Publications by authors named "Min-chao Duan"

Rearranged during transfection (RET) fusion-positive occurs in approximately 2% of non-small cell lung cancer (NSCLC). This mutation often predicts metastasis risk and poor prognosis, and current mainstream therapies provide limited patient benefit. Selective RET inhibitors Pralsetinib and Selpercatinib are targeted drugs approved by the US Food and Drug Administration for treating RET-mutated tumors.

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Chronic airway inflammation mediated by CD8 T lymphocytes contributes to the pathogenesis of Chronic obstructive pulmonary disease (COPD). Deciphering the fingerprint of the chronic inflammation orchestrated by CD8 T cells may allow the development of novel approaches to COPD management. Here, the expression of IL-27 and IFN-γ CD8 Tc1 cells were evaluated in patients with COPD and in cigarette smoke-exposed mice.

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BACKGROUND Primary pulmonary mucosa-associated lymphoma tissue lymphoma is rare and is often misdiagnosed because of its diverse and nonspecific clinical features. The aim of this study was to raise awareness among clinicians and to share our experience of treating and managing such patients. MATERIAL AND METHODS This retrospective study was conducted between 1 January 2009 and 31 October 2017 at the First Affiliated Hospital of Guangxi Medical University.

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Plasmacytoid dendritic cells (pDCs) are key cells bridging the innate with adaptive immunity. However, the phenotypic characteristics of circulating pDCs and its role in smoking related-Chronic Obstructive Pulmonary Disease (COPD) remain largely unknown. The aim of this study was analyzed the phenotype of circulating pDCs and the expression of IFN-γ producing CD8T cells and IL-17-producing CD8T cells in patients with COPD by using multi-colour flow cytometry.

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IFN-γ-producing CD4 T (Th1) cells and IL-17-producing CD4 T (Th17) cells play a critical role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the immune regulation between Th1 and Th17 cells remains unclear. Previous studies have demonstrated that interleukin-27 (IL-27)/WSX-1 exerted pro- or anti-inflammatory effects in many acute inflammatory diseases by modulating T cell-mediated immune response, but little was known about its role in chronic inflammatory disease, especially in smoking-related lung diseases.

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Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible chronic inflammatory disease associated with the accumulation of activated T cells. To date, there is little information concerning the intrinsic association among Th17, Tc17, and regulatory T (Treg) cells in COPD. The objective of this study was to investigate the variation of lungs CD4(+)Foxp3(+) Treg cells and IL-17-producing CD4 and CD8 (Th17 and Tc17) lymphocytes in mice with cigarette-induced emphysema.

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The fine balance of T help-17 (Th17)/regulatory T(Treg) cells is crucial for maintenance of immune homeostasis. However, there is little information concerning the role played in non-small cell lung cancer (NSCLC) by Th17/Treg cells. The objective of this study was to investigate the variation of Th17 and Treg cells in the peripheral blood of patients with NSCLC.

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Pathogenic mechanisms underlying the development of lung cancer are very complex and not yet entirely clarified. T lymphocytes and their immune-regulatory cytokines play a pivotal role in controlling tumor growth and metastasis. Following activation by unique cytokines, CD4+ T helper cells differentiate into Th1, Th2, Th17, and regulatory T cells (Tregs).

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Th17 and Tc17 cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a disease caused predominantly by cigarette smoking. Smoking cessation is the only intervention in the management of COPD. However, even after cessation, the airway inflammation may be present.

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Emphysema is a T-cell mediated autoimmune disease caused predominantly by cigarette smoking. Th17 cells and related cytokines may contribute to this disorder. However, the possible implication of Th17 cells in regulating inflammatory response in emphysema remains to be elucidated.

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Objective: To evaluate the expression of interleukin (IL)-21 in a cigarette smoke-induced mice model of emphysema and explore its effects on the differentiation of CD4(+)T cell.

Methods: Twenty male Balb/c mice were randomly divided into two groups: control group and smoke-exposed group. Morphological changes were evaluated by mean linear intercepts and alveolar destructive index.

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Objective: To evaluate the expression of Tc17 in a cigarette smoke-induced mice model of emphysema. To explore the probable mechanisms about how Tc17 cells to elevate in lungs of mice.

Methods: Forty male Balb/c mice were randomly divided into four groups, including control group (12 weeks, C12), control group (24 weeks, C24), smoke-exposure group (12 weeks, S12) and smoke-exposure group (24 weeks, S24), 10 mice each group, Emphysema of mice was observed by HE pigmentation.

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Objective: To evaluate the expression of Th17 cell in a cigarette smoke-induced mice model of emphysema and explore the probable mechanisms of its elevation.

Methods: Forty male Balb/c mice were randomly divided into 4 groups: control group for 12 weeks (C12), control group for 24 weeks (C24), smoke-exposure group for 12 weeks (S12) and smoke-exposure group for 24 weeks (S24)(n = 10 each). Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI).

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Objective: To evaluate the expression and the role of Th17 in cigarette smoke-induced lung inflammation and emphysema in mice.

Methods: Forty male BALB/c mice were randomly divided into 4 groups, including a control group C12, a control group C24, a smoke-exposure 12 week group (S12) and a smoke-exposure 24 week group S24 (n = 10 each). Morphological changes were evaluated by mean linear intercepts and destructive index (DI).

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