Bibliographic record
Abstract
The irritable bowel syndrome (IBS) may be defined as a painful chronic abdominal symptom complex which is usually associated with altered bowel habit, and for which there is no discernible underlying structural abnormality. It is generally accepted that symptoms are generated by abnormalities of gut function, including altered sensory perception, abnormal motility and, in some patients, abnormalities of epithelial function. Behavioural factors are important, particularly in the reporting of symptoms. What is lacking is an understanding of the pathogenetic mechanisms that alter gut function. IBS is a heterogeneous condition, not only in its clinical presentation and pathophysiology, but also in terms of its pathogenesis. While both central and peripheral factors have been implicated in the pathogenesis of IBS, this article will restrict itself to an evaluation of the evidence supporting inflammation as a basis for altered gut function in IBS. In considering the role of inflammation in IBS, one is prompted to make a comparison with asthma. Like IBS, asthma was once considered a psychosomatic disorder, particularly in non-atopic children. For more than 50 years the treatment of asthma focused on the pharmacological correction of abnormal end organ physiology (that is, airways hyperresponsiveness), an approach that is similar to current therapeutic approaches to IBS, and which are aimed at modulating motor activity or sensory perception. The subsequent discovery of inflammatory cells in the normally sterile broncheoalveolar lavage led to the recognition of asthma as an inflammatory condition. There are two reasons why a similar shift in thinking in IBS will be difficult. Firstly, the gut is normally in a state of controlled inflammation and the challenge of identifying a subtle increase in inflammatory cell number or composition is not to be underestimated. Secondly, IBS is intuitively more heterogeneous than asthma, and inflammation is unlikely to be a factor in all …
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.002 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.002 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 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 itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".