Shaanxi Province Peoples Hospital

Xi’an, China

Shaanxi Province Peoples Hospital

Xi’an, China
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Deng S.,PLA Fourth Military Medical University | Yang Y.,Shaanxi Province Peoples Hospital | Han Y.,PLA Fourth Military Medical University | Li X.,PLA Fourth Military Medical University | And 3 more authors.
PLoS ONE | Year: 2012

The Crosstalk between a tumor and its hypoxic microenvironment has become increasingly important. However, the exact role of UCP2 function in cancer cells under hypoxia remains unknown. In this study, UCP2 showed anti-apoptotic properties in A549 cells under hypoxic conditions. Over-expression of UCP2 in A549 cells inhibited reactive oxygen species (ROS) accumulation (P<0.001) and apoptosis (P<0.001) compared to the controls when the cells were exposed to hypoxia. Moreover, over-expression of UCP2 inhibited the release of cytochrome C and reduced the activation of caspase-9. Conversely, suppression of UCP2 resulted in the ROS generation (P = 0.006), the induction of apoptosis (P<0.001), and the release of cytochrome C from mitochondria to the cytosolic fraction, thus activating caspase-9. These data suggest that over-expression of UCP2 has anti-apoptotic properties by inhibiting ROS-mediated apoptosis in A549 cells under hypoxic conditions. © 2012 Deng et al.

Zhou X.B.,Xi'an Jiaotong University | Qin H.,Xi'an Jiaotong University | Li J.,ShaanXi Province Peoples Hospital | Wang B.,Xi'an Jiaotong University | And 4 more authors.
Ultrasonics | Year: 2011

Microbubbles (MBs) can augment the acoustic cavitation' (US), thereby facilitating the thrombolysis of external ultrasound. But we observed re-thrombosis after successful thrombolysis by MBs and transcutaneous ultrasound in an endothelium injury model. This study was designed to explore whether platelet-targeted MBs can prevent the reformation of thrombi. Arterial injury was induced in canine femoral arteries with balloon, and the arteries were completely thrombotically occluded. The arteries were treated with intra-arterial MBs or platelet-targeted MBs (TMB) and transcutaneous low frequency ultrasound (LFUS) to achieve complete thrombolysis. The arterial flow was monitored with angiogram for 4 h following treatment. Results showed that both MBs and TMBs produced successful dissolution of clots in the presence of ultrasound. The re-occlusion began to occur 1 h after thrombolysis in MB/LFUS treatment, and 7 of 8 arteries were re-occluded within 3 h. Most of the arteries (7 of 8) in the TMB/LFUS group remained patent for 4 h following treatment. The flow tended to decrease after thrombolysis in MB/LFUS treatment. These results indicated that platelet-targeted microbubbles were beneficial in preventing re-thrombosis in vivo and microbubbles served as good carrier of thrombolytic and anticoagulation drugs. © 2010 Elsevier B.V. All rights reserved.

Chen J.-J.,PLA Fourth Military Medical University | Gao Y.,Shaanxi Province Peoples Hospital | Tian Q.,PLA Fourth Military Medical University | Liang Y.-M.,PLA Fourth Military Medical University | Yang L.,PLA Fourth Military Medical University
British Journal of Radiology | Year: 2014

Objective: The aimof this studywas to find a newradiation protector, platelet factor 4 (PF4) and to identify its effect on haemopoietic microenvironment in vitro and in vivo.Methods: Radiation damage on bone marrow mesenchymal stem cells ex and in vitro was set up as models. Growth curve analysis, clonogenic survival assay, FACSCalibur™ (BD Immunocytometry Systems, San Jose, CA), 5-ethynyl-2′-deoxyuridine immunofluorescence staining and quantitative reverse transcription-polymerase chain reaction were employed to assess the characterization of bone marrow mesenchymal stem cells (BMSCs), proliferation, apoptosis, cell cycle and gene expression.Results: A dose- and time-dependent enhancement of cell viability and survival was observed for PF4 treatment along with 500cGy γ-radiation in vitro. The same phenomena were noted in vivo, including enhancement of adherence and proliferation ability while inhibition of cell apoptosis, which were associated with a short-term decrease in the G0/G1 ratio owing to S phase arrest. These were accompanied with enhanced Bcl-2 expression and p53/p21 loss.Conclusion: These results uncover that PF4 might be a novel therapeutic approach, which could reduce DNA damage and increase survival of BMSCs, in part, by inhibiting p53/p21 axis and facilitating DNA damage repair. Advances in knowledge: This study explores the feasibility of a new radioprotector and hence may be clinically important. © 2014 The Authors.

