Anti-SOD2 (aa 119-130) polyclonal antibody

Purpose: This study was aimed at identifying differentially expressed genes (DEGs) in bacterial and fungal keratitis. The candidate genes can be selected and quantified to distinguish between causative agents of infectious keratitis to improve therapeutic outcomes. Methods: The expression profile of bacterial or fungal infection, and normal corneal tissues were downloaded from the Gene Expression Omnibus. The limma package in R was used to screen DEGs in bacterial and fungal keratitis. The Co-Express tool was used to calculate correlation coefficients of co-expressed genes. The "Advanced network merge" function of Cytoscape tool was applied to obtain a fusional co-expression network based on bacterial and fungal keratitis DEGs. Finally, functional enrichment analysis by DAVID software and KEGG analysis by KOBAS of DEGs in fusion network were performed. Results: In total, 451 DEGs in bacterial keratitis and 353 DEGs in fungal keratitis were screened, among which 148 DEGs were found only in bacterial keratitis and 50 DEGs only in fungal keratitis. Besides, 117 co-expressed gene pairs were identified among bacterial keratitis DEGs and 87 pairs among fungal keratitis DEGs. In total, nine biological pathways and seven KEGG pathways were screened by analyzing DEGs in the fusional co-expression network. Conclusion: TLR4 is the representative DEG specific to bacterial keratitis, and SOD2 is the representative DEG specific to fungal keratitis, both of which are promising candidate genes to distinguish between bacterial and fungal keratitis.

The liver is susceptible to drug toxicity due to its vital role in xenobiotic metabolism and elimination. In addition to human leukocyte antigen (HLA) variants, which were previously determined as risk factors for drug-induced liver injury (DILI) due to co-amoxiclav, other non-HLA genes may contribute to hepatotoxicity risk. In this study, the association between DILI due to co-amoxiclav and several non-HLA genes was investigated. Association of variants in candidate genes (SOD2, GPX1, GSTM1, and GSTT1) with DILI due to various drugs was reported previously in other DILI cohorts. This study examined relevance in a co-amoxiclav-DILI cohort. One hundred sixty-five co-amoxiclav DILI cases were recruited from several European countries by two different studies (DILIGEN and iDILIC). A North-East England population group (n = 334) was used as the control group. PCR assays were used to genotype for the GSTM1 and GSTT1 null alleles with TaqMan SNP genotyping assays used for SOD2 (rs4880) and GPX1 (rs1050450). Fisher's exact test was used to assess differences in significance between cases and controls. None of the studied variants (SOD2 rs4880, GPX1 rs1050450, GSTM1 null allele, and GSTT1 null allele) was significantly associated with co-amoxiclav DILI compared with the control group. No significant differences between cases and controls were seen when combined SOD2/GPX1 genotypes and GST genotypes were considered. Despite the possible functional relevance and the previously reported contribution of the selected genes to DILI, our study failed to confirm associations between the selected genes and liver injury induced by co-amoxiclav.