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.

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Depression is intimately linked with oxidative stress. As one of the most reactive and oxidative reactive oxygen species that is overproduced during oxidative stress,t he hydroxyl radical (COH) can cause macromolecular damage and subsequent neurological diseases.However,due to the high reactivity and lowconcentration of COH, precise exploration of COH in brains remains ac hallenge.T he two-photon fluorescence probe MD-B was developed for in situ COH imaging in living systems.T his probe achieves exceptional selectivity towards COH through the one-electron oxidation of 3-methylpyrazolone as an ew specific recognition site.M D-B can be used to map COH in mouse brain, therebyr evealing that increased COH is positively correlated with the severity of depression phenotypes.F urthermore, COH has been shown to inactivate deacetylase SIRT1,therebyleading to the occurrence and development of depression phenotypes.T his work provides anew strategy for the future treatment of depression.Depression as one of the most common and disabling mental disorders,w ith aw orldwide prevalence of approximately 17 %. [1] However,u nderstanding of the pathophysiology of depression is still rudimentary due to its complex aetiology. [2] Previous findings suggest that oxidative stress contributes to the pathogenesis of depression. [3][4][5] Theh ydroxyl radical (COH) is one of the most reactive and oxidative reactive oxygen species (ROS) that is overproduced during oxidative stress. [6] Excess COH leads to irreparable damage to neural cells and potentially even to neurological disease. [7] Therefore,t here is an urgent need to develop an effective means for tracing COH in living brain to define the relationship between depression and COH levels.Recently,f luorescence imaging has become ar obust approach for real-time monitoring of molecular events in living cells and in vivo because of its non-destructive nature and spatiotemporal resolution. [8][9][10] Fluorescent probes have been developed to reveal the biological functions of COH in living cells,i nz ebrafish, and in the abdomens of mice. [11][12][13][14][15][16][17][18][19] Given the very high reactivity and low concentration of COH and the particularly complicated construction of the brain, two-photon (TP) fluorescence imaging is the most appropriate for brain imaging because it provides ah igher signal-tobackground ratio,d eeper tissue imaging, higher spatialtemporal resolution, and less specimen photodamage than one-photon (OP) fluorescence imaging. [20][21][22][23] Molecular fluorescent probes have some appealing performance characteristics in terms of stability,ease of crossing of the blood-brain barrier (BBB), and easy excretion, which is preferable for the TP in situ imaging of COH in the brains of living mice with depression-like behaviours.However,suitable TP fluorescent probes for brain imaging of COH with specificity,h igh sensitivity,and instantaneous response are still scarce.Inspired by the specific one-electron oxidation reaction between COH and 3-methyl-pyrazolone in the...

Detection of circulating tumor cells (CTCs) could be used as a "liquid biopsy" for tracking the spread of cancer. In vitro detection methods based on blood sampling and in vitro CTC capture often suffer from the small sampling volume and sampling error. Here, the in vivo capture of CTCs based on transfusion with a surface-modified vein indwelling needle is proposed. When the needle was applied to transfusion in the vein, the simultaneous capture of CTCs was performed. To investigate the actual capture efficiency of the in vivo capture method, labeled MCF-7 cells were directly injected into the veins of rabbits, wild type mice, and nude mice and could be successfully captured. Two of 5 MCF-7 cells injected into the veins of nude mice were successfully captured. To investigate the CTC capture of mouse tumor model and compare with the in vitro method, mice were subcutaneous inoculated with metastatic 4T1 cells. Seven and 21 days after inoculation, CTCs were captured for the first time using in vivo and in vitro methods, respectively. This predicted that the in vivo method could be more suitable for use of early diagnosis of cancer than the in vitro method. As CTC capture can be performed at the same time as transfusion and does not cause further bodily harm, it would be easily accepted by patients. This efficient, simple, and less damaging method involving the use of a vein indwelling needle could be popularized easily in the clinic.