Rybergomar6761
The purpose of this study was to determine the efficacy of nanoparticle-encapsulated Fidgetin-like 2 (FL2) siRNA (FL2-NPsi), a novel therapeutic agent targeting the
gene, for the treatment of corneal alkaline chemical injury.
Eighty 12-week-old, male Sprague-Dawley rats were divided evenly into 8 treatment groups prednisolone, empty nanoparticles, control-NPsi (1 µM, 10 µM, and 20 µM) and FL2-NPsi (1 µM, 10 µM, and 20 µM). An alkaline burn was induced onto the cornea of each rat, which was then treated for 14 days according to group assignment. Clinical, histopathologic, and immunohistochemical analyses were conducted to assess for wound healing. FL2-NPsi-mediated knockdown of FL2 was confirmed by in vitro quantitative polymerase chain reaction (qPCR). Toxicity assays were performed to assess for apoptosis (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling [TUNEL] assay) and nerve damage (whole mount immunochemical staining). Statistical analyses were performed keleton were used to design a therapeutic to enhance corneal cell migration, highlighting the promise of targeting microtubules to regulate corneal wound healing.
To examine the intra- and intergrader agreement on morphologic characteristics of type 3 neovascularization on optical coherence tomography angiography (OCT-A).
OCT-A images of 22 eyes from 21 patients with a new-onset, treatment-naive type 3 neovascularization were included in this cross-sectional retrospective agreement study. Each image was graded three times by two independent medical retina specialists to assess intra- and intergrader agreement. The graders scored the presence or absence of the following vascular and structural features intraretinal neovascularization (IRN), subretinal neovascularization, sub-retinal pigment epithelium (RPE) neovascularization (SRPEN), retinal choroidal anastomosis (RCA), intraretinal cysts, subretinal fluid, and pigment epithelial detachment. Agreement was analyzed for each feature using Gwet's AC
, к statistics, and percentage of agreement.
The best agreement (AC
) was found for intraretinal neovascularization (within
0.94; within
0.93 and between 1.00) and intraretinal cysts (within
, 1.00; within
, 0.97 and between, 1.00). The poorest intragrader agreements were observed for SRPEN (within
, 0.54 and within
, 0.36) and RCA (within
, 0.45 and within
, 0.52), and the poorest intergrader agreement was found for SRPEN, RCA, and pigment epithelial detachment (0.18, 0.37, and 0.15, respectively).
Although the agreement values were high for intraretinal features, considerable grader variability was found for the vascular and structural features in the deeper retina or under the RPE. Clinicians should be careful to base therapeutic decisions on qualitative OCT-A assessment, because even well-trained specialists show a considerable grader variation in their subjective evaluation.
The clinical value of OCT-A imaging largely depends on the agreement of subjective evaluations by ophthalmologists.
The clinical value of OCT-A imaging largely depends on the agreement of subjective evaluations by ophthalmologists.
We correlated quantitative fundus autofluorescence (qAF) with other fundus features in patients exhibiting central serous chorioretinopathy (CSC).
Short wavelength fundus autofluorescence (SW-AF, 488 nm excitation) was measured by qAF. Using nonnormalized images qAF values were calculated within eight concentric segments (qAF
) located at an eccentricity of 7° to 9°. Horizontal spectral domain optical coherence tomography (SD-OCT) scans and near-infrared fundus autofluorescence images (NIR-AF) were studied.
Thirty-six eyes of 20 patients (mean age 48.7± 8.5 years) diagnosed with CSC were studied. Thirteen patients had bilateral disease; four patients were female. In 22 eyes CSC was present in the macula; in one eye the lesion was in a peripapillary location, 10 involved both locations, and three were unaffected. Serous retinal detachment, retinal pigmented epithelial detachment (PED), outer retinal atrophy and subRPE hypertransmission were all features identifiable by SD-OCT. NIR-AF images were helpful in detecting foveal and parafoveal lesions. Sampling for retina-wide elevations in SW-AF intensity by measuring qAF
did not indicate a generalizable relationship amongst CSC-diagnosed eyes. However, color-coded qAF images revealed alterations in SW-AF topography and intensity relative to healthy eyes at the same locations. JG98 HSP (HSP90) inhibitor Thus zones of higher than normal qAF intensity were found in association with SD-OCT detectable PED; loss of ellipsoid zone and interdigitation zone; and hyperreflectivity in outer retina. Pronounced decreases in qAF colocalized with serous retinal detachment and with outer retinal degeneration that included hypertransmission of SD-OCT signal into the choroid.
Localized elevations in qAF reflect increased bisretinoid in association with CSC lesions.
Foci of elevated qAF at some stages of CSC contribute to the natural history of the disease.
Foci of elevated qAF at some stages of CSC contribute to the natural history of the disease.
Retinal pigment epithelial cell autophagy dysfunction, cellular senescence, and the retinal inflammatory response are key pathogenic factors in age-related macular degeneration (AMD), which has been reviewed in our previously work in 2019. This study aims to identify genes collectively involved in these three biological processes and target drugs in AMD.
The pubmed2ensembl database was used to perform text mining. The GeneCodis database was applied to analyze gene ontology biological process and the KEGG pathway. The STRING database was used to analyze protein-protein interaction analysis and hub genes were identified by the Cytoscape software. The Drug Gene Interaction Database was used to perform drug-gene interactions.
We identified 62 genes collectively involved in AMD, autophagy, cellular senescence, and inflammatory response, 19 biological processes including 42 genes, 11 enriched KEGG pathways including 37 genes, and 12 hub genes step by step via the above biomedical databases. Finally, five hub genes (IL-6, VEGF-A, TP53, IL-1β, and transforming growth factor [TGF]-β1) and their specific interaction modes were identified, corresponding with 24 target drugs with therapeutic potential for AMD.
