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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. Source


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. Source


Xu N.,Central Hospital of Nanyang | Yang Y.-R.,Central Hospital of Nanyang | Jin W.-B.,Central Hospital of Nanyang
World Chinese Journal of Digestology | Year: 2014

Aim: To observe the effects of sitagliptin and repaglinide in glycemic control and gastrointestinal hormone regulation in patients with diabetic enteropathy.Methods: Thirty diabetic enteropathy outpatients were randomly divided into either a repaglinide group or a sitagliptin group, with 15 cases in each group. The sitagliptin group was given sitagliptin phosphate orally 100 mg per day, and the repaglinide group was given repaglinide 0.5 mg, three times a day. Glycemic control effects and gastrointestinal hormone levels were determined before and after drug administration.Results: In both the sitagliptin group and repaglinide group, HbA1c, fasting plasma glucose, 2 h postprandial glucose (2 h PBG) were significantly lower after treatment than before treatment (P<0.05). Serum levels of motilin (MTL), gastrin (GAS), and somatostatin (SS) were also significantly lower after treatment than before treatment in both groups, while glucagon-like peptide-1 (GLP-1) was significantly higher after treatment than before treatment (P<0.05). After treatment, serum levels of MTL and GAS were significantly lower, and GLP-1 was significantly higher in the sitagliptin group than in the repaglinide group (P<0.05).Conclusion: Sitagliptin and repaglinide have good effects in glycemic control and modulating gastrointestinal function. Ruigelieting has a better effect in regulating gastrointestinal hormones. © 2014 Baishideng Publishing Group Inc. All rights reserved. Source


Yang Y.,Central Hospital of Nanyang | Song Z.,Central Hospital of Nanyang | Wang G.,Central Hospital of Nanyang | Liu J.,Central Hospital of Nanyang
Life Science Journal | Year: 2013

Objective To investigate the tumor marker carbohydrate antigen CA19-9 in the diagnosis of early pancreatic cancer (PCA) and to find the value and significance of early diagnosis. Methods In our hospital from February 2010 to October 2012, 35 patients among treated with pancreatic cancer, it is set to the observation group, while 40 patients healthy subjects were set as the reference group. Chemiluminescence immunoassay method for the observation group and the reference group of healthy patients with pancreatic cancer by measuring tumor markers carbohydrate antigen CA19-9 levels, and clinical correlation. Results The group of 35 patients with serum CA19-9 levels were significantly higher than the reference group of healthy subjects, the positive rate of 86.9% of the observation group, the positive rate of 7.3% in the reference group, two groups, the difference was statistically significant sex significance (P <0.05). Conclusion Early diagnosis of pancreatic cancer, on the determination of CA19-9 is very important in the clinical value, is deemed reliable indicators can improve the early diagnosis of pancreatic cancer. Source


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). Source

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