UNASSIGNED: Coronary artery disease (CAD) is a type of cardiovascular disease that greatly hurts the health of human beings. Diabetic status is one of the largest clinical factors affecting CAD-associated gene expression changes. Most of the studies focus on diabetic patients, whereas few have been done for non-diabetic patients. Since the pathophysiological processes may vary among these patients, we cannot simply follow the standard based on the data from diabetic patients. Therefore, the prognostic and predictive diagnostic biomarkers for CAD in non-diabetic patient need to be fully recognized.
UNASSIGNED: To screen out candidate genes associated with CAD in non-diabetic patients, weighted gene co-expression network analysis (WGCNA) was constructed to conduct an analysis of microarray expression profiling in patients with CAD. First, the microarray data GSE20680 and GSE20681 were downloaded from NCBI. We constructed co-expression modules via WGCNA after excluding the diabetic patients. As a result, 18 co-expression modules were screened out, including 1,225 differentially expressed genes (DEGs) that were obtained from 152 patients (luminal stenosis ≥50% in at least one major vessel) and 170 patients (stenosis of <50%). Subsequently, a Pearson\'s correlation analysis was conducted between the modules and clinical traits. Then, a functional enrichment analysis was conducted, and we used gene network analysis to reveal hub genes. Last, we validated the hub genes with peripheral blood samples in an independent patient cohort using RT-qPCR.
UNASSIGNED: The results showed that the midnight blue module and the yellow module played vital roles in the pathogenesis of CAD in non-diabetic patients. Additionally, CD40, F11R, TNRC18, and calcium/calmodulin-dependent protein kinase type II gamma (CAMK2G) were screened out and validated using enzyme-linked immunosorbent assay (ELISA) in an independent patient cohort and immunohistochemical (IHC) staining in an atherosclerosis mouse model.
UNASSIGNED: Our findings demonstrate that hub genes, CD40, F11R, TNRC18, and CAMK2G, are surrogate diagnostic biomarkers and/or therapeutic targets for CAD in non-diabetic patients and require deeper validation.

To investigate cognitive function improvement in diabetic and non-diabetic patients after the implantation of Carotid Artery Stent (CAS), 128 patients suffering severe carotid stenosis were successfully enrolled in this study. Tests including, the Mini Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Alzheimer\'s Disease Assessment Scale-Cognitive subscale (ADAS-Cog), Clock Drawing Test (CDT), Hasegawa\'s Dementia Scale-Revised (HDS-R) and the serum levels of S-100B, were all measured at baseline for 3 months after the implantation of CAS. The baseline characteristics were similar between the patients with and without diabetes. 3 months after the implantation, significant improvements in MMSE (24.8 ± 2.2 vs. 25.2 ± 2.1, p=0.003), MoCA (25.6 ± 2.0 vs. 26.1 ± 1.9, p=0.000), ADAS-Cog (6.5 ± 1.3 vs. 6.1 ± 1.3, p=0.000), and CDT (3.3 ± 0.7 vs. 3.5 ± 0.7, p=0.034) were observed in the non-diabetic group. In contrast, there was no significant improvement in any of the cognitive test for the diabetic group. Another interesting discovery was the CAS procedure significantly decreased the S-100B level in the non-diabetic group (0.11 ± 0.04 ng/mL vs. 0.10 ± 0.04 ng/mL, p=0.000), but similar phenomena were not discovered in the diabetic group. In this light, the change of the S-100B level was negatively correlated with the results in the MMSE (p<0.01) and the MoCA (p<0.01) tests, and positively correlated with the result in ADAS-Cog (p<0.05) test. Our findings suggest that the CAS-induced beneficial effects on cognitive function might have a correlation relationship with the serum level of S-100B.