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Background: In humans, methane (CH4) is exclusively produced by the intestinal microbiota and has been implicated in several conditions including cardiovascular disease. After microbial production of CH4 in the gut, it steadily crosses into the systemic circulation and reaches the lungs where it can be detected in the exhaled breath, as a surrogate measure for intestinal CH4 production. Recent reports have shown an association between CH4 and vagal dysfunction as well as the inhibition of CH4 activity on ileal contractions with atropine, suggesting its action on the parasympathetic nervous system. Given these findings, we hypothesized that CH4 may be affecting resting heart rate (HR) based on the potential effect of CH4 on the vagus nerve. Objectives: Given its possible role in the parasympathetic nervous system, we aimed to study the relationship between breath CH4 and resting HR in humans. Additionally, we performed a longitudinal study analyzing the change in HR and its association with breath CH4 over time. Methods: First, we reviewed 1,126 subjects and compared HR in subjects with detectable and undetectable breath CH4. Second, we performed a post hoc analysis of a randomized control trial to compare the change in HR for those who had an increase in breath CH4 versus those that had a decrease in breath CH4 over 14 weeks. Last, we assessed whether a larger decrease in CH4 is associated with a larger increase in HR over time. Results: In the retrospective cohort, subjects with detectable CH4 had a lower HR compared to those with undetectable CH4 (73.0 ± 0.83 vs. 76.0 ± 0.44 beats/min, p = 0.01). In the post hoc analysis, a decrease in CH4 over time was associated with an increase in HR (median ∆ = 6.5 ± 8.32 beats/min, p = 0.0006). Last, we demonstrated a biological gradient whereby a larger drop in CH4 was associated with a greater increase in HR (R = −0.31, p = 0.03). Conclusion: Our findings suggest a potential role for the microbiome (and specifically CH4 from methanogens) to regulate HR. Considering these findings, mechanistic studies are warranted to further investigate this potential novel microbiome-neurocardiac axis. [ABSTRACT FROM AUTHOR]

Herein, form‐stable phase change material fibrous composite containing nanoparticles was prepared via a single‐step green approach using single‐nozzle electrospinning for the first time. Polyethylene glycol (PEG), polyvinyl alcohol (PVA), and water were used as PCM, polymeric support and safe solvent together with simultaneous formation of nanoparticles. The introduced manner not only is free from applying organic solvents, separate addition, or buying nanoparticles and coaxial electrospinning but also it is easy and cost‐effective to use for different applications. Thermal energy storage capacity of the fabricated samples reached to 135.88 and 136.27 J/g in melting process for the nanofibers and nanofibers with nanoparticles, respectively, which are mostly higher than the reported works. Meanwhile supercooling temperature was decreased for (50% PVA/50% PEG/0.1% AgNO3/1% TiO2) nanofibers compared to the other fabricated composites and the pure PEG. The effects of different weight ratio of polymers in spinning solutions, amount of titanium dioxide nanoparticles and silver nitrate, range of phase change transition and thermal endurance and stability of the samples were further discussed in details. Altogether, this renders a single‐step safe route for producing form‐stable PCM nanofibrous composites and also a broad insight concerning the thermal behavior of such composites for diverse renewable energy applications. [ABSTRACT FROM AUTHOR]

• Mutations of coronaviruses, eg SARS-CoV-2, challenge developing effective antivirals. • Under controlled conditions, narrow-band UVA reduces SARS-CoV-2 viral load in vitro. • Narrow-band UVA intra- and extracellular antiviral effects are variant-independent. • UVA exposure activates canonical pathways, including interferon signaling. Under controlled settings, narrow-band ultraviolet A (UVA) exposure exerts antiviral effects both in vivo and in vitro. The effect is thought to be mediated via direct effect on viral particles and indirectly, by modulation of metabolic pathways of host cells. We aimed to explore the extracellular and intracellular antiviral effects of UVA exposure against Alpha, Beta, and Delta variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Vero E6 kidney normal epithelial cells and human tracheal epithelial cells were infected with Alpha, Beta, and Delta variants in a BSL-3 laboratory. To assess extracellular effects, SARS-CoV-2 variants were directly exposed to a single dose of UVA prior to infection of the host cells (Vero E6 kidney normal epithelial cells and human tracheal epithelial cells) The intracellular effects of UVA were assessed by first infecting the cells with SARS-CoV-2 variants followed by UVA treatment of infected cell monolayers. Efficacy was quantified by both plaque reduction assay and quantitative real-time polymerase chain reaction. Additionally, transcriptomic analysis was performed on exposed Vero E6 cells to assess differentially expressed genes and canonical pathways as compared to controls. SARS-CoV-2 Alpha, Beta and Delta variants are susceptible to UVA exposure prior to infection of Vero E6 cells. Importantly, the UVA-driven reduction in Delta variant load could be reproduced in human primary tracheal cells. Beta and Delta variants load also significantly decreased during Vero E6 cells intracellular experiments. UVA-driven reductions in viral loads ameliorate several host metabolic pathways, including canonical pathways related to viral infection and interferon signaling. Narrow-band UVA exhibits both extracellular effects on SARS-CoV-2 viral particles and intracellular effects on infected cells with SARS-CoV-2. Efficacy appears to be variant independent. [ABSTRACT FROM AUTHOR]