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Mi Y.,Xi'an Jiaotong University | Xiao X.,Xi'an Jiaotong University | Liu D.,Xi'an Jiaotong University | Ping N.,Xi'an Jiaotong University | And 4 more authors.
International Journal of Experimental Pathology | Year: 2016

Summary: The main vitamin K-deficient model, minidose warfarin, is different from the pathological mechanism of vitamin K deficiency, which is a shortage of vitamin K. The objective of this study was to establish a new method of vitamin K-deficient model combining a vitamin K-deficient diet with the intragastrical administration of gentamicin in rats. The clotting was assayed by an automated coagulation analyser. The plasma PIVKA-II was assayed by ELISA. The vitamin K status was detected by an HPLC-fluorescence system. In the diet- and gentamicin-induced vitamin K-deficient 14-day group, the rats had undetected vitamin K1 and vitamin K2 in the liver and a prolonged APTT. In the 21-day group, there was also a prolonged PT and a decrease of the FIX activities. In the 28-day group, the undetected vitamin K1 and vitamin K2, the prolonged PT and APTT, and the decrease of the FII, FVII, FIX, and FX activities prompted the suggestion that there were serious deficiencies of vitamin K and vitamin K-dependent coagulation in rats. It is suggested that the diet- and gentamicin-induced vitamin K-deficient 14-day or 21-day model can be used for studies related to the status of vitamin K. The vitamin K-deficient 28-day model can be applied to research involving both the status of vitamin K and of vitamin K-dependent coagulation. In conclusion, the combination of a vitamin K-deficient diet with the administration of gentamicin results in a useful model of vitamin K-deficieny. © 2016 The Authors. International Journal of Experimental Pathology © 2016 International Journal of Experimental Pathology


PubMed | Shaanxi Provincial Peoples Hospital, Xi'an Jiaotong University and The First Affiliated Hospital of Xian Medical College
Type: Journal Article | Journal: International journal of experimental pathology | Year: 2016

The main vitamin K-deficient model, minidose warfarin, is different from the pathological mechanism of vitamin K deficiency, which is a shortage of vitamin K. The objective of this study was to establish a new method of vitamin K-deficient model combining a vitamin K-deficient diet with the intragastrical administration of gentamicin in rats. The clotting was assayed by an automated coagulation analyser. The plasma PIVKA-II was assayed by ELISA. The vitamin K status was detected by an HPLC-fluorescence system. In thediet- and gentamicin-induced vitaminK-deficient 14-day group, the rats had undetected vitamin K1 and vitamin K2 in the liver and a prolonged APTT. In the 21-day group, there was also a prolonged PT and a decrease of the FIX activities. In the 28-day group, the undetected vitamin K1 and vitamin K2, the prolonged PT and APTT, and the decrease of the FII, FVII, FIX, and FX activities prompted the suggestion that there were serious deficiencies of vitamin K and vitamin K-dependent coagulation in rats. It is suggested that thediet- and gentamicin-induced vitamin K-deficient 14-day or 21-day model can be used for studies related to the status of vitamin K. The vitamin K-deficient 28-day model can be appliedto research involving both the status of vitamin K and of vitamin K-dependent coagulation. In conclusion, the combination of a vitamin K-deficient diet with the administration of gentamicin results in a useful model of vitamin K-deficieny.


Zhang S.-H.,The First Affiliated Hospital of Xian Medical College | Yang X.-F.,Xi'an Jiaotong University | Wu S.-J.,The First Affiliated Hospital of Xian Medical College | Ma S.-Y.,The First Affiliated Hospital of Xian Medical College | And 2 more authors.
Journal of Xi'an Jiaotong University (Medical Sciences) | Year: 2014

Objective: To explore the mechanism of drug resistance of ovarian cancer cells to TRAIL-induced apoptosis. Methods: We collected 3AO cells and CAOV3 cells, respectively, at 18, 24, 48 and 72 hour under 12.5, 25, 50 and 100 ng/mL concentrations of TRAIL. The rate of cell growth inhibition was checked by methyl thiazolyl tetrazolium (MTT) assay to evaluate the effect of TRAIL. Morphology of apoptotic cells was observed by TdT-mediated-dUTP nick end labeling (TUNEL). The apoptosis rate was detected by flow cytometry (FCM) and C-FLIP protein was determined by Western blotting. Results: TRAIL inhibited the growth of 3AO and CAOV3 cells. The rate of growth inhibition at 24 hour was 28% in 3AO cells and 10% in CAOV3 cells. TRAIL induced apoptosis of cells. The apoptosis rate at 24 hour was 8.5% in 3AO cells, which was higher than 5.5% in CAOV3 cells. The expression level of C-FLIP protein was higher in CAOV3 cells than in 3AO cells. Conclusion: C-FLIP protein is an important protein that regulates drug resistance of ovarian cancer cells to TRAIL-induced apoptosis.


