Extremes of sleep duration and obstructive sleep apnea (OSA) are both associated with hypertension. We aimed to explore whether sleep duration modifies the relationship between OSA and prevalent hypertension, using both objective and subjective measures of total sleep duration. A total of 7107 OSA patients and 1118 primary snorers were included in the study. Hypertension was defined based either on direct blood pressure measures or on diagnosis by a physician. Objective sleep duration was derived by polysomnography and subjective sleep duration was self-reported. Logistic regression models were used to estimate the associations between objective/subjective sleep duration and hypertension prevalence in OSA and primary snorers. Compared with primary snorers, OSA combined with objective sleep duration of 5 to 6 hours increased the odds of hypertension by 45% (odds ratio, 1.45; 95% confidence interval, 1.14-1.84), whereas OSA combined with objective sleep duration <5 hours further increased the odds of hypertension by 80% (odds ratio, 1.80; 95% confidence interval, 1.33-2.42). These results were independent of major confounding factors frequently associated with OSA or hypertension. In stratified analysis by sleep duration, risk of hypertension in those with extremely short sleep (<5 hours) was not significantly different between OSA and primary snorers, whereas odds were significant for OSA in the other 4 sleep duration strata (5-6, 6-7, 7-8, and >8 hours). No significance was evident using subjective sleep duration. We conclude that objective short sleep duration is associated with hypertension in OSA patients. Extremely short sleep duration in itself may actually be even more detrimental than OSA in terms of hypertension risk.

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BackgroundMyocardial fibrosis is a common pathophysiological process that is related to ventricular remodeling in congenital heart disease. However, the presence, characteristics, and clinical significance of myocardial fibrosis in Ebstein’s anomaly have not been fully investigated. This study aimed to evaluate myocardial fibrosis using cardiovascular magnetic resonance (CMR) late gadolinium enhancement (LGE) and T1 mapping techniques, and to explore the significance of myocardial fibrosis in adolescent and adult patients with Ebstein’s anomaly.MethodsForty-four consecutive patients with unrepaired Ebstein’s anomaly (34.0 ± 16.2 years; 18 males), and an equal number of age- and gender-matched controls, were included. A comprehensive CMR protocol consisted of cine, LGE, and T1 mapping by modified Look-Locker inversion recovery (MOLLI) sequences were performed. Ventricular functional parameters, native T1, extracellular volume (ECV), and LGE were analyzed. Associations between myocardial fibrosis and disease severity, ventricular function, and NYHA classification were analyzed.ResultsLGE was found in 10 (22.7%) patients. Typical LGE in Ebstein’s anomaly was located in the endocardium of the septum within the right ventricle (RV). The LV ECV of Ebstein’s anomaly were significantly higher than those of the controls (30.0 ± 3.8% vs. 25.3 ± 2.3%, P < 0.001). An increased ECV was found to be independent of the existence of LGE. Positive LGE or higher ECV (≥30%) was associated with larger fRV volume, aRV volume, increased disease severity, and worse NYHA functional class. In addition, ECV was significantly correlated with the LV ejection fraction (P <  0.001).ConclusionsBoth focal and diffuse myocardial fibrosis were observed in adolescent and adult patients with Ebstein’s anomaly. Increased diffuse fibrosis is associated with worse LV function, increased Ebstein’s severity, and worse clinical status.

Autophagy is prevalent in eukaryotic organisms. Massive research efforts have focused on the mechanism and functionality of autophagy in eukaryotes, for example, their role in human diseases. However, little is known about how this fundamental pathway evolved; in particular, there is an absence of research in prokaryotes.Here, we carried out a comparative genomics analysis among 84 species ranging from eukaryotes to eubacteria and archaebacteria. We found that most of the core proteins in the autophagy pathway were ubiquitous in eukaryotes, whereas the distribution of proteins involved in selective autophagy were limited. In prokaryotes, distant homologs of autophagy-related proteins were also found. Species in Cyanobacteria and Euryarchaeota possess relatively more of these homologs compared to other prokaryotes, which indicated the prokaryotic origin of some autophagyrelated proteins. Phylogenic tree analysis and the distribution of homologs suggested that the presence of proteins involved in autophagosome formation should be an important sign of autophagy. Furthermore, we found that distribution of mitochondrial protein importing-related proteins was quite similar to that of autophagy-related proteins in eukaryotes and that their phylogenic profile was closer to that of several core autophagy proteins compared with 16S/18S ribosomal RNAs, suggesting the engulfment of mitochondria may be the driving force for the evolution of autophagy. Autophagy may have evolved as a quality control system for mitochondria at the very beginning of evolution of eukaryotes. This research shed light on the prokaryotic origin of autophagy and provided a new perspective that mitochondria and autophagy may interplay during the course of eukaryotic evolution.

Bubble formation from a downward‐pointing capillary nozzle was investigated in this study. The experiments were conducted at gas flow rate of 40–5,400 ml/h and inner nozzle radius of 0.030–0.255 mm. Experimental results show that microbubbles are formed continuously at moderate Weber number, which was not reported in pervious investigations with injecting gas through an upward‐pointing capillary nozzle. High‐speed visualization indicates that the formation of microbubbles arises from the convergence of the capillary waves induced by the partial coalescence of larger bubbles. A bubbling regime map is given to identify the critical conditions for the formation of microbubbles. In the present air‐water experiments, the generated microbubbles are 20–170 μm in diameter. From experimental data, a scaling law for microbubble size is proposed as a function of Weber and Bond numbers.