Animal models for cystic fibrosis (CF) have enhanced our understanding of the pathology and contributed to the development of new treatments. In the field of CF, many animal models have been developed and described. To our knowledge, thus far, none of the reviews of CF animal models has used a systematic methodology. A systematic approach to creating model overviews can lead to an objective, evidence-based choice of an animal model for new research questions. We searched Pubmed and Embase for the currently available animal models for CF. Two independent reviewers screened the results. We included all primary studies describing an animal model for CF. After duplicate removal, 12,304 publications were left. Because of the large number of models, in the current paper, only the genetic models are presented. A total of 636 publications were identified describing genetic animal models for CF in mice, pigs, ferrets, rats and zebrafish. Most of these models have an altered Cftr gene. An overview of basic model characteristics and outcome measures for these genetic models is provided, together with advice on using these data. As far as the authors are aware, this is one of the largest systematic mapping reviews on genetic animal models for CF. It can aid in selecting a suitable model and outcome measures. In general, the reporting quality of the included publications was poor. Further systematic reviews are warranted to determine the quality and translational value of these models further.

Background and purpose — Trochanteric fractures are often treated using intramedullary fixation. In our institution, the TFN-Advanced Proximal Femoral Nailing System (TFNA) was introduced as replacement for the Gamma Trochanteric Nail (GTN3) for the treatment of these fractures as a result of a hospital-driven change of trauma implant supplier. We compared trochanteric fracture fixation failure rate between these 2 intramedullary nails. Patients and methods — All trochanteric fractures treated surgically from 2011 to 2019 were retrospectively reviewed for fixation failure. From 2016 only the TFNA was used. Fixation failure was defined as implant cut-out, implant breakage, non-union, malpositioning of the screw/blade requiring reoperation, new fracture around the nail, or miscellaneous. Propensity score matching was used to balance distribution of covariates and to compare failure rates between TFNA and GTN3 groups. Learning curve analyseswere performed. Results — After exclusion, 797 GTN3s (779 patients) and 542 (536 patients) TFNAs were available for analysis. A higher risk of fixation failure was found in the TFNA group (14%) compared with the GTN3 group (7.0%) (hazard ratio [HR] 2.0, 95% confidence interval [CI] 1.2–3.5). This was mainly attributed to a higher risk of cut-out (HR 2.2; CI 0.9–5.7), malpositioning (HR 4.7; CI 0.7–34), and new fracturearound the nail (HR 4.0; CI 1.0–16). Learning curve analyses indicated no clear learning curve effect. Interpretation — Failure of fixation increased after a switch from the GTN3 to the TFNA proximal femoral nail for the treatment of trochanteric fractures. Cut-out and malpositioning of the calcar screw or blade appeared to be the most dominant failure mechanisms. Modifications in implant design may have played a role in this increased risk of failure of fixation. In our institution a new implant device was introduced without solid clinical evidence behind it. This study may help to underline the need for medical doctors with acritical and scientific background to be involved in implant choices.

Various animal models are available to study cystic fibrosis (CF). These models may help to enhance our understanding of the pathology and contribute to the development of new treatments. We systematically searched all publications on CF animal models. Because of the large number of models retrieved, we split this mapping review into two parts. Previously, we presented the genetic CF animal models. In this paper we present the nongenetic CF animal models. While genetic animal models may, in theory, be preferable for genetic diseases, the phenotype of a genetic model does not automatically resemble human disease. Depending on the research question, other animal models may thus be more informative. We searched Pubmed and Embase and identified 12,303 unique publications (after duplicate removal). All references were screened for inclusion by two independent reviewers. The genetic animal models for CF (from 636 publications) were previously described. The non-genetic CF models (from 189 publications) are described in this paper, grouped by model type: infection-based, pharmacological, administration of human materials, xenografts and other. As before for the genetic models, an overview of basic model characteristics and outcome measures is provided. This CF animal model overview can be the basis for an objective, evidence-based model choice for specific research questions. Besides, it can help to retrieve relevant background literature on outcome measures of interest.