Publications by authors named "Zeng-tie Zhang"

Keshan disease (KD) is an endemic dilated cardiomyopathy with unclear etiology. In this study, we compared mitochondrial-related gene expression profiles of peripheral blood mononuclear cells (PBMCs) derived from 16 KD patients and 16 normal controls in KD areas. Total RNA was isolated, amplified, labeled and hybridized to Agilent human 4 × 44k whole genome microarrays.

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Objective: To investigate the changes in the expressions of Fas-associated death domain protein (FADD) and cellular-FLICE inhibitory protein (c-FLIP) in the articular cartilage of patients with Kashin-Beck disease (KBD) and the role of these proteins in the pathogenesis of KBD.

Methods: The cartilage samples were collected from patients with established diagnosis of KBD and osteoarthritis and from healthy control subjects undergoing amputation due to traffic accidents. The expressions of Fas-associated death domain protein (FADD) and cellular-FLICE inhibitory protein (c-FLIP) in the cartilage were detected by immunohistochemistry, and the positive chondrocytes were counted in different layers of the articular cartilage under microscope.

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Objective: To investigate the role of Caspase-8 and Bcl-2 in the formation of loose bodies in Kashin-Beck disease (KBD).

Methods: Specimens of cartilage loose bodies were collected from 50 adult patients with KBD, and the samples of articular cartilage were collected from 10 healthy adults to serve as control. Avidin-biotin alkaline phosphatase immunohistochemistry was employed to examine Bcl-2 and Caspase-8 positivities in the chondrocytes in the loose bodies.

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Objective: To investigate the effects of mycotoxin moniliformin (MON) on the metabolism of aggrecan and type II collagen in human chondrocytes in vitro and the relationship between MON and Kashin-Beck disease (KBD).

Methods: Human chondrocytes were isolated and cultured on bone matrix gelatin to form an artificial cartilage model in vitro with or without MON toxin. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.

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Objective: To explore the effects of selenium and/or iodine deficiency on chondrocyte apoptosis in articular cartilage in rats.

Methods: Forty-eight Sprague-Dawley rats were randomly divided into selenium deficiency group, iodine deficiency group, combined selenium and iodine deficiency group, and control group. Chondrocyte apoptosis was detected by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) method, and Bcl-2 and Bax in articular cartilage were stained by immunohistochemistry in F3 generation of rats.

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Objective: To evaluate the use of cancellous bone matrix gelatin (BMG) combined with chondrocytes in constructing tissue-engineered cartilage by observing the growth, proliferation and differentiation of chondrocytes on allogeneic cancellous BMG.

Methods: The articular chondrocytes isolated from a 1-month-old rabbit were multiplied to a monolayer and seeded onto cancellous BMG to construct tissue-engineered cartilage in vitro during a period of 6 weeks. Samples were taken from the construct after 1, 2, 4, and 6 weeks of culture and evaluated by histology, immunohistochemistry and transmission electron microscopy (TEM).

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Objective: To identify the relationship between T-2 toxin and Kashin-Beck disease (KBD), the effects of T-2 toxin on aggrecan metabolism in human chondrocytes and cartilage were investigated in vitro.

Methods: Chondrocytes were isolated from human articular cartilage and cultured in vitro. Hyaluronic acid (HA), soluble CD44 (sCD44), IL-1beta and TNF-alpha levels in supernatants were measured by enzyme-linked immunosorbent assay (ELISA).

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Objective: To observe cell apoptosis and Bcl-2 and Bax expression changes of chondrocytes induced by butenolide (BUT) and the inhibitory effect of selenium against BUT-induced chondrcyte apoptosis, to gain insights into the mechanism by which BUT induces chondrcyte apoptosis.

Methods: Cartilage tissue reestablished from human fetal articular chondrocytes in vitro were treated with BUT at the concentrations of 0.1, 1.

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Objective: To study the effect of butenolide (BUT) on cultured chondrocytes differentiation and the possible protective effects of selenium (Se).

Methods: Ex-vivo cultured chondrocytes were divided into six groups: (1) Control group (without BUT and Se); (2) Se 0.1 microg/ml control group; (3) BUT 0.

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Objective: To investigate chondrocyte apoptosis and the expressions of Bcl-2, Bax, Fas and iNOS in the articular cartilage between Kashin-Beck disease (KBD) and primary osteoarthritis (OA) and explore the difference in pathogenesis between the two diseases.

Methods: The articular cartilage specimens were collected from 15 normal human subjects, 15 adult patients with KBD and 15 with OA. Chondrocyte apoptosis was detected by TUNEL method, and the expressions of Bcl-2, Bax, Fas and iNOS in articular cartilage were examined with B-SA immunohistochemistry.

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The purpose of the current study was to investigate the abnormal expression of Col X, PTHrP, TGF-beta, bFGF, and VEGF in cartilage from patients with Kashin-Beck disease (KBD) to understand the pathogenesis of chondronecrosis in KBD. Articular cartilage and growth plate cartilage collected were divided into four groups: control children (8 samples, 5 cases), KBD children (19 samples, 9 cases), control adults (8 samples, 6 cases), and KBD adults (16 samples, 15 cases). The presence of PTHrP, TGF-beta1, bFGF, VEGF, and collagen X in articular cartilage and in growth plate cartilage was analyzed by immunohistochemistry.

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Objective: To investigate chondrocyte apoptosis and expression of Fas and inducible nitric oxide synthase (iNOS) in articular cartilage in the pathogenesis of Kashin-beck disease (KBD) and primary osteoarthritis (OA).

Methods: The collected samples of articular cartilage were divided into three groups: normal control (15 cases), KBD adults (15 cases) and OA (15 cases). Chondrocyte apoptosis was detected by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling method, and Fas and iNOS in articular cartilage were stained by immunohistochemistry.

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The present study aimed to determine the role of tissue injury in migration of mesenchymal stem cells (MSCs) intravenously transplanted into heart and to establish experimental basis for improving stem cell therapy in its targeting and effectiveness. MSCs were isolated from bone marrow of male Sprague-Dawley rats and purified by density centrifuge and adhered to the culture plate in vitro. Female rats were divided randomly into four groups.

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Objective: To investigate the characteristics of chondrocyte apoptosis and distribution of Bcl-2, Bax, Fas and iNos expressions in articular cartilage in Kashin-Beck disease (KBD).

Methods: Samples of articular cartilage were collected from 15 healthy children and 15 children with KBD diagnosed according to the Pathological Criteria of KBD Diagnosis in China. Chondrocyte apoptosis was detected by TUNEL method, and the articular chondrocytes positive for Bcl-2, Bax, Fas and iNos were stained by B-SA immunohistochemistry.

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