Predictive Value of Carotid Plaque Contrast-Enhanced Ultrasound Score and Homocysteine in Senile Metabolic Syndrome Complicated by Cerebral Infarction.

OBJECTIVE: To investigate the predictive value of the carotid plaque contrast-enhanced ultrasound (CEUS) score and blood homocysteine (HCY) in senile metabolic syndrome (MetS) complicated by cerebral infarction. STUDY DESIGN: Observational study. Place and Duration of the Study: Department of Ultrasound Imaging, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, China, from July 2020 to December 2021. METHODOLOGY: A total of 118 senile MetS patients complicated by cerebral infarction were selected as Group A, and 103 senile MetS patients without cerebral infarction were selected as Group B. Both groups were compared in terms of cardiovascular risk factors and ultrasonic examination of carotid plaques. The independent risk factors for cerebral infarction among senile MetS patients were analysed using logistic regression. An ROC curve was used to assess the predictive value of statistically significant risk factors in senile MetS complicated by cerebral infarction. RESULTS: Significant differences were observed in smoking, abdominal circumference, blood pressure, HCY, fasting blood glucose, high-density and low-density lipoprotein cholesterol, triacylglycerol, carotid plaque thickness, CEUS score, lumen stenosis, and ulcer plaque between the two groups. Logistic regression analysis showed that the plaque CEUS score and HCY were independent risk factors for senile MetS complicated by cerebral infarction. The areas under the ROC curve for the CEUS score and HCY were 0.795 and 0.812, respectively, and was 0.858 for the combined diagnosis of both. When the CEUS score was ≥2 and HCY was ≥16.45 mmol/l, the sensitivity and specificity of predicted senile MetS complicated by cerebral infarction were 83.1% and 74.8%, respectively. CONCLUSION: The carotid plaque CEUS score and blood HCY exhibit a substantial predictive capacity for cerebral infarction in elderly MetS patients. The combined diagnostic efficacy of the two is superior. KEY WORDS: Contrast-enhanced ultrasound, Homocysteine, Elderly, Metabolic syndrome, Cerebral infarction, Carotid plaque.

Downregulated lncRNA UCA1 accelerates proliferation and migration of vascular smooth muscle cells by epigenetic regulation of MMP9.

Function of long non-coding RNA urothelial carcinoma antigen 1 (lncRNA UCA1) in regulating the proliferative and migratory abilities of vascular smooth muscle cells (VSMCs) by mediating matrix metalloproteinase-9 (MMP9) level were elucidated. After treatment with different concentrations of ox-LDL for different time points, lncRNA UCA1 level in VSMCs was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Subcellular distribution of UCA1 was analyzed. Proliferative and migratory abilities of VSMCs transfected with pcDNA-UCA1 were assessed. Protein level of MMP9 in HA-VSMCs treated with different concentrations of ox-LDL for different time points was also determined. The potential interaction between UCA1 and enhancer of zeste homolog 2 (EZH2) was identified by RNA immunoprecipitation (RIP) assay. Recruitment ability of EZH2 to MMP9 promoter region influenced by UCA1 was determined by Chromatin immunoprecipitation (ChIP) assay. Finally, the potential function of MMP9 in UCA1-mediated cellular behavior of VSMCs was explored. UCA1 was time-dependently and dose-dependently upregulated in VSMCs by ox-LDL treatment. Proliferative and migratory abilities of VSMCs were enhanced by treatment of 100 mg/l ox-LDL for 48 h, which were further reduced after transfection of pcDNA-UCA1. Subcellular distribution analysis showed that UCA1 was mainly distributed in the nucleus. Protein level of MMP9 was gradually elevated with the treatment of increased concentrations of ox-LDL in VSMCs. Its level was downregulated by transfection of pcDNA-UCA1 in VSMCs. The interaction between UCA1 and EZH2 was confirmed by RIP assay. Transfection of pcDNA-UCA1 stimulated the binding of EZH2 on MMP9 promoter region. Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1. Downregulated UCA1 accelerates VSMCs to proliferate and migrate through negatively regulating MMP9 level.

The Antithrombotic Effects of Low Molecular Weight Fragment from Enzymatically Modified of Laminaria Japonica Polysaccharide.

BACKGROUND Laminaria japonica polysaccharide (LJP), a fucose enriched sulfated polysaccharide has been demonstrated to have excellent anticoagulant and antithrombotic activities. However, the antithrombotic effect of low molecular weight polysaccharide from enzymatically modified of LJP (LMWEP) remains unknown. MATERIAL AND METHODS LMWEP was prepared by fucoidanase enzymatic hydrolysis, and the antithrombotic and anticoagulant activities, and the underlying mechanism were investigated thoroughly. Rats were randomly divided into 6 groups (8 rats in each group): the blank control group, the blank control group treated with LMWEP (20 mg/kg), the model group, the model group treated with heparin (2 mg/kg), the model group treated with LJP (20 mg/kg), and the model group treated with LMWEP (20 mg/kg). After 7 days of intravenous administration, blood was collected for biochemical parameters examinations. RESULTS LMWEP increased the activated partial thromboplastin time (APTT), thrombin time (TT), prothrombin time (PT), 6-keto prostaglandin F1alpha (6-Keto-PGF1alpha), and endothelial nitric oxide synthase (eNOS). In addition, LMWEP decreased fibrinogen (FIB), endothelin-1 (ET-1), thromboxane B2 (TXB2), erythrocyte sedimentation rate (ESR), and hematocrit (HCT). CONCLUSIONS LMWEP, an enzymatically modified fragment with a molecular weight of 25.8 kDa, is a potential antithrombotic candidate for treatment of thrombosis related diseases.