Central Hospital of Nanyang

Nanyang, China

Central Hospital of Nanyang

Nanyang, China
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Gan X.,Central Hospital of Nanyang | Nan W.-L.,Zhengzhou University
Chinese Journal of Tissue Engineering Research | Year: 2016

BACKGROUND: Nerve tissue-engineered scaffolds must have axially aligned structures, that can promote oriented growth of new axons, to guarantee the effective repair and regeneration of damaged nerves. OBJECTIVE: To investigate the effect of heparin sulfate/collagen nerve tissue-engineered scaffolds on peripheral nerve injury repair. METHODS: Heparin sulfate/collagen nerve tissue-engineered scaffolds were prepared, and its internal structure and porosity was observed and measured. Then rat Schwann cells were seeded on the scaffolds to observe cell adhesion. Afterwards, 32 rats undergoing removal of left sciatic nerve were randomly divided into two groups (n=16 per group), and the rats were implanted by heparin sulfate/collagen nerve tissue-ergineered scaffolds as experimentd group, and the rats were implanted by autdogous sciatic nerve as control group. At 16 weeks after implantation, diameter, thickness of myelin sheath as well as density of myelinated nerve fiber, the percentage of neural tissue and electrophysiology was detected, respectively. RESULTS AND CONCLUSION: The tissue-engineered scaffolds whose porosity was 91% were composed of microtubules arranging parallelly along the axial direction, and the microtubule diameter was 180 µm; the scaffolds had good biocompatibility with the Schwann cells. In addition, at 16 weeks after implantation, no significant differences were found in myelin sheath thickness, myelinated nerve fiber density, as well as conduction velocity and latency of motor and sensory nerves between two groups; compared with the control group, diameter of myelinated nerve fiber, percentage of neural tissue and amplitude of motor and sensory nerves in the experimental group were significantly decreased (P < 0.05). To conclude, the heparin sulfate/collagen nerve tissue-engineered scaffold can effectively repair peripheral nerve injury, but its effect is weaker than that of autologous nerve repair. © 2016, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Cao L.N.,Central Hospital of Nanyang | Xu B.L.,Central Hospital of Nanyang
Chinese Journal of Tissue Engineering Research | Year: 2016

BACKGROUND: Skin reproducing membrane is a biomaterial used directly in contact with skin defects, so its toxicity to the body must be taken into consideration. OBJECTIVE: To systematically evaluate the biocompatibility of skin reproducing membrane of medical fibroin. METHODS: Skin irritation test: the skin defect of New Zealand white rabbit was covered with the skin reproducing membrane of medical fibroin, formaldehyde or normal saline, respectively, and erythema and edema were observed at 24 and 72 hours after treatment. Acute systematic toxicity test: the mice were given extracts of skin reproducing membrane of medical fibroin, phenol and normal saline via tail vein injection; then status of mice, toxicity grade and death were recorded at 24, 48 and 72 hours after injection. Cytotoxicity test: L-929 cells were co-cultured with 100%, 50%, 25%, 10% skin reproducing membrane of medical fibroin extracts, and absorbance values were detected by ultraviolet spectrophotometry at 2, 4 and 7 days after culture, as well as by MTT assay after 48 hours of culture, respectively. Besides, L-929 cells were co-cultured with 100% skin reproducing membrane of medical fibroin extracts, and mRNA expression of fibronectin was determined by qPCR technology after 48-hour culture. RESULTS AND CONCLUSION: Skin reproducing membrane of medical fibroin has no adverse reaction, acute cytotoxicity, skin irritation and systemic toxicity, and additionally, it does not affect mRNA expression of fibronectin. In general, skin reproducing membrane of medical fibroin has good biocompatibility. © 2016, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Zhao Y.-G.,Central Hospital of Nanyang | Li M.-M.,Zhengzhou University
Chinese Journal of Tissue Engineering Research | Year: 2016

