Coronavirus disease 2019 (COVID-19) outbreak, first reported in Wuhan, China, has rapidly swept around the world just within a month, causing global public health emergency. In diagnosis, chest computed tomography (CT) manifestations can supplement parts of limitations of real-time reverse transcription polymerase chain reaction (RT-PCR) assay. Based on a comprehensive literature review and the experience in the frontline, we aim to review the typical and relatively atypical CT manifestations with representative COVID-19 cases at our hospital, and hope to strengthen the recognition of these features with radiologists and help them make a quick and accurate diagnosis.

Background Improved chondrogenic differentiation of mesenchymal stem cells (MSCs) by genetic regulation is a potential method for regenerating articular cartilage. MiR-127-5p has been reported to promote cartilage differentiation of rat bone marrow MSCs (rMSCs); however, the regulatory mechanisms underlying hypoxia-stimulated chondrogenic differentiation remain unknown. Methods rMSCs were induced to undergo chondrogenic differentiation under normoxic or hypoxic conditions. Expression of lncRNA DNM3OS, miR-127-5p, and GREM2 was detected by quantitative real-time PCR. Proteoglycans were detected by Alcian blue staining. Western blot assays were performed to examine the relative levels of GREM2 and chondrogenic differentiation related proteins. Luciferase reporter assays were performed to assess the association among DNM3OS, miR-127-5p, and GREM2. Results MiR-127-5p levels were upregulated, while DNM3OS and GREM2 levels were downregulated in rMSCs induced to undergo chondrogenic differentiation, and those changes were attenuated by hypoxic conditions (1% O2). Further in vitro experiments revealed that downregulation of miR-127-5p reduced the production of proteoglycans and expression of chondrogenic differentiation markers (COL1A1, COL2A1, SOX9, and ACAN) and osteo/chondrogenic markers (BMP-2, p-SMAD1/2). MiR-127-5p overexpression produced the opposite results in rMSCs induced to undergo chondrogenic differentiation under hypoxic conditions. GREM2 was found to be a direct target of miR-127-5p, which was suppressed in rMSCs undergoing chondrogenic differentiation. Moreover, DNM3OS could directly bind to miR-127-5p and inhibit chondrogenic differentiation of rMSCs via regulating GREM2. Conclusions Our study revealed a novel molecular pathway (DNM3OS/miR-127-5p/GREM2) that may be involved in hypoxic chondrogenic differentiation.

In order to explore the rational use of nursing resources in the epidemic situation of COVID-19, we optimized the shift arrangement in COVID-19 isolation area and constructed a reasonable nursing schedule under the condition of limited human resources. Seventy-eight nurses were arranged in COVID-19 isolation area to work for 1 week according to 3 different shifts: 4 + 4 h, 6 h and 6 h (overlapping by 1 h). Through the form of questionnaire, the comprehensive job satisfaction of 3 different models were compared, and the nursing quality and the consumption of protective equipment under 3 different modes were analyzed. The results showed that the comprehensive job satisfaction and nursing quality of nurses in 6 h (overlapping by 1 h) shift mode were better than those in other shift modes, and the consumption of protective equipment was lower.

Purpose This study compared the biomechanics of reinserted pedicle screws using the previous entry point and trajectory with those of correctly inserted pedicle screws. Methods The study used 18 lumbar vertebrae (L1–6) from three fresh calf spines to insert 6.5 × 40-mm pedicle screws. A control screw was inserted correctly along the axis of one pedicle, while an experimental screw was reinserted completely using the previous entry point and trajectory in the other pedicle. The experimental screw was removed after being completely inserted in group A and after 80% of the total trajectory inserted in group B. And the experimental screw was removed after 60% of the total trajectory was reached in group C. The biomechanical values of the pedicle screws were measured. Results There were no significant differences in pedicle screw axial pullout strength between reinserted screws and correct screws in the 3 groups ( P A = 0.463, P B = 0.753, P C = 0.753). Stiffness measurement increased for the reinserted screw compared with that of the control screw. Fracturing was observed between the vertebral body and pedicle. Conclusion Theoretically, a surgeon can remove the pedicle screw when necessary, inspect the trajectory, and reinsert the screw using the previous entry point and trajectory.

Background The therapeutic effects of adipose-derived mesenchymal stem cell (ADSC) transplantation have been demonstrated in several models of central nervous system (CNS) injury and are thought to involve the modulation of the inflammatory response. However, the exact underlying molecular mechanism is poorly understood. Activation of the Jagged1/Notch signaling pathway is thought to involve inflammatory and gliotic events in the CNS. Here, we elucidated the effect of ADSC transplantation on the inflammatory reaction after spinal cord injury (SCI) and the potential mechanism mediated by Jagged1/Notch signaling pathway suppression.Methods Using a mouse model of compression SCI, ADSCs and Jagged1 small interfering RNA (siRNA) were injected into the spinal cord. Locomotor function, spinal cord tissue morphology and the levels of various proteins and transcripts were compared between groups.Results ADSC treatment resulted in significant downregulation of proinflammatory mediator expression and reduced ionized calcium binding adapter molecule 1 (Iba1) and ED1 staining in the injured spinal cord, promoting the survival of neurons. These changes were accompanied by improved functional recovery. The augmentation of the Jagged1/Notch signaling pathway after SCI was suppressed by ADSC transplantation. The inhibition of the Jagged1/Notch signaling pathway by Jagged1 siRNA resulted in a decrease in SCI-induced proinflammatory cytokines as well as the activation of microglia. Furthermore, Jagged1 knockdown suppressed the phosphorylation of JAK/STAT3 following SCI.Conclusion The results of this study demonstrated that the therapeutic effects of ADSCs in SCI mice were partly due to Jagged1/notch signaling pathway inhibition and a subsequent reduction in JAK/STAT3 phosphorylation.