Publications by authors named "Chengang Zhu"

Objectives: Acute type A aortic dissection is a life-threatening cardiovascular disease commonly seen in emergency department, resulting in substantial mortality and morbidity. We aimed to investigate the prognostic value of N-terminal pro-B type natriuretic peptide (NT-proBNP) among this critically ill population.

Design: The design of this study was a retrospective cohort study.

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Objectives: This study sought to validate the V-RESOLVE score system.

Background: The V-RESOLVE score was developed to predict the risk of side branch (SB) occlusion after stenting in the main vessel (MV) of coronary bifurcation lesions based on visual estimation of the angiographic data, but it needed to be validated.

Methods: From January to June 2013, 1,286 patients with 1,820 bifurcation lesions undergoing elective intervention with provisional strategy were included.

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Introduction: The intentional strategy (aggressive side branch (SB) protection strategy: elective two-stent strategy or jailed balloon technique) is thought to be associated with lower SB occlusion rate than conventional strategy (provisional two-stent strategy or jailed wire technique). However, most previous studies showed comparable outcomes between the two strategies, probably due to no risk classification of SB occlusion when enrolling patients. There is still no randomised trial compared the intentional and conventional strategy when treating bifurcation lesions with high risk of SB occlusion.

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Objectives: To investigate the predictors of and generate a risk prediction method for periprocedural myocardial infarction (PMI) after percutaneous coronary intervention (PCI) using the new PMI definition proposed by the Society for Cardiovascular Angiography and Interventions (SCAI).

Background: The SCAI-defined PMI was found to be associated with worse prognosis than the PMI diagnosed by other definitions. However, few large-sample studies have attempted to predict the risk of SCAI-defined PMI.

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ZNF300, which plays the role in human embryonic development and some diseases, is a typical KRAB/C2H2 zinc finger gene expressed only in higher mammalians. Our data showed that expression of ZNF300 changed significantly in various leukemia blasts in the bone marrow aspirates of newly diagnosed leukemia patients. To investigate the potential relationship between expression of ZNF300 and the progression of leukemia development and hematopoietic differentiation, we cloned and characterized the putative human ZNF300 gene promoter and identified its transcription start sites (TSSs).

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C3 convertase regulatory proteins, decay accelerating factor (DAF, CD55) and membrane cofactor protein (MCP, CD46), have complementary function and transfected into non-human cells might confer protection against human complement. This may be an effective strategy to alleviate C-mediated cell damage by combining the two activities. In this study, we constructed a dicistronic mammalian expression vector pcDNA3-MCPIRESDAF using the internal ribosomal entry sites (IRES) of the encephalomyocarditis virus (EMCV), and stable cell lines were obtained by G418 screening.

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The human ZNF268 gene was initially described as a gene associated with early human embryogenesis and was later implicated in human leukemia due to the identification of an alternatively splice form in leukemia patients. To systematically evaluate the correlation of ZNF268 with human hematological malignancy, expression of different alternatively spliced forms of ZNF268 mRNA in peripheral blood of 45 patients with hematological malignancies and 17 healthy donors were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and nested PCR. We demonstrated that presence of ZNF268a, ZNF268c, ZNF268f and ZNF268g were significantly different between the patients and healthy donors (P<0.

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Nonsense-mediated mRNA decay (NMD), also called RNA surveillance, is a process that degrades mRNAs with premature translation termination codons. In Saccharomyces cerevisiae, it has also been shown that NMD can regulate gene expression at the transcriptional level. To date, there has been no example where promoters are regulated by the NMD pathway in higher eukaryotes.

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The aim has been to determine whether the supernatants of mesenchymal stem cells (MSCs) transfected with adenovirus carrying human heme oxygenase-1 (hHO-1) gene protect cardiomyocytes from ischemic injury. We have found that hHO-1 infected MSCs (hHO-1-MSCs) increased expression of hHO-1 protein. Apoptosis of cultured hHO-1-MSCs exposed to hypoxia was suppressed.

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Objective: Bone marrow mesenchymal stem cells (MSCs) have the potential to repair the infarcted myocardium and improve cardiac function. However, this approach is limited by its poor viability after transplantation, and controversy still exists over the mechanism by which MSCs contribute to the tissue repair.

Methods: The human heme oxygenase-1 (hHO-1) was transfected into cultured MSCs using an adenoviral vector.

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Background: Emerging data suggest that inflammation may play an important role in the pathogenesis of coronary artery disease. However, the relation of inflammatory status to coronary vasospasm has been less investigated in patients with variant angina (VA).

Purpose: The aim of this study, therefore, was to determine peripheral circulating white blood cells as well as monocyte cells and plasma C-reactive protein (CRP) and interleukin-6 (IL-6) levels in patients with VA, and to compare patients with VA, stable coronary artery disease, and controls with angiographically normal coronary arteries.

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Expression of the human T-cell leukemia virus type 1 (HTLV-1) oncoprotein Tax is correlated with cellular transformation, contributing to the development of adult T-cell leukemia. In this study, we investigated the role of Tax in the regulation of the ZNF268 gene, which plays a role in the differentiation of blood cells and the pathogenesis of leukemia. We demonstrated that ZNF268 mRNA was repressed in HTLV-1-infected cells.

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Vascular calcification is an age-dependent, common finding in human coronary arteries and begins as early as the second decade of life, just after fatty streak formation. Previous studies have showed that the severity of coronary calcification is closely related to atherosclerotic plaque burden and cardiac event rate. In the past few decades, coronary calcification has been considered passive and degenerative.

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Background: The pathophysiological mechanism in cardiac syndrome X has been suggested as impairment in normal endothelial function of the coronary microvasculature, resulting in inadequate flow reserve. However, despite the extensive studies, the precise mechanisms in cardiac syndrome X remain unclear.

Purpose: The present study was, therefore, to investigate whether inflammatory cells and markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) might be involved in the pathogenesis of cardiac syndrome X.

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The ZNF268 gene was originally isolated from an early human embryo cDNA library. Several different transcripts have been isolated for the ZNF268 gene and developmental expression studies suggest that ZNF268 plays a role in the development of human fetal liver and the differentiation of blood cells. In our effort to study the functions of ZNF268 in different organs during development and in pathogenesis, we have now identified 3 novel splicing isoforms, ZNF268e, ZNF268f and ZNF268g, in human fetal tissues and human tumor derived cell lines.

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Human ZNF268 gene is a typical Krüppel-associated box/C2H2 zinc finger gene whose homolog has been found only in higher mammals and not in lower mammals such as mouse. Its expression profiles have suggested that it plays a role in the differentiation of blood cells during early human embryonic development and the pathogenesis of leukemia. To gain additional insight into the molecular mechanisms controlling the expression of the ZNF268 gene and to provide the necessary tools for further genetic studies of leukemia, we have mapped the 5'-end of the human ZNF268 mRNA by reverse transcription-PCR and primer extension assays.

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