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PubMed | The Fifth Affiliated Hospital of Zunyi Medical College
Type: Journal Article | Journal: Transplantation proceedings | Year: 2016

To investigate the expression of RANTES (regulated upon activation, normal T-cell-expressed and -secreted) and monocyte chemoattractant protein-1 (MCP-1) in renal allografts with chronic renal allograft dysfunction (CRAD), and explore its relationship with interstitial fibrosis and tubular atrophy (IF/TA).An immunohistochemical assay and computer-assisted, genuine colored image analysis system were used to detect the expression of RANTES and MCP-1 in renal allografts with CRAD. The relationship among the expression level of MCP-1, RANTES, and the grade of inflammatory cell infiltration, interstitial fibrosis, and tubular atrophy in renal allografts were analyzed. Ten specimens of healthy renal tissue were used as controls.Compared to the normal tissues, the expressions of RANTES and MCP-1 were significantly higher in the renal tissues with CRAD (P< .001), and the expressions tended to increase along with the pathological grade of IF/TA. The expression of RANTES and MCP-1 were positively correlated with the pathological grades of IF/TA (r= 0.940 and 0.954 respectively, P< .001 for both).In renal allograft tissue with CRAD, the up-regulated expressions of RANTES and MCP-1 may be related to the progression of chronic renal allograft dysfunction and allograft fibrosis.


Zhang S.-T.,Jilin University | Zuo C.,The Fifth Affiliated Hospital of Zunyi Medical College | Li W.-N.,Jilin University | Fu X.-Q.,Jilin University | And 2 more authors.
Archives of Gynecology and Obstetrics | Year: 2016

Purpose: To identify key genes related to the effect of estrogen on ovarian cancer. Methods: Microarray data (GSE22600) were downloaded from Gene Expression Omnibus. Eight estrogen and seven placebo treatment samples were obtained using a 2 × 2 factorial designs, which contained 2 cell lines (PEO4 and 2008) and 2 treatments (estrogen and placebo). Differentially expressed genes were identified by Bayesian methods, and the genes with P < 0.05 and |log2FC (fold change)| ≥0.5 were chosen as cut-off criterion. Differentially co-expressed genes (DCGs) and differentially regulated genes (DRGs) were, respectively, identified by DCe function and DRsort function in DCGL package. Topological structure analysis was performed on the important transcriptional factors (TFs) and genes in transcriptional regulatory network using tYNA. Functional enrichment analysis was, respectively, performed for DEGs and the important genes using Gene Ontology and KEGG databases. Results: In total, 465 DEGs were identified. Functional enrichment analysis of DEGs indicated that ACVR2B, LTBP1, BMP7 and MYC involved in TGF-beta signaling pathway. The 2285 DCG pairs and 357 DRGs were identified. Topological structure analysis showed that 52 important TFs and 65 important genes were identified. Functional enrichment analysis of the important genes showed that TP53 and MLH1 participated in DNA damage response and the genes (ACVR2B, LTBP1, BMP7 and MYC) involved in TGF-beta signaling pathway. Conclusion: TP53, MLH1, ACVR2B, LTBP1 and BMP7 might participate in the pathogenesis of ovarian cancer. © 2015, Springer-Verlag Berlin Heidelberg.


PubMed | Jilin University and The Fifth Affiliated Hospital of Zunyi Medical College
Type: Journal Article | Journal: Archives of gynecology and obstetrics | Year: 2016

To identify key genes related to the effect of estrogen on ovarian cancer.Microarray data (GSE22600) were downloaded from Gene Expression Omnibus. Eight estrogen and seven placebo treatment samples were obtained using a 22 factorial designs, which contained 2 cell lines (PEO4 and 2008) and 2 treatments (estrogen and placebo). Differentially expressed genes were identified by Bayesian methods, and the genes with P<0.05 and |log2FC (fold change)|0.5 were chosen as cut-off criterion. Differentially co-expressed genes (DCGs) and differentially regulated genes (DRGs) were, respectively, identified by DCe function and DRsort function in DCGL package. Topological structure analysis was performed on the important transcriptional factors (TFs) and genes in transcriptional regulatory network using tYNA. Functional enrichment analysis was, respectively, performed for DEGs and the important genes using Gene Ontology and KEGG databases.In total, 465 DEGs were identified. Functional enrichment analysis of DEGs indicated that ACVR2B, LTBP1, BMP7 and MYC involved in TGF-beta signaling pathway. The 2285 DCG pairs and 357 DRGs were identified. Topological structure analysis showed that 52 important TFs and 65 important genes were identified. Functional enrichment analysis of the important genes showed that TP53 and MLH1 participated in DNA damage response and the genes (ACVR2B, LTBP1, BMP7 and MYC) involved in TGF-beta signaling pathway.TP53, MLH1, ACVR2B, LTBP1 and BMP7 might participate in the pathogenesis of ovarian cancer.


