ReviewFrontiers in immunology2024
Why is it so difficult to understand why we don't understand human systemic lupus erythematosus? Contemplating facts, conflicts, and impact of "the causality cascade paradigm".
Review in Frontiers in immunology, 2024. 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
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In attempts to understand systemic lupus erythematosus (SLE), we find ourselves in the intellectual cross-point between nosology, pathogenicity-oriented science, philosophy, empiricism, and qualified conjectures. A vital consequence in science theory is that scientific hypotheses that are not critically investigated are in danger of being transformed into scientific dogmas. This statement has consequences for this study. Two central problematic aspects are discussed. For the first, we have to consider new selection principles for classification criteria-implying integration of the causality principle. Second, central historical data must be implemented if we aim to understand SLE. These data comprise famous descriptions of distinct, dynamically changing DNA structures linked to the genetic machinery. These unique structures have since their discoveries decades ago mostly been ignored in SLE research. Likewise, inconclusive dogmatic data indicate that different glomerular ligands are recognized by nephritogenic anti-dsDNA antibodies-exposed chromatin fragments or inherent membrane ligands. These incongruent models have not been comparatively and systematically investigated. Three research areas will be critically discussed: (
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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.