BackgroundRespiratory syncytial virus (RSV) infection is a common cause of pediatric hospitalization. microRNA, key regulators of the immune system, have not previously been investigated in respiratory specimens during viral infection. We investigated microRNA expression in the nasal mucosa of 42 RSV-positive infants, also comparing microRNA expression between disease severity subgroups.MethodsNasal mucosa cytology specimens were collected from RSV-positive infants and healthy controls. 32 microRNA were selected by microarray for qPCR verification in 19 control, 16 mild, 7 moderate and 19 severe disease samples.ResultsCompared to healthy controls, RSV-positive infants downregulated miR-34b, miR-34c, miR-125b, miR-29c, mir125a, miR-429 and miR-27b and upregulated miR-155, miR-31, miR-203a, miR-16 and let-7d. On disease subgroups analysis, miR-125a and miR-429 were downregulated in mild disease (p = 0.03 and 0.02, respectively), but not in severe disease (p = 0.3 and 0.3).ConclusionmicroRNA expression in nasal epithelium cytology brushings of RSV-positive infants shows a distinct profile of immune-associated miRNA. miR-125a has important functions within NF-κB signaling and macrophage function. The lack of downregulation of miR-125a and miR-429 in severe disease may help explain differences in disease manifestations on infection with RSV.

Background:We compared the current guidelines for neonatal resuscitation with alternative measures and aimed to find out whether this modulated brain inflammation. Methods: Progressive asphyxia was induced in 94 newborn pigs until asystole. With the reference being resuscitation guidelines, 30 s of initial positive-pressure ventilation before compression (c) and ventilation (V) (c:V; 3:1) in 21% oxygen, pigs were randomized to (i) ventilation for 30, 60, or 90 s before chest compressions; (ii) c:V ratios of 3:1, 9:3, or 15:2; or (iii) 21% or 100% oxygen. concentrations of inflammatory markers in the cerebrospinal fluid (csF) and gene expression in the hippocampus and frontal cortex were measured for different interventions. results: In csF, s100 was higher with 90 s than with 30 or 60 s of initial positive-pressure ventilation, whereas concentrations of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were higher with 30 than with 60 s. Matrix metalloproteinase-2 (MMP-2) and intracellular adhesion molecule 1 (IcaM-1) were higher with 30 than with 60 s. No other comparison between ratios and oxygen concentrations used yielded significant results. conclusion: With respect to signs of brain inflammation, newly born pigs at asystole should be ventilated for longer than 30 s before chest compressions start. c:V ratios of 9:3 and 15:2 as compared with 3:1, or air instead of pure oxygen, did not modulate inflammatory markers.

Antibacterial surfaces are increasingly used in the food industry. In the present study, the antibacterial effect of a triclosan-containing industrial floor was assessed. A poultry processing plant, which had a floor that contained triclosan, was visited, and the floor was sampled for bacteria. A high bacterial diversity was found on the floor. Testing showed that bacteria isolated from the floor showed a sensitivity to triclosan that covered a range of MICs from 0.07 to >40 ppm. Staphylococci were the most sensitive, and Pseudomonas fluorescens and Serratia marcescens were the most tolerant. The MICs of triclosan for the strains isolated from the floor were similar to the control strains from the corresponding genera or species of other origin. Thus, the floor seemed not to select for strains that were tolerant to triclosan or that led to the development of resistance to triclosan. Laboratory studies showed that the ability of bacteria to survive under dry conditions on coupons of the floor was similar to that for stainless steel and that the survival of the bacteria on the floor was not linked to their tolerance of triclosan, as determined by the MICs of triclosan. Adherence studies showed that bacteria were able to adhere to coupons of the floor; however, no thick biofilm developed after 3 days of incubation. In an agar plate assay, the floor produced inhibition zones against staphylococci, which are known to be very sensitive to triclosan, whereas no inhibition zones were observed for other bacteria tested. In conclusion, the antibacterial effect of the floor seemed to be very low. Because the concentration of triclosan in the floor was low compared to what has been reported for other triclosan-incorporated surfaces, sufficient amounts of triclosan may not have been available on the surface of the floor to kill the bacteria.

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