02; 95% CI 1.44-2.82), having an exaggerated blood pressure response to exercise (OR 1.878; 95% CI 1.39-2.50), mild depression symptoms (OR 2.38; 95% CI 1.68-338), and lower fitness as assessed by 6MWT (OR 5.74; 95% CI 3.18-10.37), even after controlling for age and relevant medications. Pre-frail females were also at increased odds for having CVD risk scores indicating higher risk with the FRS (OR 1.52; 95% CI 1.12-2.05), the RDS (OR 1.60; 95% CI 1.21-2.10) and the CANHEART risk score (OR 3.07; 95% CI 2.04-4.62). These odds were higher when frail females were compared to their robust peers. Frailty and pre-frailty were associated with higher odds of presenting with CVD risk factors as compared to robust females, even after controlling for age.Frailty and pre-frailty were associated with higher odds of presenting with CVD risk factors as compared to robust females, even after controlling for age. Numerous structural studies have already reported volumetric reduction in cerebellum with aging. However, there are still limited studies particularly focusing on analysis of the cerebellar resting state FC in old adults. Even so, the least related studies were unable to include some important cerebellar lobules due to limited cerebellum segmentation methods. The purpose of this study is to explore cognitive function in relation to cerebellar lobular morphometry and cortico-cerebellar connectivity changes in old adults' lifespan by incorporating previously undetected cerebellar lobules. This study includes a sample of 264 old adults subdivided into five cognitively normal age groups (G1 through G5). Cerebellum Segmentation (CERES) software was used to obtain morphometric measures and brain masks of all the 24 cerebellar lobules. We then defined individual lobules as seed regions and mapped the whole-brain to get functional connectivity maps. To analyze age group differences in cortico-cerebellar connectivity and cerebellar lobular volume, we used one way ANOVA and post hoc analysis was performed for multiple comparisons using Bonferroni method. Our results report cerebellar lobular volumetric reduction, disrupted intra-cerebellar connectivity and significant differences in cortico-cerebellar resting state FC across age groups. In addition, our results show that disrupted FC between left Crus-II and right ACC relates to well emotion regulation and cognitive decline and is associated with poor performance on TMT-B and logical memory tests in older adults. Overall, our findings confirm that as humans get older and older, the cerebellar lobular volumes as well as the cortico-cerebellar functional connectivity are affected and hence reduces cognition.Overall, our findings confirm that as humans get older and older, the cerebellar lobular volumes as well as the cortico-cerebellar functional connectivity are affected and hence reduces cognition.Cardiac aging is manifested as unfavorable geometric and functional alterations in heart. The current work was to test whether a ketogenic diet (KD) impacted aging-associated myocardial remodeling and dysfunction in mice and investigate the underlying mechanism. The young and aged male mice were fed with KD or standard chow for four months. Echocardiography results revealed that KD decreased left ventricular end systolic diameter (LVESD) and increased fractional shortening in aged mice. With KD feeding, aged mice exhibited reduced cardiomyocyte cross-sectional area, fibrosis, and mRNA expression of atrial natriuretic peptide (ANP), Col1A1 and alpha smooth muscle actin (α-SMA) in myocardium. KD enhanced activities of superoxide dismutase 2 (SOD2), glutathione peroxidase (GPx) and catalase, and reduced the levels of malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) in myocardium of aged mice. CW069 ic50 KD led to a downregulation of expression of C/EBP homologous protein (CHOP), glucose regulated protein 78 (GRP78), cleaved activated transcription factor 6 (ATF6), and spliced X box-binding protein 1 (XBP-1 s) in myocardium of aged mice. KD in aged mice reduced mitochondrial reactive oxygen species (ROS) formation, enhanced mitochondrial ATP production and mitochondrial membrane potential (MMP), and preserved activity of complex III and electron-coupling capacities between complexes I and III and between complexes II and III in myocardium. Importantly, KD in aged mice promoted autophagic flux, evidenced by reduced protein expression of p62 and enhanced protein expression of lysosome-associated membrane protein-2 (Lamp2) in myocardium. In conclusion, long-time KD intake delayed cardiac aging in male mice, possibly through abating oxidative stress, improving mitochondrial function, and promoting autophagic flux.As the coronavirus 2019 (COVID-19) pandemic marches unrelentingly, more patients with cardiac arrhythmias are emerging due to the effects of the virus on the respiratory and cardiovascular (CV) systems and the systemic inflammation that it incurs, and also as a result of the proarrhythmic effects of COVID-19 pharmacotherapies and other drug interactions and the associated autonomic imbalance that enhance arrhythmogenicity. The most worrisome of all arrhythmogenic mechanisms is the QT prolonging effect of various anti-COVID pharmacotherapies that can lead to polymorphic ventricular tachycardia in the form of torsade des pointes and sudden cardiac death. It is therefore imperative to monitor the QT interval during treatment; however, conventional approaches to such monitoring increase the transmission risk for the staff and strain the health system. Hence, there is dire need for contactless monitoring and telemetry for inpatients, especially those admitted to the intensive care unit, as well as for outpatients needing continued management. In this context, recent technological advances have ushered in a new era in implementing digital health monitoring tools that circumvent these obstacles. All these issues are herein discussed and a large body of recent relevant data are reviewed. Studies have shown that cardiac arrhythmias may occur in up to 44% of patients with severe coronavirus disease 2019 (COVID-19) and has been associated with an increased risk of death. This systematic review and meta-analysis aimed to evaluate the incidence of cardiac arrhythmias in patients with COVID-19 and their implications on patient prognosis. We performed a systematic literature search from PubMed, SCOPUS, Europe PMC, Cochrane Central Databases, and Google Scholar+Preprint Servers. The primary endpoint of the study was poor outcomes including mortality, severe COVID-19, and the need for ICU care. A total of 4 studies including 784 patients were analyzed. The incidence of arrhythmia in patients with COVID-19 was 19% (9-28%; I 91.45). Arrhythmia occurred in 48% (38-57%; I 48.08) of patients with poor outcome and 6% (1-12%; I 85.33%) of patients without poor outcome. Patients with COVID-19 experiencing arrhythmia had an increased risk of poor outcome (RR 7.96 [3.77, 16.81], p<0.001; I 71.1%).