To achieve the zero-carbon-emissions society, it is essential to increase the use of clean and renewable energy. Yet, renewable energy resources present constraints in terms of geographical locations and limited...
We evaluated genetic variation in Middle East respiratory syndrome coronavirus (MERS-CoV) imported to South Korea in 2018 using specimens from a patient and isolates from infected Caco-2 cells. The MERS-CoV strain in this study was genetically similar to a strain isolated in Riyadh, Saudi Arabia, in 2017.
ABSTRACT. Use of porcine tissues has been suggested as a promising solution for severe shortage of transplantable human organs. The immediate hurdle for xenotransplantation is acute immune/inflammatory vascular rejection of the transplant. Because endothelial cells play a key role in the initiation and the amplification of inflammation, alteration of gene expression in human endothelial cells, by various inflammatory stimulators has been studied extensively. However, transcriptional changes induced by human and other inflammatory stimulators in porcine endothelial cells have thus far not been studied. In this study, we treated porcine endothelial cells with human tumor necrosis factor (TNF)-, porcine interferon (IFN)-, H 2 O 2 and lypopolysaccharide (LPS) and profiled transcriptional change at 1 hr, 6 hr and 24 hr, using pig oligonucleotide 13K microarray. We found that mRNA species such as chemokine (C-X-C motif) ligand 6 (CXCL6) and Cathepsin S were significantly induced in porcine endothelial cells, as was previously reported with human endothelial cell. We also found that mRNA species including secreted frizzled-related protein 2 (SFRP2), radical S-adenosyl methionine domain containing 2 (RSAD2), structure specific recognition protein 1 (SSRP1) also were highly overexpressed in porcine endothelial cells. This result shows clues to understand underlying mechanisms of xenotransplantation rejection and the highly responsive porcine genes may serve as novel targets to be regulated for improving the function of grafted porcine donor organs.
Human Leukocyte Antigen (HLA), called human Major Histocompatibility Complex (MHC), performs the crucial function of antigen presentation in human immunity, and correctly matched HLA antigens improves survival and reduces immunological complications. Therefore, a precise HLA typing method is necessary for successful transplantation between donor and recipient. Until now, many methods have been developed for HLA typing, including serological and DNA-based methods. However, these previous methods have been somewhat limited due to their requirements for a large number of samples and complex experimental procedures. To resolve this problem, in this study, we developed rapid genotyping methods for HLA-C using an oligonucleotide microarray. To evaluate the performance of the HLA-C genotyping microarray, we analyzed 50 unrelated Korean individuals. The genotyping results obtained by the oligonucleotide microarray were identical with those of PCR-SBT and PCR-SSPs, at a low-resolution, 2-digit level. Therefore, this microarray method for genotyping HLA constitutes a rapid, simultaneous, and high-throughput method that can be used as an alternative to current methods.
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