ArticleJournal of pharmacokinetics and pharmacodynamics2006
Pharmacodynamic models for agents that alter production of natural cells with various distributions of lifespans.
Article in Journal of pharmacokinetics and pharmacodynamics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Reticulocyte-based estimation of red blood cell lifespan.Experimental hematology · 2013Trial
- An assessment of recombinant human erythropoietin effect on reticulocyte production rate and lifespan distribution in healthy subjects.Pharmaceutical research · 2007Trial
- The Role of Feedback Control Design in Developing Anemia Management Protocols.Annals of biomedical engineering · 2021Article
- Estimation of adult and neonatal RBC lifespans in anemic neonates using RBCs labeled at several discrete biotin densities.Pediatric research · 2017Article
- The greatly misunderstood erythropoietin resistance index and the case for a new responsiveness measure.Hemodialysis international. International Symposium on Home Hemodialysis · 2016Article
- Models for the red blood cell lifespan.Journal of pharmacokinetics and pharmacodynamics · 2016Article
- A Method to Evaluate Fetal Erythropoiesis from Postnatal Survival of Fetal RBCs.The AAPS journal · 2015Article
- Modeling of delays in PKPD: classical approaches and a tutorial for delay differential equations.Journal of pharmacokinetics and pharmacodynamics · 2014Article
- Computational approaches to analyse and predict small molecule transport and distribution at cellular and subcellular levels.Biopharmaceutics & drug disposition · 2014Review
- Solution and implementation of distributed lifespan models.Journal of pharmacokinetics and pharmacodynamics · 2013Article
- A semi-mechanistic red blood cell survival model provides some insight into red blood cell destruction mechanisms.Journal of pharmacokinetics and pharmacodynamics · 2013Article
- Population pharmacodynamic analysis of erythropoiesis in preterm infants for determining the anemia treatment potential of erythropoietin.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Lifespan based indirect response models.Journal of pharmacokinetics and pharmacodynamics · 2012Review
- Comparative performance of cell life span and cell transit models for describing erythropoietic drug effects.The AAPS journal · 2011Article
- Pharmacodynamic analysis of stress erythropoiesis: change in erythropoietin receptor pool size following double phlebotomies in sheep.Biopharmaceutics & drug disposition · 2011Article
- Interpretation of transit compartments pharmacodynamic models as lifespan based indirect response models.Journal of pharmacokinetics and pharmacodynamics · 2011Article
- Simplification of an erythropoiesis model for design of anemia management protocols in end stage renal disease.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2011Article
- Erythropoietic response to endogenous erythropoietin in premature very low birth weight infants.The Journal of pharmacology and experimental therapeutics · 2010Article
- Pharmacodynamic modeling of the effect of changes in the environment on cellular lifespan and cellular response.Journal of pharmacokinetics and pharmacodynamics · 2008Article
- Modeling time variant distributions of cellular lifespans: increases in circulating reticulocyte lifespans following double phlebotomies in sheep.Journal of pharmacokinetics and pharmacodynamics · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Indirect pharmacodynamic response (IDR) models were developed for agents which alter the generation of cell populations with arbitrary lifespan distributions. These models extend lifespan based IDR models introduced previously [J. Pharmacokinet. Biopharm. 27: 467, 1999] for cell populations with the same lifespan ("delta" distribution). Considered are cell populations exhibiting time-invariant lifespan distributions described by the probability density function l(tau). It is assumed that cell response (R) is produced at a zero-order rate (kin(t)) and is eliminated from the population when the cell lifespan expires. The cell loss rate is calculated as kin*l(t), where '*' denotes the convolution operator. Therapeutic agents can stimulate or inhibit production rates according to the Hill function: 1 +/- H(C(t)) where H(C(t)) contains the capacity (Smax) and potency (SC50) parameters and C(t) is a pharmacokinetic function. The production rate is kin(t) = kin.[ 1+/-H(C(t))]. The operational model is dR/dt = kin(t)-kin*l(t) with the baseline condition R0 = kin.TR, where TR is the mean lifespan. Single populations as well as populations with precursors were examined by simulation to establish the role of lifespan distribution parameters (mean and standard deviation) in controlling the response vs. time profile. Estimability of parameters was assessed. Numerical techniques of solving differential equations with the convolution integral were proposed. In addition, the models were applied to literature data to describe the stimulatory effects of single doses of recombinant human erythropoietin on reticulocytes in blood. The estimates of Smax and SC50 for these agents were obtained along with means and standard deviations for reticulocyte lifespan distributions. The proposed models can be used to analyze the pharmacodynamics of agents which alter natural cell production yielding parameters describing their efficacy and potency as well as means and standard deviations for cell lifespan distributions.
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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.