ArticleJournal of mathematical biology2017
Normal and pathological dynamics of platelets in humans.
Article in Journal of mathematical biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 34 citations in OpenAlex.
- The highs and lows of cyclic thrombocytopenia.British journal of haematology · 2024Review
- Numerical methods and hypoexponential approximations for gamma distributed delay differential equations.IMA journal of applied mathematics · 2022Article
- Quantitative systems pharmacology model of thrombopoiesis and platelet life-cycle, and its application to thrombocytopenia based on chronic liver disease.CPT: pharmacometrics & systems pharmacology · 2021Article
- A Blueprint for Identifying Phenotypes and Drug Targets in Complex Disorders with Empirical Dynamics.Patterns (New York, N.Y.) · 2020Article
- Importance of Stability Analysis When Using Nonlinear Semimechanistic Models to Describe Drug-Induced Hematotoxicity.CPT: pharmacometrics & systems pharmacology · 2020Article
- Evaluating the Role of Janus Kinase Pathways in Platelet Homeostasis Using a Systems Modeling Approach.CPT: pharmacometrics & systems pharmacology · 2019Article
- Response of an oscillatory differential delay equation to a periodic stimulus.Journal of mathematical biology · 2019Article
- Cyclic thrombocytopenia with statistically significant neutrophil oscillations.Clinical case reports · 2018Article
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We develop a mathematical model of platelet, megakaryocyte, and thrombopoietin dynamics in humans. We show that there is a single stationary solution that can undergo a Hopf bifurcation, and use this information to investigate both normal and pathological platelet production, specifically cyclic thrombocytopenia. Carefully estimating model parameters from laboratory and clinical data, we then argue that a subset of parameters are involved in the genesis of cyclic thrombocytopenia based on clinical information. We provide model fits to the existing data for both platelet counts and thrombopoietin levels by changing four parameters that have physiological correlates. Our results indicate that the primary change in cyclic thrombocytopenia is an interference with, or destruction of, the thrombopoietin receptor with secondary changes in other processes, including immune-mediated destruction of platelets and megakaryocyte deficiency and failure in platelet production. This study contributes to the understanding of the origin of cyclic thrombocytopenia as well as extending the modeling of thrombopoiesis.
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Registered trials
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.