Effect of ultrasound-supported wound debridement in subjects with diabetic foot ulcers: A meta-analysis.

A meta-analysis study to assess the effect of ultrasound-supported wound debridement (USSD) in subjects with diabetic foot ulcer (DFU). A comprehensive literature examination till January 2023 was implemented and 1873 linked studies were appraised. The picked studies contained 577 subjects with DFUs in the studies' baseline, 282 of them were using USSD, 204 were using standard care, and 91 were using a placebo. Odds ratio (OR) in addition to 95% confidence intervals (CIs) were used to calculate the consequence of USSD in subjects with DFUs by the dichotomous styles and a fixed or random effect model. The USSD applied to DFU caused a significantly higher wound healing rate compared with the standard care (OR, 3.08; 95% CI, 1.94-4.88, P < .001) with no heterogeneity (I2  = 0%) and the placebo (OR, 7.61; 95% CI, 3.11-18.63, P = .02) with no heterogeneity (I2  = 0%). The USSD applied to DFUs caused a significantly higher wound healing rate compared with the standard care and the placebo. Though precautions should be taken when commerce with the consequences as all of the picked studies for this meta-analysis was with low sample sizes.

Effect of honey dressing in the management of diabetic foot ulcers: A meta-analysis.

A meta-analysis study to assess the effect of honey dressing (HD) in the management of diabetic foot ulcer (DFU). A comprehensive literature examination till January 2023 was implemented and 1794 linked studies were appraised. The picked studies contained 882 subjects with DFUs were in the picked studies' baseline, 424 of them were using HD, and 458 were using a control. Odds ratio (OR) in addition to 95% confidence intervals (CIs) were used to calculate the consequence of HD in the management of DFUs after DFU by the dichotomous and continuous styles and a fixed or random model. The HD applied to DFUs caused a significantly higher wound healing rate (OR, 2.06; 95% CI, 1.45-2.93, P < .001) and lower wound healing time (MD, -10.42; 95% CI, -16.27- -4.58, P < .001) compared with the control. The HD applied to DFUs caused a significantly higher wound healing rate and lower wound healing time compared with the control. Although precautions should be taken when commerce with the consequences since most of the picked studies for this meta-analysis was with low sample sizes.

Glutamate Transporters GltS, GltP and GltI Are Involved in Escherichia coli Tolerance In Vitro and Pathogenicity in Mouse Urinary Tract Infections.

To verify the roles of GltS, GltP, and GltI in E. coli tolerance and pathogenicity, we quantified and compared the relative abundance of gltS, gltP, and gltI in log-phase and stationary-phase E. coli and constructed their knockout mutant strains in E. coli BW25113 and uropathogenic E. coli (UPEC) separately, followed by analysis of their abilities to tolerate antibiotics and stressors, their capacity for adhesion to and invasion of human bladder epithelial cells, and their survival ability in mouse urinary tracts. Our results showed that gltS, gltP, and gltI transcripts were higher in stationary phase E. coli than in log-phase incubation. Furthermore, deletion of gltS, gltP, and gltI genes in E. coli BW25113 results in decreased tolerance to antibiotics (levofloxacin and ofloxacin) and stressors (acid pH, hyperosmosis, and heat), and loss of gltS, gltP, and gltI in uropathogenic E. coli UTI89 caused attenuated adhesion and invasion in human bladder epithelial cells and markedly reduced survival in mice. The results showed the important roles of the glutamate transporter genes gltI, gltP, and gltS in E. coli tolerance to antibiotics (levofloxacin and ofloxacin) and stressors (acid pH, hyperosmosis, and heat) in vitro and in pathogenicity in mouse urinary tracts and human bladder epithelial cells, as shown by reduced survival and colonization, which improves our understanding of the molecular mechanisms of bacterial tolerance and pathogenicity.

Identification of Novel Genes Involved in Escherichia coli Persistence to Tosufloxacin.

Persisters are metabolically quiescent phenotypic variants of the wild type that are tolerant to cidal antibiotics, and the mechanisms of persister formation and survival are complex and not completely understood. To identify genes involved in persistence to tosufloxacin, which has higher activity against persisters than most other quinolones, we screened the E. coli KEIO mutant library using a different condition from most persister mutant screens (6 h) with a longer exposure of 18 h with tosufloxacin. We identified 18 mutants (acrA, acrB, ddlB, dnaG, gltI, hlpA, lpcA, recG, recN, rfaH, ruvC, surA, tatC, tolQ, uvrD, xseA, and ydfI) that failed to form tosufloxacin tolerant persisters. Among them, gltI, hlpA, ruvC, ddlB, ydfI, and tatC are unique genes involved in E. coli persistence to tosufloxacin which have not been reported before. Furthermore, deletion mutants in genes coding periplasmic proteins (surA, lpcA, hlpA, and gltI) had more defect in persistence to tosufloxacin than the other identified mutants, with surA and lpcA mutants being the most prominent. The "deep" persister phenotype of surA and lpcA mutants was further confirmed both in vitro and in vivo. Compared with the wild type strain E. coli BW25113 in vitro, the persister phenotype of the surA and lpcA mutants was decreased more than 100-1,000-fold in persistence to various antibiotics, acidic, hyperosmotic and heat conditions. In addition, in both stationary phase bacteria and biofilm bacteria infection mouse models, the surA and lpcA mutants had lower survival and persistence than the parent uropathogenic strain UTI89, suggesting that the in vitro identified persister mechanisms (surA and lpcA) are operative and valid for in vivo persistence. Our findings provide new insight into the mechanisms of persister formation and maintenance under tosufloxacin and will likely provide novel therapeutic and vaccine targets for developing more effective treatment and prevention of persistent E. coli infections.