Influence of Lifestyles on Mild Cognitive Impairment: A Decision Tree Model Study.

OBJECTIVE: To explore the effects of different lifestyle choices on mild cognitive impairment (MCI) and to establish a decision tree model to analyse their predictive significance on the incidence of MCI. METHODS: Study participants were recruited from geriatric and physical examination centres from October 2015 to October 2019: 330 MCI patients and 295 normal cognitive (NC) patients. Cognitive function was evaluated by the Mini-Mental State Examination Scale (MMSE) and Clinical Dementia Scale (CDR), while the Barthel Index (BI) was used to evaluate life ability. Statistical analysis included the χ 2 test, logistic regression, and decision tree. The ROC curve was drawn to evaluate the predictive ability of the decision tree model. RESULTS: Logistic regression analysis showed that low education, living alone, smoking, and a high-fat diet were risk factors for MCI, while young age, tea drinking, afternoon naps, social engagement, and hobbies were protective factors for MCI. Social engagement, a high-fat diet, hobbies, living condition, tea drinking, and smoking entered all nodes of the decision tree model, with social engagement as the root node variable. The importance of predictive variables in the decision tree model showed social engagement, a high-fat diet, tea drinking, hobbies, living condition, and smoking as 33.57%, 27.74%, 22.14%, 11.94%, 4.61%, and 0%, respectively. The area under the ROC curve predicted by the decision tree model was 0.827 (95% CI: 0.795~0.856). CONCLUSION: The decision tree model has good predictive ability. MCI was closely related to lifestyle; social engagement was the most important factor in predicting the occurrence of MCI.

Alginate oligosaccharide protects endothelial cells against oxidative stress injury via integrin-α/FAK/PI3K signaling.

Alginate oligosaccharide (AOS) was reported to possess antioxidant and free radical scavenging activities, but the specific effects and mechanisms remain unclear. We investigated the effects of AOS on H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells (HUVECs) and the associated mechanisms. HUVECs were treated with 100-800 µM hydrogen peroxide (H2O2) for various periods (12, 24, and 36 h) to establish an in vitro oxidative stress and apoptosis HUVEC model. AOS protects HUVEC cells against oxidative stress-induced apoptosis by decreasing the expression levels of caspase 3 and Bax, and increasing Bcl-2 expression. Microarray assay, real-time PCR and western blot results revealed that AOS was able to effectively suppress H2O2-induced apoptosis via regulated integrin-α/FAK/PI3K pathway by influencing the expression of integrin-α, FAK, PI3K, PTEN, P21, and CDK2. In conclusion, our study suggests that AOS can protect endothelial cells against oxidative stress injury caused by H2O2, providing novel alternative strategies to prevent atherosclerosis in the future.

Cyanidin-3-O-glucoside attenuates endothelial cell dysfunction by modulating miR-204-5p/SIRT1-mediated inflammation and apoptosis.

Endothelial cell (EC) dysfunction is a major symptom associated with the initiation of atherosclerosis (AS). Cyanidin-3-O-glucoside (C3G) has the potentials to attenuate AS symptoms. In the current study, the mechanism driving the effects of C3G on AS rabbits and injured ECs were explored by focusing on the changes in miR-204-5p/SIRT1 axis. AS symptoms were induced in rabbits using high-fatty diet (HFD) plus balloon catheter injured method and handled with C3G of two doses. Then the changes in artery wall structure, hemodynamics parameters, blood lipid level, systemic inflammation, and miR-204-5p/SIRT1 axis were detected. EC dysfunction was imitated by subjecting human umbilical vein endothelial cells (HUVECs) to TNF-α, which was then handled with C3G. The changes in apoptosis, inflammation, and miR-204-5p/SIRT1 axis were detected. The results showed that the administrations of C3G improved artery wall structure and hemodynamics parameters, decreased blood lipid levels, and suppressed pro-inflammatory cytokine production in HFD rabbits, which was associated with the down-regulation of miR-204-5p and the up-regulation of SIRT1. In in vitro assays, the treatments of C3G suppressed apoptosis, inhibited inflammation, down-regulated miR-204-5p level, and induced SIRT1 level in HUVECs. The overexpression of miR-204-5p impaired the protective effects of C3G on the injured HUVECs by increasing cell apoptosis and inflammation. The findings outlined in the current study confirmed the protective effects of C3G on EC function, which was associated with the down-regulation of miR-204-5p and the up-regulation of SIRT1.

Errata: Polysaccharides from Enteromorpha Prolifera Ameliorate Acute Myocardial Infarction in Vitro and in Vivo via Up-Regulating HIF-1α.

An error appeared in the article entitled "Polysaccharides from Enteromorpha Prolifera Ameliorate Acute Myocardial Infarction in Vitro and in Vivo via Up-Regulating HIF-1α" by Zongqiu Wang, Zhihua Zhang, Jing Zhao, Chunming Yong, and Yongjun Mao (Vol. 60, No. 4, 964-973, 2019).The second affiliation of the authors on the bottom of page 964 should be replaced by "2Department of Vascular Surgery, The Affiliated Central Hospital of Qingdao University, Qingdao, China".

Polysaccharides from Enteromorpha Prolifera Ameliorate Acute Myocardial Infarction in Vitro and in Vivo via Up-Regulating HIF-1α.

Acute myocardial infarction (AMI) is a serious heart disease and the main reason for heart failure and sudden death worldwide. This study investigated the effects of polysaccharides from Enteromorpha prolifera (PEP) on AMI in vitro and in vivo, as well as the underlying mechanisms.Human cardiac microvascular endothelial cells (HCMVEC) were cultured in vitro in an oxygen-glucose deprivation (OGD) environment to induce injury. The viability and apoptosis of HCMVEC were then detected using CCK-8 assay and Annexin V-FITC/PI staining, respectively. ELISA was performed to measure the concentrations of inflammatory cytokines. Cell transfection was conducted to reduce the expression of HIF-1α. Expression of key factors involving in cell proliferation, apoptosis, autophagy, MEK/ERK, and the NF-κB and mTOR pathways were evaluated using Western blotting. In vivo, Wistar rats were pre-treated by PEP and AMI was induced. The infarct size and cardiac functions (LVEDD, LVEF and LVFS) were measured.In vitro, PEP treatment significantly protected HCMVEC from OGD-induced viability loss, proliferation inhibition, apoptosis, inflammatory cytokine expression, and autophagy. Moreover, PEP enhanced the expression of HIF-1α in HCMVEC via the MEK/ERK pathway. HIF-1α participated in the protective effects of PEP on OGD-treated HCMVEC. Furthermore, PEP attenuated OGD-induced NF-κB pathway activation and promoted the mTOR pathway in HCMVEC. In vivo, PEP pre-treatment reduced the infarct size and enhanced the LVEDD, LVEF and LVFS of rats via up-regulation of HIF-1α.PEP ameliorated AMI in vitro and in vivo through up-regulation of HIF-1α. In vitro, PEP could activate the MEK/ERK and mTOR pathways, but inactivate the NF-κB pathway in OGD-treated HCMVEC.