Publications by authors named "Katharine V Rogers"
Inflammatory bowel disease (IBD) is a heterogeneic disease with a variety of treatments targeting different mechanisms. A multistate, mechanistic, mathematical model of IBD was developed in part 1 of this two-part article series. In this paper, application of the model to predict response of key clinical biomarkers following different treatment options for Crohn's disease was explored.
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- A mathematical model was created to understand inflammatory bowel disease (IBD) by focusing on biological mechanisms in the blood and gut, including cell differentiation and cytokine production.
- The model is adaptable, allowing easy updates to incorporate new biological insights or modify existing pathways between healthy individuals and those with IBD.
- Simulations using the model align with existing data and can test treatment hypotheses by analyzing the response of clinical biomarkers like C-reactive protein and fecal calprotectin to changes in the model parameters.
In this study, we present an effective model All-Trans Retinoic Acid (ATRA)-induced differentiation of HL-60 cells. The model describes reinforcing feedback between an ATRA-inducible signalsome complex involving many proteins including Vav1, a guanine nucleotide exchange factor, and the activation of the mitogen activated protein kinase (MAPK) cascade. We decomposed the effective model into three modules; a signal initiation module that sensed and transformed an ATRA signal into program activation signals; a signal integration module that controlled the expression of upstream transcription factors; and a phenotype module which encoded the expression of functional differentiation markers from the ATRA-inducible transcription factors.
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