FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2912449823> ?p ?o ?g. }

• W2912449823 endingPage "810" @default.
• W2912449823 startingPage "801" @default.
• W2912449823 abstract "PurposeTo compare functional and structural changes in the retina in patients with aquaporin-4 immunoglobulin G (AQP4-IgG)-positive neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS).DesignCross-sectional study; biochemical study of human retinas.ParticipantsA total of 181 participants, including 22 consecutive patients (44 eyes) with NMOSD, 131 patients (262 eyes) with multiple sclerosis (MS), and 28 normal subjects (56 eyes). In addition, 8 eyeballs from healthy donors were used for biochemical analysis.MethodsFull-field electroretinography (ERG) and spectral-domain OCT were performed in all the subjects. Topography of AQP4 expression and Müller glial distribution were analyzed using Western blotting and immunohistochemistry.Main Outcome MeasuresFull-field ERG parameters, including amplitudes and peak times. Tissue volume of each of the retinal layers at the fovea by OCT segmentation. Levels of AQP4 expression at different retinal regions.ResultsThe b-wave amplitude was significantly reduced in patients with AQP4-IgG+ NMOSD in scotopic ERGs (compared with AQP4-IgG- subjects, patients with MS, and normal controls) but not in photopic ERGs. Further analysis showed that this b-wave change was mainly caused by reduction of the slow PII component, suggesting specific Müller cell dysfunction. We also found thinning of specific retinal layers at the fovea in patients with AQP4-IgG+ NMOSD, in the Henle fiber outer nuclear layer (HFONL) and the inner segment (IS) layer, but not in the inner nuclear layer (INL), outer plexiform layer (OPL), or outer segment (OS) layer. Furthermore, there was a significant association between foveal HFONL-IS complex thinning and scotopic b-wave amplitude reduction (P = 0.005∼0.01, fixed-effects model). Western blotting demonstrated that Müller cell–specific AQP4 was expressed at a higher level at the fovea than the peripheral retina. Immunohistochemical studies revealed that the specific foveal thinning reflected the topography of AQP4 expression and Müller glial distribution in the human macula.ConclusionsThis study provides in vivo structural and functional evidence of Müller glial dysfunction in eyes of patients with AQP4-IgG+ NMOSD. Topography of retinal structural change is supported by distribution of Müller cells and patterns of AQP4 expression. The study suggests that visual electrophysiology and retinal imaging could be useful biomarkers to assess the potential retinal astrocytopathy in NMOSD. To compare functional and structural changes in the retina in patients with aquaporin-4 immunoglobulin G (AQP4-IgG)-positive neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). Cross-sectional study; biochemical study of human retinas. A total of 181 participants, including 22 consecutive patients (44 eyes) with NMOSD, 131 patients (262 eyes) with multiple sclerosis (MS), and 28 normal subjects (56 eyes). In addition, 8 eyeballs from healthy donors were used for biochemical analysis. Full-field electroretinography (ERG) and spectral-domain OCT were performed in all the subjects. Topography of AQP4 expression and Müller glial distribution were analyzed using Western blotting and immunohistochemistry. Full-field ERG parameters, including amplitudes and peak times. Tissue volume of each of the retinal layers at the fovea by OCT segmentation. Levels of AQP4 expression at different retinal regions. The b-wave amplitude was significantly reduced in patients with AQP4-IgG+ NMOSD in scotopic ERGs (compared with AQP4-IgG- subjects, patients with MS, and normal controls) but not in photopic ERGs. Further analysis showed that this b-wave change was mainly caused by reduction of the slow PII component, suggesting specific Müller cell dysfunction. We also found thinning of specific retinal layers at the fovea in patients with AQP4-IgG+ NMOSD, in the Henle fiber outer nuclear layer (HFONL) and the inner segment (IS) layer, but not in the inner nuclear layer (INL), outer plexiform layer (OPL), or outer segment (OS) layer. Furthermore, there was a significant association between foveal HFONL-IS complex thinning and scotopic b-wave amplitude reduction (P = 0.005∼0.01, fixed-effects model). Western blotting demonstrated that Müller cell–specific AQP4 was expressed at a higher level at the fovea than the peripheral retina. Immunohistochemical studies revealed that the specific foveal thinning reflected the topography of AQP4 expression and Müller glial distribution in the human macula. This study provides in vivo structural and functional evidence of Müller glial dysfunction in eyes of patients with AQP4-IgG+ NMOSD. Topography of retinal structural change is supported by distribution of Müller cells and patterns of AQP4 expression. The study suggests that visual electrophysiology and retinal imaging could be useful biomarkers to assess the potential retinal astrocytopathy in NMOSD." @default.
• W2912449823 created "2019-02-21" @default.
• W2912449823 creator A5001215128 @default.
• W2912449823 creator A5003148662 @default.
• W2912449823 creator A5011298369 @default.
• W2912449823 creator A5027132248 @default.
• W2912449823 creator A5027571386 @default.
• W2912449823 creator A5031675779 @default.
• W2912449823 creator A5062060255 @default.
