Central Hospital of Zhuzhou

Zhuzhou, China

Central Hospital of Zhuzhou

Zhuzhou, China
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Fu X.-Y.,Central South University | Tan D.-M.,Central South University | Liu C.-M.,Central South University | Gu B.,Second Peoples Hospital of Chenzhou | And 15 more authors.
World Journal of Gastroenterology | Year: 2017

Aim: To investigate whether hepatitis viral DNA load at 24 wk of treatment predicts response at 96 wk in patients with chronic hepatitis B. Methods: A total of 172 hepatitis B envelope antigen (HBeAg)- positive chronic hepatitis B patients who received initial treatment at 16 tertiary hospitals in Hunan Province, China were enrolled in this study. All patients received conventional doses of lamivudine and adefovir dipivoxil, telbivudine, entecavir dispersible tablets, or entecavir tablets for 96 wk. Patients who used other antiviral drugs or antitumor and immune regulation therapy were excluded. Patients were stratified into three groups according to their viral DNA load at 24 wk: < 10 IU/mL (group 1), 10-103 IU/mL (group 2), and > 103 IU/mL (group 3). Correlations of 24-wk DNA load with HBeAg negative status and HBeAg seroconversion at 96 wk were analyzed. Receiver operating characteristic curve analysis was used to test the predictive value of the HBV DNA load at 24 wk for long-term response. Results: The rates of conversion to HBeAg negative status and HBeAg seroconversion rates were 53.7% and 51.9%, respectively, in group 1; 35.21% and 32.39% in group 2; and 6.38% and 6.38% in group 3. The receiver operating characteristic curves for the three subgroups revealed that the lowest DNA load (< 10 IU/mL) was better correlated with response at 96 wk than a higher DNA load (10-103 IU/mL). Nested PCR was used for amplifying and sequencing viral DNA in patients with a viral DNA load > 200 IU/mL at 96 wk; resistance mutations involving different loci were present in 26 patients, and three of these patients had a viral DNA load 10-103 IU/mL at 96 wk. Conclusion: Hepatitis B viral DNA load at 24 wk of antiviral treatment in patients with chronic hepatitis B is a predictor of the viral load and response rate at 96 wk. © 2017 Baishideng Publishing Group Inc. All rights reserved.


Qiu Z.,Central Hospital of Zhuzhou | Yuan W.,Central Hospital of Zhuzhou | Chen T.,The First Affiliated Hospital of Guangzhou Medical University | Zhou C.,The First Affiliated Hospital of Guangzhou Medical University | And 4 more authors.
Gene | Year: 2015

The metabolic program of cancer cells is significant different from the normal cells, which makes it possible to develop novel strategies targeting cancer cells. Mevalonate pathway and its rate-limiting enzyme HMG-CoA reductase (HMGCR) have shown important roles in the progression of several cancer types. However, their roles in glioblastoma cells remain unknown. In this study, up-regulation of HMGCR in the clinical glioblastoma samples was observed. Forced expression of HMGCR promoted the growth and migration of U251 and U373 cells, while knocking down the expression of HMGCR inhibited the growth, migration and metastasis of glioblastoma cells. Molecular mechanism studies revealed that HMGCR positively regulated the expression of TAZ, an important mediator of Hippo pathway, and the downstream target gene connective tissue growth factor (CTGF), suggesting HMGCR might activate Hippo pathway in glioblastoma cells. Taken together, our study demonstrated the oncogenic roles of HMGCR in glioblastoma cells and HMGCR might be a promising therapeutic target. © 2015.


PubMed | Central Hospital of Zhuzhou and The First Affiliated Hospital of Guangzhou Medical University
Type: Journal Article | Journal: Gene | Year: 2015

The metabolic program of cancer cells is significant different from the normal cells, which makes it possible to develop novel strategies targeting cancer cells. Mevalonate pathway and its rate-limiting enzyme HMG-CoA reductase (HMGCR) have shown important roles in the progression of several cancer types. However, their roles in glioblastoma cells remain unknown. In this study, up-regulation of HMGCR in the clinical glioblastoma samples was observed. Forced expression of HMGCR promoted the growth and migration of U251 and U373 cells, while knocking down the expression of HMGCR inhibited the growth, migration and metastasis of glioblastoma cells. Molecular mechanism studies revealed that HMGCR positively regulated the expression of TAZ, an important mediator of Hippo pathway, and the downstream target gene connective tissue growth factor (CTGF), suggesting HMGCR might activate Hippo pathway in glioblastoma cells. Taken together, our study demonstrated the oncogenic roles of HMGCR in glioblastoma cells and HMGCR might be a promising therapeutic target.


