85 Hospital of PLA

Shanghai, China

85 Hospital of PLA

Shanghai, China
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Meng X.-X.,Shanghai University | Zhang Y.-Q.,85 Hospital of PLA | Liao H.-Q.,Shanghai University | Liu H.-C.,Shanghai University | And 3 more authors.
European Spine Journal | Year: 2016

Purpose: To determine if dynamic contrast-enhanced MRI (DCE-MRI) could correlate well with invasive angiography in the characterization of spinal tumor vascularity. Methods: Totally 40 patients with untreated spinal tumors underwent MRI before preoperative angiography and embolization. Tumors were assigned to hypervascular, moderate, or hypovascular groups based on angiographic appearance. Tumor vascularity was also evaluated with enhancement degree on standard MR and with DCE-MRI parameters via ROI analysis of enhanced tumor area. The Spearman correlation coefficient was calculated to determine the correlation between the degree of angiographic vascularity and enhancement on MRI and DCE-MRI parameters. ROC analysis was conducted to assess the appropriate cut-off value. Results: There were 12 hypervascular, 12 moderate, and 16 hypovascular tumors, respectively. The Spearman correlation coefficient between DCE-MRI parameter and the degree of angiographic vascularity was0.899 (RSlopemax), 0.847 (Slopemax), 0.697 (Emax), 0.694 (ERmax), and −0.587 (TTP), respectively, which showed excellent-to-moderate relationships. The RSlopemax cut-off value of 1.325 provided the highest specificity of 100 % and sensitivity of 87.5 % in predicting hypovascular tumors and the value of 1.85 provided the highest sensitivity of 100 % and specificity of 96.4 % in characterizing hypervascular ones. Conclusions: DCE-MRI is an accurate technique for the assessment of spinal tumor vascularity, which may have a potential value in the decision-making of preoperative embolization. © 2016 Springer-Verlag Berlin Heidelberg


Huang J.,85 Hospital of PLA | Jia J.,Jilin University | Tong Q.,85 Hospital of PLA | Liu J.,85 Hospital of PLA | And 4 more authors.
Tumor Biology | Year: 2015

Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently identified human oncoprotein that can stabilize some proteins by inhibiting degradation mediated by protein phosphatase 2A (PP2A), and its level in cancer is associated with resistance to chemotherapy. However, whether CIP2A could increase chemoresistance of prostate cancer (PCa) cells to chemotherapeutic agent cabazitaxel remains unclear. To determine whether CIP2A serves as a potential therapeutic target of human PCa, we utilized small interference RNA (siRNA) to knock down CIP2A expression in human PCa cells and analyzed their phenotypic changes. The data demonstrated that CIP2A was significantly elevated in mCRPC cell lines C4-2 and ARCaPM at both the mRNA and protein levels. CIP2A silencing led to decreased proliferation and enhanced chemosensitivity and apoptosis to cabazitaxel in human PCa cells, as well as reduced Akt phosphorylation. Our data suggesting critical roles of CIP2A in PCa cells chemoresistance to cabazitaxel and raising the possibility of CIP2A inhibition as a promising approach for chemosensitization of metastatic castration-resistant prostate cancer (mCRPC). © 2014, International Society of Oncology and BioMarkers (ISOBM).


Mao A.,85 Hospital of PLA | Huang H.,85 Hospital of PLA | Ding K.,85 Hospital of PLA | Xin H.,85 Hospital of PLA | And 2 more authors.
Zhonghua wei zhong bing ji jiu yi xue | Year: 2015

