Objective:To investigate the antibody-dependent cell-mediated cytotoxicity (ADCC) in plasma samples from patients with SARS-CoV-2 infection and to evaluate its correlation with antibody titer and neutralizing activity.Methods:A simple method for ADCC detection was established using HEK293T cells expressing SARS-CoV-2 spike (S) protein as target cells and FcγRⅢa-V158-expressing Jurkat cells as effector cells. It was used to analyze the ADCC activity in 38 plasma samples after the ratio of effector cells to target cells was optimized. Plasma-specific antibody was detected by capturing ELISA, which was to capture the C-terminal-tagged recombinant SARS-CoV-2 S protein with an anti-tag antibody. The neutralizing activity in plasma samples was detected using a pseudovirus neutralization assay. Mann-Whitney U test was used for comparison between different groups and non-parametric Spearman correlation test was performed for correlation analysis. Results:The seroconversion rates for antibodies specific for S protein, S1 protein and RBD were all 97.4% (37/38), and the dynamic changes in antibody titers with recovery time showed that antibody titers peaked at 3-4 weeks. Among the plasma samples with neutralizing activity, those with antibody titers >1∶320 had stronger neutralizing activity than the plasma samples with antibody titers <1∶320 [IC 50: 749.6 (396.5-3 772.0) vs 81.4 (11.6-228.4), P<0.01]. ADCC activity was detectable in 86.8% (33/38) of the plasma samples, and its dynamic change with recovery time were consistent with that of specific antibody titer with a peak at 3-4 weeks. Correlation analysis showed ADCC was positively correlated with the titers of antibodies specific for S protein, S1 protein and RBD ( r=0.686, 0.535 and 0.471, all P<0.01). A positive correlation was also found between ADCC and neutralizing activity ( r=0.573, P<0.01). Conclusions:This study established a simple method for the detection of ADCC. Results of this study suggested that SARS-CoV-2 could induce specific ADCC in plasma and the ADCC might be associated with non-neutralizing antibodies. Besides, the activity of ADCC peaked at 3-4 weeks. These findings would be of reference value for clinical treatment with convalescent plasma.

Objective To investigate the expression and significance of the endocrine gland-derived vascular endothelial growth factor (EG-VEGF) and vascular endothelial growth factor(VEGF) in adrenocortical lesions of primary aldosteronism. Methods The expressions of EG-VEGF, and VEGF were detected by immunohistochemistry and real-time fluorescence quantitative PCR in samples of 18 cases of adrenocortical adenoma, 6 adrenocortical hyperplasia, and 8 normal adrenal cortex. The correlation between the expressions of EG-VEGF, VEGF, and clinicopathological parameters was analyzed. Results The expression of EG-VEGF or VEGF in adrenocortical adenomas was higher than that in adrenocortical hyperplasia or normal adrenal cortex ( all P＜0. 05 ), and the expression of EG-VEGF or VEGF between adrenocortical hyperplasia samples and normal adrenal cortex samples was indistinctive. There was no statistically significant correlation between EG-VEGF or VEGF expression and sex, age, blood pressure, serum potassium, plasma renin activity, except in case of serum aldosterone( P＜0.05 ). A positive correlation between EG-VEGF and VEGF ( P＜0. 01 ) was found. Conclusions EG-VEGF and VEGF may play a significant role in the formation and development of adrenocortical tumors in primary aldosteronism.

AIM: To examine the effect of pretreatment with low-concentration of 11, 12-epoxyeicosatrienoic acid(EET) on myocardial ischemia/reperfusion injury in rats. METHODS: After tracheotomy, myocardial ischemia/reperfusion was produced by occlusion and release of the left anterior descending artery(LAD) of the rats. Ischemic preconditioning(IP) was made by two times of ischemia (5 min)/reperfusion (5 min). The experiment was conducted in three groups: control,IP and pretreatment with 11,12-EET(6.24?10 -8 mol/L), and each group was subdivided into two subgroups:A,the rats were subjected to ischemia (10 min)/reperfusion (10 min) and arrhythmias during the whole periods were monitored; The rats in B were subjected to ischemia (60 min)/reperfusion (30 min) and arrhythmias, cardiac funtion and myocardial infarction size were documented. RESULTS: Both IP and pretreatment with 11,12-EET could protect the heart against arrhythmias, cardiac disfunction and myocardial infarction. CONCLUSION: Pretreatment with 11,12-EET had protective effect on myocardium in case of ischemia/reperfusion, which was similar to ischemic preconditioning.