Our previous studies revealed RBM8A may play a role in various progressive neurological diseases. The present study aimed to explore the role of RBM8A in Alzheimer's disease (AD). RBM8A is significantly down-regulated in AD. Interestingly, 9186 differentially expressed genes are overlapped from comparisons of AD versus control and RBM8A-low versus RBM8A-high. Weight gene correlation analysis was performed and 9 functional modules were identified. Modules positively correlated with AD and RBM8A-low are significantly involved in the RAP1 signaling pathway, PI3K−AKT signaling pathway, hematopoietic cell lineage, autophagy and APELIN signaling pathway. Fifteen genes (RBM8A, RHBDF2, TNFRSF10B, ACP1, ANKRD39, CA10, CAMK4, CBLN4, LOC284214, NOVA1, PAK1, PPEF1, RGS4, TCEB1 and TMEM118) are identified as hub genes, and the hub gene-based LASSO model can accurately predict the occurrence of AD (AUC = 0.948). Moreover, the RBM8A-module-pathway network was constructed, and low expression of RBM8A down-regulates multiple module genes, including FIP200, Beclin 1, NRBF2, VPS15 and ATG12, which composes key complexes of autophagy. Thus, our study supports that low expression of RBM8A correlates with the decrease of the components of key complexes in autophagy, which could potentially contribute to pathophysiological changes of AD.

Competing endogenous RNA (ceRNA) and autophagy were related to neurological diseases. But the relationship among ceRNA, autophagy and Schizophrenia (SZ) was not clear. In this study, we obtained gene expression profile of SZ patients (GSE38484, GSE54578, and GSE16930) from Gene Expression Omnibus (GEO) database. Then we screened the autophagy-related differentially expressed lncRNA, miRNA, and mRNA (DElncRNA, DEmiRNA, and DEmRNA) combined with Gene database from The National Center for Biotechnology Information (NCBI). In addition, we performed enrichment analysis. The result showed that biological processes (BPs) mainly were associated with cellular responses to oxygen concentration. The enriched pathways mainly included ErbB, AMPK, mTOR signaling pathway and cell cycle. Furthermore, we constructed autophagy-related ceRNA network based on the TargetScan database. Moreover, we explored the diagnostic efficiency of lncRNA, miRNA and mRNA in ceRNA, through gene set variation analysis (GSVA). The result showed that the diagnostic efficiency was robust, especially miRNA (AUC = 0.884). The miRNA included hsa-miR-423-5p, hsa-miR-4532, hsa-miR-593-3p, hsa-miR-618, hsa-miR-4723-3p, hsa-miR-4640-3p, hsa-miR-296-5p, and hsa-miR-3943. The result of this study may be helpful for deepening the pathophysiology of SZ. In addition, our finding may provide a guideline for the clinical diagnosis of SZ.

Purpose Carotid atherosclerosis is a kind of systemic atherosclerosis in the carotid arteries. However, the efficiency of treatment is insufficient. Therefore, it is urgent to find therapeutic targets and deepen the understanding of carotid atherosclerosis. Materials and Methods In this study, we analyzed differentially expressed genes (DEGs) between atheroma plaque and macroscopically intact tissue (control samples). Furthermore, we performed Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) enrichment analysis based on the DEGs. Four methods were used to identify the hub genes in the protein–protein interaction networks of the DEGs. Furthermore, we also performed network module analysis to reveal carotid atherosclerosis-related gene modules and biological functions. Results The enrichment results showed that the biological functions were related to inflammation, immunity, chemokine and cell adhesion molecule, such as PIK-Akt signaling pathway, Rap1 signaling pathway, MAPK signaling pathway, NOD-like receptor signaling pathway and B cell receptor signaling pathway. In addition, we screened the hub genes. A total of 16 up-regulated genes (C3AR1, CCR1, CCR2, CD33, CD53, CXCL10, CXCL8, CXCR4, CYBB, FCER1G, FPR2, ITGAL, ITGAM, ITGAX, ITGB2, and LILRB2) were identified as hub genes. A total of 5 gene modules were obtained. We found that biological functions obtained for each cluster were mostly related to immunity, chemokines and cell adhesion molecules. Conclusion The present study identified key DEGs in atheroma plaque compared with control samples. The key genes involved in the development of carotid atherosclerosis may provide valuable therapeutic targets for carotid atherosclerosis.

BackgroundPolymorphisms in miR-146a (rs2910164), miR-196a2 (rs11614913), miR-149 (rs2292832) and miR-499 (rs3746444) have been associated with ischemic stroke (IS), but studies have given inconsistent results.MethodsThis meta-analysis investigated the possible association between IS risk and the four polymorphisms. A total of 14 case-control studies from Asian populations involving 6,083 cases and 7,248 controls for the four polymorphisms were included.ResultsResults showed that the GG genotype of miR-146a (rs2910164) may be associated with increased IS risk according to the recessive model (OR=1.20, 95% CI=1.02–1.42, P=0.03). Similarly, the CC genotype of miR-149 (rs2292832) may be associated with increased IS risk according to the recessive model (OR=1.28, 95% CI=1.08–1.52, P=0.005) and the homozygous model (OR=1.31, 95% CI=1.09–1.58, P=0.004). In contrast, miR-196a2 (rs11614913) and miR-499 (rs3746444) polymorphisms did not show significant association with IS risk in any of the five genetic models.ConclusionThese results indicate that the GG genotype of miR-146a (rs2910164) and CC genotype of miR-149 (rs2292832) may confer increased susceptibility to IS, while miR-196a2 (rs11614913) and miR-499 (rs3746444) polymorphisms may not be associated with IS risk in Asian populations. These conclusions should be verified in large and well-designed studies.

Our results indicate that ustekinumab is safe for patients with moderate to severe plaque psoriasis over a period of 5 years, and it is effective after 12 weeks. There was no significant superiority in efficacy between the 45 mg and 90 mg doses for short-term therapy. Results of the long-term safety evaluation are consistent with short-term reports of ustekinumab safety. More long-term studies and RCTs are needed to validate these results.