Publications by authors named "Celeste Cummings"

The pore-forming S. aureus α-toxin (Hla) contributes to virulence and disease pathogenesis. While high concentrations of toxin induce cell death, neutrophils exhibit relative resistance to lysis, suggesting that the action of Hla may not be solely conferred by lytic susceptibility.

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Transposable elements (TE) are selfish genetic elements that can cause harmful mutations. In Drosophila, it has been estimated that half of all spontaneous visible marker phenotypes are mutations caused by TE insertions. Several factors likely limit the accumulation of exponentially amplifying TEs within genomes.

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Article Synopsis
  • Nirsevimab is a monoclonal antibody shown to protect healthy infants from RSV-related lower respiratory tract infections in two clinical trials (phase 2b and MELODY), demonstrating safety similar to the existing drug palivizumab!* -
  • Infants were dosed based on weight (50 mg for those <5 kg and 100 mg for ≥5 kg) and both the pooled efficacy and safety of nirsevimab were analyzed, particularly in infants at higher risk for severe RSV infections due to health conditions or preterm birth.* -
  • The primary goal was to determine the incidence of RSV LRTI requiring medical attention within 150 days post-injection, with secondary focuses on hospital admissions and very
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  • - SARS-CoV-2 activates the host immune system in critically ill patients, highlighting the need for understanding this interaction to develop effective treatments.
  • - The study shows that the viral surface proteins spike (S) and envelope (E) can activate key immune signaling pathways, increasing reactive oxidative species and cytokine production in human and mouse immune cells.
  • - The role of these proteins, especially the envelope protein, is crucial in triggering specific inflammation in the lungs, suggesting their significance in COVID-19 pathology and potential as therapeutic targets.
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Calcium signals are initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed by opening of plasma-membrane calcium-release activated calcium (CRAC) channels. ORAI1, ORAI2, and ORAI3 are known to comprise the CRAC channel; however, the contributions of individual isoforms to neutrophil function are not well understood. Here, we show that loss of ORAI1 partially decreases calcium influx, while loss of both ORAI1 and ORAI2 completely abolishes SOCE.

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