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Background This study aimed to identify metallo-β-lactamases (MBLs) and AmpC β-lactamases-producing Escherichia coli isolates obtained from hemodialysis (HD) patients with urinary tract infections (UTI). Methods and results A total of 257 HD patients with UTI were included in this study, from which 47 E. coli isolates were collected. Antibiotic susceptibility was tested by disc diffusion method. MBLs and AmpC production were phenotypically detected by imipenem-ethylenediaminetetracetate and cefoxitin/boronic acid assays, respectively. The presence of MBLs and AmpC genes was examined by polymerase chain reaction (PCR). Fosfomycin and ampicillin were the most and the least effective antibiotics against E. coli isolates, respectively. Moreover, 61.7% (29/47) of E. coli isolates were multidrug-resistant with seven different antibiotypes. Antibiotype V (AMP–CIP–IMP–MEM–CPD–CRO–CTX–GEN–LEV–SXT–TOB) was the most prevalent profile. Besides, 24 (51.1%) isolates were simultaneously resistant to imipenem and meropenem. Phenotypic assay showed MBL production in 16 (66.7%) of the 24 carbapenem-resistant E. coli isolates. The distribution of MBL genes in carbapenem-resistant E. coli was as follows: bla IMP 18 (72%), bla VIM 7 (28%), and bla NDM 1 (4%). AmpC was detected in 61.7% (29/47) of the isolates using the phenotypic method. The presence of AmpC genes was confirmed by PCR in only 26 of 29 (86.7%) AmpC producers. The frequencies of bla DHA-1 , bla ACC , and bla CMY-2 were 6 (20.7%), 11 (37.9%), and 21 (72.4%), respectively. Conclusions The emergence of MBL and AmpC coproducing E. coli isolates calls for an urgent surveillance program for timely diagnosis and screening of these genes in our healthcare systems.

Undoubtedly, mesenchymal stem cells (MSCs) are the most common cell therapy candidates in clinical research and therapy. They not only exert considerable therapeutic effects to alleviate inflammation and promote regeneration, but also show low-immunogenicity properties, which ensure their safety following allogeneic transplantation. Thanks to the necessity of providing a sufficient number of MSCs to achieve clinically efficient outcomes, prolonged in vitro cultivation is indisputable. However, either following long-term in vitro expansion or aging in elderly individuals, MSCs face cellular senescence. Senescent MSCs undergo an impairment in their function and therapeutic capacities and secrete degenerative factors which negatively affect young MSCs. To this end, designing novel investigations to further elucidate cellular senescence and to pave the way toward finding new strategies to reverse senescence is highly demanded. In this review, we will concisely discuss current progress on the detailed mechanisms of MSC senescence and various inflicted changes following aging in MSC. We will also shed light on the examined strategies underlying monitoring and reversing senescence in MSCs to bypass the comprised therapeutic efficacy of the senescent MSCs.

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