Publications by authors named "Nicholas Choi"

Purpose: We aimed to assess whether the presence of contaminants in the pre-operative urine culture (preop-UC) predicts postoperative urinary tract infection (postop-UTI) in patients undergoing elective ureteroscopy with laser lithotripsy.

Methods: A retrospective chart review was performed from 01/2019 to 12/2021 examining patients with unilateral stone burden ≤ 2 cm who underwent ureteroscopy with laser lithotripsy and had a preop-UC within 3 months. Positive, negative, contaminated, and polymicrobial definitions for UCs were established in accordance with current guidelines.

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Objectives: To examine olfactory performance in African Americans (AA) and Whites by comparing individual scent scores on objective olfactory tests to assess potential racial-ethnic differences of scent detection.

Methods: Cross-sectional study of healthy participants, age 18+ years, and without sinonasal inflammatory disease from June 2021 to April 2022. Included participants self-identified as AA or White.

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Germinal centers (GCs), sites of antibody affinity maturation, are organized into dark (DZ) and light (LZ) zones. Here, we show a B cell-intrinsic role for signal transducer and activator of transcription 3 (STAT3) in GC DZ and LZ organization. Altered zonal organization of STAT3-deficient GCs dampens development of long-lived plasma cells (LL-PCs) but increases memory B cells (MBCs).

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MicroRNAs (miRNAs) are involved in healthy B cell responses and the loss of tolerance in systemic lupus erythematosus (SLE), although the role of many miRNAs remains poorly understood. Dampening miR-21 activity was previously shown to reduce splenomegaly and blood urea nitrogen levels in SLE-prone mice, but the detailed cellular responses and mechanism of action remains unexplored. In this study, using the TLR7 agonist, imiquimod-induced SLE model, we observed that loss of miR-21 in mice prevented the formation of plasma cells and autoantibody-producing Ab-forming cells (AFCs) without a significant effect on the magnitude of the germinal center (GC) response.

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Genome-wide association studies identified variants in the transcription factor gene and several other genes in the STAT4 signaling pathway, such as , , , and , which are associated with an increased risk of developing systemic lupus erythematosus (SLE) and other autoimmune diseases. Consistent with the genome-wide association studies data, STAT4 was shown to play an important role in autoimmune responses and autoimmunity development in SLE mouse models. Despite such important role for STAT4 in SLE development in mice and humans, little is known whether and how STAT4 may regulate extrafollicular Ab-forming cell (AFC) and follicular germinal center (GC) responses, two major pathways of autoreactive B cell development and autoantibody production.

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IL-10 producing B cells (B10 cells) play an important immunoregulatory role in various autoimmune and infection conditions. However, the factors that regulate their development and maintenance are incompletely understood. Recently, we and others have established a requirement for TLR7 in promoting autoimmune antibody forming cell (AFC) and germinal center (GC) responses.

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Although STAT1 tyrosine-701 phosphorylation (designated STAT1-pY701) is indispensable for STAT1 function, the requirement for STAT1 serine-727 phosphorylation (designated STAT1-pS727) during systemic autoimmune and antipathogen responses remains unclear. Using autoimmune-prone B6.Sle1b mice expressing a STAT1-S727A mutant in which serine is replaced by alanine, we report in this study that STAT1-pS727 promotes autoimmune Ab-forming cell (AFC) and germinal center (GC) responses, driving autoantibody production and systemic lupus erythematosus (SLE) development.

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TLR7 is associated with development of systemic lupus erythematosus (SLE), but the underlying mechanisms are incompletely understood. Although TLRs are known to activate type I IFN (T1IFN) signaling, the role of T1IFN and IFN-γ signaling in differential regulation of TLR7-mediated Ab-forming cell (AFC) and germinal center (GC) responses, and SLE development has never been directly investigated. Using TLR7-induced and TLR7 overexpression models of SLE, we report in this study a previously unrecognized indispensable role of TLR7-induced IFN-γ signaling in promoting AFC and GC responses, leading to autoreactive B cell and SLE development.

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Article Synopsis
  • * The study found that in autoimmune-prone mice, abnormal regulation of Spt-GCs is linked to autoimmune diseases, while the presence of a protein called MAVS affects Spt-GC responses and B cell development differently based on the mice's genetic background.
  • * Specifically, MAVS-deficient mice with a mixed genetic background showed significantly reduced Spt-GC activity and B cell issues, but treatment with a TLR7 booster could help, whereas MAVS-deficiency in a specific strain showed normal immune responses, unders
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Hydride abstraction from (Me3Si)3CSiMePhH by Ph3C+ affords the cation [(Me3Si)2CSiMe2-Ph-SiMe2]+, which is shown by X-ray crystallography to contain the first structurally characterised example of a Ph group bridging between two silicon atoms.

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