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Guankou, China

Chu S.-H.,Shanghai JiaoTong University | Zhou Z.-M.,Dujiangyan Medical Center | Karri S.,Harvard University | Li Z.-Q.,Wuhan University | Zhao J.-M.,Shanghai JiaoTong University
Cancer Gene Therapy | Year: 2014

Our previous study showed that solute carrier family 22 (organic cation transporter) member 18 (SLC22A18) downregulation via promoter methylation was associated with the development and progression of glioma, and the elevated expression of SLC22A18 was found to increase the sensitivity of glioma U251 cells to the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea. In this study, we investigated the possible upregulated expression of SLC22A18-induced enhancement of radiosensitivity of human glioma U251 cells in order to provide evidence in support of further clinical investigations. Stably overexpressing SLC22A18 human glioma U251 cells were generated to investigate the effect of SLC22A18 on the sensitivity of cells to irradiation in vitro using clonogenic survival assay. The apoptosis of U251 cells was examined with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. DNA damage and repair were measured using γH2AX foci. The effect of SLC22A18 on the in vivo tumor radiosensitivity was investigated in the orthotopic mice model. Upregulated expression of SLC22A18 enhanced the radiosensitivity of glioma U251 cells and also enhanced irradiation-induced apoptosis of U251 cells, but irradiation-induced apoptosis did not correlate with radiosensitizing effect of upregulated expression of SLC22A18. The repair of irradiation-induced double-strand-breaks was retarded in stably overexpressing SLC22A18 U251 cells. In the orthotopic mice model, the upregulated expression of SLC22A18 in U251 cells enhanced the effect of irradiation treatment and increased the survival time of mice. These results show that upregulated expression of SLC22A18 radiosensitizes human glioma U251 cells by suppressing DNA repair capacity. © 2014 Nature America, Inc. All rights reserved. Source

Yuan Z.,Chongqing Medical University | Tang Z.,University of Sichuan | He C.,Dujiangyan Medical Center | Tang W.,Chongqing Medical University
Journal of Diabetes | Year: 2015

Herein we review and discuss epidemiological, clinical, and experimental studies on diabetic cystopathy, a common chronic complication of diabetes mellitus with a variety of lower urinary tract symptoms, providing directions for future research. A search of published epidemiological, clinical, or preclinical trial literature was performed using the key words "diabetes", "diabetic cystopathy", "diabetic bladder dysfunction", "diabetic lower urinary tract dysfunction", "diabetic detrusor instability". The classic symptoms of diabetic cystopathy are decreased bladder sensation, increased bladder capacity, and impaired bladder emptying with resultant increased post-void residual volume. However, recent clinical evidence indicates a presence of storage symptoms, such as overactive bladder symptoms. The pathophysiology of diabetic cystopathy is multifactorial, including disturbances of the detrusor, neuron, urothelium, and urethra. Hyperglycemia, oxidative stress, and polyuria play important roles in inducing voiding dysfunction in diabetic individuals. Treatment choice depends on clinical symptoms and urodynamic abnormalities. Urodynamic evaluation is the cornerstone of diagnosis and determines management strategies. Diabetes mellitus could cause a variety of lower urinary tract symptoms, leading to diabetic cystopathy with broadly varied estimates of the prevalence rates. The exact prevalence and pathogenesis of diabetic cystopathy remains to be further investigated and studied in multicenter, large-scaled, or randomized basic and clinical trials, and a validated and standardized workup needs to be made, improving diabetic cystopathy management in clinical practice. Further studies involving only female diabetics are recommended. © 2015 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd. Source

Chu S.-H.,Shanghai JiaoTong University | Zhou Z.-M.,Dujiangyan Medical Center | Feng D.-F.,Shanghai JiaoTong University | Ma Y.-B.,Shanghai JiaoTong University
Molecular Biology Reports | Year: 2014

