Use of Radiology Procedure Codes in Health Care: The Need for Standardization and Structure.

Radiology procedure codes are a fundamental part of most radiology workflows, such as ordering, scheduling, billing, and image interpretation. Nonstandardized unstructured procedure codes have typically been used in radiology departments. Such codes may be sufficient for specific purposes, but they offer limited support for interoperability. As radiology workflows and the various forms of clinical data exchange have become more sophisticated, the need for more advanced interoperability with use of standardized structured codes has increased. For example, structured codes facilitate the automated identification of relevant prior imaging studies and the collection of data for radiation dose tracking. The authors review the role of imaging procedure codes in radiology departments and across the health care enterprise. Standards for radiology procedure coding are described, and the mechanisms of structured coding systems are reviewed. In particular, the structure of the RadLex™ Playbook coding system and examples of the use of this system are described. Harmonization of the RadLex Playbook system with the Logical Observation Identifiers Names and Codes standard, which is currently in progress, also is described. The benefits and challenges of adopting standardized codes-especially the difficulties in mapping local codes to standardized codes-are reviewed. Tools and strategies for mitigating these challenges, including the use of billing codes as an intermediate step in mapping, also are reviewed. In addition, the authors describe how to use the RadLex Playbook Web service application programming interface for partial automation of code mapping. © RSNA, 2017.

Inhibitory effects of hepatocyte growth factor and interleukin-6 on transforming growth factor-beta1 mediated vocal fold fibroblast-myofibroblast differentiation.

OBJECTIVES: The role of myofibroblasts in vocal fold scarring has not been extensively studied, partly because of the lack of a robust in vitro model. The objective of this investigation was to develop and characterize a myofibroblast in vitro model that could be utilized to investigate the molecular mechanism of myofibroblast differentiation and function in injured vocal fold tissue. METHODS: Differentiation of human primary vocal fold fibroblasts (hVFFs) to myofibroblasts was stimulated with 5, 10, or 20 ng/mL of recombinant transforming growth factor-beta1 (TGF-beta1). Cultures were analyzed by immunofluorescence and Western blotting, with an alpha-smooth muscle actin (alpha-SMA) antibody used as a myofibroblast marker. Normal rabbit vocal folds were treated with 10 ng/mL of TGF-beta1 for 7 days for in vivo corroboration. The effects of interleukin-6 (IL-6) and hepatocyte growth factor (HGF) on myofibroblast differentiation were studied with Western blots. RESULTS: The hVFFs demonstrated positive alpha-SMA labeling in cells stimulated by 10 and 20 ng/mL TGF-beta1, indicating that hVFFs were capable of differentiation to myofibroblasts. Transforming growth factor-beta1 induced the largest increase in alpha-SMA at 10 ng/mL on day 5 of treatment. Both HGF and IL-6 suppressed the expression of TGF-beta1-induced alpha-SMA. CONCLUSIONS: Our work characterizes a useful in vitro model of TGF-beta1-mediated vocal fold fibroblast-myofibroblast differentiation. The extent of differentiation appears to be attenuated by HGF, suggesting a potential mechanism to support prior work indicating that HGF plays a protective role in reducing scar formation in vocal fold injuries. Paradoxically, IL-6, which has been shown to play a profibrotic role in dermal studies, also attenuated the TGF-beta1 response.