Sheng X.-D.,The First Affiliated Hospital of Xian Medical College | Chen H.,PLA Fourth Military Medical University | Wang H.,The First Affiliated Hospital of Xian Medical College | Ding Z.-B.,The First Affiliated Hospital of Xian Medical College | And 5 more authors.
Asian Pacific Journal of Cancer Prevention | Year: 2015

Fibulin-5 has recently been considered as a potential tumor suppressor in human cancers. Several studies have shown that it is down-regulated in a variety of tumor types and inhibits tumor growth and metastasis. This study was aimed to investigate the clinical significance of fibulin-5 in glioma and its role in cell proliferation and invasion. We found that the expression of fibulin-5 in glioma tissues was significantly lower than those in normal brain (NB) tissues. Negative expression was significantly correlated with advanced clinical stage (grade III+IV) . Furthermore, Fibulin-5 negative expression was correlated with a shorter overall survival of glioma patients. Multivariate Cox repression analysis indicated that fibulin-5 was an independent factor for predicting overall survival of glioma patients. Overexpression obviously inhibited cell proliferation in U251 and U87 cells. Furthermore, it significantly reduced the number of migrating and invading glioma cells. In conclusion, impaired expression of fibulin-5 is correlated with the advanced tumor stage in glioma. Otherwise, Fibulin-5 is an independent prognostic marker for predicting overall survival of glioma patients. Mechanistically, it may function as a tumor suppressor via inhibiting cell proliferation and invasion in gliomas.


Zhang H.,The First Affiliated Hospital Of Xian Medical College | Cao H.,The First Affiliated Hospital Of Xian Medical College | Xu D.,The First Affiliated Hospital Of Xian Medical College | Zhu K.,The Second Affiliated Hospital Of Xian Jiaotong University
OncoTargets and Therapy | Year: 2016

MicroRNAs have been confirmed to be a group of important regulators during the pathogenesis of nasopharyngeal carcinoma (NPC). This study confirmed that the expression of microRNA-92a (miR-92a) was significantly upregulated in NPC as compared to noncancerous nasopharyngeal epithelial tissues. Furthermore, high expression of miR-92a was observed in all NPC cell lines, especially in high metastatic cell lines. Clinical analysis indicated that high expression of miR-92a was associated with adverse clinicopathological features including the advanced tumor-node-metastasis stage and distant metastasis, and conferred poor prognosis of patients. In vitro assays showed that miR-92a overexpression potentiated the migration and invasion of 6-10B cells, and miR-92a silencing reduced the number of migrated and invaded 5-8F cells. Phosphatase and tensin homolog (PTEN) was confirmed as a direct downstream target of miR-92a in NPC cells. Otherwise, alteration of miR-92a expression regulated PTEN/AKT pathway in NPC cells. Mechanistically, miR-92a exerted its promoting effects on the metastatic behaviors of NPC cells through suppressing PTEN/AKT pathway. Taken together, this study demonstrates that miR-92a is a promising prognostic biomarker for patients with NPC, and may be a potential therapeutic target to prevent the metastasis of NPC. © 2016 Zhang et al.


PubMed | the First Affiliated Hospital of Xian Medical College
Type: Journal Article | Journal: Hepatitis monthly | Year: 2015

To systematically evaluate the effects of hepatoprotective agents, when delivered either alone or in combination with other antiviral or non-antiviral drugs in patients with hepatitis B and hepatic fibrosis.The current randomized controlled clinical trials aimed to evaluate the efficacy of combinations of antiviral and non-antiviral hepatoprotective agents on indexes of liver function and liver fibrosis in patients with hepatitis B.Published literatures in Chinese and English on hepatoprotective treatment strategies for chronic hepatitis B and liver fibrosis were searched in three databases and randomized controlled clinical trials were selected.Data were extracted according to a variety of inclusion and exclusion criteria. Meta-analysis was employed to analyze the data.A total of 22 randomized controlled trials encompassing 1,714 cases were considered in the meta-analysis. The obtained results indicated that the combination of antiviral drug and hepatoprotective agent was better than antiviral drug alone to improve liver function. Similarly, regarding liver fibrosis, using two different hepatoprotective agents was better than using one agent. The normalization rates of Aminotransferase (ALT) and total Bilirubin (TBil) were improved 25.7% by two hepatoprotective agents compared to the single agent. Acetylcysteine was superior to ursodeoxycholic acid or silibinin to reduce ALT. Ursodeoxycholic acid was superior to acetylcysteine or silibinin to reduce TBIL.Hepatoprotective agents combined with antiviral drugs can significantly improve liver function and liver fibrosis parameters in patients with hepatitis B.


PubMed | the First Affiliated Hospital of Xian Medical College
Type: Journal Article | Journal: Asian Pacific journal of cancer prevention : APJCP | Year: 2015

Fibulin-5 has recently been considered as a potential tumor suppressor in human cancers. Several studies have shown that it is down-regulated in a variety of tumor types and inhibits tumor growth and metastasis. This study was aimed to investigate the clinical significance of fibulin-5 in glioma and its role in cell proliferation and invasion. We found that the expression of fibulin-5 in glioma tissues was significantly lower than those in normal brain (NB) tissues. Negative expression was significantly correlated with advanced clinical stage (grade III+IV). Furthermore, Fibulin-5 negative expression was correlated with a shorter overall survival of glioma patients. Multivariate Cox repression analysis indicated that fibulin-5 was an independent factor for predicting overall survival of glioma patients. Overexpression obviously inhibited cell proliferation in U251 and U87 cells. Furthermore, it significantly reduced the number of migrating and invading glioma cells. In conclusion, impaired expression of fibulin-5 is correlated with the advanced tumor stage in glioma. Otherwise, Fibulin-5 is an independent prognostic marker for predicting overall survival of glioma patients. Mechanistically, it may function as a tumor suppressor via inhibiting cell proliferation and invasion in gliomas.

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