Song W.,PLA Fourth Military Medical University | Song W.,Shaanxi Province Peoples Hospital | Sun J.,PLA Fourth Military Medical University | Su B.,PLA Fourth Military Medical University | And 3 more authors.
Journal of Thoracic and Cardiovascular Surgery | Year: 2013

Background: It is well known that ischemic postconditioning reduces ischemic-reperfusion injury, but the underlying mechanism is not fully understood. The current study investigated the role of reactive oxygen species-mediated upregulation of endogenous antioxidant enzymes in the generation of a protective effect induced by ischemic postconditioning against spinal cord reperfusion injury in the rabbit. Methods: New Zealand White rabbits were randomly allocated to sham, ischemia-reperfusion, and postconditioning groups (3 cycles of 30 seconds of reperfusion and 30 seconds of occlusion during the onset of reperfusion). Spinal cord ischemia was induced by clamping the infrarenal abdominal aorta for 20 minutes in the ischemia-reperfusion and postconditioning groups. Forty-eight hours after reperfusion, the neurologic status of the lower limbs was assessed. Blood samples were collected for analysis of serum neuron-specific enolase levels, and the lumbar spinal cord segments (L5-7) were harvested for histopathologic and antioxidant enzyme activities and mRNA analysis with or without administration of N-2-mercaptopropionylglycine (an effective oxygen free radical scavenger) given at different reperfusion times. Results: Continuous administration of N-2-mercaptopropionylglycine for 13 minutes, starting at 10 minutes before (but not 10 minutes after) the beginning of reperfusion, attenuated the neuroprotective effect of postconditioning against spinal cord ischemia and reversed the increase in activity of the antioxidant enzymes superoxide dismutase and catalase in spinal cord tissue subjected to ischemic postconditioning. Conclusions: The results indicate that reactive oxygen species-triggered upregulation of endogenous antioxidant enzyme activities may be involved in the mechanism of neuroprotection of ischemic postconditioning. © 2013 by The American Association for Thoracic Surgery.

Song W.,PLA Fourth Military Medical University | Song W.,Shaanxi Province Peoples Hospital | Huo T.,PLA Fourth Military Medical University | Guo F.,PLA Fourth Military Medical University | And 6 more authors.
Neuroscience | Year: 2013

Recent studies indicate that adiponectin can attenuate cerebral ischemic lesions via its functional area located in the C-terminal globular domain, which is called globular adiponectin (gAD). However, the mechanisms underlying this action remain unclear. In this study, we investigated the antioxidant properties of gAD during cerebral ischemia. Adult male C57BL/6 mice received an intracerebral injection of gAD with or without tetrabromocinnamic acid (TBCA, a NADPH oxidase activator). Mice were subjected to middle cerebral artery occlusion (MCAO) after gAD injection. Infarct volume, neurological function, the activity of antioxidant enzymes (superoxide dismutase [SOD], catalase), the content of malondialdehyde (MDA), and the expression of Bax, Bcl-2, cleaved caspase-3 and NADPH oxidase 2 (NOX2) were examined at 24. h after MCAO. Infarct volume was attenuated in gAD-transduced mice when compared with mice in the MCAO group, with significant improvement in neurological function. In addition, neuronal apoptosis was attenuated, along with the expression of Bax/Bcl-2 and cleaved caspase 3. Furthermore, the activities of SOD and catalase increased, and the content of MDA reduced. However, TBCA blocked the effect of gAD on cerebral protection and its antioxidant abilities. Taken together, these results demonstrate that the neuroprotective action of gAD may result from the promotion of antioxidant capacity by inhibiting the NOX2 signaling system. © 2013 IBRO.

