ArticlebioRxiv : the preprint server for biology2025
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Introduction: Mounting evidence links Methods: Sixteen, fully sequenced Results: Although genetically indistinguishable, the isolates differed markedly in their effects on dysplastic oral keratinocytes (DOK) with isolates from dysplastic lesions demonstrating enhanced proliferation, migration, and invasion of DOK in proportion to the dysplasia severity of their clinical origin. Strikingly, amyloid-like FadA levels were also significantly higher in dysplasia-associated "high-risk" isolates and correlated with their pro-carcinogenic effects. RNA-seq further showed upregulation of heme acquisition genes in high risk isolates. Transcriptome and cytokine profiling of DOK revealed a uniform pro-inflammatory response across all isolates, independent of origin, but genes and pathways related to proliferation correlated with dysplasia severity. Supporting this, 45% of the most severity-correlated host genes identified Conclusion: These results show, for the first time, that clinical oral isolates of
Identifiers
What Socratic 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 Socratic graph.