Publications by authors named "Yong-zhi Deng"

Background: Coronary artery bypass graft (CABG) and percutaneous coronary intervention (PCI) are the main treatment methods for left main artery disease (LMAD) and triple-vessel coronary artery disease (TVCAD).

Objective: This study aimed to evaluate the five-year post-treatment effects of CABG and PCI in patients with severe coronary vasculopathy.

Methods: A total of 430 patients with LMAD and/or triple-vessel coronary artery disease from November 2014 to July 2015 were enrolled retrospectively in the affiliated cardiovascular hospital of Shanxi Medical University and divided into the CABG group and PCI group.

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Ovarian cancer is the most deadly malignancy among women, but its complex pathogenesis is unknown. Most patients with ovarian cancer have a poor prognosis due to high recurrence rates and chemotherapy resistance as well as the lack of effective early diagnostic methods. The tumor microenvironment mainly includes extracellular matrix, CAFs, tumor angiogenesis and immune-associated cells.

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Severe acute lung injury (ALI) cause significant morbidity and mortality worldwide. MicroRNAs (miRNAs) are possible biomarkers and therapeutic targets for ALI. We aimed to explore the role of miR-762, a known oncogenic factor, in the pathogenesis of ALI.

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Background: spontaneous esophageal rupture (Boerhaave's syndrome) is a rare and challenging clinical condition.

Objective: to evaluate the outcome of different surgical treatments for patients with Boerhaave's syndrome with an early diagnosis (< 24 h) and delayed diagnosis (> 24 h), using a retrospective cohort study in a tertiary referral center.

Patients And Methods: eighty-eight patients with Boerhaave's syndrome who underwent surgical treatment were identified from March 1994 to March 2019 in the First Hospital of Shanxi Medical University.

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Autophagy is implicated in the maintenance of cardiac homeostasis. Autophagy is activated in heart failure, in which reactive oxygen species (ROS) are increased. Exogenous ROS have been shown to induce cardiomyocyte autophagy alterations.

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It has been reported that resistin induces, whereas apelin inhibits cardiac hypertrophy. However, the underlying molecular mechanisms of apelin inhibiting resistin-induced cardiac hypertrophy remain unclear. The aim of the current study is to investigate the effects of apelin on resistin-induced cardiomyocyte hypertrophy and elucidate the underlying molecular mechanism.

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Resistin has been previously demonstrated to induce cardiac hypertrophy, however, the underlying molecular mechanisms of resistin-induced cardiac hypertrophy remain unclear. Using H9c2 cells, the present study investigated the liver kinase B1 (LKB1)/adenosine monophosphate-activated protein kinase (AMPK) signaling pathway for a potential role in mediating resistin-induced cardiomyocyte hypertrophy. Treatment of H9c2 cells with resistin increased cell surface area, protein synthesis, and expression of hypertrophic marker brain natriuretic peptide and β-myosin heavy chain.

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Cytokines and chemokines play an important role in defense against viral infection and modulating immune response. However, expression prolife of serum cytokines and chemokines, which were associated with the outcome of patients in response to anti-HCV treatment have not been fully elucidated. The current study aimed to determine the expression pattern of cytokines and chemokines in chronic HCV infection and their association with outcome in response to therapy.

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Aim: To investigate the effects of H2-Bl gene on biological behaviour of mouse vascular smooth muscle cells (VSMCs) including apoptosis, proliferation and anti-cytolysis to peripheral blood mononuclear cells (PBMCs), then speculate the possible mechanism of immunological rejection after heart transplantation in maternal-fetal immune tolerance.

Methods: The mouse VSMC were transfected with 0.5 mg/L of pEGFP-N1 plasmid vector, 0.

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Objective: To investigate the potential cell sources of neointimal cells in autologous vein graft in rat model.

Methods: Vein graft neointimal cell origins were investigated using a model of vein-to-artery interposition modal. Slides were stained with hematoxylin and eosin, immunohistochemical staining was also performed with primary antibodies alpha-smooth actin or CD34.

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Objective: To investigate whether knockdown Pik3cb p110beta subunit by shRNA in autologous vein grafts can reduce intimal hyperplasia.

Methods: 180 adult SD rats underwent carotid artery bypass graft surgery by using the autologous branch of jugular vein, and they were randomly divided into 6 equal groups: Group A (with the jugular vein grafts treated with 25% Pluronic F-127 only), Group B (with the graft treated with the plasmid encoding shRNA targeting Pik3cb p110beta subunit, pU6-Pik3cb-shRNA-1), Group C (with the graft treated with the plasmid encoding shRNA targeting Pik3cb p110beta subunit, pU6-Pik3cb-shRNA-2), Group D (with the graft treated with the half pU6-Pik3cb-shRNA-1 and pU6-Pik3cb-shRNA-2), and Group E (with the graft treated with the pGenesil-1 scramble shRNA), and Group F (with the jugular vein grafts treated with wortmannin). Specimens of jugular vein graft were harvested 1, 3, 7, 14, and 28 days after surgery to assess the neointimal hyperplasia.

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Aim: To investigate inhibitory effects of RNA interference on MyD88 expression in murine myeloid dendritic cells(DCs) and detect the biological activity of DCs.

Methods: Three pairs of myeloid differentiation factor 88(MyD88) siRNA were synthesized and transfected into DCs by RNAi-mate. The mRNA and protein expression of MyD88 were analyzed by semi-quantified RT-PCR and Western blot.

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