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‘Recurrence’ of coronavirus disease 2019 (COVID-19) has triggered numerous discussions of scholars at home and abroad. A total of 44 recurrent cases of COVID-19 and 32 control cases admitted from 11 February to 29 March 2020 to Guanggu Campus of Tongji Hospital affiliated to Tongji Medical College Huazhong University of Science and Technology were enrolled in this study. All the 44 recurrent cases were classified as mild to moderate when the patients were admitted for the second time. The gender and mean age in both cases (recurrent and control) were similar. At least one concomitant disease was observed in 52.27% recurrent cases and 34.38% control cases. The most prevalent comorbidity among them was hypertension. Fever and cough being the most prevalent clinical symptoms in both cases. On comparing both the cases, recurrent cases had markedly elevated concentrations of alanine aminotransferase (ALT) (P = 0.020) and aspartate aminotransferase (AST) (P = 0.007). Moreover, subgroup analysis showed mild to moderate abnormal concentrations of ALT and AST in recurrent cases. The elevated concentrations of ALT and AST may be recognised as predictive markers for the risk of ‘recurrence’ of COVID-19, which may provide insights into the prevention and control of COVID-19 in the future.

The effects of air temperature and relative humidity (RH) on the drying kinetics of two kinds of flue-cured tobacco strips (C3F and B3F) were studied using a thermogravimetric device in this work. The drying experiments were carried out with drying air temperatures of 60, 70, 80, and 90 °C and RH values of 0, 10, 20, 30, and 40% at a constant airflow. Taking the effect of RH into consideration, a modified Arrhenius-type equation of diffusivity was proposed. In addition, comparing five thin-layer drying models and five equilibrium moisture content models to describe the drying kinetics and the desorption isotherms of tobacco strips, high coefficients of determination (R2) and low reduced Chi-square (χ2) and residual sum of squares (RSS) values indicated that the Logarithmic model and the Modified Oswin model appeared to be the most suitable for predicting the moisture ratio and the moisture desorption relationship of tobacco strips. The effective moisture diffusion coefficient under different temperatures and RHs ranged from 1.68 × 10−11 to 6.81 × 10−11 m2 s−1 for C3F and from 1.62 × 10−11 to 6.68 × 10−11 m2 s−1 for B3F. A modified Arrhenius-type equation with an RH term was found to be effective for describing the drying behavior of two flue-cured tobacco strips, and the activation energy (Ea) values were 34.6 and 35.2 kJ mol−1 for C3F and B3F, respectively.

To investigate the influence of leptin receptor (LEPR) gene K109R polymorphism on the risk of nonalcoholic fatty liver disease (NAFLD) and its interaction with PNPLA3 I148M polymorphism in the Han Chinese population in Qingdao, China.Blood samples were collected from 296 NAFLD patients and 321 healthy controls, and the genotypes of these patients were determined by PCR and genotyping. Related statistical analyses were performed to compare genotypes, alleles, and clinical data between the two groups. Generalized multifactor dimensionality reduction (GMDR) was used to investigate the interaction between LEPR K109R and PNPLA3 I148M genes.The distribution of LEPR K109R genotypes and alleles showed no significant differences between the NAFLD group and the control group (P0.05). PNPLA3 I148M gene polymorphisms were closely associated with the risk of NAFLD, and the risk of NAFLD in G mutant gene carriers was 2.07 times that in patients who did not carry this gene (OR = 2.07, 95% CI 1.423-3.013, P0.001). The joint action of LEPR K109R and PNPLA3 I148M significantly increased the risk of NAFL (OR = 3.393, 95% CI 1.856-6.201, P0.001).In the Han Chinese population in Qingdao, LEPR K109R gene polymorphism is not associated with the risk of NAFLD, but its interaction with PNPLA3 I148M polymorphism can significantly increase the risk of NAFLD.

To investigate the effect of chitooligosaccharide (COS) on hepatic triglyceride (TG) metabolism and related mechanisms.The LO2 cells treated by 1 mmol/L fatty acid were used as model group, the cells treated by 1 mmol/L fatty acid and 0.5 mg/ml COS were used as COS group, and the untreated cells were used as control group. The TG content in cells was measured. RT-PCR and Western blot were used to measure the mRNA and protein expression of sterol regulatory element binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and carnitine palmityl transferase 1A (CPT1A) in each group. Male C57BL/6J mice were randomized into control group, high-fat group, and COS group to receive different treatments. Sixteen weeks later, the liver was harvested for HE and oil red O staining to measure the content of TG in the liver. The t-test or one-way analysis of variance was used for comparison of data between groups, and the SNK method was used for comparison of data between any two groups.The LO2 cells in the model group had an increased number of lipid droplets and an increased TG content, and after COS treatment, the TG content was low. The COS group had significantly lower relative mRNA expression of SREBP-1c and FAS compared with the model group (1.135 ± 0.177 vs 2.322 ± 0.198,F= 60.457,P0.01; 1.226 ± 0.150 vs 1.801 ± 0.159,F= 24.753,P0.01), while compared with the control group, the COS group had significantly higher mRNA expression of CPT1A (1.254 ± 0.156 vs 1.908 ± 0.087,F= 31.734,P0.01). The COS group had significantly lower protein expression of SREBP-1c and FAS than the model group (0.161 ± 0.081 vs 0.351±0.016,F= 188.920,P0.01; 0.332 ± 0.023 vs 1.238 ± 0.051,F= 624.069,P0.01), and significantly higher protein expression of CPT1A than the model group (1.014 ± 0.033 vs 0.561 ± 0.046,F= 193.793,P0.01). COS reduced the TG content in the liver in rats on high-fat diet.COS can reduce the accumulation of TG in the hepatocyte model of nonalcoholic fatty liver disease and in the liver in rats on high-fat diet, and the possible mechanism may be related to inhibiting the expression of SREBP-1c and downstream FAS, reducing the synthesis of TG, increasing the expression of CPT1A, and accelerating the breakdown of TG.