ArticleExperimental and therapeutic medicine2018
Immunohistochemical profile of long-standing traumatic retinal detachment in atrophic globe in a young patient.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Endoplasmic reticulum stress: New insights into the pathogenesis and treatment of retinal degenerative diseases.Progress in retinal and eye research · 2020Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Photoreceptor cell death is the ultimate cause of irreversible vision loss in retinal detachment (RD). The present study aimed to investigate the retinal changes in a case of long-standing traumatic RD in a young patient. The RD-induced atrophic globe was examined following enucleation. A control eye acquired from a deceased donor (normal histology; age- and sex-matched) was evaluated correspondingly. Frozen sections of retina tissue were assessed by immunofluorescence staining. The atrophic retina demonstrated structural disruption along with reduction in the retinal outer nuclear layer/inner nuclear layer thickness ratio. Photoreceptor degeneration was noted with complete loss of the outer segment of short-wavelength sensitive (S) cones. In addition, Müller cell hypertrophy was observed across the retinal nuclear layers. These results indicate that RD without successful medical treatment may lead to retinal atrophy associated with disruption of retinal integrity, dramatic S cones loss and subretinal gliosis. Further clarifications of the mechanisms underlying photoreceptor cell death and glial cell reprogramming may facilitate the design of novel therapeutic strategies for RD.
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Registered trials
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