• W2912449823 creator A5064279529 @default.
• W2912449823 creator A5067245074 @default.
• W2912449823 creator A5073656496 @default.
• W2912449823 creator A5083626547 @default.
• W2912449823 creator A5083946982 @default.
• W2912449823 creator A5088174174 @default.
• W2912449823 creator A5088864000 @default.
• W2912449823 creator A5089004523 @default.
• W2912449823 date "2019-06-01" @default.
• W2912449823 modified "2023-10-18" @default.
• W2912449823 title "Evidence of Müller Glial Dysfunction in Patients with Aquaporin-4 Immunoglobulin G–Positive Neuromyelitis Optica Spectrum Disorder" @default.
• W2912449823 cites W1878669653 @default.
• W2912449823 cites W2001110565 @default.
• W2912449823 cites W2026191355 @default.
• W2912449823 cites W2036172456 @default.
• W2912449823 cites W2055375414 @default.
• W2912449823 cites W2065372694 @default.
• W2912449823 cites W2075584671 @default.
• W2912449823 cites W2092102896 @default.
• W2912449823 cites W2096230518 @default.
• W2912449823 cites W2107941546 @default.
• W2912449823 cites W2113184411 @default.
• W2912449823 cites W2122545833 @default.
• W2912449823 cites W2128418445 @default.
• W2912449823 cites W2129229339 @default.
• W2912449823 cites W2144469764 @default.
• W2912449823 cites W2154221129 @default.
• W2912449823 cites W2155112931 @default.
• W2912449823 cites W2162576364 @default.
• W2912449823 cites W2255944078 @default.
• W2912449823 cites W2345156418 @default.
• W2912449823 cites W2401147790 @default.
• W2912449823 cites W2504824509 @default.
• W2912449823 cites W2538300479 @default.
• W2912449823 cites W2564793794 @default.
• W2912449823 cites W2590635473 @default.
• W2912449823 cites W2605873020 @default.
• W2912449823 cites W2744545444 @default.
• W2912449823 cites W2767373868 @default.
• W2912449823 cites W2770793064 @default.
• W2912449823 cites W2774907396 @default.
• W2912449823 cites W2789474544 @default.
• W2912449823 cites W2808813455 @default.
• W2912449823 cites W2883382613 @default.
• W2912449823 cites W2908976211 @default.
• W2912449823 doi "https://doi.org/10.1016/j.ophtha.2019.01.016" @default.
• W2912449823 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30711604" @default.
• W2912449823 hasPublicationYear "2019" @default.
• W2912449823 type Work @default.
• W2912449823 sameAs 2912449823 @default.
• W2912449823 citedByCount "39" @default.
• W2912449823 countsByYear W29124498232019 @default.
• W2912449823 countsByYear W29124498232020 @default.
• W2912449823 countsByYear W29124498232021 @default.
• W2912449823 countsByYear W29124498232022 @default.
• W2912449823 countsByYear W29124498232023 @default.
• W2912449823 crossrefType "journal-article" @default.
• W2912449823 hasAuthorship W2912449823A5001215128 @default.
• W2912449823 hasAuthorship W2912449823A5003148662 @default.
• W2912449823 hasAuthorship W2912449823A5011298369 @default.
• W2912449823 hasAuthorship W2912449823A5027132248 @default.
• W2912449823 hasAuthorship W2912449823A5027571386 @default.
• W2912449823 hasAuthorship W2912449823A5031675779 @default.
• W2912449823 hasAuthorship W2912449823A5062060255 @default.
• W2912449823 hasAuthorship W2912449823A5064279529 @default.
• W2912449823 hasAuthorship W2912449823A5067245074 @default.
• W2912449823 hasAuthorship W2912449823A5073656496 @default.
• W2912449823 hasAuthorship W2912449823A5083626547 @default.
• W2912449823 hasAuthorship W2912449823A5083946982 @default.
• W2912449823 hasAuthorship W2912449823A5088174174 @default.
• W2912449823 hasAuthorship W2912449823A5088864000 @default.
• W2912449823 hasAuthorship W2912449823A5089004523 @default.
• W2912449823 hasBestOaLocation W29124498231 @default.
• W2912449823 hasConcept C103796816 @default.
• W2912449823 hasConcept C118487528 @default.
• W2912449823 hasConcept C142724271 @default.
• W2912449823 hasConcept C15755913 @default.
• W2912449823 hasConcept C169760540 @default.
• W2912449823 hasConcept C203014093 @default.
• W2912449823 hasConcept C2777093970 @default.
• W2912449823 hasConcept C2777506830 @default.
• W2912449823 hasConcept C2777585161 @default.
• W2912449823 hasConcept C2778231335 @default.
• W2912449823 hasConcept C2779113765 @default.
• W2912449823 hasConcept C2780188069 @default.
• W2912449823 hasConcept C2780592520 @default.
• W2912449823 hasConcept C2780640218 @default.
• W2912449823 hasConcept C2780827179 @default.
• W2912449823 hasConcept C2781099447 @default.

• next