RESUMO
BACKGROUND: Research has shown that up to 33% of pressure ulcers (PUs) acquired in hospitals result from the application of a medical device. Cervical collars (C-collars) have been implicated in causing PUs, due to the mechanical force they apply to the skin. In order to improve our understanding of collar-related PUs, the present study aimed to assess the biomechanical, biochemical, and microclimate effects of C-collar design and fitting tension. METHODS: A cohort of 15 healthy volunteers was fit with two different C-collars according to the manufacturer guidelines. Two further collar tensions were also defined as loose and tight for each device. Each collar condition was applied for 15 minutes, with a 10 minute refractory period. Measurements at the device-skin interface included interface pressures, inflammatory biomarkers, microclimate, range of cervical motion, and comfort scores. RESULTS: The interface pressures at each tissue site increased monotonically with greater collar tension (p<0.01), irrespective of collar design. Biomarker analysis revealed that inflammatory cytokines (IL-1a) were elevated during collar application, with the highest increase during the tight fit condition, representing over a fourfold increase from unloaded conditions. Regardless of collar tension or type, there was an increase in temperature 1.5°C ±0.8°C compared to baseline values. Range of motion significantly decreased with greater strap tension (p<0.05), with an associated increase in discomfort. CONCLUSION: The present findings revealed that increasing C-collar tensions caused elevated contact pressures at the device-skin interface, with a corresponding inflammatory response at the skin. These peak contact pressures were highest at the occiput, corresponding with reported PU locations. Devices should be designed to uniformly distribute pressures, and appropriate guidance is needed for their application.
RESUMO
MicroRNA (miRNA) target recognition is largely dictated by short 'seed' sequences, and single miRNAs therefore have the potential to regulate a large number of genes. Understanding the contribution of specific miRNA-target interactions to the regulation of biological processes in vivo remains challenging. Here we use transcription activator-like effector nuclease (TALEN) and clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 technologies to interrogate the functional relevance of predicted miRNA response elements (MREs) to post-transcriptional silencing in zebrafish and Drosophila. We also demonstrate an effective strategy that uses CRISPR-mediated homology-directed repair with short oligonucleotide donors for the assessment of MRE activity in human cells. These methods facilitate analysis of the direct phenotypic consequences resulting from blocking specific miRNA-MRE interactions at any point during development.
