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Background and Aim: Although resting heart rate (RHR) is associated with prevalence and incidence of diabetes, whether it is associated with undiagnosed diabetes is still unclear. We aimed to investigate whether the RHR is associated with the prevalence of undiagnosed diabetes in a large Korean national dataset., Methods and Results: The Korean National Health and Nutrition Examination Survey data from 2008 to 2018 were used. After screening, 51,637 participants were included in this study. The odds ratios and 95% confidence intervals (CIs) for undiagnosed diabetes were calculated using multivariable-adjusted logistic regression analyses. Analyses showed that participants with a RHR of ≥90 bpm showed a 4.00- (95% CI: 2.77-5.77) and 3.21-times (95% CI: 2.01-5.14) higher prevalence of undiagnosed diabetes for men and women, respectively, than those with a RHR of <60 bpm. The linear dose-response analyses showed that each 10-bpm increment in RHR was associated with a 1.39- (95% CI: 1.32-1.48) and 1.28-times (95% CI: 1.19-1.37) higher prevalence of undiagnosed diabetes for men and women, respectively. In the stratified analyses, the positive association between RHR and the prevalence of undiagnosed diabetes was tended to be stronger among those who were younger (age: <40 years) and lean (BMI: <23 kg/m 2 )., Conclusions: Elevated RHR was significantly associated with a higher prevalence of undiagnosed diabetes in Korean men and women, independent of demographic, lifestyle, and medical factors. Accordingly, the value of RHR as a clinical indicator and health marker, especially in reducing the prevalence of undiagnosed diabetes, is suggestible., Competing Interests: Declaration of competing interest The authors declare that they have no conflicts of interest., (Copyright © 2022 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Background: Although epicardial adipose tissue (EAT) volume is associated with increased incidence of coronary artery disease (CAD), its role in myocardial systolic dysfunction is unclear. The present study aimed to identify independent determinants of EAT volume in patients without obstructive CAD, and to evaluate the association between EAT volume (vs other measures of obesity) and myocardial systolic strain analysis., Methods: We prospectively recruited 130 patients without obstructive CAD on contrast-enhanced cardiac computed tomography imaging and normal left ventricular ejection fraction on 3-dimensional (3D) echocardiography. EAT volume was quantified from cardiac computed tomography imaging, and 3D multidirectional (longitudinal, circumferential, radial, and area) strain were measured., Results: The mean EAT volume was 97.5 ± 43.7 cm 3 . In multivariable analysis, measures of obesity (body mass index [P = 0.007] and waist/hip ratio [P = 0.001]) were independently associated with larger EAT volume. EAT volume was correlated with 3D global longitudinal (r = 0.601; P < 0.001), circumferential (r = 0.375; P < 0.001), radial (r = -0.546; P < 0.001), and area (r = 0.558; P < 0.001) strain. In multivariable analyses, epicardial fat volume was the strongest predictor of 3D global longitudinal (standardized β = 0.512; P < 0.001), circumferential (standardized β = 0.242; P = 0.006), radial (standardized β = -0.422; P < 0.001), and area (standardized β = 0.428; P < 0.001) strain. In contrast, other measures of obesity including body mass index and waist/hip ratio were not independent determinants of 3D multidirectional global strain (all P > 0.05)., Conclusions: EAT volume is independently associated with impaired myocardial systolic function despite preserved 3D left ventricular ejection fraction and absence of obstructive CAD, and might play a significant role in the pathophysiology of diabetic, obesity, and metabolic heart disease., (Copyright © 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Vibrio vulnificus, a pathogenic bacterium causing primary septicemia, exhibited cytotoxicity towards Jurkat cells of T-lymphocytes through intracellular reactive oxygen species (ROS) production. Pretreatment of Jurkat T-cells with diphenyleneiodonium chloride (DPI) abolished V. vulnificus-induced ROS generation and bacterial ability to cause cell death. Jurkat T-cells expressing dominant-negative protein of Rac subunit of NADPH oxidase (NOX) did not show increased ROS production and cell death by V. vulnificus. Vibrio vulnificus also triggered phosphorylation of mitogen-activated protein kinases (MAPKs) including p38 and ERK1/2 in Jurkat T-cells. Experiments using inhibitors or small interfering RNAs for each MAPK showed that both MAPKs are involved in V. vulnificus-induced cell death. DPI only blocked the phosphorylation of p38 MAPK in Jurkat T-cells exposed by V. vulnificus. This study demonstrates that V. vulnificus induces death of Jurkat T-cells via ROS-dependent activation of p38 MAPK, and that NOX plays a major role in ROS generation in V. vulnificus-exposed cells.