BACKGROUND: It has been reported that tissue-engineered acellular matrix can induce and promote epithelial cells and smooth muscle cells to evolve into a part of body in vivo compared with the normal extracellular matrix. OBJECTIVE: To investigate the effect of tissue-engineered acellular matrix in articular cartilage repair. METHODS: Totally 30 New Zealand rabbits were randomly allotted to fibroid tissue and acellular matrix groups (n=15 per group), and then articular cartilage defect models, 4 mm in diameter, were established at the white rabbit femoral condyle. Acellular cartilage matrix scaffold was prepared using bovine knee cartilage, and model rats in the acellular matrix group were repaired with acellular cartilage matrix scaffold and the others in the fibroid tissue group repaired with fibroid tissues. Finally, repair effects between two groups were compared. RESULTS AND CONCLUSION: The dark blue and porous tissue-engineered acellular matrix material could be found, with a diameter of 5 mm and moderate hardness, and exhibited certain flexibility after cross-linking. Hematoxylin-eosin staining showed that cell debris, blue-stained nuclear materials and residual extracellular matrix disappeared. Toluidine blue staining found that the porosity of the blue scaffold was 90%, and the swelling ratio was (1 314±337)%. The absorbance value in the acellular matrix group was significantly higher than that in the fibroid tissue group at 1, 3, 5, 7 and 9 days (P < 0. 05). In the fibroid tissue group, defects filled with newborn fibrous scars were overt. By contrast, in the acellular matrix group, the white tissues covered the defect region with smooth surface, and the wound was basically healed, with an unclear boundary after 12 weeks. Moreover, blue-stained, small flattened cells appeared, subchondral bone structure was connected well with the cartilage, and the scaffold was directly degraded. In conclusion, the tissue-engineered acellular matrix material exhibits good biocompatibility, cell adsorption and hydrophilicity, and can promote the defect repair after articular cartilage injury. Therefore, it is a suitable substitute for articular cartilage repair. © 2017, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Wang X.,Central Hospital of Nanyang | Tong X.-B.,Central Hospital of Karamay | Liu C.-M.,Xinjiang Medical University
Chinese Journal of Tissue Engineering Research | Year: 2016

BACKGROUND: Due to their inability to be degraded, the traditional repair materials for chest wall defects require a long-term stay in the body. Therefore, severe tissue reaction and the high incidence of complications make the traditional materials unable to meet the requirements of restoration. OBJECTIVE: To prepare an artificial reticular chest wall using biodegradable materials, and to analyze its performance and application in the repair of chest wall defect. METHODS: Mixture of silk fiber and polycaprolactone was used to prepare the biodegradable chest wall, and its porosity and modulus of elasticity were measured. Twenty-two rabbits were selected to build chest wall defect models, which were randomized into two groups. The artificial reticular chest wall was implanted into experimental group, and polycaprolactone implanted into control group. At 4 weeks after implantation, the chest defect was observed by hematoxylin-eosin staining; at 2 months, the chest defect region was observed by CT examination. RESULTS AND CONCLUSION: The holes were uniformly distributed in the artificial chest wall, with the porosity of 54.4% and the diameter of 200-300 μm, fiber distribution in the material was relatively stable, and the modulus of elasticity was significantly higher than that of the polycaprolactone (P < 0.05). CT showed that in the experimental group, the implant material was in close contact with the rib ends, and new tissues appeared between the chest wall plate and visceral pleura; in the control group, the material contacted the broken ends with unclear border, and a visible high density. Hematoxylin-eosin staining showed that in the experimental group there were numerous fibroblasts and a small amount of inflammatory cells, and collagen fibers were loose; in the control group, the boundary between the muscle fiber membrane and the muscle became obscure, accompanied by appearance of edema and more inflammatory cells. These results show that the artificial reticular chest wall made of biodegradable materials can promote the chest wall repair. © 2017, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Wang A.,Central Hospital of Nanyang | Zhang B.,Central Hospital of Nanyang | Zhang J.,Central Hospital of Nanyang | Wu W.,Jilin University | Wu W.,Wenzhou Medical College
Oncology Reports | Year: 2013

Brain glioma is the most common malignant intracranial tumor and has become the focus of research on diseases of the central nervous system due to its high incidence and poor prognosis. As a small-molecule inhibitor of X-linked inhibitor of apoptosis protein (XIAP), embelin has the ability to specifically inhibit XIAP to control and regulate the apoptosis of various types of tumor cells. However, to date, the mechanism of action for this effect is not well understood. The aim of this study was to investigate the role that the mitochondrial pathway plays in embelin-induced brain glioma cell apoptosis and the effect of embelin on the cell cycle. Brain glioma cells were treated with different doses of embelin. The MTT method was used to determine cell proliferation, and flow cytometry was used to determine apoptosis, as well as changes in the cell cycle and cell mitochondrial membrane potential. Western blot analysis was performed to determine the expression levels of apoptosis-associated proteins, Bcl-2, Bcl-xL, Bax and Bak as well as cytochrome c. We found that embelin induced a time- and dose-dependent apoptosis of brain glioma cells, and that it could arrest the cell cycle in the G0/G1 phase. Embelin also caused changes in brain glioma cell mitochondrial membrane potential. Additionally, embelin regulated the shifting of Bax and Bcl-2 to promote the mitochondrial release of cytochrome c, thus activating the caspase proteins to cause apoptosis. Thus, embelin induces apoptosis in brain glioma cells which is closely associated with the mitochondrial pathway.


