Publications by authors named "D Leaffer"

Background: Environmental low frequency noise (LFN < 125 Hz), ubiquitous in urban areas, is an understudied area of exposure science and an overlooked threat to population health. Environmental noise has historically been measured and regulated by A-weighted decibel (dBA) metrics, which more heavily weight frequencies between 2000 and 5000 Hz. Limited research has been conducted to measure and characterize the LFN components of urban environmental noise.

View Article and Find Full Text PDF

Alveolar type I (TI) cells are large squamous cells that cover >95% of the internal surface area of the lung; type II (TII) cells are small cuboidal cells with distinctive intracellular surfactant storage organelles. Based on autoradiographic studies in the 1970s, the long-held paradigm of alveolar epithelial development has been a linear progression from undifferentiated progenitor cells through TII cells to TI cells. Subsequent data support the existence of more complex pathways.

View Article and Find Full Text PDF

Epidemiological studies have linked both traffic-related air pollution (TRAP) and noise to adverse health outcomes, including increased blood pressure, myocardial infarction, and respiratory health. The high correlation between these environmental exposures and their measurement challenges have constrained research on how simultaneous exposure to TRAP and traffic noise interact and possibly enhance each other's effect. The objective of this study was to deploy two novel personal sensors for measuring ultrafine particles (UFP, <100 nm diameter) and noise to concurrently monitor real-time exposures.

View Article and Find Full Text PDF

We have developed a transgenic mouse expressing enhanced green fluorescent protein (EGFP) in virtually all type II (TII) alveolar epithelial cells. The CBG mouse (SPC-BAC-EGFP) contains a bacterial artificial chromosome modified to express EGFP within the mouse surfactant protein (SP)-C gene 3' untranslated region. EGFP mRNA expression is limited to the lung.

View Article and Find Full Text PDF

P38alpha is a protein kinase that regulates the expression of inflammatory cytokines, suggesting a role in the pathogenesis of diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus. Here, we describe the preclinical pharmacology of pamapimod, a novel p38 mitogen-activated protein kinase inhibitor. Pamapimod inhibited p38alpha and p38beta enzymatic activity, with IC(50) values of 0.

View Article and Find Full Text PDF