Aims: It remains unknown whether the treatment of hypertension influences the mortality of patients diagnosed with coronavirus disease 2019 (COVID-19). Methods and results: This is a retrospective observational study of all patients admitted with COVID-19 to Huo Shen Shan Hospital. The hospital was dedicated solely to the treatment of COVID-19 in Wuhan, China. Hypertension and the treatments were stratified according to the medical history or medications administrated prior to the infection. Among 2877 hospitalized patients, 29.5% (850/2877) had a history of hypertension. After adjustment for confounders, patients with hypertension had a two-fold increase in the relative risk of mortality as compared with patients without hypertension [4.0% vs. 1.1%, adjusted hazard ratio (HR) 2.12, 95% confidence interval (CI) 1.17–3.82, P = 0.013]. Patients with a history of hypertension but without antihypertensive treatment (n = 140) were associated with a significantly higher risk of mortality compared with those with antihypertensive treatments (n = 730) (7.9% vs. 3.2%, adjusted HR 2.17, 95% CI 1.03–4.57, P = 0.041). The mortality rates were similar between the renin–angiotensin–aldosterone system (RAAS) inhibitor (4/183) and non-RAAS inhibitor (19/527) cohorts (2.2% vs. 3.6%, adjusted HR 0.85, 95% CI 0.28–2.58, P = 0.774). However, in a study-level meta-analysis of four studies, the result showed that patients with RAAS inhibitor use tend to have a lower risk of mortality (relative risk 0.65, 95% CI 0.45–0.94, P = 0.20). Conclusion: While hypertension and the discontinuation of antihypertensive treatment are suspected to be related to increased risk of mortality, in this retrospective observational analysis, we did not detect any harm of RAAS inhibitors in patients infected with COVID-19. However, the results should be considered as exploratory and interpreted cautiously.

Antioxidants have shown great promise in stroke prevention. Diarylheptanoids (also known as diphenylheptanoids) are a small class of plant secondary metabolites that possess antioxidant activity greater than that of α-tocopherol. Curcumin is the best known member and is mainly extracted from turmeric. This study aimed to explore whether curcumin has a preventive effect on stroke. Stroke-prone spontaneously hypertensive rats (SHRsp) were randomly divided into control group (n = 10) and curcumin group (n = 10), and saline or curcumin (100 mg/kg/day) was administrated daily. Vascular endothelial function was examined by the relaxation of the artery in response to acetylcholine (ACH). The levels of reactive oxygen species (ROS) and nitric oxide (NO) were measured by using dihydroethidium (DHE) and 4, 5-diaminofluorescein (DAF-2 DA), respectively. The expression of uncoupling protein 2 (UCP2) was examined by RT-PCR and immunoblotting. Administration of curcumin significantly delayed the onset of stroke and increased the survival of SHRsp, which was ascribed to decreased ROS and improved endothelial dependent relaxation of carotid arteries. In the presence of UCP2 inhibitor genipin, both curcumin-mediated decrease of ROS and increase of NO production were blocked. Our study suggests that curcumin exerts a stroke preventive effect by attenuating oxidative stress to improve vascular endothelial function, which might be associated with UCP2 signaling.

The worldwide epidemic of metabolic diseases, especially obesity and other diseases caused by it, has shown a dramatic increase in incidence. A great deal of attention has been focused on the underlying mechanisms of these pathological processes and potential strategies to solve these problems. Chronic inflammation initiated by abdominal adipose tissues and immune cell activation in obesity is the major cause of the consequent development of complications. In addition to adipocytes, macrophages and monocytes, natural killer (NK) cells have been verified to be vital components involved in shaping the inflammatory microenvironment, thereby leading to various obesity-related metabolic diseases. Here, we provide an overview of the roles of NK cells and the interactions of these cells with other immune and nonimmune cells in the pathological processes of metabolic diseases. Finally, we also discuss potential therapeutic strategies targeting NK cells to treat metabolic diseases.

