Ruijun Ji's research while affiliated with Capital University and other places

Background and purpose Studies showed that patients with hemorrhagic stroke are at a higher risk of developing deep vein thrombosis (DVT) than those with ischemic stroke. We aimed to develop a risk score (intracerebral hemorrhage-associated deep vein thrombosis score, ICH-DVT) for predicting in-hospital DVT after ICH. Methods The ICH-DVT was developed based on the Beijing Registration of Intracerebral Hemorrhage, in which eligible patients were randomly divided into derivation (60%) and internal validation cohorts (40%). External validation was performed using the iMCAS study (In-hospital Medical Complication after Acute Stroke). Independent predictors of in-hospital DVT after ICH were obtained using multivariable logistic regression, and β-coefficients were used to generate a scoring system of the ICH-DVT. The area under the receiver operating characteristic curve (AUROC) and the Hosmer–Lemeshow goodness-of-fit test were used to assess model discrimination and calibration, respectively. Results The overall in-hospital DVT after ICH was 6.3%, 6.0%, and 5.7% in the derivation (n = 1,309), internal validation (n = 655), and external validation (n = 314) cohorts, respectively. A 31-point ICH-DVT was developed from the set of independent predictors including age, hematoma volume, subarachnoid extension, pneumonia, gastrointestinal bleeding, and length of hospitalization. The ICH-DVT showed good discrimination (AUROC) in the derivation (0.81; 95%CI = 0.79–0.83), internal validation (0.83, 95%CI = 0.80–0.86), and external validation (0.88; 95%CI = 0.84–0.92) cohorts. The ICH-DVT was well calibrated (Hosmer–Lemeshow test) in the derivation (P = 0.53), internal validation (P = 0.38), and external validation (P = 0.06) cohorts. Conclusion The ICH-DVT is a valid grading scale for predicting in-hospital DVT after ICH. Further studies on the effect of the ICH-DVT on clinical outcomes after ICH are warranted.

Objective: MicroRNAs (miRNAs) in exosomes had been implicated differentially expressed in patient with moyamoya disease (MMD), but the miRNAs expression in circulating leukocytes remains unclear. This study was investigated on the differential expression of miRNAs in peripheral leukocytes between MMD patients and healthy adults, and among patients with subtypes of MMD. Materials and methods: A total of 30 patients with MMD and 10 healthy adults were enrolled in a stroke center from October 2017 to December 2018. The gene microarray was used to detect the differential expression profiles of miRNA in leukocytes between MMD patients and controls, and the differentially expressed miRNAs were verified by the method of real-time PCR. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to explore the key signaling pathways and possible pathogenesis of MMD. Results: The microarray results showed 12 differentially expressed miRNAs in leukocytes of MMD patients compared with controls (fold change >2.0, p < 0.05 and FDR <0.05), of which 8 miRNAs were upregulated (miRNA-142-5p, miRNA-29b-3p, miRNA-424-5p, MiRNA-582-5p, miRNA-6807-5p, miRNA-142-3p, miRNA-340-5p, miRNA-4270), and 4 miRNAs were downregulated (miRNA-144-3p, miRNA-451a, miRNA-486-5p, miRNA-363-3p). The real-time PCR confirmed seven differentially expressed miRNAs (p < 0.05), of which 4 miRNAs (miRNA-29b-3p, miRNA-142-3p, miRNA-340-5p, miRNA-582-5p) were upregulated, and 3 miRNAs (miRNA-363-3p, miRNA-451a and miRNA-486-5p) were downregulated. Both GO and KEGG analysis suggested that the Wnt signaling pathway may be involved in the pathogenesis of MMD. In addition, miRNAs were also differentially expressed among patients with subtypes of MMD. Conclusion: This study indicated that miRNAs are differentially expressed in peripheral leukocytes between MMD patients and healthy adults, and among patients with subtypes of MMD. The Wnt signaling pathway is probably involved in the pathogenesis of MMD.

