the novel coronavirus disease 2019 (COVID-19) that emerged in Wuhan city has spread rapidly around the world. The risk for poor outcome dramatically increases once a patient progresses to the severe or critical stage. The present study aims to investigate the risk factors for disease progression in individuals with mild to moderate COVID-19. Methods: We conducted a cohort study that included 1007 individuals with mild to moderate COVID-19 from three hospitals in Wuhan. Clinical characteristics and baseline laboratory findings were collected. Patients were followed up for 28 days for observation of disease progression. The end point was the progression to a more severe disease stage. Results: During a follow up of 28 days, 720 patients (71.50%) had recovered or were symptomatically stable, 222 patients (22.05%) had progressed to severe disease, 22 patients (2.18%) had progressed to the critically ill stage and 43 patients (4.27%) had died. Multivariate Cox proportional hazards models identified that increased age (hazard ratio (HR) 2.56, 95% CI 1.97e3.33), male sex (HR 1.79, 95% CI 1.41 e2.28), presence of hypertension (HR 1.44, 95% CI 1.11e1.88), diabetes (HR 1.82, 95% CI 1.35e2.44), chronic obstructive pulmonary disease (HR 2.01, 95% CI 1.38e2.93) and coronary artery disease (HR 1.83, 95% CI 1.26e2.66) were risk factors for disease progression. History of smoking was protective against disease progression (HR 0.56, 95% CI 0.34e0.91). Elevated procalcitonin (HR 1.72, 95% CI 1.02e2.90), urea nitrogen (HR 1.72, 95% CI 1.21e2.43), a-hydroxybutyrate dehydrogenase (HR 3.02, 95% CI 1.26e7.21) and D-dimer (HR 2.01, 95% CI 1.12e3.58) at baseline were also associated with risk for disease progression. Conclusions: This study identified a panel of risk factors for disease progression in individuals with mild to moderate COVID-19.

Background: Mechanical forces regulate gene expression. The mechanisms are not well understood. Results: A HES-1 site in the promoter of h2-calponin gene is a tension-regulated repressor responsive to Notch signaling. Conclusion: Notch regulation plays a role in the mechanoregulation of h2-calponin. Significance: The findings demonstrated a novel mechanism in the mechanoregulation of h2-calponin gene expression.

Cardiomyocyte-like cells have been reported in thoracic veins of rodents and other mammals, but their differentiation state and relationship to the muscle mass in the heart remain to be characterized. Here we investigated the distribution, ultrastructure, and the expression and developmental regulation of myofilament proteins in mouse and rat pulmonary and azygos venous cardiomyocytes. Tracing cardiomyocytes in transgenic mouse tissues with a lacZ reporter gene driven by cloned rat cardiac troponin T promoter demonstrated scattered distribution of cardiomyocytes discontinuous from the atrial sleeves. The longitudinal axis of venous cardiomyocytes is perpendicular to that of the vessel. These cells contain typical sarcomere structures and intercalated discs as shown in electron microscopic images and express cardiac isoforms of troponin T, troponin I and myosin. The expression of troponin I isoform genes and the alternative splicing of cardiac troponin T in thoracic venous cardiomyocytes are regulated during postnatal development in a precise synchrony with that in the heart. Nonetheless, the patterns of cardiac troponin T splicing in adult rat thoracic venous cardiomyocytes are slightly but clearly distinct from those in the atrial and ventricular muscles. The data indicate that mouse and rat thoracic venous cardiomyocytes residing in extra-cardiac tissue possess a physiologically differentiated state and an intrinsically preset developmental clock, which are apparently independent of the very different hemodynamic environments and functional features of the vessels and heart.

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