Mutations in the gene encoding the main cardiac sodium channel (SCN5A) are the commonest genetic cause of Brugada syndrome (BrS). However, the effect of SCN5A mutations on the outcomes of ventricular fibrillation (VF) and syncope remains uncertain. To clarify this relationship, a meta‐analysis was performed. A comprehensive search was conducted to identify all eligible studies from PubMed, MEDLINE, EBSCO, ProQuest, Science Direct, Clinical Key, and Cochrane database for cohort studies of BrS populations that had been systematically tested for SCN5A mutations. We did meta‐analysis to see the relationship between SCN5A mutations and the occurrence of VF and/or syncope using RevMan 5.3. Five clinical studies met our criteria and included a total of 665 BrS patients. These studies included 45 patients with VF and 178 patients with syncope. We found that in BrS patients with SCN5A mutations the rate of VF event was 30.7% while in patients without mutations was 28.5% (Risk Ratio [RR] = 1.11, [95% CI: 0.61, 2.00], P = 0.73, I
2 = 0%). The occurrence of syncope events was 35.9% in patients with SCN5A mutations and 34.5% in patients without mutations (RR = 1.12, [95% CI: 0.87, 1.45], P = 0.37, I
2 = 39%). Furthermore, the occurrence of combined VF and syncope events were similar between the 2 groups (RR = 1.12, [95% CI: 0.89, 1.42], P = 0.34, I
2 = 11%). BrS patients with SCN5A mutations exhibit a similar risk of future occurence of VF and/or syncope as compared to those without SCN5A mutations.
The reduced number and function of Endothelial Progenitor Cells (EPC) in stable coronary artery disease (SCAD) patients aggravate endothelial dysfunction and inhibit neovascularization, thus leading to atherosclerosis. Garlic is currently believed to increase the number and function of EPCs. Therefore, this in vitro study was conducted to analyse the effect of garlic extract (Allicin) on the proliferation of EPCs in patients with SCAD. Mononuclear cells were isolated from peripheral blood of eight SCAD patients and cultured on CFU-Hill media for three days. Samples were divided into 2 groups: a group treated with Allicin and a control group. The treatment group was then divided into 3 subgroups which received 10, 50, and 100 mg/ml of doses and incubated for 48 hours. EPC proliferation was assessed using MTT Cell Proliferation Assay. Immunohistochemical method of CD34+ were performed for EPC identification. Data was analysed using an independent T test and ANOVA. MTT Assay showed significant increase in EPC proliferation in Allicin group compared to control group (0.2811±0.008 vs 0.194±0.151, p<0.05) and significant improvements were observed in each dose increment. CFU-Hill quantification shows the addition of EPC colony in high-dose Allicin. Immunohistochemical method shows positive CD34+ expression. Allicin increases EPC proliferation dose-dependently from peripheral blood of SCAD patients.
BACKGROUND: The reduced number and function of endothelial progenitor cell (EPC) in stable coronary artery disease (SCAD) patients aggravate endothelial dysfunction and inhibit neovascularization, thus lead to atherosclerosis. Garlic is currently believed to increase the number and function of EPC.
AIM: Therefore, this in vitro study was conducted to analyze the effect of garlic extract (allicin) on the proliferation of EPC in patients with SCAD.
METHODS: Mononuclear cells were isolated from peripheral blood of eight SCAD patients and cultured on colony-forming unit (CFU)-Hill medium for 3 days. Samples were divided into two groups: Group treated with allicin and control group. The treatment group was then divided into three subgroups which received 10, 50, and 100 mg/ml of doses and incubated for 48 h. EPC proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay. Immunohistochemical method of CD34+ was performed for EPC identification. Data were analyzed using independent t-test and ANOVA.
RESULTS: MTT assay showed a significant increase in EPC proliferation in the allicin group compared to the control group (0.2811 ± 0.008 vs. 0.194 ± 0.151, p < 0.05) and significant improvements were observed in each dose increment. CFU-Hill quantification shows the addition of EPC colony in high-dose allicin. Immunohistochemical method shows positive CD34+ expression.
CONCLUSION: Allicin increases EPC proliferation dose-dependently from peripheral blood of SCAD patients.
<p><strong>Aim <br /></strong>The infection of the SARS-CoV-2 virus potentially causes a cytokine storm with elevated IL-6 and IL-1&beta; levels. Statin therapy was common among COVID-19 patients due to their cardiovascular comorbidities. However, the effect of statins on COVID-19 infection is unclear. The aim of this study was to evaluate the impact of statin administration on IL-6 and IL-1&beta; level in peripheral blood mononuclear cells (PBMCs) after SARS-CoV-2 spike protein stimulation.<br /><strong>Methods</strong> <br />The PBMCs were isolated from a hypertensive patient and stimulated by the SARS-CoV-2 subunit S1 spike protein. The<br />PBMCs were then divided into four treatment groups and treated with simvastatin at various doses (10 &micro;M, 25 &micro;M, 50 &micro;M,<br />and control). IL-6 and IL-1&beta; were measured from the supernatant using the ELISA method.<br /><strong>Results</strong> <br />The stimulation of SARS-CoV-2 spike protein in PBMC cell culture statistically increased IL-6 and IL1&beta; expression of 5.2<br />and 35.07 fold, respectively (p&lt;0.05). The expressions of IL-6 and IL-1&beta; were not statistically significant among three simvastatin doses and control.<br /><strong>Conclusion</strong> <br />Statin administration did not have significant effect on IL-6 and IL-1&beta; levels in PBMCs after SARS-CoV-2 spike protein stimulation in this study, a further study is needed.</p>
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