Low‐pressure plasma‐polymerized ethylene film coatings rich in bonded oxygen groups (L‐PPE:O) were deposited on poly(ethylene terephthalate; PET) in order to act as hosts for antimicrobial drugs. Increasing O2 content in the ethylene (C2H4)/Ar–diluted oxygen (O2) gas mixture reduced the deposition rate, but increased the concentration of bonded oxygen, [O], including that of carboxylic acid groups, [COOH], as determined by X‐ray photoelectron‐ (XPS) and Fourier transform infrared (FTIR) spectroscopies, and by toluidine blue O (TBO) assays. L‐PPE:O coatings took up and sustained the release of ciprofloxacin for several hours. Steric hindrance impeded vancomycin penetration into the cross‐linked L‐PPE:O coatings. Ciprofloxacin‐loaded L‐PPE:O coatings inhibited in vitro the growth of Staphylococcus aureus. Deposition of L‐PPE:O on medical devices may endow them with ability to prevent nosocomial infections.

Atraumatic subtrochanteric and diaphyseal (atypical) femoral fractures are a rare, but important adverse event in patients treated with potent anti-resortive agents. The mechanisms involved are unknown and particularly the association with genetic variants has not been explored. The aim of the study was to identify rare genetic variants that could be associated with the occurrence of these fractures. We performed a genome-wide analysis of up to 300,000 variants, mainly distributed in gene coding regions, in 13 patients with atypical femoral fractures and 268 control women, either healthy or with osteoporosis. Twenty one loci were more frequent in the fracture group, with a nominal p value between 1 × 10(-6) and 2.5 × 10(-3). Most patients accumulated two or more allelic variants, and consequently the number of risk variants was markedly different between patients and controls (p = 2.6 × 10(-22)). The results of this pilot study suggest that these fractures are polygenic and are associated with the accumulation of changes in the coding regions of several genes.

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Several studies have identified single-nucleotide polymorphisms (SNPs) associated with adverse effects in non-small-cell lung cancer (NSCLC) patients treated with radiation therapy. Here, using an independent cohort, we aimed to validate the reported associations. We selected 23 SNPs in 17 genes previously associated with radiation-induced oesophagitis for validation in a cohort of 178 Spanish NSCLC patients. Of them, 18 SNPs were finally analysed, following the methods described in the original published studies. Two SNPs replicated their association with radiation-induced oesophagitis (rs7165790 located in the BLM gene: odds ratio (OR) = 0.16, 95% CI = 0.04–0.65, p-value = 0.010; rs4772468 at FGF14: OR = 4.36, 95% CI = 1.15–16.46, p-value = 0.029). The SNP rs2868371 at HSPB1 was also validated but displayed an opposite effect to the formerly described (OR = 3.72; 95% CI = 1.49–9.25; p-value = 0.004). Additionally, we tested a meta-analytic approach including our results and the previous datasets reported in the referenced publications. Twelve SNPs (including the two previously validated) retained their statistically significant association with radiation-induced oesophagitis. This study strengthens the role of inflammation and DNA double-strand break repair pathways in the risk prediction of developing radiation-induced oesophagitis in NSCLC patients. The validated variants are good candidates to be evaluated in risk prediction models for patient stratification based on their radiation susceptibility.