Nantong Third Peoples Hospital

Nantong, China

Nantong Third Peoples Hospital

Nantong, China
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Yao Y.,Nantong University | Xue H.-W.,Nantong Third Peoples Hospital | Zhao J.,Shanghai University | Zhang F.,Nantong University | And 4 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2017

BACKGROUND: Santoni put forward the cortical bone trajectory technology by changing the traditional pedicle screw placement for lumbar internal fixation in order to obtain better control of the screw and bone in 2009. OBJECTIVE: To analyze biomechanical stability of cortical bone trajectory system in the lumbar fusion. METHODS: Twenty fresh newborn calf L3/4, L5/6 motion segment specimens were obtained, and their ranges of motion were detected under different states, as normal controls. Subsequently, twenty samples were divided into cortical bone trajectory screw group and traditional pedicle screw group, which underwent cortical bone trajectory screw fixation combined with posterior lumbar fusion and traditional pedicle screw fixation combined with posterior lumbar fusion, respectively. Without destruction, ranges of motion were detected under different states in both groups. In the revision group, after the test in the traditional pedicle screw group, screw was withdrawn, and corical bone trajectory screw was used to detect its range of motion under different states. RESULTS AND CONCLUSION: Ranges of motion at bending to the left and right, anteflexion, posterior extension and axial rotation were significantly lower in the cortical bone trajectory screw group and traditional pedicle screw group than in the normal control group (P < 0.05). No significant difference in bending to the left and right, anteflexion, posterior extension and axial rotation was detected between the cortical bone trajectory screw and revision groups and traditional pedicle screw group (P > 0.05). These results confirmed that cortical bone trajectory technology combined with posterior lumbar fusion can obtain identical stability as the traditional pedicle screw fixation combined with posterior lumbar fusion. Simultaneously, it is a new choice for revision after traditional pedicle screw fixation. © 2017, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


PubMed | Nantong Third peoples Hospital and Shanghai JiaoTong University
Type: | Journal: Scientific reports | Year: 2016

Thalidomide is used in clinical practice to treat gastrointestinal vascular malformation (GIVM), but the pathogenesis of GIVM is not clear. Hypoxia inducible factor 1 alpha (HIF-1) and 2 alpha (HIF-2/EPAS1) are in the same family and act as master regulators of the adaptive response to hypoxia. HIF-1 and HIF-2 are up-regulated in vascular malformations in intestinal tissues from GIVM patients, but not in adjacent normal vessels. Therefore, we investigated the role of HIF-1 and HIF-2 during angiogenesis and the mechanism of thalidomide action. In vitro experiments confirmed that vascular endothelial growth factor (VEGF) was a direct target of HIF-2 and that HIF-1 and HIF-2 regulated NOTCH1, Ang2, and DLL4, which enhanced vessel-forming of endothelial cells. Thalidomide down-regulated the expression of HIF-1 and HIF-2 and inhibited angiogenesis. In vivo zebrafish experiments suggested that HIF-2 overexpression was associated with abnormal subintestinal vascular (SIV) sprouting, which was reversed by thalidomide. This result indicated that thalidomide regulated angiogenesis via the inhibition of HIF-1 and HIF-2 expression, which further regulated downstream factors, including VEGF, NOTCH1, DLL4, and Ang2. The abnormally high expression of HIF-1 and HIF-2 may contribute to GIVM.


