Predicting cerebral white matter lesions based on the platelet-to-white blood cell ratio in hypertensive patients.

Hypertension is a common chronic disease affecting many people. White matter lesions (WMLs) are one of the imaging features of cerebrovascular disease. Predicting the possibility of developing syncretic WMLs in patients with hypertension may contribute to the early identification of serious clinical conditions. This study aims to build a model to identify patients who suffered from moderate-to-severe WMLs by using recognized WMLs risk factors including age and history of diabetes and a new factor named platelet-to-white blood cell ratio (PWR). A total of 237 patients were included in this study. The Affiliated ZhongDa Hospital of Southeast University Research Ethics Committee approved this study (Ethics No. 2019ZDSYLL189-P01). We developed a nomogram to predict the risk of syncretic WMLs in patients with hypertension using the above factors. Higher total scores on the nomogram indicated a higher risk of syncretic WMLs. This means older age, smaller PWR, and patients suffering from diabetes contributed to a greater chance for the patient to suffer from syncretic WMLs. We used a decision analysis curve(DCA) to determine the net benefit of the prediction model. The DCA we constructed showed that using our model to decide whether patients suffered from syncretic WMLs or not was better than assuming they all suffered from syncretic WMLs or all WMLs-free. As a result, the area under the curve of our model was 0.787. By integrating PWR, history of diabetes, and age, we could estimate integrated WMLs in hypertensive patients. This study provides a potential tool to identify cerebrovascular disease in patients with hypertension.

Role of ferroptosis in the process of diabetes-induced endothelial dysfunction.

BACKGROUND: Endothelial dysfunction, a hallmark of diabetes, is a critical and initiating contributor to the pathogenesis of diabetic cardiovascular complications. However, the underlying mechanisms are still not fully understood. Ferroptosis is a newly defined regulated cell death driven by cellular metabolism and iron-dependent lipid peroxidation. Although the involvement of ferroptosis in disease pathogenesis has been shown in cancers and degenerative diseases, the participation of ferroptosis in the pathogenesis of diabetic endothelial dysfunction remains unclear. AIM: To examine the role of ferroptosis in diabetes-induced endothelial dysfunction and the underlying mechanisms. METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with high glucose (HG), interleukin-1ß (IL-1ß), and ferroptosis inhibitor, and then the cell viability, reactive oxygen species (ROS), and ferroptosis-related marker protein were tested. To further determine whether the p53-xCT (the substrate-specific subunit of system Xc-)-glutathione (GSH) axis is involved in HG and IL-1ß induced ferroptosis, HUVECs were transiently transfected with p53 small interfering ribonucleic acid or NC small interfering ribonucleic acid and then treated with HG and IL-1ß. Cell viability, ROS, and ferroptosis-related marker protein were then assessed. In addition, we detected the xCT and p53 expression in the aorta of db/db mice. RESULTS: It was found that HG and IL-1ß induced ferroptosis in HUVECs, as evidenced by the protective effect of the ferroptosis inhibitors, Deferoxamine and ferrostatin-1, resulting in increased lipid ROS and decreased cell viability. Mechanistically, activation of the p53-xCT-GSH axis induced by HG and IL-1ß enhanced ferroptosis in HUVECs. In addition, a decrease in xCT and the presence of de-endothelialized areas were observed in the aortic endothelium of db/db mice. CONCLUSION: Ferroptosis is involved in endothelial dysfunction and p53-xCT-GSH axis activation plays a crucial role in endothelial cell ferroptosis and endothelial dysfunction.

Effects of hyperglycaemia and elevated glycosylated haemoglobin on contrast-induced nephropathy after coronary angiography.

In patients undergoing percutaneous coronary intervention after acute myocardial infarction, hyperglycaemia on admission is associated with an increased risk of contrast-induced nephropathy (CIN). However, the effects of hyperglycaemia and elevated glycosylated haemoglobin (HbA1c) on CIN have remained to be fully elucidated. Therefore, a prospective cohort study was performed, comprising 258 patients who underwent coronary angiography between May 2017 and November 2017 at Zhongda Hospital affiliated with Southeast University (Nanjing, China). According to the diagnostic criteria for CIN (increase of serum creatinine by >44.2 µmol/l or by 25% within 48-72 h of using contrast agent), the patients were divided into two groups: CIN (45 cases) and non-CIN (213 cases). For all patients, the baseline data, medical history, laboratory parameters, medication history and intraoperative situation were recorded and assessed using single-factor analysis and multiple logistic regression analysis to analyse the risk factors of CIN. The incidence of CIN in the hyperglycaemia group (blood glucose on admission, >11.1 mmol/l) was 25%, compared with 13.8% in the non-hyperglycaemia group (P=0.026). Furthermore, the incidence of CIN in the elevated HbA1c group (HbA1c on admission, upper limit of normal) was 26.1%, compared with 14.3% in the group without elevated HbA1c (P=0.027). Hyperglycaemia was present on hospital admission in 84 of 258 patients (32.6%). The percentage of patients with elevated HbA1c was 26.7%. Age, estimated glomerular filtration rate, pre-operative blood cholesterol, hyperglycaemia on admission and elevated HbA1c were all identified to be associated with CIN. According to the multivariate logistic regression analysis, hyperglycaemia was an independent predictor of CIN (odds ratio, 2.815; 95% confidence interval, 1.042-4.581; P=0.029). In the acute coronary syndrome (ACS) and diabetes subgroups, hyperglycaemia was significantly associated with CIN. In the ACS subgroup, the incidence of CIN was 38.1%. It was indicated that hyperglycaemia is an independent risk factor for CIN, particularly in patients with ACS or diabetes. Trial registration no. ChiCTR-OOC-17011466.