Analysis on the Clinical Characteristics of 10 Cases of Asymptomatic SARS-CoV-2 Novel Coronavirus Infection

Objective:To analyze the clinical features of asymptomatic patients infected with the SARS-CoV-2 novel coronavirus.Methods:The clinical data of 10 asymptomatic cases and 12 symptomatic cases of COVID-19 diagnosed during February 2020 to April 2020 was collected and the clinical features of the two groups of patients were compared.Results:10 cases of asymptomatic infection and 12 cases of symptomatic patients were tested positive for the novel coronavirus nucleic acid test.There was no significant difference in gender distribution between the two groups(P>0.05);the average age of patients in the asymptomatic group was lower than that of the symptomatic group(P<0.05),the difference in clinical classification between the two groups was statistically significant(P<0.05);there was no statistically significant difference in the results of chest CT examination involving lung lobes between the two groups(P>0.05),and there was no statistically significant difference in mortality between the two groups(P>0.05).Conclusion:The average age of asymptomatic novel coronavirus infections was lower than that of confirmed cases of COVID-19,mainly among young people.There was no significant difference in clinical classification,mortality and chest CT examination results between symptomatic and asymptomatic cases.

Focal adhesion protein Kindlin-2 regulates bone homeostasis in mice

Our recent studies demonstrate that the focal adhesion protein Kindlin-2 is critical for chondrogenesis and early skeletal development. Here, we show that deleting Kindlin-2 from osteoblasts using the 2.3-kb mouse Col1 a1-Cre transgene minimally impacts bone mass in mice, but deleting Kindlin-2 using the 10-kb mouse Dmp1-Cre transgene, which targets osteocytes and mature osteoblasts, results in striking osteopenia in mice. Kindlin-2 loss reduces the osteoblastic population but increases the osteoclastic and adipocytic populations in the bone microenvironment. Kindlin-2 loss upregulates sclerostin in osteocytes,downregulates β-catenin in osteoblasts, and inhibits osteoblast formation and differentiation in vitro and in vivo. Upregulation ofβ-catenin in the mutant cells reverses the osteopenia induced by Kindlin-2 deficiency. Kindlin-2 loss additionally increases the expression of RANKL in osteocytes and increases osteoclast formation and bone resorption. Kindlin-2 deletion in osteocytes promotes osteoclast formation in osteocyte/bone marrow monocyte cocultures, which is significantly blocked by an anti-RANKLneutralizing antibody. Finally, Kindlin-2 loss increases osteocyte apoptosis and impairs osteocyte spreading and dendrite formation.Thus, we demonstrate an important role of Kindlin-2 in the regulation of bone homeostasis and provide a potential target for the treatment of metabolic bone diseases.