Evidence map›Paper›PMID 22102145›Full record

ArticleThe Journal of comparative neurology2012

Rearrangement of the cone mosaic in the retina of the rat model of retinitis pigmentosa.

Yerina Ji, Colleen L Zhu, Norberto M Grzywacz, Eun-Jin Lee

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of comparative neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 39 citations in OpenAlex.

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  9. Early detection of cone photoreceptor cell loss in retinitis pigmentosa using adaptive optics scanning laser ophthalmoscopy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019
    Article
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  17. Genetically engineered pig models for human diseases.Annual review of animal biosciences · 2013
    Review
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yerina JiNeuroscience Graduate Program, University of Southern California, Los Angeles, California 90089-1111, USA.
Colleen L Zhu
Norberto M Grzywacz
Eun-Jin Lee
University of Southern California · US

Funding

Mid-Level Vision Systems for Low VisionR01EY016093 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GRZYWACZ, NORBERTO M · 2007 to 2011
$6.0M
Development of Retinal Receptive FieldsR01EY011170 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GRZYWACZ, NORBERTO M · 1997 to 2006
$2.0M
NEI NIH HHS EY016093NEI NIH HHS EY11170NEI NIH HHS R01 EY011170NEI NIH HHS R01 EY016093
6 · The paper itself

Abstract

In retinitis pigmentosa (RP), the death of cones normally follows some time after the degeneration of rods. Recently, surviving cones in RP have been studied and reported in detail. These cones undergo extensive remodeling in their morphology. Here we report an extension of the remodeling study to consider possible modifications of spatial-distribution patterns. For this purpose we used S334ter-line-3 transgenic rats, a transgenic model developed to express a rhodopsin mutation causing RP. In this study, retinas were collected at postnatal (P) days P5-30, 90, 180, and P600. We then immunostained the retinas to examine the morphology and distribution of cones and to quantify the total cone numbers. Our results indicate that cones undergo extensive changes in their spatial distribution to give rise to a mosaic comprising an orderly array of rings. These rings first begin to appear at P15 at random regions of the retina and become ubiquitous throughout the entire tissue by P90. Such distribution pattern loses its clarity by P180 and mostly disappears at P600, at which time the cones are almost all dead. In contrast, the numbers of cones in RP and normal conditions do not show significant differences at stages as late as P180. Therefore, rings do not form by cell death at their centers, but by cone migration. We discuss its possible mechanisms and suggest a role for hot spots of rod death and the remodeling of Müller cell process into zones of low density of photoreceptors.

Indexed as

AgingAnimalsAntibodiesCell DeathCell LineColoring AgentsDisease ProgressionHematoxylinImmunohistochemistryIn Situ Nick-End LabelingOpsinsProliferating Cell Nuclear AntigenRatsRats, Sprague-DawleyRats, TransgenicRetinaAntibodiesColoring AgentsHematoxylinOpsinsProliferating Cell Nuclear AntigenRhodopsin

Identifiers

PMID22102145
PMCPMC3934420
OpenAlexW2089419695

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.