Wang C.,Southern Medical University | Wang C.,The Fifth Affiliated Hospital of Zunyi Medical College | Wang C.,Shandong University | Chen S.,The Fifth Affiliated Hospital of Zunyi Medical College | And 2 more authors.
Cell Biochemistry and Biophysics | Year: 2014

The aim of this study is to characterize and dynamically monitor the progress of peripheral neuropathy induced by n-hexane by electromyography and nerve conduction velocity (NCV-EMG). Twenty-five patients with n-hexane poisoning from an electronic company were investigated in the year 2009. The occupational history of these workers was collected, and toxic substance exposure was identified. Neurologic inspection and regular NCV-EMG inspection were performed for all patients upon hospital admission and after 3, 6, and 12 months of treatment. NCV-EMG results shown that patients with n-hexane poisoning have simultaneous damage on motor and sensory nerves, of which sensory nerve damage was more severe. Motor nerves of the lower limbs were severe damaged than those of the upper limbs; whereas injury of sensory nerve in the upper limbs was more severe than that of the lower limbs. After treatment, clinical signs and symptoms of the patients were significantly improved. NCV-EMG result showed a delayed worsening at 3 months then gradually recovered after 12 months. Recovery of the motor nerve was better compared with sensory nerve, with upper limbs faster than that of the lower limbs. © 2014 Springer Science+Business Media New York.


Wang Z.J.,The Fifth Affiliated Hospital of Zunyi Medical College | An R.Z.,The Fifth Affiliated Hospital of Zunyi Medical College | Zhao J.Y.,The Fifth Affiliated Hospital of Zunyi Medical College | Zhang Q.,The Fifth Affiliated Hospital of Zunyi Medical College | And 7 more authors.
Genetics and Molecular Research | Year: 2014

After injury, inflammation, or degeneration, articular cartilage has limited self-repair ability. We aimed to explore the feasibility of repair of articular cartilage defects with tissue-engineered cartilage constructed by acellular cartilage matrices (ACMs) seeded with adipose-derived stem cells (ADSCs). The ADSCs were isolated from 3-month-old New Zealand albino rabbit by using collagenase and cultured and amplified in vitro. Fresh cartilage isolated from adult New Zealand albino rabbit were freeze-dried for 12 h and treated with Triton X-100, DNase, and RNase to obtain ACMs. ADSCs were seeded in the acellular cartilaginous matrix at 2 × 107/mL, and cultured in chondrogenic differentiation medium for 2 weeks to construct tissue-engineered cartilage. Twenty-four New Zealand white rabbits were randomly divided into A, B, and C groups. Engineered cartilage was transplanted into cartilage defect position of rabbits in group A, group B obtained ACMs, and group C did not receive any transplants. The rabbits were sacrificed in week 12. The restored tissue was evaluated using macroscopy, histology, immunohistochemistry, and transmission electron microscopy (TEM). In the tissue-engineered cartilage group (group A), articular cartilage defects of the rabbits were filled with chondrocyte-like tissue with smooth surface. Immunohistochemistry showed type II-collagen expression and Alcian blue staining was positive. TEM showed chondrocytes in the recesses, with plenty of secretary matrix particles. In the scaffold group (group B), the defect was filled with fibrous tissue. No repaired tissue was found in the blank group (group C). Tissue-engineered cartilage using ACM seeded with ADSCs can help repair articular cartilage defects in rabbits. © FUNPEC-RP.


PubMed | The Fifth Affiliated Hospital of Zunyi Medical College
Type: Journal Article | Journal: Genetics and molecular research : GMR | Year: 2014

After injury, inflammation, or degeneration, articular cartilage has limited self-repair ability. We aimed to explore the feasibility of repair of articular cartilage defects with tissue-engineered cartilage constructed by acellular cartilage matrices (ACMs) seeded with adipose-derived stem cells (ADSCs). The ADSCs were isolated from 3-month-old New Zealand albino rabbit by using collagenase and cultured and amplified in vitro. Fresh cartilage isolated from adult New Zealand albino rabbit were freeze-dried for 12 h and treated with Triton X-100, DNase, and RNase to obtain ACMs. ADSCs were seeded in the acellular cartilaginous matrix at 2x10(7)/mL, and cultured in chondrogenic differentiation medium for 2 weeks to construct tissue-engineered cartilage. Twenty-four New Zealand white rabbits were randomly divided into A, B, and C groups. Engineered cartilage was transplanted into cartilage defect position of rabbits in group A, group B obtained ACMs, and group C did not receive any transplants. The rabbits were sacrificed in week 12. The restored tissue was evaluated using macroscopy, histology, immunohistochemistry, and transmission electron microscopy (TEM). In the tissue-engineered cartilage group (group A), articular cartilage defects of the rabbits were filled with chondrocyte-like tissue with smooth surface. Immunohistochemistry showed type II-collagen expression and Alcian blue staining was positive. TEM showed chondrocytes in the recesses, with plenty of secretary matrix particles. In the scaffold group (group B), the defect was filled with fibrous tissue. No repaired tissue was found in the blank group (group C). Tissue-engineered cartilage using ACM seeded with ADSCs can help repair articular cartilage defects in rabbits.

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