Publications by authors named "G A Neil"

Purpose: NRL is an influential transcription factor and central to animal modeling in ophthalmology. Disrupting NRL abrogates rod development and produces an excess of S-cones (also known as "UV cones" or "short-wavelength-sensitive1 [SWS1] cones"). Strikingly, mutations in zebrafish tbx2b produce the exact opposite phenotypes (excess rods and loss of SWS1 cones).

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Article Synopsis
  • The study explored barriers and facilitators to using a chatbot tool for collecting family cancer history (FCH) in clinical settings and aimed to understand clinicians' views on its implementation.
  • It involved surveys and interviews to assess the chatbot's acceptability and integration into clinical workflows, gathering feedback from a range of healthcare providers and staff.
  • Results indicated strong support for the chatbot, highlighting the need for customizable implementation strategies to better fit different clinical workflows and enhance the adoption of FCH tools.
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Advances in understanding the physiologic functions of the tumor necrosis factor superfamily (TNFSF) of ligands, receptors, and signaling networks are providing deeper insight into pathogenesis of infectious and autoimmune diseases and cancer. LIGHT (TNFSF14) has emerged as an important modulator of critical innate and adaptive immune responses. LIGHT and its signaling receptors, herpesvirus entry mediator (TNFRSF14), and lymphotoxin β receptor, form an immune regulatory network with two co-receptors of herpesvirus entry mediator, checkpoint inhibitor B and T lymphocyte attenuator, and CD160.

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BACKGROUNDSevere coronavirus disease 2019 (COVID-19) is associated with a dysregulated immune response, which can result in cytokine-release syndrome and acute respiratory distress syndrome (ARDS). Patients with COVID-19-associated ARDS have elevated free serum levels of the cytokine lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT; also known as TNFSF14). Such patients may benefit from LIGHT-neutralization therapy.

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Cellular Prion Protein (PrP) is a well-studied protein as the substrate for various progressive untreatable neurodegenerative diseases. Normal functions of PrP are poorly understood, though recent proteomic and transcriptomic approaches have begun to reveal common themes. We use our compound and knockout mutant zebrafish at three days post fertilization to take a transcriptomic approach to investigating potentially conserved PrP functions during development.

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