The genetic control of airway responsiveness and the effect of resiquimod treatment on allergic asthma
Why this work is in the frame
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
Bibliographic record
Abstract
Asthma is a heterogeneous airway disease caused by a mixture of genetic and environmental factors which result in improper immune responses to innocuous antigens.Toll-like receptors (TLR) are pathogen associated pattern recognition receptors which form homo-or heterodimers which bind specific ligands leading to activation and modulation of immune responses.The present study examined the effect of resiquimod, a synthetic toll-like receptor 7 ligand, on the development of allergic asthma pathology in animal models.Resiquimod treatment of ovalbumin sensitized mice prevented the subsequent development of airway hyperresponsiveness and inflammation, increased plasma IgE levels, and both T H 1 and T H 2 cytokine production.This effect was independent of the Mapkapk2 gene but was ineffective in Myd88 knockout mice.A defining feature of asthmatic airways is airway wall remodelling which is characterized by an increase in airway smooth muscle mass, goblet cell hyperplasia, and the deposition of extra-cellular matrix components.The effects of resiquimod treatment on the development of airway remodelling were examined in Brown Norway rats.Resiquimod treatment prevented the increase in airway smooth muscle mass and goblet cell hyperplasia observed in control animals.These effects were associated with a reduction in the number of proliferating airway cells and were preceded by an abrogation of the allergic inflammatory reaction.Employing gene expression microarray analysis, the transcriptome of resiquimod treated, and untreated asthmatic A/J and C57BL/6 mice, was characterized.Asthma induction resulted in the up-regulation of genes involved with the control of cell cycle progression, the complement and coagulation cascades, and chemokine signalling, findings which are consistent with previous reports.Treatment with resiquimod resulted in the normalization of asthma induced genes related to airway remodelling and chemokine signalling.
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Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.002 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.002 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.001 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it