Song L.,Nantong University | Jiang W.,Nantong Third Peoples Hospital | Liu W.,Nantong University | Ji J.-H.,Nantong Third Peoples Hospital | And 3 more authors.
Acta Paediatrica, International Journal of Paediatrics | Year: 2016

Aim Protein tyrosine phosphatases receptor type D (PTPRD) is a tumour suppressor gene, and its epigenetic silencing is frequently found in glioblastoma. As aberrant deoxyribonucleic acid (DNA) methylation patterning has been shown to play a role in leukaemogenesis, we studied the promoter methylation, expression profiles and molecular functions of PTPRD in paediatric patients with acute myeloid leukaemia (AML). Methods Bone marrow specimens were obtained from 32 Chinese patients with a mean age of 7.2 years (range 1.1-16.5). PTPRD and methylation status were evaluated by real-time polymerase chain reaction (PCR) and methylation-specific PCR. Western blot and flow cytometry techniques were also used. Results PTPRD expression was decreased by promoter region methylation in six AML cells and methylated in 21 (65.6%) of the 32 samples. In addition, PTPRD expression could be induced by the DNA demethylating agent 5-aza-2′-deoxycytidine. Furthermore, functional studies showed that overexpression of PTPRD in AML cells inhibited cell proliferation and clonogenicity as well as inducing apoptosis. However, PTPRD knockdown increased cell proliferation. These effects were associated with downregulation of cyclin D1, c-myc and upregulation of Bax. Conclusion The results of this study demonstrated that PTPRD was a potential tumour suppressor gene inactivated by DNA methylation in paediatric AML. ©2015 Foundation Acta Pædiatrica. Published by John Wiley & Sons Ltd.


Ding Y.,Nantong University | Wang Y.,Nantong University | Ju S.,Nantong University | Wu X.,Nantong University | And 3 more authors.
Molecular Medicine Reports | Year: 2014

Cancerous inhibitor of protein phosphatase 2A (CIP2A) has been identified as an oncoprotein that is able to promote the proliferation of cancer cells. The role of CIP2A in the anticancer activity of bortezomib in colon cancer remains to be elucidated. In the present study, the antitumor effect of bortezomib was investigated and the role of CIP2A in determining the effect on colon cancer cells was identified. In the present study, bortezomib demonstrated an antitumor effect, as observed by WST-1 assay and flow cytometry. In addition, the mRNA and protein level of CIP2A was inhibited in a dose-dependent manner by bortezomib with quantitative PCR (qPCR) and western blotting. Furthermore, the inhibition of CIP2A with small interfering RNA by treatment with bortezomib inhibited proliferation, increased apoptosis and attenuated the invasion of the cells. Finally, the in vivo data demonstrated that bortezomib was able to decrease the growth of tumors, and that CIP2A was downregulated in the LoVo tumors treated with bortezomib. Therefore, CIP2A was shown to be important in the bortezomib-induced inhibitory effect on colon cancer.


PubMed | Nantong Third Peoples Hospital and Nantong University
Type: Journal Article | Journal: Acta paediatrica (Oslo, Norway : 1992) | Year: 2016

Protein tyrosine phosphatases receptor type D (PTPRD) is a tumour suppressor gene, and its epigenetic silencing is frequently found in glioblastoma. As aberrant deoxyribonucleic acid (DNA) methylation patterning has been shown to play a role in leukaemogenesis, we studied the promoter methylation, expression profiles and molecular functions of PTPRD in paediatric patients with acute myeloid leukaemia (AML).Bone marrow specimens were obtained from 32 Chinese patients with a mean age of 7.2 years (range 1.1-16.5). PTPRD and methylation status were evaluated by real-time polymerase chain reaction (PCR) and methylation-specific PCR. Western blot and flow cytometry techniques were also used.PTPRD expression was decreased by promoter region methylation in six AML cells and methylated in 21 (65.6%) of the 32 samples. In addition, PTPRD expression could be induced by the DNA demethylating agent 5-aza-2-deoxycytidine. Furthermore, functional studies showed that overexpression of PTPRD in AML cells inhibited cell proliferation and clonogenicity as well as inducing apoptosis. However, PTPRD knockdown increased cell proliferation. These effects were associated with downregulation of cyclin D1, c-myc and upregulation of Bax.The results of this study demonstrated that PTPRD was a potential tumour suppressor gene inactivated by DNA methylation in paediatric AML.

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