Long Y.,Central Hospital of Zhuzhou | Wu Z.,Affiliated Hospital of Guiyang Medical College | Yang X.,Central Hospital of Zhuzhou | Chen L.,Central Hospital of Zhuzhou | And 5 more authors.
Molecular Medicine Reports | Year: 2016

MicroRNAs (miRs) have important roles in the parthenogenesis of malignancies. While it has been suggested that deregulation of miR-101 is involved in bladder cancer, the underlying mechanisms have remained largely elusive. The present study aimed to investigate the roles of miR-101 in the regulation of bladder cancer cell proliferation and invasion. Reverse-transcription quantitative polymerase chain reaction analysis revealed that the expression of miR-101 was significantly reduced in the HT-1376, BIU87, T24 and 5637 several human bladder cancer cell lines compared to that in the SV-HUC-1 normal bladder epithelial cell line. Furthermore, a Targetscan search and a luciferase assay were used to identify c-FOS as a novel target of miR-101, and western blot analysis indicated that the protein expression of c-FOS was shown to be negatively regulated by miR-101 in bladder cancer T24 cells; however, c-FOS mRNA expression was not affected. In addition, plasmid-mediated overexpression of miR-101 and small hairpin RNA-mediated inhibition of c-FOS significantly inhibited the proliferation and invasive capacity of T24 cells, as indicated by an MTT and a Transwell assay, respectively. However, plasmid-mediated overexpression of c-FOS reversed the inhibitory effects of miR-101 overexpression on T24-cell proliferation and invasion. In conclusion, the present study demonstrated that miR-101 inhibits the proliferation and invasion of bladder cancer cells, at least partly via targeting c-FOS, suggesting that miR-101/c-FOS signaling may represent a potential therapeutic target for bladder cancer.


Fu Y.,Central South University | Zhang Y.,Central South University | Gao M.,Central South University | Quan L.,Central Hospital of Zhuzhou | And 2 more authors.
Molecular Medicine Reports | Year: 2016

Alisertib, a potent and selective Aurora kinase A inhibitor, has been demonstrated to exert potent anti-cancer effects in pre-clinical and clinical studies. However, mechanisms of action of alisertib, including the molecular pathways involved in alisertib-induced apoptosis and autophagy of leukemic cells, have remained elusive. The aim of the present study was to investigate the effects of alisertib on cell growth, apoptosis and autophagy and to delineate the possible molecular mechanisms in leukemic cells. Acid phosphatase, MTT and Annexin V/propidium iodide staining assays as well as immunostaining for light chain 3B showed that treatment of the REH leukemia cell line with alisertib exerted potent growth inhibitory effects, and induced apoptosis and autophagy in a dose-dependent manner. Western blot analysis indicated that these effects may be attributed to the suppression of the activity of the Akt/mammalian target of rapamycin/5'-AMP-dependent kinase/p38 mitogen-activated protein kinase signaling pathways in REH cells. The present study confirmed that alisertib may represent a promising autophagy-inducing drug for the treatment of leukemia and shed light on its molecular mechanism of action.


Li Y.,Central South University | Fu Q.,Central Hospital of Zhuzhou | Liu A.,Central South University | Zheng Z.,Hunan Provincial Peoples Hospital | And 4 more authors.
Journal of Central South University (Medical Sciences) | Year: 2014

Iliac arteriovenous fistula (AVF) usually manifests in a wide range of symptoms similar to typical deep venous thrombosis (DVT), which often lead to delayed diagnosis or misdiagnosis. We reported a 51-year old woman who was performed lumbar discectomy and showed a progressive abdominal distention, dyspnea, and swollen left leg. She was initially diagnosed as deep vein thrombosis and the final diagnosis was arteriovenous fistula. The fistula was successfully sealed by an endovascular covered stent. No further recurrence was found after a half year's follow-up. This article summarized the experience regarding iliac arteriovenous fistula misdiagnosed, and discussed the differential diagnosis between arteriovenous fistula and pulmonary thromboembolism caused by deep vein thrombosis.


