Evidence map›Paper›PMID 23140121›Full record

ReviewCritical reviews in biomedical engineering2012

Pharmacokinetic/pharmacodynamic modeling in inflammation.

Hoi-Kei Lon, Dongyang Liu, William J Jusko

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in biomedical engineering, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Metabolites · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Interrelationships between Infliximab and Recombinant Tumor Necrosis Factor-Drug metabolism and disposition: the biological fate of chemicals · 2017
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Moving from basic toward systems pharmacodynamic models.Journal of pharmaceutical sciences · 2013
    Review
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

3 authors at 1 institution in 1 country.

Hoi-Kei LonDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, Buffalo, NY 14214, USA.
Dongyang Liu
William J Jusko
University at Buffalo, State University of New York · US

Funding

Corticosteroid Pharmacokinetics and PharmacodynamicsR37GM024211 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI JUSKO, WILLIAM J. · 2005 to 2014
$6.4M
CORTICOSTEROID PHARMACOKINETICS/DYNAMICSR01GM024211 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI JUSKO, WILLIAM J. · 1985 to 2018
$4.7M
NIGMS NIH HHS GM24211NIGMS NIH HHS R01 GM024211NIGMS NIH HHS R37 GM024211
6 · The paper itself

Abstract

Inflammation is an array of immune responses to infection and injury. It results from a complex immune cascade and is the basis of many chronic diseases such as arthritis, diabetes, and cancer. Numerous mathematical models have been developed to describe the disease progression and effects of anti-inflammatory drugs. This review illustrates the state of the art in modeling the effects of diverse drugs for treating inflammation, describes relevant biomarkers amenable to modeling, and summarizes major advantages and limitations of the published pharmacokinetic/ pharmacodynamic (PK/PD) models. Simple direct inhibitory models are often used to describe in vitro effects of anti-inflammatory drugs. Indirect response models are more mechanism based and have been widely applied to the turnover of symptoms and biomarkers. These, along with target-mediated and transduction models, have been successfully applied to capture the PK/PD of many anti-inflammatory drugs and describe disease progression of inflammation. Biologics have offered opportunities to address specific mechanisms of action, and evolve small systems models to quantitatively capture the underlying physiological processes. More advanced mechanistic models should allow evaluation of the roles of some key mediators in disease progression, assess drug interactions, and better translate drug properties from in vitro and animal data to patients.

Indexed as

Models, BiologicalAnimalsAnti-Inflammatory AgentsComputer SimulationCytokinesHumansInflammationAnti-Inflammatory AgentsCytokines

Identifiers

PMID23140121
PMCPMC3538354
OpenAlexW2009115805

What OpenQuestion holds

Textmetadata
LicenceTDM
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.