mucus extract stress inhibited the primary metabolic pathways of S. aureus by inducing the tricarboxylic acid cycle and amino acid biosynthesis, which further affected the normal physiological functions of biofilms. In conclusion, the antimicrobial effect of the skin mucus extract is achieved by disrupting cell membrane functions to induce an intracellular metabolic imbalance. Hence, these results conduce to amass novel insights into the antimicrobial mechanism of the skin mucus extract of C. argus against S. aureus. [ABSTRACT FROM AUTHOR]

Liver cirrhosis remains a significant global public health concern, with liver transplantation standing as the foremost effective treatment currently available. Therefore, investigating the pathogenesis of liver cirrhosis and developing novel therapies is imperative. Mitochondrial dysfunction stands out as a pivotal factor in its development. This study aimed to elucidate the relationship between mitochondria dysfunction and liver cirrhosis using bioinformatic methods to unveil its pathogenesis. Initially, we identified 460 co-expressed differential genes (co-DEGs) from the GSE14323 and GSE25097 datasets, alongside their combined datasets. Functional analysis revealed that these co-DEGs were associated with inflammatory cytokines and cirrhosis-related signaling pathways. Utilizing weighted gene co-expression network analysis (WCGNA), we screened module genes, intersecting them with co-DEGs and oxidative stress-related mitochondrial genes. Two algorithms (least absolute shrinkage and selection operator (LASSO) regression and SVE-RFE) were then employed to further analyze the intersecting genes. Finally, COX7A1 and IFI27 emerged as identifying genes for liver cirrhosis, validated through a receiver operating characteristic (ROC) curve analysis and related experiments. Additionally, immune infiltration highlighted a strong correlation between macrophages and cirrhosis, with the identifying genes ( COX7A1 and IFI27 ) being significantly associated with macrophages. In conclusion, our findings underscore the critical role of oxidative stress-related mitochondrial genes ( COX7A1 and IFI27 ) in liver cirrhosis development, highlighting their association with macrophage infiltration. This study provides novel insights into understanding the pathogenesis of liver cirrhosis.

The antidiabetic activities of bitter melon powders produced with lyophilization/superfine grinding and hot air drying/normal grinding were investigated in vivo for selecting a suitable bitter melon processing procedure. After a five-week treatment, bitter melon lyophilized superfine grinding powder (BLSP) had a higher antidiabetic activity with reducing fasting blood glucose levels from 21.40 to 12.54 mmol/L, the serum insulin levels from 40.93 to 30.74 mIU/L, and restoring activities of SOD compared with those in the bitter melon hot air drying powder (BAP) treated group. Furthermore, BLSP protected pancreatic tissues including islet beta cells and reduced the loss of islet cells. Combined with the difference of compositions in BLSP and BAP, it could be concluded that superfine grinding and lyophilization processes were beneficial for presenting the antidiabetic activity, which will provide a reference for direct utilization of bitter melon as a suitable functional food to relieve symptoms of diabetes.