Publications by authors named "Oluwakemi Phillips"

Background: The purpose of this study is to report the clinical features and outcomes of Black/African American (AA) and Latino Hispanic patients with Coronavirus disease 2019 (COVID-19) hospitalized in an inter-city hospital in the state of New Jersey.

Methods: This is a retrospective cohort study of AA and Latino Hispanic patients with COVID-19 admitted to a 665-bed quaternary care, teaching hospital located in Newark, New Jersey. The study included patients who had completed hospitalization between March 10, 2020, and April 10, 2020.

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Article Synopsis
  • * E1A-immortalized murine embryonic fibroblasts (MEFs) from both POLG-deficient and wild-type (WT) mice showed a pyruvate dependency, with POLG-deficient MEFs being more affected by mitochondrial inhibitors and producing higher levels of reactive oxygen species (ROS).
  • * The study examined how activating AMPK with AICAR and inhibiting mTOR with rapamycin affected mitochondrial function; results indicated varying impacts on respiration and ATP levels depending on the treatment and MEF type, highlighting
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Background: Inflammation is a key hallmark of ALI and is mediated through ungoverned cytokine signaling. One such cytokine, interleukin-1beta (IL-1β) has been demonstrated to be the most bioactive cytokine in ALI patients. Macrophages are the key players responsible for IL-1β secretion into the alveolar space.

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Acute lung injury (ALI), which presents as acute respiratory failure, is a major clinical problem that requires aggressive care, and patients who require prolonged oxygen exposure are at risk of developing this disease. Although molecular determinants of ALI have been reported, the molecules involved in disease catabasis associated with oxygen toxicity have not been well studied. It has been reported that lung mucosa is rich in omega-3 fatty acid dicosahexanoic acid (DHA), which has antiinflammatory properties.

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Hyperoxic acute lung injury (HALI) is characterized by inflammation and epithelial cell death. CLOCK genes are master regulators of circadian rhythm also implicated in inflammation and lung diseases. However, the relationship of CLOCK genes in hyperoxia-induced lung injury has not been studied.

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