We look to understand the enhancement and spatial resolution of a tip-enhanced Raman scattering (TERS) system containing a metal tip and plasmonic substrate.
As 2 S 3 :Cd films with nominal Cd content x up to 4 at.% were prepared by thermal evaporation. Their amorphous structure is confirmed by Raman spectroscopy. The film surface roughness estimated from atomic force microscopy does not exceed 1 nm. Energy-dispersive X-ray spectroscopy and X-ray photoelectron spectroscopy show a strong decrease of Cd content with the film depth. Peaks of CdS longitudinal optical phonon and its overtones emerging in the Raman spectra of films with x ! 2 at.% Cd are the evidence for the laser irradiation-induced formation of CdS crystallites in the As 2 S 3 :Cd films. The downward shift of the CdS Raman peak frequencies is mainly explained by tensile strain undergone by the CdS crystallites in the films caused by material transfer from the laser spot due to the photoplastic effect.
It has been widely shown that biomaterial surface topography can modulate host immune response, but a fundamental understanding of how different topographies contribute to pro-inflammatory or anti-inflammatory responses is still lacking. To investigate the impact of surface topography on immune response, we undertook a systematic approach by analyzing immune response to eight grades of medical grade polyurethane of increasing surface roughness in three in vitro models of the human immune system. Polyurethane specimens were produced with defined roughness values by injection molding according to the VDI 3400 industrial standard. Specimens ranged from 0.1 μm to 18 μm in average roughness (Ra), which was confirmed by confocal scanning microscopy. Immunological responses were assessed with THP-1-derived macrophages, human peripheral blood mononuclear cells (PBMCs), and whole blood following culture on polyurethane specimens. As shown by the release of pro-inflammatory and anti-inflammatory cytokines in all three models, a mild immune response to polyurethane was observed, however, this was not associated with the degree of surface roughness. Likewise, the cell morphology (cell spreading, circularity, and elongation) in THP-1-derived macrophages and the expression of CD molecules in the PBMC model on T cells (HLA-DR and CD16), NK cells (HLA-DR), and monocytes (HLA-DR, CD16, CD86, and CD163) showed no influence of surface roughness. In summary, this study shows that modifying surface roughness in the micrometer range on polyurethane has no impact on the pro-inflammatory immune response. Therefore, we propose that such modifications do not affect the immunocompatibility of polyurethane, thereby supporting the notion of polyurethane as a biocompatible material.
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