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Objective To analyze IgG test results of serum SARS-CoV-2 antibody in people after booster vaccinations against SARS-CoV-2, and to provide a basis for the booster vaccination. Methods There were 314 healthy individuals who had been vaccinated with the COVID-19 vaccine. Depending on their inoculation situation, they were divided into three groups:the booster injection group(1 week to 2 months after booster vaccination)of 205 cases, <180 days after two doses group(<180 days after two doses of COVID-19 vaccine)of 49 cases, and >180 days after two doses group(>180 days after two doses of COVID-19 vaccine)of 60 cases. The positive rate of IgG in serum of the three groups was measured using the colloidal gold method. Results The serum COVID-19 antibody IgG positive rates were 83.9% in the booster injection group, 18.4% in the <180 days after two doses group, and 5.0% in the >180 days after two doses group, with statistically significant difference between any two groups(all P < 0.05). In the booster injection group, the serum COVID-19 antibody IgG positive rate was 85.2% in people who received a booster injection more than a month, while those who received a booster injection less than a month had a positive rate of 75.9%, and there was no significant difference between these two groups(P > 0.05). In the booster injection group, the positive rates of serum COVID-19 antibody IgG were 85.1% in males and 82.4% in females, with no significant difference(P > 0.05). In the booster injection group, people at the age of 18 and 50 had a positive serum COVID-19 antibody IgG rate of 86.0%, while those over 50 had a positive rate of 58.3%, and there was significant difference between them(P < 0.05). Conclusions Compared with two injections of the COVID-19 vaccine, the booster injection can significantly increase the positive rate of the antibody IgG of COVID-19, which results in a stronger immune response. There is a lower IgG positive rate of COVID-19 antibodies in those aged over 50 years following the booster dose of COVID-19 vaccine than in those aged 18- 50 years.
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BACKGROUND: Severe sepsis and its subsequent complications cause high morbidity and mortality rates worldwide. The lung is one of the most vulnerable organs sensitive to the sepsis-associated inflammatory storm and usually develops into acute respiratory distress syndrome (ARDS)/acute lung injury (ALI). The pathogenesis of sepsis-associated ALI is accompanied by coordinated transmembrane signal transduction and subsequent programmed cell death; however, the underlying mechanism remains largely unclear. RESULTS: Here we find that the expression of serine incorporator 2 (Serinc2), a protein involved in phosphatidylserine synthesis and membrane incorporation, is upregulated in cecal ligation and puncture (CLP)-induced ALI. Furthermore, the Serinc2-knockout (KO) mouse line is generated by the CRISPR-cas9 approach. Compared with wild-type mice, the Serinc2-KO mice exhibit exacerbated ALI-related pathologies after CLP. The expressions of pro-inflammatory factors, including IL1ß, IL6, TNFα, and MCP1, are significantly enhanced by Serinc2 deficiency, concurrent with over-activation of STAT3, p38 and ERK pathways. Conversely, Serinc2 overexpression in RAW264.7 cells significantly suppresses the inflammatory responses induced by lipopolysaccharide (LPS). Serinc2 KO aggravates CLP-induced apoptosis as evidenced by increases in TUNEL-positive staining, Bax expression, and cleaved caspase-3 and decreases in BCL-2 expression and Akt phosphorylation, whereas these changes are suppressed by Serinc2 overexpression in LPS-treated RAW264.7 cells. Moreover, the administration of AKTin, an inhibitor of Akt, abolishes the protective effects of Serinc2 overexpression against inflammation and apoptosis. CONCLUSIONS: Our findings demonstrate a protective role of Serinc2 in the lung through activating the Akt pathway, and provide novel insight into the pathogenesis of sepsis-induced ALI.
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Objective: To investigate a reasonable threshold d total bilirubin for the diagnosis of hepatitis B virus - related acute - on -chronic liver failure (HBV - ACLF), and to realize accurate early diagnosis.