ABSTRACT
A pterygium is a common conjunctival degeneration and inflammatory condition. It grows onto the corneal surface or limbus, causing blurred vision and cosmetic issues. Ultraviolet is a well-known risk factor for the development of a pterygium, although its pathogenesis remains unclear, with only limited understanding of its hereditary basis. In this study, we collected RNA-seq from both pterygial tissues and conjunctival tissues (as controls) from six patients (a total of twelve biological samples) and retrieved publicly available data, including eight pterygium samples and eight controls. We investigated the intrinsic gene regulatory mechanisms closely linked to the inflammatory reactions of pterygiums and compared Asian (Korea) and the European (Germany) pterygiums using multiple analysis approaches from different perspectives. The increased expression of antioxidant genes in response to oxidative stress and DNA damage implies an association between these factors and pterygium development. Also, our comparative analysis revealed both similarities and differences between Asian and European pterygiums. The decrease in gene expressions involved in the three primary inflammatory signaling pathways-JAK/STAT, MAPK, and NF-kappa B signaling-suggests a connection between pathway dysfunction and pterygium development. We also observed relatively higher activity of autophagy and antioxidants in the Asian group, while the European group exhibited more pronounced stress responses against oxidative stress. These differences could potentially be necessitated by energy-associated pathways, specifically oxidative phosphorylation.
Subject(s)
Inflammation , Oxidative Phosphorylation , Oxidative Stress , Pterygium , RNA-Seq , Pterygium/genetics , Pterygium/metabolism , Humans , Oxidative Stress/genetics , Inflammation/genetics , Conjunctiva/metabolism , Conjunctiva/pathology , Male , Female , Gene Expression Regulation , Middle Aged , Signal Transduction/geneticsABSTRACT
Surface plasmon resonances of metallic nanostructures offer great opportunities to guide and manipulate light on the nanoscale. In the design of novel plasmonic devices, a central topic is to clarify the intricate relationship between the resonance spectrum and the geometry of the nanostructure. Despite many advances, the design becomes quite challenging when the desired spectrum is highly complex. Here we develop a theoretical model for surface plasmons of interacting nanoparticles to reduce the complexity of the design process significantly. Our model is developed by combining plasmon hybridization theory with transformation optics, which yields an efficient way of simultaneously controlling both global and local features of the resonance spectrum. As an application, we propose a design of metasurface whose absorption spectrum can be controlled over a large class of complex patterns through only a few geometric parameters in an intuitive way. Our approach provides fundamental tools for the effective design of plasmonic metamaterials with on-demand functionality.
ABSTRACT
The LPS-induced inflammation model is widely used for studying inflammatory processes due to its cost-effectiveness, reproducibility, and faithful representation of key hallmarks. While researchers often validate this model using clinical cytokine markers, a comprehensive understanding of gene regulatory mechanisms requires extending investigation beyond these hallmarks. Our study leveraged multiple whole-blood bulk RNA-seq datasets to rigorously compare the transcriptional profiles of the well-established LPS-induced inflammation model with those of several human diseases characterized by systemic inflammation. Beyond conventional inflammation-associated systems, we explored additional systems indirectly associated with inflammatory responses (i.e., ISR, RAAS, and UPR) using a customized core inflammatory gene list. Our cross-condition-validation approach spanned four distinct conditions: systemic lupus erythematosus (SLE) patients, dengue infection, candidemia infection, and staphylococcus aureus exposure. This analysis approach, utilizing the core gene list aimed to assess the model's suitability for understanding the gene regulatory mechanisms underlying inflammatory processes triggered by diverse factors. Our analysis resulted in elevated expressions of innate immune-associated genes, coinciding with suppressed expressions of adaptive immune-associated genes. Also, upregulation of genes associated with cellular stresses and mitochondrial innate immune responses underscored oxidative stress as a central driver of the corresponding inflammatory processes in both the LPS-induced and other inflammatory contexts.
ABSTRACT
Myopia is a substantial global public health concern primarily linked to the elongation of the axial length of the eyeball. While numerous animal models have been employed to investigate myopia, the specific contributions of genetic factors and the intricate signaling pathways involved remain incompletely understood. In this study, we conducted RNA-seq analysis to explore genes and pathways in two distinct myopia-inducing mouse models: form-deprivation myopia (FDM) and lens-induced myopia (LIM). Comparative analysis with a control group revealed significant differential expression of 2362 genes in FDM and 503 genes in LIM. Gene Set Enrichment Analysis (GSEA) identified a common immune-associated pathway between LIM and FDM, with LIM exhibiting more extensive interactions. Notably, downregulation was observed in OxPhos complex III of FDM and complex IV of LIM. Subunit A of complex I was downregulated in LIM but upregulated in FDM. Additionally, complex V was upregulated in LIM but downregulated in FDM. These findings suggest a connection between alterations in energy metabolism and immune cell activation, shedding light on a novel avenue for understanding myopia's pathophysiology. Our research underscores the necessity for a comprehensive approach to comprehending myopia development, which integrates insights from energy metabolism, oxidative stress, and immune response pathways.
Subject(s)
Myopia , Animals , Mice , Myopia/genetics , Eye , Disease Models, Animal , Energy Metabolism/genetics , RNA/metabolismABSTRACT
This paper is concerned with the inverse problem of reconstructing small and local perturbations of a planar surface using the field interaction between a known plasmonic particle and the planar surface. The aim is to perform a super-resolved reconstruction of these perturbations from shifts in the plasmonic frequencies of the particle-surface system. In order to analyse the interaction between the plasmonic particle and the planar surface, a well-chosen conformal mapping, which transforms the particle-surface system into a coated structure, is used. Then the even Fourier coefficients of the transformed domain are related to the shifts in the plasmonic resonances of the particle-surface system. A direct reconstruction of the perturbations of the planar surface is proposed. Its viability and limitations are documented by numerical examples.
ABSTRACT
In this paper, we derive an impedance boundary condition to approximate the optical scattering effect of an array of plasmonic nanoparticles mounted on a perfectly conducting plate. We show that at some resonant frequencies the impedance blows up, allowing for a significant reduction of the scattering from the plate. Using the spectral properties of a Neumann-Poincaré type operator, we investigate the dependency of the impedance with respect to changes in the nanoparticle geometry and configuration.