“Evaluation of: Parks QM, Young RL, Poch KR, Malcolm KC, V


“Evaluation of: Parks QM, Young RL, Poch KR, Malcolm KC, Vasil Ill Nick JA: Neutrophil enhancement of Pseudomonas aeruginosa biofilm development: human F-actin and DNA as targets for therapy. J. Med. Microbiol. 58(4), 492-502 (2009). Pseudomonas aeruginosa infection and biofilm formation in the cystic fibrosis lung occurs in association with an exuberant inflammatory response in a neutrophil-rich environment. The presence of DNA/F-actin bundles,

formed by components released from necrotic neutrophils, was shown to stimulate biofilm formation by P. aeruginosa. Soluble polyvalent anions can sequester polyvalent cations and dissolve DNA/F-actin bundles, and treatment with polyvalent anions was shown to disrupt neutrophil-induced P. aeruginosa biofilms. In addition, polyvalent anions could also www.selleckchem.com/products/Adriamycin.html prevent the formation of neutrophil-induced P. aeruginosa biofilms. While young neutrophil-induced P. aeruginosa biofilms could be disrupted by treatment with polyvalent anions or DNase, older neutrophil-induced biofilms, or biofilms formed by a mucold P. aeruginosa variant, were less susceptible to treatment with polyvalent Elafibranor concentration anions or DNase but they could be efficiently disrupted by polyvalent anion-DNase combination treatment. The synergistic effect of the combined polyvalent anion-DNase treatment is most likely

due,to the capacity of polyvalent anions to dissociate DNA/F-actin bundles with bacteria and polysaccharides, leading to exposure of a greater number of DNase cleavage sites on the extracellular DNA. It is conceivable that treatment with soluble polyvalent anions as an adjunct to DNase treatment will represent an improvement in cystic fibrosis therapy.”
“P>We followed up 550 primary kidney transplant recipients in an observational retrospective cohort to evaluate the impact of three consecutive cytomegalovirus (CMV) prevention strategies. In period 1 (1996-2000; n = 190), no anti-CMV prophylaxis

was given; in period 2 (2000-2004; n = 173), 6-month Selleckchem SRT2104 valacyclovir was given and in period 3 (> 2004; n = 187), 6-month valganciclovir was given. Cytomegalovirus disease significantly decreased from 33.2% in period 1 to 13.9% in period 2 and to 8.6% in period 3; onset was significantly prolonged with valganciclovir (228 days) compared with valacyclovir (93 days) and with no prophylaxis (33 days). After Cox regression adjustments, both valganciclovir and valacyclovir were similarly protective factors for CMV disease. Cytomegalovirus diseases encountered in both valacyclovir and valganciclovir groups were primary infections (79.2 and 93.8% respectively) as compared with a significant low number (39.7%) in the nonprophylaxis group. Two cases of valganciclovir resistance were recorded in the valganciclovir group and no resistance was seen with valacyclovir.

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