Purpose: This study aimed to investigate sub-health status (SHS) of people living in China during the Coronavirus disease 2019 (COVID-19) COVID-19 pandemic. COVID-19 is a severe acute respiratory syndrome coronavirus (SARS-CoV) infection-induced acute infectious disease, which is featured by universal susceptibility and strong infectivity, and SHS (a status of low quality health) refers to a status of low-quality health. COVID-19 has gradually developed into a global pandemic, making the public in a high stress situation in physiological, psychological and social states in the short term. Methods: From March 6 to 11, 2020, a large-scale cross-sectional survey was conducted by convenient sampling, and SHS assessment scale was used in the questionnaire. The ordinal logistic regression analysis was used to identify the factors affecting SHS. Results: In this study, 17,078 questionnaires were delivered with 16,820 effective questionnaires collected, and 10,715 subjects (63.7%) were found with SHS, with moderate SHS primarily. Physiological sub-scale scored the highest, followed by psychological and social sub-scales. Ordinal logistic regression analysis indicated that man, only-child, workers and farmers were risk factors of SHS. Protective factors of SHS included living in rural areas and townships, laid-off retirees and education degree. Conclusion It shows many people in China place in a poor health status during COVID-19 pandemic. It is necessary that relevant departments pay more attention to people with poor health such as men, only-child, urban people, workers and farmers, and groups with high education degree during and after pandemic stabilization.

Objective To establish a liver-specific Rbp4 gene knockout mouse model and to explore the effect of liver Rbp4 gene deletion on glucose metabolism.Methods Cre-LoxP technology was used to construct a liver-specific Rbp4 gene knockout mouse model using C57/BL6J and Alb-Cre mice.The genotype of the mice was identified by polymerase chain reaction and agarose gel electrophoresis.Ten 18 week old C57/BL6J male mice were included in the WT group,10 flox homozygous and Alb-Cre negative mice of the same age were included in the experimental control group(Rbp4flox/flox:Cre-),and 10 flox homozygous and Alb-Cre positive mice of the same age were included in the experimental group(Rbp4flox/flox:Cre+).Expression levels of RBP4 protein and mRNA in the liver were verified by Western Blot and quantitative reverse transcription-polymerase chain reaction(qRT-PCR),respectively,and expression levels of Rbp4 mRNA in other tissues were detected by qRT-PCR.Morphological changes in liver tissue were detected by hematoxylin and eosin staining.Blood glucose values were detected in mouse tail vein blood samples using a blood glucose meter,and glucose tolerance and insulin tolerance were determined.Expression levels of the liver glucose metabolism genes phosphoenolpyruvate carboxylase(Pepck)and glucose-6-phosphatase(G6pase)were detected by qRT-PCR.Results Liver-specific Rbp4 knockout mice were successfully bred and identified.RBP4 protein and mRNA levels were significantly decreased in the liver of Rbp4flox/flox:Cre+mice(P＜0.05),but there was no significant difference in the relative expression levels of Rbp4 mRNA in fat,kidney,pancreas,spleen,heart,or muscle tissues among the three groups(P＞0.05).Liver-specific Rbp4 knockout had no significant effect on liver morphology,glucose tolerance,or insulin tolerance(P＞0.05).Pepck mRNA levels in the liver differed significantly among the three groups(P＜0.05),and pairwise comparison showed that liver Pepck mRNA levels were significantly lower in Rbp4flox/flox:Cre+mice compared with levels in Rbp4flox/flox:Cre-mice(P＜0.05).There was no significant difference in liver glucose-6-phosphatase(G6pase)mRNA expression among the three groups(P＞0.05).Conclusions We successfully constructed a liver-specific Rbp4 knockout mouse model.Deletion of Rbp4 in the liver inhibited expression of Pepck mRNA in the liver,thus providing a basis for further exploration of the role of this gene in glucose metabolism in mice.