Objective: The aim of this study was to investigate the correlation between the Trial of Org 10172 in acute stroke treatment classification and the National Institutes of Health Stroke Scale score of acute cerebral infarction as well as acute cerebral infarction's risk factors. Methods: The clinical data of 3,996 patients with acute cerebral infarction hospitalized in Hebei Renqiu Kangjixintu Hospital from January 2014 to November 2018 were analyzed retrospectively. According to Trial of Org 10172 in acute stroke treatment, they were divided into five groups: arteriosclerosis, cardio cerebral embolism, arterial occlusion, other causes, and unknown causes. Through questionnaire design, routine physical examination, and physical and chemical analysis of fasting venous blood samples, the risk factors were evaluated, and the correlation between Trial of Org 10172 in acute stroke treatment classification and National Institutes of Health Stroke Scale classification was analyzed using multivariate logistic regression. In addition, the relationship between National Institutes of Health Stroke Scale score and risk factors in different groups was compared, and the correlation between Trial of Org 10172 in acute stroke treatment classification and National Institutes of Health Stroke Scale score was analyzed. Results: Multivariate logistic regression analysis showed that diabetes, atrial fibrillation or stroke history, age, and education level were related to Trial of Org 10172 in acute stroke treatment classification. In the National Institutes of Health Stroke Scale comparison, the scores of the cardio cerebral embolism group were significantly higher than those of the other four groups, and patients with diabetes, atrial fibrillation, or stroke history had a high share, especially atrial fibrillation (33.06%). Conclusions: The nerve function defect is more serious after acute cerebral infarction with cardiogenic cerebral embolism, indicating a poor prognosis.

The early hematoma expansion of intracerebral hemorrhage (ICH) indicates a poor prognosis. This paper studies the relationship between cerebral blood flow (CBF) around the hematoma and hematoma expansion (HE) in the acute stage of intracerebral hemorrhage. A total of 50 patients with supratentorial cerebral hemorrhage were enrolled in this study. They underwent baseline whole-brain CTP within 6 h after intracerebral hemorrhage, and non-contrast CT within 24 h. Absolute hematoma growth and relative hematoma growth were calculated, respectively. A relative growth of Hematoma volume >33% was considered to be hematoma expansion. The Ipsilateral peri-edema CBF and Ipsilateral edema CBF were calculated by CTP maps in patients with and without hematoma expansion, respectively. In this study the incidence of hematoma expansion in the early stage of supratentorial cerebral hemorrhage was 32%; The CBF of the hematoma expansion group was higher than that of the patients without hematoma expansion (23.5 ± 12.5 vs. 15.1 ± 7.4, P = 0.004). After adjusting for age, gender, Symptom onset to NCCT and Baseline hematoma volume, ipsilateral peri-edema CBF was still an independent risk factor for early HE (or = 1.095, 95% CI = 1.01–1.19, P = 0.024). Here, we concluded that higher cerebral blood flow predicts early hematoma expansion in patients with intracerebral hemorrhage.

To systematically compare 27 ICH models with regard to mortality and functional outcome at 1-month, 3-month and 1-year after ICH. The validation cohort was derived from the Beijing Registration of Intracerebral Hemorrhage. Poor functional outcome was defined as modified Rankin Scale score (mRS) ≥3 at 1-month, 3-month and 1-year after ICH, respectively. The area under the receiver operating characteristic curve (AUROC) and Hosmer-Lemeshow goodness-of-fit test were used to assess model discrimination and calibration. A total number of 1575 patients were included. The mean age was 57.2 ± 14.3 and 67.2% were male. The median NIHSS score on admission was 11 (IQR: 3–21). For predicting mortality at 3-month after ICH, AUROC of 27 ICH models ranged from 0.604 to 0.856. In pairwise comparison, the ICH-FOS (0.856, 95%CI = 0.835–0.878, P < 0.001) showed statistically better discrimination than other models for mortality at 3-month after ICH (all P < 0.05). For predicting poor functional outcome (mRS≥3) at 3-month after ICH, AUROC of 27 ICH models ranged from 0.602 to 0.880. In pairwise comparison with other prediction models, the ICH-FOS was superior in predicting poor functional outcome at 3-month after ICH (all P < 0.001). The ICH-FOS showed the largest Cox and Snell R-square. Similar results were verified for mortality and poor functional outcome at 1-month and 1-year after ICH. Several risk models are externally validated to be effective for risk stratification and outcome prediction after ICH, especially the ICH-FOS, which would be useful tools for personalized care and clinical trial in ICH.

