ArticleEmergency medicine international2022
A Signature of Genes Featuring
Article in Emergency medicine international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Retracted: A Signature of Genes FeaturingEmergency medicine international · 2024Article
- An updated review of the immunological mechanisms of keloid scars.Frontiers in immunology · 2023Review
Corrections and comments
- Retraction · 2024-01-24Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Peer Review · Informed/Patient Consent - None/Withdrawn · Investigation by Journal/Publisher · Investigation by Third Party · Lack of IRB/IACUC Approval and/or Compliance · Paper Mill · Computer-Aided Content or Computer-Generated Content · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloid is a fibroproliferative disorder in the skin, which manifested with extensive deposition of collagen and extracellular matrix. Its etiology remains a mystery and its recurrence rate remains high despite combinative treatment regimens. Current hypotheses of its pathogenesis centered on the role of inflammatory processes as well as immune infiltration in the microenvironment. However, there are a lot of discrepancies when it comes to the verification of certain well-recognized pathways involved in the dysfunctional fibroblast. Further exploration and characterization are required to reveal the driving force and even leading genes responsible for keloid formation. In this study, we provided supportive evidence of the immunologic nature of keloids distinct from normal fibroblasts and physiological scars by incorporating multiple available expressional profiles in the Gene Expression Omnibus (GEO). Through differential analyses and functional analyses, we identified a set of genes that successfully captures the dissimilarities between keloid lesions and nonlesions. They were differentially regulated in keloid samples and had opposite behavior in exposure to hydrocortisone. A key signature of six genes featuring
Identifiers
What OpenQuestion holds
Registered trials
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.