Myotonic dystrophy type 1 (DM1) lacks non-invasive and easy to measure biomarkers, still largely relying on semi-quantitative tests for diagnostic and prognostic purposes. Muscle biopsies provide valuable data, but their use is limited by their invasiveness. microRNA (miRNAs) are small non-coding RNAs regulating gene expression that are also present in biological fluids and may serve as diseases biomarkers. Thus, we tested plasma miRNAs in the blood of 36 DM1 patients and 36 controls. First, a wide miRNA panel was profiled in a patient subset, followed by validation using all recruited subjects. We identified a signature of nine deregulated miRNAs in DM1 patients: eight miRNAs were increased (miR-133a, miR-193b, miR-191, miR-140-3p, miR-454, miR-574, miR-885-5p, miR-886-3p) and one (miR-27b) was decreased. Next, the levels of these miRNAs were used to calculate a "DM1-miRNAs score". We found that both miR-133a levels and DM1-miRNAs score discriminated DM1 from controls significantly and Receiver-Operator Characteristic curves displayed an area under the curve of 0.94 and 0.97, respectively. Interestingly, both miR-133a levels and DM1-miRNAs score displayed an inverse correlation with skeletal muscle strength and displayed higher values in more compromised patients. In conclusion, we identified a characteristic plasma miRNA signature of DM1. Although preliminary, this study indicates miRNAs as potential DM1 humoral biomarkers.
Objective:Recently, many articles reported increased incidence of urinary tract infection (UTI) due to Extended-Spectrum Beta-Lactamase (ESBL)-producing E. coli. No data are available to date regarding patients presenting with complicated upper ESBL-positive E. coli UTI and sepsis. We report the clinical presentation, management, and outcomes in seven cases.Materials and Methods:This prospective study was carried out between January 2008 and September 2011. Follow-ups varied in patients according to their disease presentation and clinical outcomes. All strains were cultured and identified by the Clinical Microbiology Laboratory and were recovered from blood and urine cultures. In-vitro presence of ESBL was confirmed with Clinical and Laboratory Standard Institute double disc method.Results:In the study period, 49 patients needed hospitalization for upper UTI. Overall, in 25 patients (51%), cultures were negative. In the remaining, seven patients (14.3%) presented positive blood and urine-culture for ESBL + E. coli. Of these, four were female and three were male. Their median age was 73 years (range 66-84). The median hospital stay of these patients was 23 days (range 13 to 45 days).Conclusions:The current situation of multiple bacterial antibiotic resistance has become a worrisome issue in UTI. Multi-drug-resistant E. coli can be readily encountered in hospital settings during daily clinical practice, and urologist should act timely. The management of such infections is extremely important for the future, with particular reference to prevention of new antibiotic resistance patterns.
Escherichia coli are developing new drug resistances. Early recognition of patients who harbor MDRO E. coli in their rectum or in the urine could be an important strategy for preventing sepsis. If a patient who has recently undergone transrectal prostate biopsy shows clinical signs of sepsis in the 48 h, a multiresistant E. coli infection must be suspected. The patient must be admitted urgently to the hospital, and carbapenem antibiotic therapy should be started.
Frequent use of carbapenems has contributed to the increase to K. pneumoniae strains resistant to this class of antibiotics (CRKP), causing a problem in the clinical treatment of patients. This investigation reports the epidemiology, genetic diversity, and clinical implication of the resistance to drugs mediated by CRKP in our hospital. A total of 280 K. pneumoniae strains were collected; in particular 98/280 (35%) were CRKP. Sequencing analysis of CRKP isolated strains showed that 9/98 of MBL-producing strains carried the bla VIM-1 gene and 89/98 of the isolates were positive for bla KPC-2. Antimicrobial susceptibility tests revealed a complete resistance to third-generation cephalosporins and a moderate resistance to tigecycline, gentamicin, and fluoroquinolones with percentages of resistance of 61%, 64%, and 98%, respectively. A resistance of 31% was shown towards trimethoprim-sulfamethoxazole. Colistin was the most active agent against CRKP with 99% of susceptibility. Clonality was evaluated by PFGE and MLST: MLST showed the same clonal type, ST258, while PFGE analysis indicated the presence of a major clone, namely, pulsotype A. This finding indicates that the prevalent resistant isolates were genetically related, suggesting that the spread of these genes could be due to clonal dissemination as well as to genetic exchange between different clones.
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