This novel method feasibly could be used to map tear film thickness, and it provides a valuable means to investigate the spatial distribution of tear film.
Background/Aims: Lipocalin 2 (LCN2), an important mediator of a variety of cellular processes, is involved in regulating the inflammatory response, but its roles in different inflammatory diseases are controversial. Because the role of LCN2 in ocular inflammation has been unclear until now, we explored the function of LCN2 in lipopolysaccharide (LPS)-induced ocular inflammation in vivo and in vitro. Methods: Endotoxin-induced uveitis (EIU) was induced in male Sprague Dawley rats by the intravitreal injection of LPS. The expression and location of LCN2 in the retina were detected with western blotting and immunohistochemistry, respectively. We determined the clinical scores for anterior inflammation, quantified the infiltrated inflammatory cells, and measured the pro-inflammatory factors to determine the anti-inflammatory effects of LCN2 in EIU eyes. Cultured primary rat Müller cells were stimulated with LPS and the expression and secretion of LCN2 were measured with real-time PCR, western blotting, and an ELISA. After Müller cells were cotreated with LPS and LCN2 or PBS, the expression and secretion of TNF-α, IL-6, and MCP-1 were examined with realtime PCR, western blotting, and ELISAs. Western blotting and immunofluorescence were used to detect the phosphorylation and cellular distribution of nuclear factor kappaB (NF-κB) subunit p65. Results: In EIU, the expression of LCN2 was significantly upregulated in the retina, especially in the outer nuclear layer (mainly composed of Müller cells). LPS stimulation of cultured Müller cells also markedly elevated LCN2 expression. Intravitreal injection of LCN2 significantly reduced the clinical scores, inflammatory infiltration, and protein leakage in EIU, which correlated with the reduced levels of proinflammatory factors in the aqueous humor and retina. LCN2 treatment also reduced the expression and secretion of TNF-α, IL-6, and MCP-1 in LPS-stimulated Müller cells. LCN2 inhibited the inflammatory response by inhibiting the phosphorylation and translocation of NF-κB p65. Conclusions: LCN2 protects against ocular inflammation, at least in part, by negatively regulating the activation of the NF-κB signaling pathway. LCN2 may be a promising anti-inflammatory therapy for ocular diseases, such as uveitis.
The elevated MMP/TIMP ratio and MMP activity may play a role in the pathogenesis of human high myopia. Large prospective studies are needed to further investigate the effect of MMPs in the pathogenesis of human high myopia.
Purpose:The aim was to study the dynamic properties of wavefront aberrations and visual acuity in normal and dry eyes. Methods: Thirty dry-eye patients and 27 normal subjects participated in this study. Multi-file mode of a Hartmann-Shack wavefront sensor was used to measure dynamic wavefront aberrations for a period of 45 seconds. Dynamic measurements of visual acuity (VA) were made for 150 seconds using a multi-functional VA tester. Standard deviation of the measurements (RMS or VA) over the testing period was used to estimate instability of the dynamic wavefront aberration and VA. Results: For most subjects, both wavefront aberration and VA changed over time and the instability varied substantially among individuals. Blink-dependent fluctuation in wavefront aberration or VA was observed for some dry-eye subjects. On average, the dry-eye group had greater instability than the normal group in either the higher order wavefront aberrations (t = 2.09, p = 0.03, for OD; t = 3.76, p = 0.001, for OS) or the VA (t = 2.09, p = 0.02, for OD; t = 204, p = 0.03, for OS). Instability of VA in the dry-eye group was significantly correlated with blink rate (r = 0.28, p = 0.02). Conclusion: Dynamic changes in wavefront aberrations and VA are highly individual dependent, while the dry eye tends to be less stable than the normal eye. The results suggest that tear-film fluctuation might play a role in determining dynamic wavefront aberration and VA, however, contributions from other factors should not be overlooked. For dry eye, dynamic change in VA depends on blink rate. The human eye is not static in either its optical properties or its visual performance. Therefore, it is, interesting to understand the factors that are contributing to the dynamic changes in both the optical properties and the visual performance of the eye. The thin layer of precorneal tear film is perhaps the most influential factor affecting the stability of the optical quality of the eye as fast change of the tear-film could alter the pathway of the light entering the eye and thus induce additional ocular aberrations.To assess the effect of dynamic change of the tear-film on the optical qualities of the eye, wavefront technique has been employed in several studies. Using a Hartmann-Shack wavefront sensor, Koh and associates 1 measured wavefront aberrations in the whole eye for 20 normal subjects before and after break-up of the tear film and found a significant increase in root-mean-square (RMS) of higher order aberrations (HOAs) after tear-film break-up, compared to the level of aberrations with a complete tear-film. The tearlinked changes in HOA were described as the changes in Zernike aberrations, such as the coma-like and spherical-like aberrations. Montéa-Micó and colleagues 2,3 used
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