Liu L.,Fudan University | Liu L.,Central Hospital of Nanyang | Wu H.,Xian XD Group Hospital | Wang Q.,Fudan University | And 4 more authors.
Endocrine Journal | Year: 2012

Autoimmune thyroid disease (AITD) is a multifactorial disease with a genetic susceptibility and environmental factors. The thyroid stimulating hormone receptor gene (TSHR) which is expressed on the surface of the thyroid epithelial cell is thought to be the main auto-antigen and a significant candidate for genetic susceptibility to AITD. This case-control study aimed at evaluating the association between single nucleotide polymorphisms (SNP) of TSHR and AITD in a Chinese Han population. We recruited 404 patients with Graves' disease (GD), 230 patients with Hashimoto's thyroiditis (HT) and 242 healthy controls. The Matrix Assisted Laser Desorption Ionization-Time of Flight Mass Spectrometer (MALDI-TOFMS) Platform was used to detect five SNPs (rs179247, rs12101255, rs2268475, rs1990595, and rs3783938) in TSHR gene. The frequencies of allele T and TT genotype of rs12101255 in GD patients were significantly increased compared with those of the controls (P=0.004/0.015, OR=1.408/1.446). The allele A frequency of rs3783938 was greater in HT patients than in the controls (P=0.025, OR=1.427). The AT haplotype (rs179247-rs12101255) was associated with an increased risk of GD (P=0.010, OR=1.368). The allele A of rs179247 was associated with ophthalmopathy in GD patients. These data suggest that the polymorphisms of rs12101255 and rs3783938 are associated with GD and HT, respectively. © The Japan Endocrine Society.


PubMed | PLA 81 Hospital, Central Hospital of Nanyang and China Pharmaceutical University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Xanthine oxidase (XOD) and paraoxonase1 (PON1) are important enzymes in redox reactions invivo, and are predominantly synthesized by the liver. The aim of the present study was to investigate the redox state in nonalcoholic fatty liver disease, and determine the association between the activities of XOD and PON1 and the severity of NAFLD. SpragueDawley rats were randomly divided into control, model and lipoic acid (high and low dose) groups. The rats in the NAFLD model were induced by feeding a high fat diet for 12weeks and the invitro cell model of hepatocyte steatosis was induced by treating L02 cells with oleic acid for 24h. The body weight, liver function, lipid and oxidative stress indices, and histological features of the liver were examined in the rats. Compared with the control group, the rats in the NAFLD model group showed impaired liver function, lipid disorders and damage from oxidative stress. The serum activity of XOD increased significantly from the 4th week and was markedly higher, compared with that in the control group, reaching a peak in the 12th week. The activity of PON1 was negatively correlated with that of XOD. Compared with the control cells, the activity of XOD and levels of freefatty acids were significantly higher, and the activity of PON1 was significantly lower in the NAFLD L02 cell model. All the above indicators were significantly improved by treatment with the antioxidant, lipoic acid. The activities of XOD and PON1 may be promising as markers in a noninvasive approach for detecting the severity of NAFLD clinically. lipoic acid had protective effects on the NAFLD rats, and the potential mechanism may be associated with the inhibition of oxidative stress and lipid peroxidation.


Zhou J.,Central Hospital of Nanyang | Zhang B.-C.,Central Hospital of Nanyang
Chinese Journal of Tissue Engineering Research | Year: 2015

BACKGROUND: Previous studies have found that the expression level of miR-486 in glioma stem cells CD133+) is significantly down-regulated compared with that in glioma non-stem cells CD133), but the effect of down-regulation of miR-486 on CD133+ cells remains unclear. OBJECTIVE: To explore the effect of miR-486 on CD133+ cells. METHODS: CD133+ glioma stem cells and CD133 glioma cells were separated from U87 cells by flow cytometer. miR-486 overexpression glioma stem cells were constructed by lipofection transfection. RESULTS AND CONCLUSION: After sorting and purification, the content of the CD133+ fraction was enriched up to 83. 5%. The expression level of miR-468 in CD133+ glioma stem cells was obviously down-regulated compared with that in CD133 glioma cells. CD133+ glioma stem cells overexpressing miR-486 were fabricated successfully. Results from in vitro experiments showed that miR-486 overexpression could dramatically decrease the proliferation of glioma stem cells, induce a cell cycle arrest in G1/S phase for CD133+ glioma stem cells and promote cell apoptosis. These findings suggest that miR-486 can be a suppressor of glioma stem cells, which offers a novel potential therapeutic target for glioma stem cells and human glioma. © 2015, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Zhang Z.,Central Hospital of Nanyang | Yan Z.,Central Hospital of Nanyang | Yuan Z.,Central Hospital of Nanyang | Sun Y.,Central Hospital of Nanyang | And 2 more authors.
Tumor Biology | Year: 2015

