Abstract Background We aimed to clarify high-risk factors for coronavirus disease 2019 (COVID-19) with multivariate analysis and establish a predictive model of disease progression to help clinicians better choose a therapeutic strategy. Methods All consecutive patients with COVID-19 admitted to Fuyang Second People’s Hospital or the Fifth Medical Center of Chinese PLA General Hospital between 20 January and 22 February 2020 were enrolled and their clinical data were retrospectively collected. Multivariate Cox regression was used to identify risk factors associated with progression, which were then were incorporated into a nomogram to establish a novel prediction scoring model. ROC was used to assess the performance of the model. Results Overall, 208 patients were divided into a stable group (n = 168, 80.8%) and a progressive group (n = 40,19.2%) based on whether their conditions worsened during hospitalization. Univariate and multivariate analyses showed that comorbidity, older age, lower lymphocyte count, and higher lactate dehydrogenase at presentation were independent high-risk factors for COVID-19 progression. Incorporating these 4 factors, the nomogram achieved good concordance indexes of .86 (95% confidence interval [CI], .81–.91) and well-fitted calibration curves. A novel scoring model, named as CALL, was established; its area under the ROC was .91 (95% CI, .86–.94). Using a cutoff of 6 points, the positive and negative predictive values were 50.7% (38.9–62.4%) and 98.5% (94.7–99.8%), respectively. Conclusions Using the CALL score model, clinicians can improve the therapeutic effect and reduce the mortality of COVID-19 with more accurate and efficient use of medical resources.

It was also supported by grants from ANRS (Agence Nationale de Recherche sur le Sida et les hépatites virales).

Dexmedetomidine attenuates isoflurane-induced injury in the developing brain, providing neurocognitive protection. Isoflurane-induced injury in vitro appears to be independent of activation of the gamma-amino-butyric-acid type A receptor. If isoflurane-induced neuroapoptosis proves to be a clinical problem, administration of dexmedetomidine may be an important adjunct to prevent isoflurane-induced neurotoxicity.

Although fibroblasts are responsible for the production and deposition of extracellular matrix in renal fibrosis, their origin is controversial. Circulating fibroblast precursors may contribute to the pathogenesis of renal fibrosis, but the signaling mechanisms underlying the recruitment of bone marrow-derived fibroblast precursors into the kidney in response to injury are incompletely understood. Here, in the unilateral ureteral obstruction model of renal fibrosis, tubular epithelial cells upregulated the chemokine CXCL16 in obstructed kidneys, and circulating fibroblast precursors expressed the CXCL16 receptor, CXCR6. Compared with wild-type mice, CXCL16-knockout mice accumulated significantly fewer bone marrow-derived fibroblast precursors in obstructed kidneys. CXCL16-knockout mice also exhibited significantly fewer CD45-, collagen I-, and CXCR6-triple-positive fibroblast precursors in injured kidneys. Furthermore, targeted deletion of CXCL16 inhibited myofibroblast activation, reduced collagen deposition, and suppressed expression of collagen I and fibronectin. In conclusion, CXCL16 contributes to the pathogenesis of renal fibrosis by recruiting bone marrow-derived fibroblast precursors.