Publications by authors named "Bihua Xu"

The function of transient receptor potential vanilloid (TRPV) cation channels governing B cell activation remains to be explored. We present evidence that TRPV2 is highly expressed in B cells and plays a crucial role in the formation of the B cell immunological synapse and B cell activation. Physiologically, TRPV2 expression level is positively correlated to influenza-specific antibody production and is low in newborns and seniors.

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Background: Smad7 is protective in a mouse model of rheumatoid arthritis. Here we investigated whether Smad7-expressing CD4 T cells and the methylation of gene in CD4 T cells contribute to the disease activity of RA in patients.

Methods: Peripheral CD4 T cells were collected from 35 healthy controls and 57 RA patients.

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Rheumatoid arthritis (RA) is a common disease worldwide and is treated commonly with methotrexate (MTX). CS12192 is a novel JAK3 inhibitor discovered by Chipscreen Biosciences for the treatment of autoimmune diseases. In the present study, we examined the therapeutic effect of CS12192 against RA and explored if the combinational therapy of CS12192 and MTX produced a synergistic effect against RA in rat collagen-induced arthritis (CIA).

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An excellent flushing efficiency evaluation device is indispensable for studying the cementing flushing fluid. However, the existing flushing efficiency evaluation device cannot simulate the formation and flushing process of the downhole mud cake. Therefore, this paper proposes a novel flushing efficiency evaluation device that can simulate the formation and flushing of downhole mud cakes.

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Objective: NLRP3 inflammasome regulates T cell responses. This study examined the roles of NLRP3 inflammasome activation in the regulation of T follicular helper (Tfh) cells during humoral response to T dependent antigens and in systemic lupus erythematosus (SLE).

Methods: NLRP3 inflammasome activation of Tfh cells was studied in B6, MRL/lpr and NZM2328 mice and in SLE patients and healthy controls using a fluorescence-labelled caspase-1 inhibitor probe.

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Transforming growth factor-β (TGF-β) plays a critical role in the pathological processes of various diseases. However, the signaling mechanism of TGF-β in the pathological response remains largely unclear. In this review, we discuss advances in research of Smad7, a member of the I-Smads family and a negative regulator of TGF-β signaling, and mainly review the expression and its function in diseases.

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Article Synopsis
  • The study investigates the role of Smad3 signaling in beta cell function and type 2 diabetes by using genetically modified mice with Smad3 deletion.
  • The research found that Smad3 deficiency prevents diabetes-induced beta cell loss and dysfunction, identifying over 8,000 genes that are differentially expressed in response to Smad3.
  • The preservation of Pax6, a crucial mediator for beta cell development, due to Smad3 deficiency enhances both beta cell proliferation and insulin secretion, suggesting Smad3 as a potential therapeutic target for type 2 diabetes.
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Background: Transforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise role of Smad3 in the pathogenesis of diabetic nephropathy remains unclear.

Methods: Smad3 knockout (KO)-db/db mice were generated by intercrossing of male and female double-heterozygous Smad3 db/m mice. Renal functions including urinary albumin excretion and serum creatinine were determined.

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Follicular T regulatory (Tfr) cells inhibit follicular T helper (Tfh) cells mediated B cell responses. Tfh cells are involved in the pathogenesis of systemic lupus erythematosus (SLE). However, the role of Tfr cells in SLE remains unclear.

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Objective: Development of proteinuria in lupus nephritis (LN) is associated with podocyte dysfunction. The NLRP3 inflammasome has been implicated in the pathogenesis of LN. The purpose of this study was to investigate whether NLRP3 inflammasome activation is involved in the development of podocyte injury in LN.

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Lysosomal membrane permeabilization (LMP) has been shown to cause the release of cathepsins and other hydrolases from the lysosomal lumen to the cytosol and initiate a cell death pathway. Whether proteinuria triggers LMP in renal tubular epithelial cells (TECs) to accelerate the progression of renal tubulointerstitial injury remains unclear. In the present study, we evaluated TEC injury as well as changes in lysosomal number, volume, activity, and membrane integrity after urinary protein overload in vivo and in vitro.

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The present study aimed to evaluate the effects of an individualized, low-dose multi-drug immunosuppressive regimen for the treatment of immunoglobulin A nephropathy (IgAN). A preliminary investigation of the course of IgAN following immunosuppressive treatment was conducted based on repeat renal biopsies. Clinical and pathological data of 17 patients with IgAN who received repeat renal biopsies were analyzed retrospectively.

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