Objective: Severe or critical patients with coronavirus disease 2019 (COVID-19) are at increased risk for developing acute kidney injury (AKI). However, the rate of AKI in patients of different severities and independent predictive factors associated with AKI are not well understood. Patients and Methods: We enrolled 107 severely or critically ill elderly patients with COVID-19 who were admitted to the intensive care unit (ICU) in Wuhan, China. AKI was defined according to the 2012 KDIGO criteria. We explored the association between AKI and in-hospital mortality using logistic regression. A predictive nomogram was formulated to predict the AKI development of patients with COVID-19 based on multivariate logistic regression. Results: A total of 107 elderly patients were enrolled during the study period. The mean age was 70 (64– 78) years, and 69 (64.5%) were men. For the 107 patients, the degree of severity of COVID-19 was categorized as 37 patients with the severe type (34.6%) and 70 patients with the critical type (65.4%). Overall, 48 of the 107 patients (44.9%) developed AKI during their hospitalization, while AKI occurred in 7 (18.9%) out of the 37 severe patients and 41 (44.9%) out of the 70 critical patients. Of the AKI patients, 35.4% (17/48) required continuous renal replacement therapy, including 14.3% of AKI patients in severe cases and 39.0% of AKI patients in critical cases. Kaplan–Meier analysis demonstrated that patients with AKI had a significantly higher risk for in-hospital mortality than severely and critically ill patients without AKI. Multivariate logistic regression analysis showed that AKI (OR = 33.74; 95% CI = 3.34– 341.29; P = 0.003), septic shock (OR = 15.58; 95% CI = 2.08– 116.78; P = 0.008), invasive mechanical ventilation (OR = 18.44; 95% CI = 2.35– 144.69; P = 0.006), and oxygenation index (OR = 0.99; 95% CI = 0.98– 1.000; P = 0.014) were independent risk factors for in-hospital mortality. A nomogram was established based on the multivariate analysis results. The C-index for the developed AKI model was 0.935 (95% CI, 0.892– 0.978); when 10-fold cross validation was used to validate the model, the corrected C-index was 0.825. Conclusion: AKI is common among COVID-19 patients admitted to the ICU and is recognized as a marker of disease severity. The proposed nomogram accurately predicted AKI development in ICU patients with COVID-19 based on individual characteristics. Therefore, the strategy for kidney protection against severe or critical pneumonia is appropriate.

This study aims to explore the predictive noninvasive biomarker for obstructive coronary artery disease (CAD). By using the data set GSE90074, weighted gene co‐expression network analysis (WGCNA), and protein–protein interactive network, construction of differentially expressed genes in peripheral blood mononuclear cells was conducted to identify the most significant gene clusters associated with obstructive CAD. Univariate and multivariate stepwise logistic regression analyses and receiver operating characteristic analysis were used to predicate the diagnostic accuracy of biomarker candidates in the detection of obstructive CAD. Furthermore, functional prediction of candidate gene biomarkers was further confirmed in ST‐segment elevation myocardial infarction (STEMI) patients or stable CAD patients by using the datasets of GSE62646 and GSE59867. We found that the blue module discriminated by WGCNA contained 13 hub‐genes that could be independent risk factors for obstructive CAD ( P < .05). Among these 13 hub‐genes, a four‐gene signature including neutrophil cytosol factor 2 (NCF2, P = .025), myosin‐If (MYO1F, P = .001), sphingosine‐1‐phosphate receptor 4 (S1PR4, P = .015), and ficolin‐1 (FCN1, P = .012) alone or combined with two risk factors (male sex and hyperlipidemia) may represent potential diagnostic biomarkers in obstructive CAD. Furthermore, the messenger RNA levels of NCF2, MYO1F, S1PR4, and FCN1 were higher in STEMI patients than that in stable CAD patients, although S1PR4 showed no statistical difference ( P > .05). This four‐gene signature could also act as a prognostic biomarker to discriminate STEMI patients from stable CAD patients. These findings suggest a four‐gene signature (NCF2, MYO1F, S1PR4, and FCN1) alone or combined with two risk factors (male sex and hyperlipidemia) as a promising prognostic biomarker in the diagnosis of STEMI. Well‐designed cohort studies should be implemented to warrant the diagnostic value of these genes in clinical purpose.

Obesity plays an important role in the pathogenesis of hypertension. Renal dopamine D1-like receptor-mediated diuresis and natriuresis are impaired in the obese Zucker rat, an obesity-related hypertensive rat model. The role of arterial D1 receptors in the hypertension of obese Zucker rats is not clear.