Objective:To investigate the correlation between serum cystatin C (CysC), blood lipids and the risk of intracranial aneurysm (IA) rupture.Methods:Patients with saccular IA admitted to the First Affiliated Hospital of Xinjiang Medical University from December 2017 to May 2019 were enrolled retrospectively. The patients were divided into the ruptured group and the unruptured group. The correlation between CysC, lipids and IA rupture was identified by univariate and multivariate logistic regression analyses. Results:A total of 392 patients were enrolled, including 143 (36.5%) males and 249 (63.5%) females. Two hundred and seventy-eight patients (70.9%) were ruptured IAs, 114 (29.1%) were unruptured IAs. Univariate analysis showed that triglyceride (1.26±0.94 mmol/L vs. 2.12±1.45 mmol/L; t=5.872, P<0.001), apolipoprotein A-Ⅰ (0.95±0.29 g/L vs. 1.08±0.34 g/L; t=3.744, P<0.001 ), CysC (0.63±0.20 mg/L vs. 0.80±0.48 mg/L; t=3.650, P<0.001) level, and the proportions of hypertension (46.8% vs. 61.4%; χ2=6.938, P=0.008), hyperlipidemia (19.4% vs. 48.2%; χ2=32.493, P<0.001) and aneurysm diameter >7 mm (24.4% vs. 41.2%; χ2=11.504, P<0.001) of the ruptured group were significantly lower than those of the unruptured group, while the level of apolipoprotein B was significantly higher than that of the unruptured group (1.07±0.29 g/L vs. 0.99±0.30 g/L; t=2.417, P=0.016). Multivariate logistic regression analysis showed that aneurysm diameter ≤7 mm (odds ratio [ OR] 2.281, 95% confidence interval [ CI] 1.342-3.876; P=0.002), and the serum levels of triacylglycerol ( OR 0.484, 95% CI 0.333-0.705; P<0.001), apolipoprotein A-Ⅰ ( OR 0.248, 95% CI 0.105-0.587; P=0.002) and CysC ( OR 0.130, 95% CI 0.038-0.444; P=0.001) were significantly independently correlated with the risk of IA rupture. Conclusions:CysC, apolipoprotein A-Ⅰ and triacylglycerol are protective markers for IA rupture, and aneurysm diameter ≤7 mmis associated with IA rupture.

Objective: To identify biomolecular markers closely related to the occurrence of kidney renal clear cell carcinoma (KIRC) and verify their expression levels in clinical samples. Methods: Stage Ⅰ KIRC mRNA sequencing data were obtained from The Cancer Genome Atlas (TCGA).Principal component analysis (PCA) was used for dimensionality reduction to screen differentially expressed genes (DEGs)，which then underwent GO and KEGG analyses.Weighted gene co-expression network analysis (WGCNA) was used to screen genes significantly related to KIRC，and a protein-protein interaction (PPI) network was constructed to screen hub genes.The diagnostic value of hub genes was evaluated with receiver operating characteristic (ROC) curve，and their prognostic value was analyzed using survival curve plots.The correlation between the mRNA expressions of hub genes and the pathological stages of KIRC was analyzed.Clinical samples of 20 patients with stage Ⅰ KIRC treated in our hospital were included，and the expressions of the hub genes in cancerous and adjacent tissues were detected with reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR)，Western blotting，and enzyme-linked immunosorbent assay (ELISA). Results: A total of 8223 DEGs were screened out，including 4092 up-regulated ones and 4131 down-regulated ones.GO analysis showed that DEGs were related to bioadhesion，plasma membrane composition，and transporter activity.KEGG analysis showed that DEGs were related to pathways such as cell adhesion molecules，cytokine-cytokine receptor interactions，and interactions between viral proteins and cytokines and cytokine receptors.WGCNA analysis obtained 171 genes that were significantly related to stage Ⅰ KIRC.The hub gene，lymphocyte cytosolic protein 2 (LCP2)，screened out by the PPI network，was significantly related to stage Ⅰ KIRC.The area under the ROC curve was 0.96.The expression level was negatively correlated with the overall survival rate of patients.The expression of LCP2 was related to the stage and lymph node metastasis.Clinical verification showed that the mRNA and protein relative expressions of LCP2 in KIRC tissues were significantly higher than those in adjacent tissues (P<0.000 1). Conclusion: LCP2 is significantly up-regulated in stage Ⅰ KIRC tissues and can be used as a potential biomarker for the early diagnosis and treatment of KIRC.