PubMed | Shaanxi Province Peoples Hospital, Xi'an Jiaotong University and PLA Fourth Military Medical University
Type: Journal Article | Journal: Technology in cancer research & treatment | Year: 2016

A specific protein profile that accompanies neoplastic transformation in the premalignant airway epithelium could provide an opportunity for early diagnosis of lung cancer. The aim of this study was to screen and identify early candidate biomarkers of non-small cell lung cancer. Thirteen non-small cell lung cancer samples were obtained within 30 minutes after a surgical resection. Laser capture microdissection was performed to enrich the normal lung cell and squamous metaplasia or atypical adenomatous hyperplasia cell populations. The resulting tandem mass spectrum was automatically searched for proteins against International Protein Index (IPI) human protein database using the TurboSEQUEST searching engine. The molecular function and biological processes of identified proteins were determined based on universal bioinformatics tools. The 2 proteins of interest, focal adhesion kinase and C-terminal Src kinase, were validated using Western blot method. A total of 863 proteins were identified by automatically searching the tandem mass spectrum, among which 427 were dysregulated expression in premalignant airway epithelium compared with those of normal lung cells. The 427 proteins were mainly distributed in 24 sorts of cellular components, 22 molecular function, 15 biological processes, and 10 significant perturbations of pathways. The most significant network included 48 genes and was related to energy production, cell cytoskeleton, cell adhesion, metabolism, oxidative stress, and small molecule biochemistry. Focal adhesion kinase and C-terminal Src kinase were significantly overexpressed in premalignant lung lesion cells compared with the normal lung cells in 13 cases. We identified that there were 427 proteins involved in non-small cell lung cancer carcinogenic process and confirmed the key biological pathways in premalignant lung tissue. The significantly upregulated focal adhesion kinase and C-terminal Src kinase could be considered as molecular biomarkers for early diagnosis and prognosis of non-small cell lung cancer.

PubMed | Shaanxi Province Peoples Hospital and Xi'an Jiaotong University
Type: Journal Article | Journal: Oncology reports | Year: 2016

Anginex is an artificial synthetic small molecule -sheet-formingpeptide shown to have anti-angiogenesis and antitumor effects in various solid tumors. However, its molecular mechanism remains largely unclear and efficient delivery methods for anginex remains to be developed. We report on the development of recombinant adeno-associated virus (rAAV2)-delivered anginex and the underlying mechanism of anti-angiogenesis and antitumor effects of anginex. We have successfully developed the rAAV2 vector to efficiently express anginex (rAAV2anginex). Transduction of rAAV2-anginex significantly induced apoptosis, and inhibited the proliferation, migration, invasion and tube formation of human umbilical vein endothelial cells invitro. Western blot analysis revealed that rAAV2anginex inhibited the phosphorylation of Akt, while inducing the phosphorylation of JNK and activation of the NF-B signaling pathway. In an invivo CAM assay and xenograft model of SKOV3, rAAV2-anginex significantly reduced microvessel density (MVD) and vascular endothelial growth factor165 (VEGF165), as demonstrated by immunohistochemistry analysis. Importantly, rAAV2-anginex inhibited tumor growth in an ovarian cancer SKOV3 cell nude mouse xenograft model. Our results suggest that rAAV2-anginex may inhibit tumor angiogenesis and growth through regulating Akt, JNK and NF-B signaling pathways.

PubMed | Inner Mongolia University, Shaanxi Province Peoples Hospital, Northwest University, China, Xi'an Jiaotong University and Xian Chest Hospital
Type: Journal Article | Journal: Oncotarget | Year: 2016

The distribution and levels of TNIP1 in malignant and normal gastric mucosa are different, but it is not known whether TNIP1 polymorphisms are related to gastric carcinogenesis. To assess the association between four TNIP1 SNPs (rs3792792, rs4958881, rs7708392, rs10036748) and carcinogenesis, we used Sequenom Mass-ARRAY technology to determine the genotypes of 302 gastric carcinoma patients and 300 healthy controls in a Northwest Chinese Han population. These data were then compared using the Chi-square test/Fishers exact test, genetic model analysis, and haplotype analysis. Odds ratios (OR) and 95% confidence intervals (CI) were used to evaluate the correlation. We observed that patients with the G allele of rs7708392 and the C allele of rs10036748 showed an increased risk of gastric carcinoma (OR= 1.335, 95%CI: 1.021-1.745, P= 0.035; OR= 1.358, 95%CI: 1.039-1.774, P= 0.025, respectively). Conversely, the haplotype CT of TNIP1 (rs7708392-rs10036748) may act as a genetic protective factor for gastric carcinoma (adjusted OR= 0.731, 95%CI: 0.552-0.970, P= 0.030). Our results are the first to suggest that genetic variation in TNIP1 gene is associated with gastric carcinoma, though, this finding must be confirmed in other populations with larger sample size.

