How Could Physical Activity Reduce Inflammation and Inflammatory Gene Expression in Rheumatoid Arthritis?
Bibliographic record
Abstract
Exposure to adverse life events and acute physical injury such as that caused by trauma or infection trigger activation of the sympathetic nervous system (SNS) in response to direct signaling from the brain.1-3 This instantly results in enhanced production of adrenaline and noradrenaline by the adrenal glands. Within minutes, the hypothalamic-pituitary-adrenal (HPA) axis is stimulated, leading to increased adrenal gland cortisol secretion. The SNS and HPA axis comprise the main components of the stress system. Stress system activation also involves reduced growth hormone, insulin-like growth factor-1 (IGF-1), androgen and thyroid hormone production, decreased vagal nerve activity, and increased renin-angiotensin-aldosterone system (RAAS) activation. The purpose of these neuroendocrine changes is to orchestrate the release of energy from its stores including the liver, adipose tissue, and muscle in the form of glucose, free fatty acids, and amino acids, and provide it to the activated immune system. This engenders an adequate inflammatory response and its subsequent resolution to reestablish homeostasis. Rheumatoid arthritis (RA) is a prototypic chronic inflammatory disease. Whereas the stress system is also activated in response to RA activity, it does not succeed in resolving the inflammatory process and is therefore unable to restore homeostasis.4 Even though cortisol levels are normal or slightly elevated in patients with RA who have not been treated with exogenous glucocorticoids (GCs), these levels appear to be too low to fully suppress the inflammatory process. This low GC level is thought to be due to cytokine-mediated desensitization of the HPA axis in RA. Additionally, some patients with RA experience GC resistance that may, at least in part, be genetically mediated. This seemingly inadequate cortisol response to RA-induced chronic inflammation may, however, serve to protect patients against persistent hypercortisolemia-induced sepsis. Still, HPA axis sensitivity to stressors other than inflammation, such as hypoglycemia stress, … Address correspondence to Dr. P.H. Dessein, Departments of Medicine and Physiology, University of the Witwatersrand Medical School, 7 York Road, Parktown, 2193, Johannesburg, South Africa. Email: patrick.dessein22{at}gmail.com.
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How this classification was reachedexpand
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 | 0.001 | 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 | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.003 |
| 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 itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, 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".