Liu Q.,Hunan Traditional Chinese Medical College | Liu J.,Hunan Traditional Chinese Medical College | Liu Y.,Central Hospital of Zhuzhou
Journal of Practical Oncology | Year: 2016

Objective: To study the expression of S-phase kinase-associated protein 2 (Skp2) and p27kip1 in human cervical squamous cell carcinoma and its relationship with human papilloma virus (HPV) infection. Methods: The expressions of Skp2 and p27kip1 were detected by immunohistochemistry in 50 cases of squamous cell carcinoma of cervix (SCC), 40 cases of cervical intraepithelial neoplasias (CINs) and 15 cases of chronic cervicitis (CC). The expression of HPV16/18 was detected by in situ hybridization. The association of Skp2 and p27kip1 expression with clinicopathological features and with HPV16/18 expression in cervical carcinoma was analyzed. Results: The positive rate of Skp2 protein expression in SCC was 76.0%, which was significantly higher than those in CC (13.3%, P<0.01) and CINs (57.5%, P<0.05). The positive rate of p27kip1 expression in SCC group was 24.0%, which was significantly lower than those in CC (92.6%, P<0.01) and CINs (52.5%, P<0.05). The expression levels of Skp2 and p27kip1 were significantly associated with lymph node metastasis (P<0.05), but not with age, differentiation degree or clinical stage (P>0.05). The positive rate of HPV16/18 DNA in SCC was 74.0%, which was higher than that in CC (13.3%, P<0.01), but was not significantly different to that in CINs (62.5%, P>0.05). HPV16/18 infection was positively correlated with the expression of Skp2 (r=0.238, P<0.05), and negatively correlated with the level of p27kip1 (r=-0.245, P<0.05) in cervical carcinoma. Conclusion: High expression of Skp2 and low expression of p27kip1 are closely related to lymph node metastasis of cervical squamous cell carcinoma and HPV infection. © 2016, Editorial Board of Journal of Practical Oncology. All right reserved.


PubMed | Central Hospital of Zhuzhou and Central South University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Alisertib, a potent and selective Aurora kinaseA inhibitor, has been demonstrated to exert potent anti-cancer effects in pre-clinical and clinical studies. However, mechanisms of action of alisertib, including the molecular pathways involved in alisertib-induced apoptosis and autophagy of leukemic cells, have remained elusive. The aim of the present study was to investigate the effects of alisertib on cell growth, apoptosis and autophagy and to delineate the possible molecular mechanisms in leukemic cells. Acid phosphatase, MTT and AnnexinV/propidium iodide staining assays as well as immunostaining for light chain 3B showed that treatment of the REH leukemia cell line with alisertib exerted potent growth inhibitory effects, and induced apoptosis and autophagy in a dosedependent manner. Western blot analysis indicated that these effects may be attributed to the suppression of the activity of the Akt/mammalian target of rapamycin/5-AMP-dependent kinase/p38 mitogen-activated protein kinase signaling pathways in REH cells. The present study confirmed that alisertib may represent a promising autophagy-inducing drug for the treatment of leukemia and shed light on its molecular mechanism of action.


PubMed | Central Hospital of Zhuzhou and P.A. College
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

MicroRNAs (miRs) have important roles in the parthenogenesis of malignancies. While it has been suggested that deregulation of miR101 is involved in bladder cancer, the underlying mechanisms have remained largely elusive. The present study aimed to investigate the roles of miR101 in the regulation of bladder cancer cell proliferation and invasion. Reversetranscription quantitative polymerase chain reaction analysis revealed that the expression of miR101 was significantly reduced in the HT1376, BIU87, T24 and 5637 several human bladder cancer cell lines compared to that in the SVHUC1 normal bladder epithelial cell line. Furthermore, a Targetscan search and a luciferase assay were used to identify cFOS as a novel target of miR101, and western blot analysis indicated that the protein expression of cFOS was shown to be negatively regulated by miR101 in bladder cancer T24 cells; however, cFOS mRNA expression was not affected. In addition, plasmidmediated overexpression of miR101 and small hairpin RNAmediated inhibition of cFOS significantly inhibited the proliferation and invasive capacity of T24 cells, as indicated by an MTT and a Transwell assay, respectively. However, plasmidmediated overexpression of cFOS reversed the inhibitory effects of miR101 overexpression on T24cell proliferation and invasion. In conclusion, the present study demonstrated that miR101 inhibits the proliferation and invasion of bladder cancer cells, at least partly via targeting cFOS, suggesting that miR-101/cFOS signaling may represent a potential therapeutic target for bladder cancer.

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