Mechanisms for Reduced Fibrin Clot Formation on Liquid-Infused Surfaces.

Biomedical devices are prone to blood clot formation (thrombosis), and liquid-infused surfaces (LIS) are effective in reducing the thrombotic response. However, the mechanisms that underpin this performance, and in particular the role of the lubricant, are not well understood. In this work, it is investigated whether the mechanism of LIS action is related to i) inhibition of factor XII (FXII) activation and the contact pathway; ii) reduced fibrin density of clots formed on surfaces; iii) increased mobility of proteins or cells on the surface due to the interfacial flow of the lubricant. The chosen LIS is covalently tethered, nanostructured layers of perfluorocarbons, infused with thin films of medical-grade perfluorodecalin (tethered-liquid perfluorocarbon), prepared with chemical vapor deposition previously optimized to retain lubricant under flow. Results show that in the absence of external flow, interfacial mobility is inherently higher at the liquid-blood interface, making it a key contributor to the low thrombogenicity of LIS, as FXII activity and fibrin density are equivalent at the interface. The findings of this study advance the understanding of the anti-thrombotic behavior of LIS-coated biomedical devices for future coating design. More broadly, enhanced interfacial mobility may be an important, underexplored mechanism for the anti-fouling behavior of surface coatings.

Clinical and Histopathologic Features of Interstitial Lung Disease in Erdheim⁻Chester Disease.

Limited information is available regarding interstitial lung disease (ILD) in Erdheim⁻Chester disease (ECD), a rare multisystemic non-Langerhans cell histiocytosis. Sixty-two biopsy-confirmed ECD patients were divided into those with no ILD (19.5%), minimal ILD (32%), mild ILD (29%), and moderate/severe ILD (19.5%), based on computed tomography (CT) findings. Dyspnea affected at least half of the patients with mild or moderate/severe ILD. Diffusion capacity was significantly reduced in ECD patients with minimal ILD. Disease severity was inversely correlated with pulmonary function measurements; no correlation with BRAF V600E mutation status was seen. Reticulations and ground-glass opacities were the predominant findings on CT images. Automated CT scores were significantly higher in patients with moderate/severe ILD, compared to those in other groups. Immunostaining of lung biopsies was consistent with ECD. Histopathology findings included subpleural and septal fibrosis, with areas of interspersed normal lung, diffuse interstitial fibrosis, histiocytes with foamy cytoplasm embedded in fibrosis, lymphoid aggregates, and focal type II alveolar cell hyperplasia. In conclusion, ILD of varying severity may affect a high proportion of ECD patients. Histopathology features of ILD in ECD can mimic interstitial fibrosis patterns observed in idiopathic ILD.