Publications by authors named "Nicholas D Boespflug"
Article Synopsis
- The ATF3 gene is triggered by TLR signaling and acts to inhibit pro-inflammatory genes driven by TLRs, playing a significant role in regulating immune responses.
- In studies with mice, deleting ATF3 led to increased CXCL1 production in response to LPS, but surprisingly, it did not result in higher levels of neutrophils in the airways post-challenge.
- ATF3-deficient neutrophils displayed impaired movement due to reduced TIAM2 levels, affecting their ability to migrate, suggesting ATF3 has a complex role in both suppressing inflammation and facilitating neutrophil movement.
Article Synopsis
- CYP1 monooxygenases are involved in the biosynthesis and inactivation of lipid mediators, but their specific metabolic roles are not fully understood. Researchers used advanced techniques to analyze lipid mediator profiles in knockout mice lacking CYP1 genes compared to wild-type mice.
- In the absence of CYP1 enzymes, no significant differences in untreated mice were observed regarding cell counts or CYP1 activity; however, during inflammation induced by zymosan, knockout mice displayed increased neutrophil recruitment and altered levels of various lipid mediators.
- The study found significant changes in the metabolomic profiles of lipid mediators due to zymosan stimulation, revealing that CYP1 enzymes play a critical role in regulating these mediators and influencing
Introduction: A large proportion of clinical islet transplant recipients fail to initially achieve or sustain meaningful independence from exogenous insulin use. We hypothesized that immediate allograft injury is a key constraint on independence from exogenous insulin use.
Methods: Standard human leukocyte antigen genotyping was reviewed to identify nonshared polymorphisms between 21 prospectively recruited islet transplant recipients from a single institution and their respective donors.
Background: There is no reliable serum marker available to monitor incipient pancreas or islet-cell rejection. We tested the hypothesis that quantification of donor-specific genomic DNA in serum (from tissue damage) can serve as a marker of rejection.
Methods: Using a recently developed panel of HLA-specific quantitative PCR assays (Q-PCR), we tested 158 sera from 42 pancreas-kidney transplant recipients.