Publications by authors named "M C Albright"

Centers for Medicare & Medicaid Services provides reimbursement through Hierarchical Condition Category (HCC) coding. Medical systems strive toward risk adjustment optimization, often implementing costly chart review processes. Previously, our organization implementing countermeasures through workflows was complex and performed in silos.

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Article Synopsis
  • Titanium dioxide nanoparticles (TiO NPs) are widely used in food coloring, cosmetics, and industrial materials, with over 1 million metric tons produced globally.
  • The research focuses on comparing three types of TiO NPs (P25, E171, R101) to understand their effects on inflammation, particularly observing the pro-inflammatory response of P25 in both cellular and animal studies.
  • Findings indicate that P25 TiO NPs provoke more inflammation due to their smaller particle size, resulting in a higher number of particles at mass-matched concentrations, which is critical in understanding their inflammatory potential.
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Lung inflammation, caused by acute exposure to ozone (O), one of the six criteria air pollutants, is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung, and their number increases after O exposure. However, the role of AMØs in promoting or limiting O-induced lung inflammation has not been clearly defined.

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Inhalation is a major exposure route to nanoparticles. Following inhalation, nanoparticles first interact with the lung lining fluid, a complex mixture of proteins, lipids, and mucins. We measure the concentration and composition of lung fluid proteins adsorbed on the surface of titanium dioxide (TiO) nanoparticles.

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Lung inflammation, caused by acute exposure to ozone (O) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O exposure. However, the role of AMØs in promoting or limiting O-induced lung inflammation has not been clearly defined.

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