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BACKGROUND The identification of risk factors for recurrence in patients with minor ischemic stroke (MIS) is a critical medical need. AIM To develop a nomogram for individualized prediction of in-hospital recurrence in MIS patients. METHODS Based on retrospective collection, a single-center study was conducted at the First Affiliated Hospital of Anhui Medical University from January 2014 to December 2019. Univariate and multivariate logistic regression analyses were used to determine the risk factors associated with MIS recurrence. The least absolute shrinkage and selection operator regression was performed for preliminary identification of potential risk factors. Uric acid, systolic blood pressure, serum total bilirubin (STBL), and ferritin were integrated for nomogram construction. The predictive accuracy and calibration of the nomogram model were assessed by the area under the receiver operating characteristic curve (AUC-ROC) and Hosmer-Lemeshow test, respectively. RESULTS A total of 2216 MIS patients were screened. Among them, 155 were excluded for intravascular therapy, 146 for unknown National Institutes of Health Stroke Scale score, 195 for intracranial hemorrhage, and 247 for progressive stroke. Finally, 1244 patients were subjected to further analysis and divided into a training set (n = 796) and a validation set (n = 448). Multivariate logistic regression analysis revealed that uric acid [odds ratio (OR): 0.997, 95% confidence interval (CI): 0.993-0.999], ferritin (OR: 1.004, 95%CI: 1.002-1.006), and STBL (OR: 0.973, 95%CI: 0.956-0.990) were independently associated with in-hospital recurrence in MIS patients. Our model showed good discrimination; the AUC-ROC value was 0.725 (95%CI: 0.646-0.804) in the training set and 0.717 (95%CI: 0.580-0.785) in the validation set. Moreover, the calibration between nomogram prediction and the actual observation showed good consistency. Hosmer-Lemeshow test results confirmed that the nomogram was well-calibrated (P = 0.850). CONCLUSION Our present findings suggest that the nomogram may provide individualized prediction of recurrence in MIS patients.

Background Cerebral proliferative angiopathy (CPA) is a rare vascular disease characterized by the presence of diffuse vascular proliferation, progressive vascular hyperflow and vasodilation of multiple vessels in the normal brain parenchyma. Unlike cerebral arteriovenous malformations, CPA has a mixed appearance between that of lesions with cell proliferation and endothelial proliferation. To date, the pathogenesis of CPA is unclear, in which changes induced by cortical ischemia in the elastic layer of the blood supply artery and smooth muscle cells may be involved. Case summary In this article, we retrospectively analyzed a case of hemorrhagic transformation of ischemic CPA diagnosed by digital subtraction angiography and reviewed the related literature for further exploration of its pathogenesis, diagnosis and treatment. Conclusion The information in the present case report may facilitate further clinical research on this cerebrovascular disease.

The study aims to explore how microRNA-146a/b (miR-146a/b) regulates the function of endothelial progenitor cells (EPCs) in acute ischemic stroke in mice. Eighty male SPF C57BL/6J mice were evenly divided into the model-6 h, model-12 h, model-24 h (mice suffered from middle cerebral artery occlusion [MCAO] for 6 h, 12 h and model-24 h) and normal groups. EPCs were transfected and assigned into the control, MCAO, MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. The qRT-PCR was used to detect miR-146a/b expression in EPCs. Expressions of tumor necrosis factor receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK1) were detected using western blotting. Cell proliferation and migration of EPCs were testified using CCK-8 assay and scratch test, respectively. Angiogenesis ability of EPCs was observed under microscope. MiR-146a and miR-146b expressions were lower in the model groups than the normal group. There were up-regulated TRAF6 and IRAK1 expressions in the model-6 h, model-12 h and model-24 h groups compared with the normal group. And there were down-regulated TRAF6 and IRAK1 expressions in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups than in the MCAO group. Compared with the control group, the proliferation, migration and angiogenesis ability of EPCs were significantly lower in the MCAO group, but higher in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. Besides, the miR-146a/b group showed more enhancement than the MCAO-miR-146a and MCAO-miR-146b groups. MiR-146a/b could down-regulate the TRAF6 and IRAK1 expressions and promote proliferation, migration and angiogenesis ability of EPCs, which was important for recovery of patients with hyperacute ischemic stroke.

BACKGROUND This study aimed to investigate the diagnostic values of serum levels of Hcy and UA for predicting vascular mild cognitive impairment (VMCI) in patients with cerebral small vessel disease (SVD). MATERIAL AND METHODS We selected 172 cerebral SVD patients and divided them into a VMCI group and a non-VMCI group. Eighty-six healthy individuals without nervous system diseases were selected as the control group. Enzymatic cycling method was performed to detect serum Hcy and UA levels. Serum levels of folic acid (FOA) and vitamin B12 (VitB12) were detected by chemiluminescence immunoassay. Montreal cognitive assessment (MoCA) was applied to evaluate the cognitive function. The ROC curve was used to evaluate the diagnostic values of serum Hcy and UA levels for predicting VMCI. Logistic regression analysis was used to determine the possible risk factors. RESULTS Compared with the non-VMCI and control groups, serum FOA and VitB12 levels were lower and serum Hcy and UA levels were higher in the VMCI group. AUC values of serum Hcy and UA levels were 0.703 and 0.829, respectively. Serum Hcy and UA levels were negatively correlated with serum FOA and VitB12 levels, total MoCA score, and subscores on visuospatial ability and executive function, on language ability and on delayed recall, and they were positively correlated with serum cholesterol (CH) level. Serum Hcy and UA levels were indicated as risk factors for VMCI in cerebral SVD patients. CONCLUSIONS These results suggest that serum Hcy and UA levels may serve as predictive factors for VMCI in cerebral SVD patients.