The blood Hg level in Korean adults is higher than that in USA and other Western countries, while it is similar to or lower than that in other Asian countries. The blood Hg level is influenced by sociodemographic factors and individual lifestyles including dietary habits. Furthermore, blood Hg is associated with metabolic syndrome, in which Hg exposure may play a role as a possible risk factor for cardiovascular diseases.
In a meta-analysis of three GWAS for susceptibility to Kawasaki disease (KD) conducted in Japan, Korea, and Taiwan and follow-up studies with a total of 11,265 subjects (3428 cases and 7837 controls), a significantly associated SNV in the immunoglobulin heavy variable gene (IGHV) cluster in 14q33.32 was identified (rs4774175; OR = 1.20, P = 6.0 × 10 −9). Investigation of nonsynonymous SNVs of the IGHV cluster in 9335 Japanese subjects identified the C allele of rs6423677, located in IGHV3-66, as the most significant reproducible association (OR = 1.25, P = 6.8 × 10 −10 in 3603 cases and 5731 controls). We observed highly skewed allelic usage of IGHV3-66, wherein the rs6423677 A allele was nearly abolished in the transcripts in peripheral blood mononuclear cells of both KD patients and healthy adults. Association of the highexpression allele with KD strongly indicates some active roles of B-cells or endogenous immunoglobulins in the disease pathogenesis. Considering that significant association of SNVs in the IGHV region with disease susceptibility was previously known only for rheumatic heart disease (RHD), a complication of acute rheumatic fever (ARF), these observations suggest that common B-cell related mechanisms may mediate the symptomology of KD and ARF as well as RHD.
Febrile seizures (FS) are the most common seizures found in pediatric patients. Recently, microRNA (miRNA) have been used as a novel biomarker for the diagnosis of various diseases. This study aims to explore the exosomal miRNA expression profile of the cerebrospinal fluid (CSF) in atypical FS patients. Methods: This is a case-control study including CSF specimens of 41 pediatric patients. The CSF specimens were categorized into FS and a control group. Microarray assays were performed to evaluate the CSF exosomal miRNA expression profile. Quantitative PCR (qPCR) assays were conducted to validate the microarray assay result. Bioinformatic analysis was performed to analyze the result. Results: Thirteen (62%) patients in the FS group experienced complex FS. A total of 96 miRNAs were significantly expressed in the CSF study samples and 95 amongst them, exhibited higher expression in FS than in the control group. Further validation qPCR test indicated that the top 5 highly expressed miRNA (miR-4486, miR-6850-5p, miR-642b-3p, miR-7107-5p, miR-4281) showed same results as in the microarray assay. Bioinformatic analysis identified 455 target genes in the FS group. Conclusion: FS patients displayed higher CSF exosomal miRNA profiles than the control. These altered miRNA profiles appeared to be related to complex FS.
-This study examined whether or not a pretreatment with dehydroepiandrosterone (DHEA) has an effect on indomethacin-induced gastric mucosal damage. The DHEA group, male Sprague-Dawley rats, was administrated with DHEA orally at a dose of 4 mg/day for one week before inducing gastritis with indomethacin (50 mg/kg, p.o.). Histological assay, lipid peroxidation assay, superoxide dismutase (SOD), glutathione peroxidase (GPx) and Catalase activities were determined. Interestingly, it was found that the DHEA pretreatment attenuated the gastric lesion area induced by indomethacin. Rather, the pretreatment with high dose of DHEA led to submucosal edema, leukocyte infiltration in submucosa and mucosal necrosis. The levels of MDA in the DHEA pretreatment were also higher than those in the rats given with vehicle pretreatment. This suggests that the DHEA pretreatment deteriorates severe inflammation in indomethacin-induced gastritis. DHEA supplementation significantly increased SOD activity in the gastric mucosa. However, the catalase and GPx activities were not altered by DHEA. The co-administration of DHEA with an indomethacin might not offer a protective effect against the acute gastritis induced by indomethacin.
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