Publications by authors named "Yuwei Zhan"

Breast cancer is a prevalent global disease that requires the development of effective therapeutic approaches. The occurrence of 5-fluorouracil (5-FU) resistance in breast cancer is emerging, which urgently needs new way to overcome the obstacle. In this study, we validated that the expression of LINC00467 is up-regulated in the breast cancer patients and breast cancer cells.

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Dysregulated maturation and activation of dendritic cells (DCs) play a significant role in the progression of systemic lupus erythematosus (SLE). The autophagy-lysosome pathway has been identified as a potential mechanism to inhibit DC activation and maturation, but its precise workings remain unclear. We investigated the role and regulatory mechanism of TLR9 in modulating the autophagy-lysosome pathway and DCs activation.

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Background: Cardiovascular diseases (CVD) occurrence were associated with rheumatoid arthritis (RA) and Mediterranean diet (MD), but few studies have been conducted to explore the combined effect. This study was to outline the relationship of coexistence of RA and MD on the risk of CVD based on the National Health and Nutrition Examination Survey (NHANES) database.

Methods: The data of this cross-sectional study was from the NHANES 2005-2010.

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Background: Sirtuin 1 (SIRT1) is reported downregulated in rheumatoid arthritis (RA), and the protective effects of SIRT1 on tissue damage and organ failure may be related to cellular ferroptosis. However, the exact mechanism by which SIRT1 regulates RA remains unclear.

Methods: Quantitative real-time PCR (qPCR) and western blot assays were performed to explore the expressions of SIRT1 and Yin Yang 1 (YY1).

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Background: Alterations in oral microbiota in patients with systemic lupus erythematosus (SLE) is less evaluated. The aim of this study was to compare the characteristics of the oral microbiome in SLE patients and healthy controls, and construct an SLE classifier based on the oral microbiota.

Methods: We sequenced tongue-coating samples of individuals in treatment-naïve SLE (n = 182) and matched healthy controls (n = 280).

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Background: Researches have confirmed that the abnormal signals of OX40 and PD-1 lead to the changes of T cell biological behavior, thus participating the immunopathological process of RA. However, the pathogenesis of RA immunopathological process has not been clarified yet.

Methods: 30 DBA/1 mice were randomly divided into 5 groups (6 mice per group): control group, collagen-induced arthritis (CIA) group, PD-1-Fc/CIA group, OX40-Fc/CIA group, and PD-1-Fc + OX40-Fc/CIA group.

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The Anderson localization transition in a two-dimensional AIIsystem is studied by eigenvalue statistics and then confirmed by the multifractal analysis of the wave functions at the transition point. The system is modeled by a two-dimensional lattice structure with real-quaternion off-diagonal elements and complex on-site energies, whose real and imaginary parts are two independent random variables. Via finite-size scaling analysis of eigenvalue spacing ratios, we find the non-Hermiticity reduces the critical disorder and give an estimate of the critical exponent= 1.

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Introduction: Rheumatoid arthritis (RA) is an autoimmune disease that affects millions of people. Fibroblast-like synoviocytes (FLSs) located in rheumatoid panni play a pivotal role in the formation of RA. The long noncoding RNA (lncRNA) is reportedly downregulated in rheumatoid arthritis.

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Rheumatoid arthritis (RA) is a T lymphocyte-mediated autoimmune disease, although its immune mechanism has not been fully studied. In this study, healthy controls (HC), osteoarthritis patients (OA), and RA patients were enrolled, and mice were evenly divided into control, collagen-induced arthritis (CIA), PD-1 Fc/CIA (PD-1 Fc membrane fusion protein administered to CIA mice), OX40 Fc/CIA (OX40 Fc membrane fusion protein administered to CIA mice), and PD-1 Fc + OX40 Fc/CIA groups. The expressions of programmed death-1 (PD-1) and OX40 in CD4 T lymphocytes and the levels of sPD-1, immunoglobulin, and proinflammatory factors in patients and mice were measured.

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