Realism-based assessment of the efficacy of potassium peroxymonosulphate on Stenotrophomonas maltophilia biofilm control.

The potential of pentapotassium bis(peroxymonosulphate) bis(sulphate) (OXONE) to control biofilms in drinking water distribution systems (DWDS) was evaluated and compared to chlorine disinfection. Mature biofilms of drinking water (DW)-isolated Stenotrophomonas maltophilia were formed using a simulated DWDS with a rotating cylinder reactor (RCR). After 30 min of exposure, OXONE at 10 × minimum bactericidal concentration (MBC) caused a significant 4 log reduction of biofilm culturability in comparison to the unexposed biofilms and a decrease in the number of non-damaged cells below the detection limit (4.8 log cells/cm2). The effects of free chlorine were restricted to approximately 1 log reduction in both biofilm culturability and non-damaged cells. OXONE in synthetic tap water (STW) at 25 ºC was more stable over 40 days than free chlorine in the same conditions. OXONE solution exhibited a disinfectant decrease of about 10% of the initial concentration during the first 9 days, and after this time the values remained stable. Whereas possible reaction of chlorine with inorganic and organic substances in STW contributed to free chlorine depletion of approximately 48% of the initial concentration. Electron paramagnetic resonance (EPR) spectroscopy studies confirmed the presence of singlet oxygen and other free radicals during S. maltophilia disinfection with OXONE. Overall, OXONE constitutes a relevant alternative to conventional DW disinfection for effective biofilm control in DWDS.

Performance of Graphene/Polydimethylsiloxane Surfaces against S. aureus and P. aeruginosa Single- and Dual-Species Biofilms.

The increasing incidence of implant-associated infections has prompted the development of effective strategies to prevent biofilm formation on these devices. In this work, pristine graphene nanoplatelet/polydimethylsiloxane (GNP/PDMS) surfaces containing different GNP loadings (1, 2, 3, 4, and 5 wt%) were produced and evaluated on their ability to mitigate biofilm development. After GNP loading optimization, the most promising surface was tested against single- and dual-species biofilms of Staphylococcus aureus and Pseudomonas aeruginosa. The antibiofilm activity of GNP/PDMS surfaces was determined by the quantification of total, viable, culturable, and viable but nonculturable (VBNC) cells, as well as by confocal laser scanning microscopy (CLSM). Results showed that 5 wt% GNP loading reduced the number of total (57%), viable (69%), culturable (55%), and VBNC cells (85%) of S. aureus biofilms compared to PDMS. A decrease of 25% in total cells and about 52% in viable, culturable, and VBNC cells was observed for P. aeruginosa biofilms. Dual-species biofilms demonstrated higher resistance to the antimicrobial activity of GNP surfaces, with lower biofilm cell reductions (of up to 29% when compared to single-species biofilms). Still, the effectiveness of these surfaces in suppressing single- and dual-species biofilm formation was confirmed by CLSM analysis, where a decrease in biofilm biovolume (83% for S. aureus biofilms and 42% for P. aeruginosa and dual-species biofilms) and thickness (on average 72%) was obtained. Overall, these results showed that pristine GNPs dispersed into the PDMS matrix were able to inhibit biofilm growth, being a starting point for the fabrication of novel surface coatings based on functionalized GNP/PDMS composites.

Aggregation behavior of aqueous dioctadecyldimethylammonium bromide/monoolein mixtures: a multitechnique investigation on the influence of composition and temperature.

A recently described non-viral gene delivery system [dioctadecyldimethylammonium bromide (DODAB)/monoolein (MO)] has been studied in detail to improve knowledge on the interactions between lamellar (DODAB) and non-lamellar-forming (MO) lipids, as a means to enhance their final cell transfection efficiency. Indeed, the morphology, fluidity, and size of these cationic surfactant/neutral lipid mixtures play an important role in the ability of these systems to complex nucleic acids. The different techniques used in this work, namely dynamic light scattering (DLS), fluorescence spectroscopy, differential scanning calorimetry (DSC), cryogenic transmission electron microscopy (cryo-TEM), light microscopy (LM), and surface pressure-area isotherms, allowed fully characterization of the phase behavior and aggregate morphology of DODAB/MO mixtures at different molar ratios. Overall, the results indicate that the final morphology of DODAB/MO aggregates depends on the balance between the tendency of DODAB to form zero-curvature bilayer structures and the propensity of MO to form non-bilayer structures with negative curvature. These results also show that in the MO-rich region, an increase in temperature has a similar effect on aggregate morphology as an increase in MO concentration.

Proteomic analysis of naphthalene-induced airway epithelial injury and repair in a cystic fibrosis mouse model.

Combined results from laser capture microdissection of mouse airway epithelial cells followed by high power (MALDI-FTICR) MS, and fluorescent two-dimensional gel elctrophoresis (2D-DIGE) of the whole lung, allowed us to identify proteins differentially expressed after naphthalene induced airway injury. Further, we discovered several novel aspects of Cystic Fibrosis (CF) lung pathology in an F508del-Cftr mouse model using this approach. The combined MALDI-FTICR-MS and 2D-DIGE data show that lung carbonyl reductase (CBR2), involved in prostaglandin metabolism, converting PGE2 to PGF2alpha, is localized to airway cells and is reduced 2-fold in mutant mice compared to normal, both before and after challenge. Further, we observe a downregulation of two key enzymes of retinoic acid metabolism after injury, which is more pronounced in CF mutant mice. These data show that state-of-the-art proteomics can be used to evaluate airway injury in small cell samples. Further, the results suggest the involvement of prostaglandin and retinoic acid metabolism in the abnormal responses of CF mutant mice to injury.