Publications by authors named "Benjamin Stephenson"
N95 filtering facepiece respirator contamination with SARS-CoV-2 following reuse and extended use.
Infect Control Hosp Epidemiol
July 2025
Objective: During the COVID-19 pandemic, the United States Centers for Disease Control and Prevention provided strategies, such as extended use and reuse, to preserve N95 filtering facepiece respirators (FFR). We aimed to assess the prevalence of N95 FFR contamination with SARS-CoV-2 among healthcare personnel (HCP) in the Emergency Department (ED).
Design: Real-world, prospective, multicenter cohort study.
Ghrelin circulates in acylated (AG) and deacylated (DAG) isoforms and both may impact endothelial function (EF). Although acute exercise has been shown to modulate ghrelin levels and EF, data on the impact of exercise intensity on these parameters are scarce. To investigate the effect of exercise intensity and sex on EF and ghrelin levels, nine males (age: 43.
View Article and Find Full Text PDFContext: Ghrelin circulates in acylated (AG) and deacylated (DAG) forms, which are known to affect appetite. Although acute exercise has been shown to modulate ghrelin levels, data on the impact of exercise intensity on AG and DAG levels and their effects on appetite are sparse and primarily limited to males.
Objective: To investigate the effect of exercise intensity and sex on ghrelin levels and appetite in untrained humans.
Introduction: We reported that Ca-independent phospholipase Aβ (iPLAβ)-derived lipids (iDLs) contribute to type 1 diabetes (T1D) onset. As CD4 and CD8 T cells are critical in promoting β-cell death, we tested the hypothesis that iDL signaling from these cells participates in T1D development.
Methods: CD4 and CD8 T cells from wild-type non-obese diabetic () and .
Article Synopsis
- - Type 1 diabetes (T1D) is caused by autoimmune destruction of insulin-producing β-cells, with macrophages playing a key role in this process through lipid signaling.
- - Reducing myeloid-iPLA2β in NOD mice leads to less inflammation, encourages a shift to anti-inflammatory macrophages, and decreases T-cell activation, which is linked to lower T1D rates.
- - Targeting iPLA2β in macrophages presents a promising strategy to slow down or prevent the onset of T1D by modulating inflammatory responses.
Background: Traumatic brain injury (TBI) causes neuroinflammation and can lead to long-term neurological dysfunction, even in cases of mild TBI (mTBI). Despite the substantial burden of this disease, the management of TBI is precluded by an incomplete understanding of its cellular mechanisms. Sphingolipids (SPL) and their metabolites have emerged as key orchestrators of biological processes related to tissue injury, neuroinflammation, and inflammation resolution.
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