Comparison of the Antibody Responses Following Vaccination with AstraZeneca and Sinopharm.

BACKGROUND: Vaccines are the most effective way to prevent Coronavirus 2 severe acute respiratory syndrome (SARS-CoV-2). OBJECTIVES: To compare the antibody response of healthy individuals vaccinated with either the AstraZeneca (ChAdOx1 nCoV-19) or the Sinopharm (BBIBP-CorV) vaccine, in those who had no prior infection with SARS-CoV-2. METHODS: Thirty seven participants were included, of which 17 were administered the AstraZeneca (ChAdOx1 nCoV-19) vaccine, while 20 were given the Sinopharm (BBIBP-CorV) vaccine. SARS-CoV-2 neutralizing antibody and anti-receptor-binding domain (RBD) IgG levels were checked 4 weeks after giving the first and the second dose of either vaccine using the enzyme-linked immunosorbent assay (ELISA) technique. RESULTS: The AstraZeneca (ChAdOx1 nCoV-19) vaccine exhibited a higher levels of anti-(RBD) IgG compared with the Sinopharm (BBIBP-CorV) in both the first (14.51 µg/ml vs. 1.160 µg/ml) and the second (46.68 µg/ml vs. 11.43 µg/ml) doses. About neutralizing Abs, the titer of the antibody was higher in the AstraZeneca (ChAdOx1 nCoV-19) recipients than in the Sinopharm (BBIBP-CorV) subjects after the first (7.77 µg/ml vs. 1.79 µg/ml, p < 0.0001) and the second dose (10. 36 µg/ml vs. 4.88 µg/ml, p < 0.0001). CONCLUSIONS: Recipients vaccinated with two doses of the AstraZeneca (ChAdOx1 nCoV-19) had superior quantitative antibody levels than Sinopharm (BBIBP-CorV)-vaccinated subjects. These data suggest that a booster dose may be needed for the Sinopharm (BBIBP-CorV) recipients, to control the COVID-19 pandemic.

The role of magnesium in different inflammatory diseases.

Magnesium deficiency (MgD) can cause inflammation in human body. The known mechanisms of inflammation caused by MgD include activation of phagocytic cells, opening of calcium channels, activation of the N-methyl-D-aspartate (NMDA) receptor, and activation of nuclear factor (NF)-κB. In addition, MgD causes systemic stress response through neuroendocrinological pathways. The inflammation caused by MgD can result in pro-atherogenic changes in the metabolism of lipoproteins, endothelial dysfunction, and high blood pressure. Studies suggest that magnesium may play an important role in the pathophysiology of some inflammatory diseases. Several clinical trials and laboratory studies have been done on the functional role of magnesium. In this study, we review some inflammatory diseases, in which the magnesium has a role in their pathophysiology. Among these diseases, diabetes, asthma, preeclampsia, atherosclerosis, heart damage, and rheumatoid arthritis have been highlighted.

Absence of autoantibodies against oral and vascular-related cell lines in the sera of patients with Behcet's disease.

BACKGROUND: Behcet's disease (BD) is an autoinflammatory disease with unclear pathogenesis. The oral and vascular tissue are the main target organs in BD. The role of humoral immunity in pathogenesis of oral and vascular lesions in BD patients has not been well studied. Therefore, the aim of this study was to investigate the presence of autoantibodies in the sera of BD patients using oral and vascular tissue related cell lines. METHODS: Proteins from oral (KB, HGF-1) and vascular (HUVEC) related cell lines as well as C2C12 (a muscle myoblast cell line) were extracted as representatives of oral and vascular tissue antigens and the presence of autoantibodies in BD's sera were investigated using high throughput two dimensional electrophoresis (2DE) and immunoblotting techniques. Sera of other autoimmune diseases (RA and SLE) and normal individuals were used as controls. RESULTS: After silver staining of 2DE gels, 2831, 2195, 1732, and 1839 spots were detectable in the proteome map of HUVEC, KB, HGF-1, and C2C12 cell lines, respectively. The majority of spots were in the pH range of 5 - 8 and the molecular weight range of 14 - 66 Kd. The immunoreactivity of BD, RA, SLE, and normal sera were not different with separated proteins of the cell lines. CONCLUSIONS: According to our results, it seems that humoral immunity is not significantly involved in BD pathogenesis. Therefore, investigation of the role of cellular immunity, especially TH1 and TH17 cells and their cytokine profiles, in the pathogenesis of BD is recommended for future studies.

Bcl-2 associated athanogene-1 overexpression in diffuse large B-cell lymphoma.

BACKGROUND: Apoptosis and cell cycle regulation play an important role in pathogenesis and tumor progression in patients with Diffuse Large B-Cell Lymphoma (DLBCL). Bcl-2 associated athanogene-1 (BAG-1) is an antiapoptotic protein as well as a regulator of cell growth. There is no conclusive evidence about BAG-1 protein expression in this disease. OBJECTIVE: To investigate the expression level of BAG-1 protein in DLBCL. METHODS: Thirty patients diagnosed from 1997-2004, as having DLBCL, were selected. Also 30 normal lymph nodes were included as normal counterparts in this study. BAG-1 expression was determined by immunohistochemical staining in both DLBCL and normal lymph node samples. RESULTS: Of the 30 DLBCLs examined, 100% were positive for nuclear and 83% were positive for cytoplasmic BAG-1 staining. Of the 30 normal lymph nodes investigated, 20% were positive for nuclear and 0% were positive for cytoplasmic BAG-1 staining. Nuclear staining in DLBCL samples was significantly higher than those of normal lymph nodes (100% versus 20%, p <0.001). Besides, cytoplasmic staining in DLBCL samples was significantly higher than those of normal lymph nodes (83% versus 0%, p <0.001). There was no association between BAG-1 staining and patients' overall survival. CONCLUSION: Our data indicated that BAG-1 protein was deregulated in this disease similar to some other malignancies such as breast and colon cancer. Overexpression of BAG-1 in DLBCL suggests that this protein probably plays an important role in the pathogenesis of DLBCL. Besides, higher nuclear BAG-1 staining might be correlated with poor prognosis.