Colistin exhibited excellent activity against Escherichia coli and E. cloacae (MIC(90) = 0 5 mg l(-1)). In contrast, colistin was less active against Klebsiella pneumoniae (MIC(90) = 16 mg l(-1)). Resistance rates varied from 0% in E. coli to 1.8% in E. cloacae and 13% in K. pneumoniae. High rates of very major errors were observed in the disc diffusion test using either the criteria of the Comite de l’antibiogramme

de la Societe Francaise de Microbiologie (CA-SFM) or the criteria of the Clinical and Laboratory Standards Institute (CLSI), respectively, 3.5 and 2.5%. When the criteria of Gales et al. were applied, the number of very major errors Evofosfamide mw was reduced to one (0.5%). The Etest showed good concordance with agar dilution method.

Conclusion: Disc susceptibility testing methods are

unreliable on detecting colistin resistance. MIC should be determined to confirm the susceptibility results by disc diffusion.

Significance and Impact of the study: We recommend the determination of MIC by Etest for all multidrug-resistant Enterobacteriaceae when colistin is required for the treatment.”
“The cell adhesion molecule L1 (L1CAM) was originally identified as a neural adhesion molecule essential for neurite outgrowth and axon guidance. Many studies have now shown that L1CAM is overexpressed in human carcinomas and associated with poor prognosis. So far, L1CAM-mediated cellular FAK inhibitor signaling has been largely attributed to an association with growth factor receptors, referred to as L1CAM-’assisted’ signaling. New data demonstrate that L1CAM can signal via two additional mechanisms: ‘forward’ signaling via regulated

intra-membrane proteolysis and ‘reverse’ signaling VAV2 via the activation of the transcription factor nuclear factor (NF)-kappa B. Taken together, these findings lead to a new understanding of L1CAM downstream signaling that is fundamental for the development of anti-L1CAM antibody-mediated therapeutics in human tumor cells.”
“Background

Women with cystic fibrosis are at increased risk for mucoid conversion of Pseudomonas aeruginosa, which contributes to a sexual dichotomy in disease severity.

Methods

We evaluated the effects of estradiol and its metabolite estriol on P. aeruginosa in vitro and in vivo and determined the effect of estradiol on disease exacerbations in women with cystic fibrosis.

Results

Estradiol and estriol induced alginate production in P. aeruginosa strain 01 and in clinical isolates obtained from patients with and those without cystic fibrosis. After prolonged exposure to estradiol, P. aeruginosa adopted early mucoid morphology, whereas short-term exposure inhibited bacterial catalase activity and increased levels of hydrogen peroxide, which is potentially damaging to DNA. Consequently, a frameshift mutation was identified in mucA, a key regulator of alginate biosynthesis in P. aeruginosa.