OBJECTIVE: To study the modulation in number and function of endothelial progenitor cell (EPC) in multiple organ dysfunction syndrome (MODS) after trauma in swine, and to investigate its pathogenesis.METHODS: Forty pigs were divided into sham group and MODS group (each, n=20). The model of MODS of "two-hit" injury, namely hemorrhagic shock and endotoxemia, was reproduced. The peripheral blood was collected before hemorrhage (T1) and endotoxin injection (T2), and 1 hour (T3), 24 hours (T4), 48 hours (T5) after endotoxin injection. Phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK ) in mononuclear cell was determined by Western Blot, the content of tumor necrosis factor-α (TNF-α) was determined with enzyme linked immunosorbent assay (ELISA), and the number of EPC was determined with flow cytometry.RESULTS: Model of MODS was successfully reproduced in 17 pigs. In model group, the expression of p-p38MAPK (A value) peaked at T3 (4.83±0.52), and gradually declined at T4 and T5 (4.36±0.43, 1.93±0.33), and the expression of p-p38MAPK at T3-T5 was significantly higher than that at T1 (1.00±0.22, all P<0.01). The plasma concentration of TNF-α (ng/L) at T3 in MODS group was obviously elevated compared with that of sham group (532.43±52.17 vs. 129.03±20.45, t=31.163, P<0.001), and it peaked at T3, it then gradually lowered, and it was significantly higher at T4 and T5 than that in sham group (T4: 398.93±35.75 vs. 131.12±29.53, t=26.562, P<0.001; T5: 287.48±27.26 vs. 126.44±26.96, t=17.861, P<0.001). The number of EPC (×10(7)/L) was apparently increased in MODS group at T3 compared with sham group (4.832±0.624 vs. 3.545±0.363, t=9.542, P<0.001), and it peaked at T3, then gradually decreased, and the number of EPC at T4 and T5 was significantly lower than that in sham group (T4: 2.628±0.627 vs. 3.442±0.325, t=5.043, P<0.001; T5: 2.203±0.711 vs. 3.471±0.323, t=2.972, P<0.001).CONCLUSIONS: Phosphorylation of p38MAPK could increase the plasma concentration of TNF-αand decrease the quantity of EPC in MODS,which may be one of the mechanisms of MODS.


PubMed | 85 Hospital of PLA
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2015

Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently identified human oncoprotein that can stabilize some proteins by inhibiting degradation mediated by protein phosphatase 2A (PP2A), and its level in cancer is associated with resistance to chemotherapy. However, whether CIP2A could increase chemoresistance of prostate cancer (PCa) cells to chemotherapeutic agent cabazitaxel remains unclear. To determine whether CIP2A serves as a potential therapeutic target of human PCa, we utilized small interference RNA (siRNA) to knock down CIP2A expression in human PCa cells and analyzed their phenotypic changes. The data demonstrated that CIP2A was significantly elevated in mCRPC cell lines C4-2 and ARCaP(M) at both the mRNA and protein levels. CIP2A silencing led to decreased proliferation and enhanced chemosensitivity and apoptosis to cabazitaxel in human PCa cells, as well as reduced Akt phosphorylation. Our data suggesting critical roles of CIP2A in PCa cells chemoresistance to cabazitaxel and raising the possibility of CIP2A inhibition as a promising approach for chemosensitization of metastatic castration-resistant prostate cancer (mCRPC).


PubMed | 85 Hospital of PLA
Type: Journal Article | Journal: Zhonghua wei zhong bing ji jiu yi xue | Year: 2015

To study the modulation in number and function of endothelial progenitor cell (EPC) in multiple organ dysfunction syndrome (MODS) after trauma in swine, and to investigate its pathogenesis.Forty pigs were divided into sham group and MODS group (each, n=20). The model of MODS of two-hit injury, namely hemorrhagic shock and endotoxemia, was reproduced. The peripheral blood was collected before hemorrhage (T1) and endotoxin injection (T2), and 1 hour (T3), 24 hours (T4), 48 hours (T5) after endotoxin injection. Phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK ) in mononuclear cell was determined by Western Blot, the content of tumor necrosis factor- (TNF-) was determined with enzyme linked immunosorbent assay (ELISA), and the number of EPC was determined with flow cytometry.Model of MODS was successfully reproduced in 17 pigs. In model group, the expression of p-p38MAPK (A value) peaked at T3 (4.830.52), and gradually declined at T4 and T5 (4.360.43, 1.930.33), and the expression of p-p38MAPK at T3-T5 was significantly higher than that at T1 (1.000.22, all P<0.01). The plasma concentration of TNF- (ng/L) at T3 in MODS group was obviously elevated compared with that of sham group (532.4352.17 vs. 129.0320.45, t=31.163, P<0.001), and it peaked at T3, it then gradually lowered, and it was significantly higher at T4 and T5 than that in sham group (T4: 398.9335.75 vs. 131.1229.53, t=26.562, P<0.001; T5: 287.4827.26 vs. 126.4426.96, t=17.861, P<0.001). The number of EPC (10(7)/L) was apparently increased in MODS group at T3 compared with sham group (4.8320.624 vs. 3.5450.363, t=9.542, P<0.001), and it peaked at T3, then gradually decreased, and the number of EPC at T4 and T5 was significantly lower than that in sham group (T4: 2.6280.627 vs. 3.4420.325, t=5.043, P<0.001; T5: 2.2030.711 vs. 3.4710.323, t=2.972, P<0.001).Phosphorylation of p38MAPK could increase the plasma concentration of TNF-and decrease the quantity of EPC in MODS,which may be one of the mechanisms of MODS.

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