Il1r2 and Tnfrsf12a in transcranial magnetic stimulation effect of ischemic stroke via bioinformatics analysis.

Ischemic stroke refers to ischemic necrosis or softening of localized brain tissue. Transcranial magnetic stimulation (TMS) is a painless, noninvasive and green treatment method, which acts on the central nervous system through a pulsed magnetic field to assist in the treatment of central nervous system injury diseases. However, the role of Il1r2 and Tnfrsf12a in this is unknown. The ischemic stroke datasets GSE81302 and TMS datasets GSE230148 were downloaded from Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis (WGCNA) was performed. The construction and analysis of protein-protein interaction (PPI) network and functional enrichment analysis were performed. Draw heat map gene expression. Through the Comparative Toxicogenomics Database (CTD) to find the most relevant and core gene diseases. TargetScan was used to screen miRNAs regulating DEGs. A total of 39 DEGs were identified. According to gene ontology (GO) analysis results, in biological process (BP) analysis, they were mainly enriched in the positive regulation of apoptosis process, inflammatory response, positive regulation of p38MAPK cascade, and regulation of cell cycle. In cellular component (CC) analysis, they were mainly enriched in the cell surface, cytoplasm, and extracellular space. In Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, they were mainly enriched in nf-κB signaling pathway, fluid shear stress and atherosclerosis, P53 signaling pathway, TNF signaling pathway, and apoptosis. Among the enrichment items of metascape, negative regulation of T cell activation, hematopoietic cell lineage, positive regulation of apoptotic process, fluid shear stress and atherosclerosis were observed in GO enrichment items. Five core genes (Socs3, Irf1, Il1r2, Ccr1, and Tnfrsf12a) were obtained, which were highly expressed in ischemic stroke samples. Il1r2 and Tnfrsf12a were lowly expressed in TMS samples. CTD analysis found that the core gene (Socs3, Irf1 and Il1r2, Ccr1, Tnfrsf12a) and ischemic stroke, atherosclerosis, hypertension, hyperlipidemia, thrombosis, stroke, myocardial ischemia, myocardial infarction, and inflammation. Il1r2 and Tnfrsf12a are highly expressed in ischemic stroke, but lowly expressed in TMS samples.

Higher expression of PLEK and LY86 as the potential biomarker of carotid atherosclerosis.

Carotid atherosclerosis (AS) occurs in atherosclerotic lesions of the carotid artery, which can lead to transient ischemic attack and stroke in severe cases. However, the relationship between pleckstrin (PLEK) and lymphocyte antigen 86 (LY86) and carotid AS remains unclear. The carotid AS datasets GSE43292 and GSE125771 were downloaded from the gene expression omnibus database. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. Construction and analysis of protein-protein interaction network. Functional enrichment analysis, gene set enrichment analysis and comparative toxicogenomics database analysis were performed. TargetScan screened miRNAs that regulated central DEGs. A total of 305 DEGs were identified. According to gene ontology analysis, they were mainly enriched in immune system processes, extracellular regions and cytokine binding. Kyoto encyclopedia of genes and genomes analysis showed that the target cells were mainly enriched in Rap1 signal pathway, B cell receptor signal pathway and PPAR signal pathway. In the enrichment project of metascape, the reaction to bacteria, cell activation and chemotaxis can be seen in the enrichment project of gene ontology. Total 10 core genes (TYROBP, FCER1G, PLEK, LY86, IL10RA, ITGB2, LCP2, FCGR2B, CD86, CCR1) were obtained by protein-protein interaction network construction and analysis. Core genes (PLEK, LY86, IL10RA, ITGB2, and LCP2) were highly expressed in carotid AS samples and lowly expressed in normal samples. Comparative toxicogenomics database analysis showed that 5 genes were associated with pneumonia, inflammation, necrosis, and drug allergy. PLEK and LY86 genes are highly expressed in carotid AS. The higher the expression of PLEK and LY86, the worse the prognosis is.

The value of RPS15 and MRPS27 in ischemic stroke.

Ischemic stroke is caused by insufficient blood supply to the brain. It has acute onset, often disturbance of consciousness, and high mortality and disability rate. However, relationship between ribosomal proteins (RP)-S15 and mitochondrial ribosomal proteins (MRP)-S27 and ischemic stroke remains unclear. The ischemic stroke datasets GSE22255, GSE16561, and GSE199435 were downloaded from gene expression omnibus generated by GPL6883, GPL11154, and GPL570. Differentially expressed genes (DEGs) were screened, and the construction and analysis of protein-protein interaction network, functional enrichment analysis and gene set enrichment analysis were performed. The gene expression heat map was drawn. Comparative toxicogenomics database analysis were performed to find the disease most related to core gene. TargetScan screened miRNAs that regulated central DEGs. Five hundred DEGs were identified. According to gene ontology analysis, they were mainly enriched in leukocyte activation, myoid cell activation involved in immune response, cell membrane, mitochondria, secretory vesicles, catalytic activity, enzyme binding, ribonucleic acid binding, splicing. Gene set enrichment analysis showed that the enrichment items are similar to the enrichment items of differentially expressed genes. And 20 core genes were obtained. Comparative toxicogenomics database analysis showed that 6 genes (RPS15, RPS2, RPS3, MRPS27, POLR2A, MRPS26) were found to be associated with chemical and drug-induced liver injury, necrosis, delayed prenatal exposure, nephropathy, hepatomegaly and tumor. RPS15 and MRPS27 are the core genes of ischemic stroke and play an important role in ischemic stroke.

Application of Transcranial Magnetic Stimulation with Electroencephalography in the Evaluation of Brain Function Changes after Stroke.

Objective: Based on transcranial magnetic stimulation (TMS) with electroencephalography technology, this study analyzed the rehabilitation mechanism of patients' motor function reconstruction and nerve remodeling after stroke. It revealed the function of the cerebral cortex network at a deeper level and established a set of prognostic marker evaluation indicators for the reconstruction of motor function after stroke. Methods: Twenty-one patients treated at the Beijing Rehabilitation Hospital of Capital Medical University because of ischemic stroke in the territory supplied by the middle cerebral artery were selected as the experimental group. Neurophysiological evaluation, motor function evaluation, and clinical evaluation were performed 30 and 180 d after the onset of ischemic stroke. In the control group, neurophysiological evaluation was also performed as a reference index to evaluate the changes in cortical patterns after stroke. Results: The brain topographic map showed the changes in energy or power spectral density (PSD) at 1,000 ms after stimulation as compared with before stimulation, but no difference was detected in these patients. The time-frequency analysis showed that when the left primary motor cortex (M1) area was stimulated using TMS, the PSD values of the left and right M1 and posterior occipital cortex areas produced an 8-40 Hz wave band in patients S1-S11. There was no significant energy change in patients S12-S16. Conclusions: For patients with different injury types, degrees of injury, and different onset periods, individualized intervention methods should be adopted. The evaluation methods should be as diverse as possible, and the rehabilitation effects of patients should be assessed from multiple perspectives to avoid the limitations of single factors. Possible mechanism: After brain injury, the nervous system can change its structure and function through different ways and maintain it for a certain period of time. This plasticity change will change with the course of the disease.