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Full-Text Articles in Physical Sciences and Mathematics
Identifying Important Parameters In The Inflammatory Process With A Mathematical Model Of Immune Cell Influx And Macrophage Polarization, Marcella Torres, Jing Wang, Paul J. Yannie, Shobha Ghosh, Rebecca A. Segal, Angela M. Reynolds
Identifying Important Parameters In The Inflammatory Process With A Mathematical Model Of Immune Cell Influx And Macrophage Polarization, Marcella Torres, Jing Wang, Paul J. Yannie, Shobha Ghosh, Rebecca A. Segal, Angela M. Reynolds
Mathematics and Applied Mathematics Publications
In an inflammatory setting, macrophages can be polarized to an inflammatory M1 phenotype or to an anti-inflammatory M2 phenotype, as well as existing on a spectrum between these two extremes. Dysfunction of this phenotypic switch can result in a population imbalance that leads to chronic wounds or disease due to unresolved inflammation. Therapeutic interventions that target macrophages have therefore been proposed and implemented in diseases that feature chronic inflammation such as diabetes mellitus and atherosclerosis. We have developed a model for the sequential influx of immune cells in the peritoneal cavity in response to a bacterial stimulus that includes macrophage …
Role Of Bcl-2 Family Members To Promote Glucocorticoid –Induced Apoptosis By Mek Inhibitors In Leukemic Cells, Anila Rambal
Role Of Bcl-2 Family Members To Promote Glucocorticoid –Induced Apoptosis By Mek Inhibitors In Leukemic Cells, Anila Rambal
Theses and Dissertations
Glucocorticoids (GC) are common components of many chemotherapeutic regimens for lymphoid malignancies. GC-induced apoptosis involves an intrinsic BCL-2 family-regulated pathway. It has been shown that BIM (BCL-2 interacting mediator of cell death), a BH3-only pro-apoptotic protein, is up-regulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia (ALL) cells. Furthermore, BIM is inactivated by extracellular signal-regulated kinase (ERK)-mediated phosphorylation. We therefore hypothesized co-treatment with Dex and MEK/ERK inhibitors would promote apoptosis in ALL cells through BIM up-regulation and activation. We show here that a MEK inhibitor, PD184352 synergistically enhances Dex lethality in CCRF-CEM (T-ALL) cells. Co-treatment with Dex and PD184352 results …