We described the predictive role of cytokines in fatality of Crimean Congo Hemorrhagic Fever Virus (CCHFV) infection by using daily clinical sera samples. Consequent serum samples of the selected patients in different severity groups and healthy controls were examined by using human cytokine 17-plex assay. We included 12 (23%) mild, 30 (58%) moderate, 10 (19%) severe patients, and 10 healthy volunteers. The mean age of the patients was 52 (sd 15), 52% were female. Forty-six patients (88%) received ribavirin. During disease course, the median levels of IL-6, IL-8, IL-10, IL-10/12, IFN-γ, MCP-1, and MIP-1b were found to be significantly higher among CCHF patients than the healthy controls. Within the first 5 days after onset of disease, among the fatal cases, the median levels of IL-6 and IL-8 were found to be significantly higher than the survived ones (Fig. 3), and MCP-1 was elevated among fatal cases, but statistical significance was not detected. In receiver operating characteristic (ROC) analysis, IL-8 (92%), IL-6 (92%), MCP-1 (79%) were found to be the most significant cytokines in predicting the fatality rates in the early period of the disease (5 days). IL-6 and IL-8 can predict the poor outcome, within the first 5 days of disease course. Elevated IL-6 and IL-8 levels within first 5 days could be used as prognostic markers.
In urinary tract infections, the E. coli ST131 clone seems to be a consistent predictor of treatment failure.
Bloodstream infections caused by Escherichia coli ST131 and ST131 H30-Rx subclones have emerged worldwide. This study was carried out to evaluate the prevalence of the ST131-Rx subclone and characterize the virulence properties of the Rx isolates among the bloodstream E. coli isolates. A total of 297 non-duplicated E. coli bloodstream isolates were studied. Antibiotic susceptibilities were tested using the disc diffusion method. PCR amplification and sequencing was used to identify ST131 and H30-Rx, the virulence gene, the b-lactamase and virotype. Quinolone resistance among bacteraemic E. coli strains was 51 %, and it was 98 % among E. coli ST131 isolates. The ST131 isolates accounted for 16 % (49) of all isolates and all ST131 isolates belonged to the extraintestinal pathogenic E. coli. The proportion of H30 subclone among the ST131 isolates was 98 %, and 75 % of H30 isolates belonged to the H30-Rx subclone. The prevalence of ST131 increased from 13 to 23 % in 4 years; however, there was a decrease in the ratio of H30-Rx infections. CTX-M-15 was detected in 85 % of ST131 and all of the H30-Rx isolates. The virulence genes associated with adhesion, cell protection, iron uptake and toxins ( papA, iha, kpsMTII, iut and sat) were more common in ST131 than in non-ST131 isolates. Most of the ST131 and H30-Rx isolates were of the C virotype. All papA-positive isolates were in virotype C. The E. coli ST131 clone has increased rapidly among bloodstream isolates. However, a decrease in the proportion of the H30-Rx subclone in the quinolone-resistant population suggests the possibility of dissemination of other virulent and quinolone-resistant subclones in hospital settings. INTRODUCTIONEscherichia coli is one of the major causative agents of bloodstream infections (BSI). Management of BSIs caused by E. coli has become complicated due to the emergence of antimicrobial resistance and highly virulent clones Peirano & Pitout, 2014;Rogers et al., 2011). Several studies in the past two decades have reported antimicrobial resistance of E. coli strains against quinolones, cephalosporins and carbapenems (Dhanji et al., 2010;Ló pez-Cerero et al., 2014;Olesen et al., 2013;Wu et al., 2014).Extraintestinal pathogenic E. coli (ExPEC) are strains that carry special virulence factors and usually cause A detailed subST analysis of ST131 isolates is important to understand the ongoing emergence of fluoroquinoloneresistant E. coli. However, there is limited information available on the global distribution, virotypes and METHODSA total of 297 non-duplicated consequential E. coli strains isolated from patients with bloodstream infections at the Baskent University Hospital, Ankara, during a three-year period from 1 January 2010 to 1 July 2013 were included in this study. Susceptibility testing was performed using the disc diffusion method according to the Clinical and Laboratory Standards Institute (CLSI) guidelines (M2-A11) (CLSI, 2010). ESBL production was determined based on the CLSI standards (CLSI, 2010).PCR amplification and sequenci...
Background: The detection rate of clinically significant prostate cancer has improved with the use of multiparametric magnetic resonance imaging (mpMRI).Yet, even with MRI-guided biopsy 15%-35% of high-risk lesions (Prostate Imaging-Reporting and Data System [PI-RADS] 4 and 5) are histologically benign. It is unclear if these false positives are due to diagnostic/sampling errors or pathophysiological alterations. To better understand this, we tested histologically benign PI-RAD 4 and 5 lesions for common malignant epigenetic alterations. Materials and Methods: MRI-guided in-bore biopsy samples were collected from 45 patients with PI-RADS 4 (n = 31) or 5 (n = 14) lesions. Patients had a median clinical follow-up of 3.8 years. High-risk mpMRI patients were grouped based on their histology into biopsy positive for tumor (BPT; n = 28) or biopsy negative for tumor (BNT; n = 17). From these biopsy samples, DNA methylation of well-known tumor suppressor genes (APC, GSTP1, and RARβ2) was quantified.Results: Similar to previous work we observed high rates of promoter methylation at GSTP1 (92.7%), RARβ2 (57.3%), and APC (37.8%) in malignant BPT samples but no methylation in benign TURP chips. Interestingly, similar to the malignant samples the BNT biopsies also had increased methylation at the promoter of GSTP1 (78.8%) and RARβ2 (34.6%). However, despite these epigenetic alterations none of these BNT patients developed prostate cancer, and those who underwent repeat mpMRI (n = 8) demonstrated either radiological regression or stability.Conclusions: Histologically benign PI-RADS 4 and 5 lesions harbor prostate cancerassociated epigenetic alterations.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.