Evidence map›Paper›PMID 27221115›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2016

Mathematical modeling of the circadian dynamics of the neuroendocrine-immune network in experimentally induced arthritis.

R Rao, D DuBois, R Almon, W J Jusko, I P Androulakis

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Pain mechanism and management strategy of rheumatoid arthritis.Frontiers in pain research (Lausanne, Switzerland) · 2025
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  17. Chronopharmacology of glucocorticoids.Advanced drug delivery reviews
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

R RaoDepartment of Chemical and Biochemical Engineering, Rutgers State University of New Jersey, Piscataway, New Jersey;
D DuBoisDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, New York; Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York; and.
R AlmonDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, New York; Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York; and.
W J JuskoDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, New York;
I P AndroulakisDepartment of Chemical and Biochemical Engineering, Rutgers State University of New Jersey, Piscataway, New Jersey; Department of Biomedical Engineering, Rutgers State University of New Jersey, Piscataway, New Jersey yannis@rci.rutgers.edu.
University at Buffalo, State University of New York · USRutgers, The State University of New Jersey · US

Funding

CORTICOSTEROID PHARMACOKINETICS/DYNAMICSR01GM024211 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI JUSKO, WILLIAM J. · 1985 to 2018
$4.7M
NIGMS NIH HHS R01 GM024211
6 · The paper itself

Abstract

The circadian dynamics of important neuroendocrine-immune mediators have been implicated in progression of rheumatoid arthritis pathophysiology, both clinically as well as in animal models. We present a mathematical model that describes the circadian interactions between mediators of the hypothalamic-pituitary-adrenal (HPA) axis and the proinflammatory cytokines. Model predictions demonstrate that chronically elevated cytokine expression results in the development of adrenal insufficiency and circadian variability in paw edema. Notably, our model also predicts that an increase in mean secretion of corticosterone (CST) after the induction of the disease is accompanied by a decrease in the amplitude of the CST oscillation. Furthermore, alterations in the phase of circadian oscillation of both cytokines and HPA axis mediators are observed. Therefore, by incorporating the circadian interactions between the neuroendocrine-immune mediators, our model is able to simulate important features of rheumatoid arthritis pathophysiology.

Indexed as

Circadian RhythmAdrenocorticotropic HormoneAnimalsArthritis, ExperimentalArthritis, RheumatoidCorticosteroneCorticotropin-Releasing HormoneCytokinesHypothalamo-Hypophyseal SystemModels, TheoreticalPituitary-Adrenal SystemReceptors, GlucocorticoidRodentiaAdrenocorticotropic HormoneCorticosteroneCorticotropin-Releasing HormoneCytokinesReceptors, Glucocorticoidexperimentally induced arthritisHPA axismathematical modelingneuroendocrine-immune networkproinflammatory cytokines

Identifiers

PMID27221115
PMCPMC5005970
OpenAlexW2408020614

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.