The limitations of traditional statistical analyses of randomized clinical trials which follow the frequentist inference paradigm have been increasingly noted. This article discusses the Bayesian approach to statistical inference in randomized clinical trials, demonstrating its functioning, utility, and limitations through an examination of current cardiovascular examples. A simplified overview of the mechanics of Bayesian inference and a glossary of the Bayesian terminology is first provided. The duality of the Bayesian approach providing both an evidential calculus based on the likelihood ratio and a belief calculus that incorporates our prior beliefs with the current data is presented. Specific cardiovascular trials are re-analysed with Bayesian methods. It is claimed that the Bayesian approach by providing an enhanced ability to appreciate and model uncertainty leads to an enriched understanding of the strength and quantification of the evidence, of the distinction between statistical and clinical significance, of the within and between trial variability, of subgroup analyses, of the utility of informative priors and of our ability to synthesize and update our knowledge base. Ultimately, it is argued that the Bayesian approach is more intuitive, transparent, permits enhanced data analysis and interpretation, and may lead to improved decision making not only by trialists but also by practicing clinicians, guideline writers, and even expert regulatory advisory consultants.A 65-year-old man developed three-vessel stent thrombosis after percutaneous coronary intervention with aspirin and clopidogrel. Platelet tests revealed clopidogrel resistance, which resolved after changing clopidogrel to ticagrelor. Although routine platelet tests after stenting are not recommended, these tests may be considered to identify the cause of stent thrombosis and modify antiplatelet therapy.Cardiac arrest is common in critically-ill patients with coronavirus disease 2019 (COVID-19) and is associated with poor survival. Simulation is frequently used to evaluate and train code teams with the goal of improving outcomes. All participants engaged in a training on personal protective equipment donning and doffing for suspected or confirmed COVID-19 cases. Thereafter, simulations of in-hospital cardiac-arrest of COVID-19 patients, so-called "protected code blue", were conducted at a quaternary academic center. The primary endpoint was the mean time-to-defibrillation. A total of 114 individuals participated in 33 "protected code blue" simulations over 8 weeks 10 were senior residents, 17 were attending physicians, 86 were nurses and 5 were respiratory therapists. Mean time-to defibrillation was 4.38 minutes. Mean time-to-room-entry, time-to-intubation, time-to-first-chest-compression and time-to-epinephrine were 2.77, 5.74, 6.31 and 6.20 minutes respectively. 92.84% of the 16 criteria evaluating the proper management of a COVID-19 cardiac arrest patient were met. Mean time-to-defibrillation was longer than guidelines-expected time during "protected code blue" simulations. While adherence to the modified advanced cardiovascular life support protocol was high, breaches that carry an additional infectious risk and reduce the efficacy of the resuscitation team were observed.Calcium ions (Ca2+) act as secondary messengers in a plethora of cellular processes and play crucial role in cellular organelle function and homeostasis. The average resting concentration of Ca2+ is nearly 100 nM and in certain cells it can reach up to 1 µM. The high range of Ca2+ concentration across the plasma membrane and intracellular Ca2+ stores demands a well-coordinated maintenance of free Ca2+ via influx, efflux, buffering and storage. Endoplasmic Reticulum (ER) and Mitochondria depend on Ca2+ for their function and also serve as major players in intracellular Ca2+ homeostasis. The ER-mitochondria interplay helps in orchestrating cellular calcium homeostasis to avoid any detrimental effect resulting from Ca2+ overload or depletion. Since Ca2+ plays a central role in many biological processes it is an essential component of the virus-host interactions. The large gradient across membranes enable the viruses to easily modulate this buffered environment to meet their needs. Viruses exploit Ca2+ signaling to establish productive infection and evade the host immune defense. In this review we will detail the interplay between the viruses and cellular & ER-mitochondrial calcium signaling and the significance of these events on viral life cycle and disease pathogenesis.Mitochondrial RNA degradation plays an important role in maintenance of the mitochondria genetic integrity. buy AZD9291 Mitochondrial localization of p53 was observed in non-stressed and stressed cells. p53, as an RNA-binding protein, exerts 3'→5' exoribonuclease activity. The data suggest that in non-stressed cells, mitochondrial matrix-localized p53, with exoribonuclease activity, may play a housekeeping positive role. p53, through restriction the formation of new RNA/DNA hybrid and processing R-loop, might serve as mitochondrial R-loop suppressor. Conversely, stress-induced matrix-p53 decreases the amount of mitochondrial single-stranded RNA transcripts (including polyA- and non-polyA RNAs), thereby leading to the decline in the amount of mitochondria-encoded oxidative phosphorylation components.Epileptogenesis is most commonly associated with neurodegeneration and a bioenergetic defect attributing to the fact that mitochondrial dysfunction plays a key precursor for neuronal death. Mitochondria are the essential organelle of neuronal cells necessary for certain neurophysiological processes like neuronal action potential activity and synaptic transmission. The mitochondrial dysfunction disrupts calcium homeostasis leading to inhibitory interneuron dysfunction and increasing the excitatory postsynaptic potential. In epilepsy, the prolonged repetitive neuronal activity increases the excessive demand for energy and acidosis in the brain further increasing the intracellular calcium causing neuronal death. Similarly, the mitochondrial damage also leads to the decline of energy by dysfunction of the electron transport chain and abnormal production of the ROS triggering the apoptotic neuronal death. Thus, the elevated level of cytosolic calcium causes the mitochondria DNA damage coinciding with mtROS and releasing the cytochrome c binding to Apaf protein further initiating the apoptosis resulting in epileptic encephalopathies.