Special AT-rich sequence-binding protein-1 (SATB1) has been reported to be over-expressed in many human tumors and knockdown of SATB1 can inhibit tumor growth. The present study was designed to determine the role of SATB1 in the growth of human glioma U251 cells using the plasmid-based SATB1 short hairpin RNA (shRNA) delivered by hydroxyapatite nanoparticles in vitro and in vivo. The in vitro growth, invasion and angiogenesis assays of human glioma U251 cells were done. U251 cells tumor blocks were transplanted into the nude mice. CaCl2-modified hydroxyapatite nanoparticles carrying shRNA-SATB1 plasmids were injected into the tumors. The apoptosis of the tumor U251 cells was examined with TUNEL assay and flow cytometer (FCM). The tumor growth and immunohistochemistry were measured. The expression level of SATB1 mRNA was investigated by RT-PCR. The expression levels of SATB1, Cyclin D1, MMP-2, VEGF, Bax and Caspase-9 protein were determined by western blot analysis. The results showed that hydroxyapatite nanoparticles-delivered shRNA-SATB1 could significantly inhibit the growth, invasion and angiogenesis of U251 cells in vitro and the growth of U251 cells in vivo. FCM results showed that Nano HAP-shRNA-SATB1-induced apoptosis (up to 67.8%). SATB1 expression was strongly down-regulated in the tumor U251 cells. Cyclin D1, MMP-2 and VEGF were also down-regulated in the tumor tissues that also displayed significant increased in Bax expression and Caspase-9 activity. These results show that Nano HAP-shRNA-SATB1 can inhibit the growth of human glioma U251 cells in vitro and in vivo, and hydroxyapatite nanoparticles can be used for the in vitro and in vivo delivery of plasmid-based shRNAs into U251 cells. © Springer Science+Business Media 2013. Source

Gao R.,Chongqing Medical University | Gao R.,Dujiangyan Medical Center | Zhou X.,Chongqing Medical University | Yang Y.,Chongqing Medical University | And 2 more authors.
Ultrasound in Medicine and Biology | Year: 2014

Using ultrasound-targeted microbubble destruction (UTMD), we transfected both wild-type p53 (wtp53) and Rb94 genes into retinoblastomas (RBs) of nude mice to investigate the inhibitory role of these two genes in RB development. The 40 tumor-bearing mice, which had been established by sub-retinal injection of an HXO-Rb44cell suspension, were randomly divided into five groups: blank control group (C); blank plasmid group (M); wtp53 plasmid group (p53); Rb94 plasmid group (Rb94); wtp53+Rb94 plasmid group (p53+Rb94). For preparation of the DNA-loaded microbubbles, a pre-determined amount of blank plasmid, pVIVO1-p53, pVIVO1-Rb94 or pVIVO1-p53-Rb94 was added and mixed with the microbubbles. Then, these DNA-loaded microbubbles were respectively transfected into the animal model by UTMD. Vascular endothelial growth factor level and microvessel density of the tumor were determined by immunohistochemical staining. Apoptosis of tissues was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Expression of wtp53 and Rb94 at both the gene and protein levels was detected by RT-PCR (reverse transcription polymerase chain reaction) and Western blot, respectively. Transfection of both genes had greater inhibitory effects on RB development and resulted in lower levels of vascular endothelial growth factor, lower microvessel density and more obvious apoptosis than single-gene transfection (p<0.05). The results indicate that the transfection of both genes into the RB by UTMD more strongly inhibited RB growth than transfection of a single gene. © 2014 World Federation for Ultrasound in Medicine & Biology. Source

Liang Q.-L.,Hubei University of Medicine | Mo Z.-Y.,Hubei University of Medicine | Wang P.,Hubei University of Medicine | Li X.,Hubei University of Medicine | And 3 more authors.
Medical Oncology | Year: 2014

Hepatocyte growth factor (HGF) has been shown to be overexpressed in gliomas, and high-grade gliomas (glioblastoma multiforme) express more HGF than lower-grade astrocytoma, and HGF enhances their resistance to radiotherapy. To examine the effect of serum HGF levels on the likelihood of response to radiotherapy and the disease-free survival in patients with glioma, the blood samples of the patients were collected before commencing treatment and serum HGF was measured by quantitative ELISA in 48 patients with glioma grade I–IV, and all patients underwent primary conventionally fractionated radiotherapy. For statistical analysis, SPSS Version 13.0 software was used. Thirty-eight of the 48 patients had a response to treatment, and ten patients had persistent disease at 3 months. Overall, the median serum HGF level was 1,219.5 pg/ml (range 650.4–2,264.7 pg/ml). Eight patients with local failure had HGF levels >1,219.5 pg/ml, and 28 patients with response had serum HGF level of ≤1,219.5 pg/ml (P = 0.01). The median time to progression was 6 months in patients with HGF level of >1,219.5 pg/ml compared with 17 months in patients with HGF level of ≤1,219.5 pg/ml (log-rank, P = 0.041). In multivariate analysis, serum HGF, the KPS, tumour size and pathological grade, but not the patient’s age, gender and oligodendroglial component influenced the progression-free survival. Elevated pre-therapeutic serum HGF levels are associated with poor response and a shorter time to progression in patients with glioma undergoing primary radiotherapy. © 2014, Springer Science+Business Media New York. Source

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