The role of thoracic CT (computerized tomography) in monitoring disease course of COVID-19 is controversial. The purpose of this study is to investigate the risk factors and predictive value of deterioration on repeatedly performed CT scan during hospitalization. All COVID-19 patients treated in our isolation ward, from January 22, 2020 to February 7, 2020, were reviewed. Patients included were categorized into RD (Radiological Deterioration) group or NRD (No Radiological Deterioration) group according to the manifestation on the CT routinely performed during the hospitalization. All clinical data and CT images were analyzed. Forty three patients were included in our study. All are moderate cases with at least 4 CT scans each. Eighteen (42.9%) patients had radiological deteriorations which were all identified in CT2 (the first CT after admission). Patients in RD group had lower leukocyte count ( P = .003), lymphocyte count ( P = .030), and higher prevalence ( P = .012) of elevated C-reactive protein (CRP) at admission. NRD patients had a lower prevalence of reticulations ( P = .034) on baseline CT (CT1, performed within 2 days before admission) and a longer duration between symptom onset and the time of CT2 ( P < .01). There was no significant difference in hospital stay or fibrotic change on CT4 (follow-up CT scan performed 4 weeks after discharge) between 2 groups. Shorter duration between symptom onset and CT2 time (odds ratio [OR], 0.436; 95% confidence interval: 0.233–0.816; P < .01) and lower leukocyte count in baseline evaluation (OR, 0.316; 95% CI: 0.116–0.859; P < .05) were associated with increased odds of radiological deterioration on CT image during hospitalization. For moderate COVID-19 patients, the value of routinely performed CT during the treatment is limited. We recommend avoiding using CT as a routine monitor in moderate COVID-19 patients.

Hepatocellular carcinoma (HCC) is a kind of malignant tumor derived from hepatocytes and hepatobiliary cells, and its occurrence is prevalent worldwide. Although medical technology is developing rapidly, the therapeutic efficacy of HCC is still poor. Emerging evidence manifests that microRNAs (miRNAs) play a crucial role in various cancers and have been regarded as cancer suppressor gene. However, the regulatory mechanisms mediated by miR-647 involved in HCC remain unclear. Hence, to clarify the regulatory mechanisms mediated by miR-647 in HCC, we studied the independent effects of miR-647 and explored protein tyrosine phosphatase receptor type F (PTPRF) in the constructed HCC cell line (HCV-huh7.5). Thereafter, we used dual-luciferase gene reporting and Western blot to investigate the relationship between PTPRF and miR-647. Furthermore, we studied the mechanism of miR-647 on PTPRF in HCV-huh7.5. We found that miR-647 could not only promote the proliferation and invasion of HCV-huh7.5 cells but also facilitate cell migration, while PTPRF has the opposite effect. Besides, the results of cell function experiment implied that the overexpression of miR-647 or inhibition of PTPFRF remarkably influenced the Erk signaling pathway, which could regulate cell proliferation, migration, and invasion. In addition, the dual luciferase reporting identified PTPRF as a direct target of miR-647. We further demonstrated that miR-647 inhibitor or PTPRF knockdown administration boosted HCV-huh7.5 cell proliferation, migration, and invasion by targeting PTPRF. These findings provided clues for the mechanism of miR-647 in promoting the biology of HCV-huh7.5 cells by inhibiting the expression level of PTPRF.

Unfolded protein response (UPR) plays an important role in the pathogenesis of many liver diseases. BMI1 has a liver protection effect, but whether it participates in the regulation of hepatocyte death through UPR is not well defined. Herein, the endoplasmic reticulum stress model was established by inducing hepatocyte line (MIHA) with tunicamycin (TM, 5 µg/ml). Cell counting kit-8 assay and flow cytometry were used to evaluate the viability and apoptosis of hepatocytes. The expression levels of BMI1, KAT2B, and proteins related to UPR (p-eIF2α, eIF2α, ATF4, and ATF6), NF-κB (p65 and p-p65), apoptosis (cleaved caspase-3, bcl-2, and bax) and necroptosis (p-MLKL and MLKL) were determined by Western blot. The relationship between KAT2B and BMI1 was determined by co-immunoprecipitation and ubiquitination assay. The results showed that TM not only promoted UPR, apoptosis, and necroptosis in hepatocytes but also upregulated the expression levels of BMI1 and KAT2B and activated NF-κB pathway. BAY-117082 reversed the effects of TM on viability, apoptosis, NF-κB pathway, and BMI1 but strengthened the effects of TM on KAT2B/MLKL-mediated necroptosis. BMI1 promoted the ubiquitination of KAT2B, and BMI1 overexpression reversed the effects of TM on viability, apoptosis, and KAT2B/MLKL-mediated necroptosis. In summary, overexpression of BMI1 promotes the ubiquitination of KAT2B to block the MLKL-mediated necroptosis of hepatocytes.