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Matthew Farag,Sophie Riddell,John Daffy,Lih-Ming Wong 대한비뇨의학회 2019 Investigative and Clinical Urology Vol.60 No.1
Purpose: To examine the incidence of infective complications post Transrectal Ultrasound Guided Prostate Biopsy (TRUSPB), after transition to preoperative administration of single dose oral ciprofloxacin. Materials and Methods: A retrospective study of 766 consecutive patients undergoing TRUSPB at St Vincent's Hospital Melbourne (2002–2016). Antibiotic prophylaxis between 2002–2014 consisted of 3 days of perioperative oral norfloxacin±intravenous (IV) antibiotics (Group A, n=687). From November 2014 patients received a single dose of oral 750 mg ciprofloxacin pre-biopsy (Group B, n=79), to align with the American Urological Association (AUA) and a Cochrane Database Systematic Review on Antibiotic Prophylaxis for TRUSPB. Groups were compared for all postoperative complications requiring representation and/or readmission within 30 days of biopsy. Results: In Group A, 10 of 687 patients (1.5%) re-presented with post-procedural fever (temperature >38℃), requiring readmission and IV antibiotic treatment, compared to 4 of the 79 patients (5.1%) in Group B (p=0.02). Positive blood cultures were isolated in 0.9% (n=6, Group A) versus 3.8% (n=3, Group B) (p=0.02). The 4 infectious readmissions in Group B had no prior genitourinary infections, no recent travel and all had a Charlson Comorbidity Index scores <2. Two patients in Group B cultured Escherichia coli sensitive to ciprofloxacin despite receiving preoperative ciprofloxacin. Conclusions: Antibiotic prophylaxis using single dose ciprofloxacin is associated with higher infective complications post TRUSPB. The episodes of ciprofloxacin sensitive E. coli bacteraemia in Group B suggest consideration of a longer course of perioperative antibiotic prophylaxis.
Redox Regulation Facilitates Optimal Peptide Selection by MHC Class I during Antigen Processing
Park, Boyoun,Lee, Sungwook,Kim, Eunkyung,Cho, Kwangmin,Riddell, Stanley R.,Cho, Sunglim,Ahn, Kwangseog Elsevier 2006 Cell Vol.127 No.2
<P><B>Summary</B></P><P>Activated CD8<SUP>+</SUP> T cells discriminate infected and tumor cells from normal self by recognizing MHC class I-bound peptides on the surface of antigen-presenting cells. The mechanism by which MHC class I molecules select optimal peptides against a background of prevailing suboptimal peptides and in a considerably proteolytic ER environment remained unknown. Here, we identify protein disulfide isomerase (PDI), an enzyme critical to the formation of correct disulfide bonds in proteins, as a component of the peptide-loading complex. We show that PDI stabilizes a peptide-receptive site by regulating the oxidation state of the disulfide bond in the MHC peptide-binding groove, a function that is essential for selecting optimal peptides. Furthermore, we demonstrate that human cytomegalovirus US3 protein inhibits CD8<SUP>+</SUP> T cell recognition by mediating PDI degradation, verifying the functional relevance of PDI-catalyzed peptide editing in controlling intracellular pathogens. These results establish a link between thiol-based redox regulation and antigen processing.</P>
Kim, Sungchul,Lee, Sanghyun,Shin, Jinwook,Kim, Youngkyun,Evnouchidou, Irini,Kim, Donghyun,Kim, Young-Kook,Kim, Young-Eui,Ahn, Jin-Hyun,Riddell, Stanley R,Stratikos, Efstratios,Kim, V Narry,Ahn, Kwangs Nature Publishing Group, a division of Macmillan P 2011 NATURE IMMUNOLOGY Vol.12 No.10
Major histocompatibility complex (MHC) class I molecules present peptides on the cell surface to CD8<SUP>+</SUP> T cells, which is critical for the killing of virus-infected or transformed cells. Precursors of MHC class I??presented peptides are trimmed to mature epitopes by the aminopeptidase ERAP1. The US2??US11 genomic region of human cytomegalovirus (HCMV) is dispensable for viral replication and encodes three microRNAs (miRNAs). We show here that HCMV miR-US4-1 specifically downregulated ERAP1 expression during viral infection. Accordingly, the trimming of HCMV-derived peptides was inhibited, which led to less susceptibility of infected cells to HCMV-specific cytotoxic T lymphocytes (CTLs). Our findings identify a previously unknown viral miRNA??based CTL-evasion mechanism that targets a key step in the MHC class I antigen-processing pathway.