The Corona Virus Disease 2019 (COVID-19) is rapidly spreading throughout the world. Aerosol is a potential transmission route. We conducted the quantitative microbial risk assessment (QMRA) to evaluate the aerosol transmission risk by using the South China Seafood Market as an example. The key processes were integrated, including viral shedding, dispersion, deposition in air, biologic decay, lung deposition, and the infection risk based on the dose–response model. The available hospital bed for COVID-19 treatment per capita (1.17 × 10–3) in Wuhan was adopted as a reference for manageable risk. The median risk of a customer to acquire SARS-CoV-2 infection via the aerosol route after 1 h of exposure in the market with one infected shopkeeper was about 2.23 × 10–5 (95% confidence interval: 1.90 × 10–6 to 2.34 × 10–4). The upper bound could increase and become close to the manageable risk with multiple infected shopkeepers. More detailed risk assessment should be conducted in poorly ventilated markets with multiple infected cases. The uncertainties were mainly due to the limited information on the dose–response relation and the viral shedding which need further studies. The risk rapidly decreased outside the market due to the dilution by ambient air and became below 10–6 at 5 m away from the exit.

Mechanical stimulation and histone deacetylases (HDACs) have essential roles in regulating the osteogenic differentiation of bone marrow stromal cells (BMSCs) and bone formation. However, little is known regarding what regulates HDAC expression and therefore the osteogenic differentiation of BMSCs during osteogenesis. In this study, we investigated whether mechanical loading regulates HDAC expression directly and examined the role of HDACs in mechanical loading-triggered osteogenic differentiation and bone formation. We first studied the microarrays of samples from patients with osteoporosis and found that the NOTCH pathway and skeletal development gene sets were downregulated in the BMSCs of patients with osteoporosis. Then we demonstrated that mechanical stimuli can regulate osteogenesis and bone formation both in vivo and in vitro. NOTCH signaling was upregulated during cyclic mechanical stretch (CMS)-induced osteogenic differentiation, whereas HDAC1 protein expression was downregulated. The perturbation of HDAC1 expression also had a significant effect on matrix mineralization and JAG1-mediated Notch signaling, suggesting that HDAC1 acts as an endogenous attenuator of Notch signaling in the mechanotransduction of BMSCs. Chromatin immunoprecipitation (ChIP) assay results suggest that HDAC1 modulates the CMS-induced histone H3 acetylation level at the JAG1 promoter. More importantly, we found an inhibitory role of Hdac1 in regulating bone formation in response to hindlimb unloading in mice, and pretreatment with an HDAC1 inhibitor partly rescued the osteoporosis caused by mechanical unloading. Our results demonstrate, for the first time, that mechanical stimulation orchestrates genes expression involved in the osteogenic differentiation of BMSCs via the direct regulation of HDAC1, and the therapeutic inhibition of HDAC1 may be an efficient strategy for enhancing bone formation under mechanical stimulation.