This work investigated the size distribution of the droplet nuclei and coughed droplets by test subjects. The size distributions of droplet nuclei coughed by test subjects were determined with an aerodynamic particle sizer (APS) and scanning mobility particle sizer (SMPS) system (system 1). Coughed droplets were only sampled with the APS system (system 2). Two different schemes were employed in system 2. Furthermore, the size distribution of coughed droplets of different ages and gender was investigated to identify the effects of age and gender on droplet size distribution. Results indicated the total average size distribution of the droplet nuclei was 0.58-5.42 microm, and 82% of droplet nuclei centered in 0.74-2.12 microm. The entire average size distribution of the coughed droplets was 0.62-15.9 microm, and the average mode size was 8.35 microm. The size distribution of the coughed droplets was multimodal. The size distribution of coughed droplets showed three peaks at approximately 1 microm, 2 microm, and 8 microm. These analytical findings indicate that variation for average droplet size among the three age groups was insignificant (p > 0.1). Moreover, the variation in average droplet size between males and females was also insignificant (p > 0.1). Also, the variation in droplet concentration between males and females was significant (p > 0.1). Droplet nuclei concentrations from male subjects were considerably higher than that from females. Comparison of the droplet concentrations for subjects in different age groups demonstrated that subjects in the 30-50-year age group have the largest droplet concentrations.

Oxidative stress in depression is a prime cause of neurotransmitter metabolism dysfunction in the brain. Acetylcholinesterase (AChE), a key hydrolase in the cholinergic system, directly determines the degradation of neurotransmitters. However, due to the complexity of the brain and lack of appropriate in situ imaging tools, the mechanism underlying the changes in AChE activity in depression remains unclear. Hence, we generated a twophoton fluorescence probe (MCYN) for real-time visualization of AChE with excellent sensitivity and selectivity. AChE can specifically recognize and cleave the carbamic acid ester bond in MCYN, and MCYN emits bright fluorescence at 560 nm by two-photon excitation at 800 nm. By utilizing MCYN to monitor AChE, we discovered a significant increase in AChE activity in the brains of mice with depression phenotypes. Notably, with the assistance of a two-photon fluorescence imaging probe of the superoxide anion radical (O 2•− ), in vivo visualization for the first time revealed the positive correlation between AChE and O 2•− levels associated with depressive behaviors. This finding suggests that oxidative stress may induce AChE overactivation, leading to depression-related behaviors. This work provides a new and rewarding perspective to elucidate the role of oxidative stress regulating AChE in the pathology of depression.

CKD is an independent risk factor for cardiovascular disease (CVD). The accumulation of uremic toxins in CKD induces oxidative stress and endothelial dysfunction. MicroRNA-92a (miR-92a) is induced by oxidative stress in endothelial cells (ECs) and involved in angiogenesis and atherosclerosis. We investigated a role for oxidative stress-responsive miR-92a in CKD. Our study of patients at three clinical sites showed increased serum miR-92a level with decreased kidney function. In cultured ECs, human CKD serum or uremic toxins (such as indoxyl sulfate), compared with non-CKD serum, induced the levels of miR-92a and suppressed the expression of miR-92a targets, including key endothelial-protective molecules. The antioxidant -acetylcysteine inhibited these vasculopathic properties. In rats, adenine-induced CKD associated with increased levels of miR-92a in aortas, serum, and CD144 endothelial microparticles. Furthermore, CD144 microparticles from human uremic serum contained more miR-92a than those from control serum. Additional analysis showed a positive correlation between serum levels of miR-92a and indoxyl sulfate in a cohort of patients with ESRD undergoing hemodialysis. Collectively, our findings suggest that the uremic toxins accumulated in CKD can upregulate miR-92a in ECs, which impairs EC function and predisposes patients to CVD.

We have developed a new fluorescent and photoacoustic dual-mode probe, ER-P, for the detection of ER polarity of liver tissues in normal and diabetic mice.