Viral contamination on the surfaces of the personal protective equipment among health care professionals working in COVID-19 wards: A single-center prospective, observational study.

OBJECTIVE: To evaluate potential viral contamination on the surfaces of personal protective equipment (PPE) in COVID-19 wards. METHODS: Face shields, gloves, the chest area of PPE and shoe soles were sampled at different time points. The samples were tested for the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by PCR, and the cycle threshold (CT) values were recorded. RESULTS: The positive rate was 74.7% (239/320) for all PPE specimens. The CT values of the samples were ranked in the following order: face shields > chests > gloves > shoe soles (37.08±1.38, 35.48±2.02, 34.17±1.91 and 33.52±3.16, respectively; P for trend < .001). After disinfection, the CT values of shoe soles decreased compared with before disinfection (32.78±3.47 vs. 34.3±2.61, P = .037), whereas no significant effect of disinfection on the CT values of face shields, chests and gloves was observed. After disinfection, the CT values of specimens collected from shoe soles gradually increased; before disinfection, the CT values of shoe sole specimens were all less than 35. CONCLUSIONS: SARS-CoV-2 can attach to the surfaces of the PPE of healthcare professionals in COVID-19 wards, especially the shoe soles and undisinfected gloves. Shoe soles had the highest SARS-CoV-2 loads among all tested PPE items.

CUL4B promotes proliferation and inhibits apoptosis of human osteosarcoma cells.

Cullin 4B (CUL4B) is a component of the Cullin4B-Ring E3 ligase complex (CRL4B) that functions in proteolysis and is implicated in tumorigenesis. Here, we report that CUL4B is associated with tumorigenesis by promoting proliferation and inhibiting apoptosis of human osteosarcoma cells. We performed RNA interference (RNAi) with a lentiviral vector system to silence the CUL4B gene using osteosarcoma SAOS-2 cells. The negative control included the normal target cells infected with the negative control virus whereas the knockdown cells included the normal target cells transfected with the RNAi target virus. We assessed the inhibition resulting from the decreased expression of the CUL4B gene on the proliferation rate of SAOS-2 cells, and also evaluated the cell cycle distribution, apoptosis and clonability. Compared with the negative control, the CUL4B gene expression was significantly inhibited in the SAOS-2 cells at the mRNA and protein levels in the knockdown group (P<0.01). Furthermore, in the knockdown group, the cell proliferation rate and clonability were also significantly inhibited (P<0.01). The apoptosis rate increased significantly (P<0.05). A significant decrease in the number of cells in the G1 phase (P<0.01) and significant increases in the S (P<0.01) and G2 phases (P<0.05) were observed. The silencing of CUL4B gene expression can effectively inhibit osteosarcoma cell proliferation and induce apoptosis. These findings may provide a novel biomarker for the treatment of osteosarcoma.