Objective. MicroRNAs have been revealed to be involved in the development of atherosclerosis. The present study is aimed at exploring the potential of miR-99a-5p as a therapy for atherosclerosis. We suspected that miR-99a-5p might inhibit NLRP3 inflammasome activation and promote macrophage autophagy via constraining mTOR, therefore, alleviating atherosclerosis. Methods. The cell viability in ox-LDL-induced THP-1 macrophages was assessed by CCK-8 assay. Bioinformatic analysis was used to predict the target genes of miR-99a-5p. The binding between miR-99a-5p and mTOR was confirmed by luciferase reporter assay. In vivo, a high-fat-diet-induced atherosclerosis model was established in apolipoprotein E knockout mice. Hematoxylin-eosin, oil red O, and Sirius red staining were performed for the determination of atherosclerotic lesions. MTOR and associated protein levels were detected by Western blot analysis. Results. miR-99a-5p inhibited NLRP3 inflammasome activation and promoted macrophage autophagy by targeting mTOR. Enforced miR-99a-5p significantly reduced the levels of inflammasome complex and inflammatory cytokines. Furthermore, miR-99a-5p overexpression inhibited the expression of mTOR, whereas mTOR overexpression reversed the trend of the above behaviors. In vivo, the specific overexpression of miR-99a-5p significantly reduced atherosclerotic lesions, accompanied by a significant downregulation of autophagy marker CD68 protein expression. Conclusion. We demonstrated for the first time that miR-99a-5p may be considered a therapy for atherosclerosis. The present study has revealed that miR-99a-5p might inhibit NLRP3 inflammasome activation and promote macrophage autophagy by targeting mTOR, therefore, alleviating atherosclerosis.

Background: Transcranial color-coded duplex ultrasonography (TCCD) is an important diagnostic tool in the investigation of cerebrovascular diseases. TCCD is often hampered by the temporal window that ultrasound cannot penetrate. Rapidly determine whether ultrasound can penetrate the temporal window in order to determine whether to use other acoustic windows to complete the examination process. In this study, Skull thickness can be measured simultaneously during TCCD examination, which makes it possible to use skull thickness to rapidly determine whether the temporal window is penetrated by ultrasound. Methods: This retrospective study included 301 patients with clinical symptoms of cerebrovascular diseases. These 301 patients were divided into an impenetrable temporal window (ITW) group and a penetrable temporal window group according to the results of the TCCD examination. Results: The area under the receiver operating characteristic (ROC) curve (AUC) for skull thickness was 0.887 (cutoff value 1.045 cm). Following multivariate logistic regression, sex, age, and skull thickness were used to develop a nomogram. The AUC for the nomogram was 0.923 (cutoff value 0.407). Conclusions: The skull thickness at the temporal window was measured by ultrasound, which was convenient and accurate. The probability of ITW in females was higher than that in males, and it increased with age. In this study, a prediction model incorporating sex, age and skull thickness could predict ITW probability well. If the patient’s temporal window was rapidly predicted as an ITW, other acoustic window examinations were used to complete the TCCD examination process to optimize the TCCD examination process of cerebrovascular diseases and facilitate the popularization of TCCD in clinical application.