PubMed | Shaanxi Province Peoples Hospital, Xi'an Jiaotong University, GY Highland Biotech LLC and Gaoling County Women and Childrens Hospital
Type: Journal Article | Journal: Asia-Pacific journal of clinical oncology | Year: 2016

A newly developed cervical cancer screening method - folate receptor-mediated epithelium staining utilizes methylene blue internalized by folate receptor-mediated endocytosis to stain cervical intra-epithelial neoplasia. We test the clinical feasibility of this method in this study.A total of 14344 women who were at least 21 years old and had been sexually active, participated in the study. In gynecological clinics, participants underwent cervical cancer screening with folate receptor-mediated epithelium staining followed by cytology sampling. The color change of methylene blue in the cervical neoplastic epithelium can then be detected by the cotton swabs placed inside the cervix. A change of color to blue, bluish black or black is positive, whereas a change of color to green or no color change indicates negative result. Three hundred and twenty-three women who were positive with either or both tests had histopathologic diagnosis.The sensitivity, specificity, positive predictive value and negative predictive value of folate receptor-mediated epithelium staining for cervical intra-epithelial neoplasia grade 2 and worse was 85.7%, 76.4%, 61.3% and 92.5%, respectively. Folate receptor-mediated epithelium staining had moderate agreement with cytology thresholded at atypical squamous cells, unable to exclude a high grade intra-epithelial lesion and was more sensitive that the later (85.7% vs 74.5% for intra-epithelial neoplasia grade 2 and worse; 89.2% vs 75.4% for intra-epithelial neoplasia grade 3 and worse).Folate receptor-mediated epithelium staining is capable of detecting cervical precancerous and cancerous lesions rapidly and cost-effectively.

PubMed | Shaanxi Province Peoples Hospital and Xi'an Jiaotong University
Type: | Journal: Medical science monitor : international medical journal of experimental and clinical research | Year: 2016

BACKGROUND This aim of this study was to investigate the expression of BMP-7 in atrial fibrillation and illuminate the role of BMP-7 and TGF-/Smads signaling in myocardial fibrosis. MATERIAL AND METHODS Fibrosis of myocardial fibroblasts was induced by TGF-1 and the optimal condition was determined by the MTT assay. Cells with TGF-1 treatment were sub-divided into 4 groups: TGF-1 group, TGF-1 + Smad3 siRNA group, TGF-1 + BMP-7 group, and TGF-1 + BMP-7 + Smad1/5 siRNA group. Cells were then analyzed by detecting the expression of epithelial cadherin (E-cadherin), collagen I, alpha smooth muscle cell actin (-SMA), and activated Smads using Western blot. Mice were injected daily with Ach-CaCl2 with or without the addition of BMP-7 and Smad1/5 siRNA over a period of 4 weeks. Cardiac functions were tested by echocardiogram assay and fibrosis was diagnosed by histopathological examination. Finally, molecule biomarkers were detected using standard procedures. RESULTS TGF-1 treatment significantly down-regulated E-cadherin expression and up-regulated expressions of Collagen I, -SMA, and pSmad3 (P<0.05). The effects of TGF-1 treatment can be significantly suppressed by Smad3 siRNA (P<0.05). Cells in the BMP-7 group exhibited significantly higher expression levels of E-cadherin and pSmad1/5 together with lower expression levels of pSmad3, collagen I, and a-SMA (P<0.05). Moreover, Smad1/5 siRNA can substantially repress the effects of BMP-7 (P<0.05) and results from the mice model coincided with those in myocardial fibroblasts. CONCLUSIONS BMP-7 can regulate TGF-1/Smad3 by targeting Smad1/5 to antagonize fibrosis in myocardial fibroblasts resulting from atrial fibrillation.

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