SLC26A7

Tunchang pigs are an indigenous pig population in China known for their high tolerance to roughage, delicious meat, and fecundity. However, the number of Tunchang pigs has been declining due to the influence of commercial breeds and African swine fever, which could potentially lead to inbreeding. To assess the inbreeding level and the genetic basis of important traits in Tunchang pigs, our research investigated the patterns in "runs of homozygosity" (ROHs) using whole genome resequencing data from 32 Tunchang pigs. The study aimed to determine the length, number, coverage, and distribution model of ROHs in Tunchang pigs, as well as genomic regions with high ROH frequencies. The results of the study revealed that a total of 20,499,374 single-nucleotide polymorphisms (SNPs) and 1953 ROH fragments were recognized in 32 individuals. The ROH fragments in Tunchang pigs were predominantly short, ranging from 0.5 to 1 megabases (Mb) in length. Furthermore, the coverage of ROHs varied across chromosomes, with chromosome 3 having the highest coverage and chromosome 11 having the lowest coverage. The genetic diversity of Tunchang pigs was found to be relatively high based on the values of H_E (expected heterozygosity), H_O (observed heterozygosity), pi (nucleotide diversity), Ne (effective population size), and MAF (minor allele frequency). The average inbreeding coefficients of Tunchang pigs, as determined by three different methods (F_HOM, F_GRM, and F_ROH), were 0.019, 0.0138, and 0.0304, respectively. These values indicate that the level of inbreeding in Tunchang pigs is currently low. Additionally, the study identified a total of 13 ROH islands on all chromosomes, which in total contained 38,913 SNPs and 120 genes. These ROH islands included genes associated with economically important traits, including meat quality (GYS1, PHLPP1, SLC27A5, and CRTC1), growth and development (ANKS1A, TAF11, SPDEF, LHB, and PACSIN1), and environmental adaptation (SLC26A7). The findings of this research offer valuable perspectives on the present status of Tunchang pig resources and offer a reference for breeding conservation plans and the efficient utilization of Tunchang pigs in the future. By understanding the inbreeding level and genetic basis of important traits in Tunchang pigs, conservation efforts can be targeted towards maintaining genetic diversity and promoting the sustainable development of this indigenous pig population.

This study aims to investigate the molecular mechanisms underlying the interaction of major depressive disorder (MDD) and COVID-19, and on this basis, diagnostic biomarkers and potential therapeutic drugs are further explored.

Differential gene expression analysis and weighted gene co-expression network analysis (WGCNA) were employed to identify common key genes involved in the pathogenesis of COVID-19 and MDD. Correlations with clinical features were explored. Detailed mechanisms were further investigated through protein interaction networks, GSEA, and immune cell infiltration analysis. Finally, Enrichr's Drug Signature Database and Coremine Medical were used to predict the potential drugs associated with key genes.

The study identified 18 genes involved in both COVID-19 and MDD. Four key genes (MBP, CYP4B1, ERMN, and SLC26A7) were selected based on clinical relevance. A multi-gene prediction model showed good diagnostic efficiency for the two diseases: AUC of 0.852 for COVID-19 and 0.915 for MDD. GO and GSEA analyses identified specific biological functions and pathways associated with key genes in COVID-19 (axon guidance, metabolism, stress response) and MDD (neuron ensheathment, biosynthesis, glutamatergic neuron differentiation). The key genes also affected immune infiltration. Potential therapeutic drugs, including small molecules and traditional Chinese medicines, targeting these genes were identified.

This study provides insights into the complex biological mechanisms underlying COVID-19 and MDD, develops an effective diagnostic model, and predicts potential therapeutic drugs, which may contribute to the prevention and treatment of these two prevalent diseases.

Recent studies have advanced our understanding of the pathophysiology of autoimmune gastritis, particularly its molecular aspects. The most noteworthy recent advancement lies in the identification of several candidate genes implicated in the pathogenesis of pernicious anemia through genome-wide association studies. These genes include PTPN22, PNPT1, HLA-DQB1, and IL2RA. Recent studies have also directed attention towards other genes such as ATP4A, ATP4B, AIRE, SLC26A7, SLC26A9, and BACH2 polymorphism. In-depth investigations have been conducted on lymphocytes and cytokines, including T helper 17 cells, interleukin (IL)-17A, IL-17E, IL-17F, IL-21, IL-19, tumor necrosis factor-α, IL-15, transforming growth factor-β1, IL-13, and diminished levels of IL-27. Animal studies have explored the involvement of roseolovirus and H. pylori in relation to the onset of the disease and the process of carcinogenesis, respectively. Recent studies have comprehensively examined the involvement of autoantibodies, serum pepsinogen, and esophagogastroduodenoscopy in the diagnosis of autoimmune gastritis. The current focus lies on individuals demonstrating atypical presentations of the disease, including those diagnosed in childhood, those yielding negative results for autoantibodies, and those lacking the typical endoscopic characteristics of mucosal atrophy. Here, we discuss the recent developments in this field, focusing on genetic predisposition, epigenetic modifications, lymphocytes, cytokines, oxidative stress, infectious agents, proteins, microRNAs, autoantibodies, serum pepsinogen, gastrin, esophagogastroduodenoscopy and microscopic findings, and the risk of gastric neoplasm.