Background and purpose- MicroRNAs (miRNAs) in exosomes had been implicated differentially expressed in MMD patients, but the miRNAs expression in circulating leukocytes remains unclear. This study was investigated on the differential expression of miRNAs in peripheral leukocytes between MMD patients and healthy adults, and among patients with subtypes of MMD. Methods- A total of 30 patients with MMD and 10 healthy adults were enrolled in a stroke center from October 2017 to December 2018. The gene microarray was used to detect the differential expression profiles of miRNA in leukocytes between MMD patients and controls, and the differentially expressed miRNAs were verified by the method of real-time PCR. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to explore the key signaling pathways and possible pathogenesis of MMD. Results- The microarray results showed 12 differentially expressed miRNAs in leukocytes of MMD patients compared with controls (fold change > 2.0 and P < 0.05), of which 7 miRNAs were up-regulated (miRNA-142-5p, miRNA-29b-3p, miRNA-424-5p, MiRNA-582-5p, miRNA-6807-5p, miRNA-142-3p, miRNA-340-5p), and 5 miRNAs were down-regulated (miRNA-144-3p, miRNA-144-5p, miRNA-451a, miRNA-486-5p, miRNA-363-3p). The real-time PCR confirmed 7 differentially expressed miRNAs (P<0.05), of which 4 miRNAs (miRNA-29b-3p, miRNA-142-3p, miRNA-340-5p, miRNA-582-5p) were up-regulated, and 3 miRNAs (miRNA-363-3p, miRNA-451a and miRNA-486-5p) were down-regulated. Both GO and KEGG analysis suggested that the Wnt signaling pathway may be involved in the pathogenesis of MMD. In addition, miRNAs were also differentially expressed among patients with subtypes of MMD. Conclusion- This study indicated that miRNAs are differentially expressed in peripheral leukocytes between MMD patients and healthy adults, and among patients with subtypes of MMD. The Wnt signaling pathway is probably involved in the pathogenesis of MMD.

Background: High plasma levels of trimethylamine N-oxide (TMAO) and its precursor choline have been linked to stroke; however, their association with cerebral small vessel disease remains unclear. Here we evaluated the association of plasma levels of TMAO and choline with imaging markers of cerebral small vessel disease, including white matter hyperintensities, lacunes, and cerebral microbleeds. Methods: We performed a baseline cross-sectional analysis of a multicenter hospital-based cohort study from 2015 to 2018. The data were collected from 30 hospitals in China and included 1,098 patients with ischemic stroke/transient ischemic attack aged ≥18 years. White matter hyperintensities, lacunes, and cerebral microbleeds were evaluated with the patients' demographic, clinical, and laboratory information removed. White matter hyperintensities were rated using the Fazekas visual grading scale, while the degree of severity of the lacunes and cerebral microbleeds was defined by the number of lesions. Results: Increased TMAO levels were associated with severe white matter hyperintensities [adjusted odds ratio (aOR) for the highest vs. lowest quartile, 1.5; 95% confidence interval (CI), 1.0–2.1, p = 0.04]. High TMAO levels were more strongly associated with severe periventricular white matter hyperintensities (aOR for the highest vs. lowest quartile, 1.6; 95% CI, 1.1–2.3, p = 0.009) than deep white matter hyperintensities (aOR for the highest vs. lowest quartile, 1.3; 95% CI, 0.9–1.9, p = 0.16). No significant association was observed between TMAO and lacunes or cerebral microbleeds. Choline showed trends similar to that of TMAO in the association with cerebral small vessel disease. Conclusions: In patients with ischemic stroke or transient ischemic attack, TMAO and choline appear to be associated with white matter hyperintensities, but not with lacunes or cerebral microbleeds; TMAO and choline were associated with increased risk of a greater periventricular, rather than deep, white matter hyperintensities burden.