Sphingosine kinase 1 (SphK1) is an oncogenic enzyme promoting transformation, proliferation, and angiogenesis of a number of human tumors. However, its effect on hepatocellular carcinoma (HCC) behavior has not been fully clarified. The purpose of this study was to determine the correlation between HCC and SphK1, and to evaluate the effect of SphK1 inhibitor N,N-dimethylsphingosine (DMS) in HCC. The expression of SphK1 was measured in tissue samples from 76 HCC and paired adjacent noncancerous liver tissues (NT) by immunohistochemistry, quantitative real-time PCR, and Western blotting analysis. The effect of DMS was tested on HCC cells by evaluating cell viability in vitro. Transwell cell migration and invasion assay were carried out for functional analysis. Furthermore, Western blotting analysis was performed to examine the impact of DMS on the PI3K/Akt/NF-kB signaling. High expression of Sphk1 was observed in 84.21 % (64/76) of the HCC versus 15.79 % (12/76) of the adjacent non-tumorous liver tissues; the difference of Sphk1 expression between HCC and the adjacent non-tumorous liver tissues was statistically significant (P < 0.001). The results were confirmed by Western blot analyses and quantitative real-time PCR. DMS inhibited the proliferation of SK-Hep1 and MHCCLM3 cells which have a relatively high level of SphK1 in a time- and concentration-dependent manner, and the invasion and migration of SK-Hep1 cells were distinctly suppressed after undergoing treatment with DMS. Furthermore, DMS markedly suppressed the expression of phosphorylations of Akt and NF-κB in HCC cells. Our data suggest that the pathogenesis of human HCC maybe mediated by Sphk1, and the specific Sphk1 inhibitor DMS can play a therapeutic role in the treatment of HCC and thus, Sphk1 could represent selective targets for the molecularly targeted treatments of HCC. © 2014, International Society of Oncology and BioMarkers (ISOBM).


Zhang S.-J.,Central Hospital of Nanyang | Wang G.-Z.,Central Hospital of Nanyang
World Chinese Journal of Digestology | Year: 2015

AIM: To compare the clinical effects of laparoscopic vs open surgery for repair of gastroduodenal ulcer perforation. METHODS: Nine ty- two pa t i ent s wi t h gastroduodenal ulcer perforation were divided into a study group (45 cases) and a control group (47 cases). The study group received laparoscopic surgery, and the control group received open surgery. The operation situation, pos toperat ive recovery, pos toperat ive hospitalization duration, total treatment cost, the rate of complications, and ulcer healing were compared for the two groups. RESULTS: The operation time for the study group was significantly longer than that for the control group (118.21 min ± 32.58 min vs 91.06 min ± 19.12 min, P < 0.05), and the length of incision and intraoperative blood loss for the study group were significantly lower than those for the control group (3.43 cm ± 0.86 cm vs 16.22 cm ± 2.17 cm, 15.76 mL ± 2.38 mL vs 95.23 mL ± 14.79 mL, P < 0.05). The visual analogue scale score and the times to recovery of gastrointestinal function and ambulation for the study group were significantly better than those for the control group (3.01 ± 1.06 vs 6.69 ± 1.21, 80.26 h ± 16.11 h vs 122.08 h ± 20.87 h, 1.92 d ± 0.68 d vs 3.39 d ± 1.07 d, P < 0.05). The rate of complications for the study group was significantly lower than that for the control group (4.44% vs 25.53%, P < 0.05). The duration of hospital stay for the study group was significantly lower than that for the control group (5.15 d ± 1.52 d vs 9.09 d ± 2.21 d, P < 0.05). The total treatment cost for the study group was significantly higher than that for the control group (23989.44 yuan ± 388.26 yuan vs 19151.06 yuan ± 226.75 yuan, P < 0.05). There was no significant difference in the rate of ulcer healing situation (37.78% vs 36.17%, 13.33% vs 10.64%, 31.11% vs 34.04%, 17.78% vs 19.15%, P > 0.05). CONCLUSION: Laparoscopic repair of gastroduodenal ulcer perforation is associated with minimal trauma, faster postoperative recovery, fewer complications, and shorter hospitalization time than open surgery. © 2015 Baishideng Publishing Group Inc. All rights reserved.

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