First Affiliated Hospital Of Xian Medical University

Xi’an, China

First Affiliated Hospital Of Xian Medical University

Xi’an, China
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Li S.-L.,First Affiliated Hospital of Xian Medical University | Ye Y.,First Affiliated Hospital of Xian Medical University | Yuan X.-H.,First Affiliated Hospital of Xian Medical University
PLoS ONE | Year: 2017

Background: A number of studies have investigated the effect of perioperative blood transfusion (PBT) for patients after radical prostatectomy (RP), with some reporting conflicting results. A systematic review of the literature and a meta-analysis were conducted to explore the association between PBT (autologous or allogeneic) and biochemical recurrence-free survival (BRFS), overall survival (OS) and cancer-specific survival (CSS) in patients undergoing RP. Methods: The PubMed, Medline, Cochrane Library, and Embase databases were searched for published controlled clinical studies on perioperative allogeneic or autologous blood transfusion (BT) and patient survival after RP. STATA software version 12.0 was used for data analysis. We used hazard ratios (HRs) and 95% confidence intervals (CIs) to test the correlation between BT and patient survival after RP. Results: Data from a total of 26,698 patients in ten published studies were included in the meta-analysis. The meta-analysis results showed that autologous BT was not associated with BRFS (HR: 1.06; 95% CI: 0.96±1.18; Z = 1.17; P = 0.24), OS (HR: 0.86; 95% CI: 0.71±1.04; Z = 1.58; P = 0.11), or CSS (HR: 0.98; 95% CI: 0.49±1.96; Z = 0.05; P = 0.96). Allogeneic BT exhibited a significant association with worse BRFS (HR: 1.09; 95% CI: 1.01±1.16; Z = 2.37; P = 0.02), OS (HR: 1.43; 95% CI: 1.24±1.64; Z = 4.95; P<0.01) and CSS (HR: 1.74; 95% CI: 1.18±2.56; Z = 2.81; P = 0.005). Conclusion: Our data showed an association between allogeneic BT and reduced BRFS, OS and CSS in patients after RP. These findings indicate that perioperative blood conservation strategies are important for decreasing the allogeneic BT rate. Copyright © 2017 Li et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Ning L.,Tianjin Medical University | Li Z.,Tianjin Medical University | Wei D.,Tianjin Medical University | Chen H.,Tianjin Medical University | Yang C.,First Affiliated Hospital of xiAn Medical University
Cancer Biomarkers | Year: 2017

BACKGROUND: The long non-coding RNAs (lncRNAs) are emerging as important regulators in cancer progression. Clear cell renal cell carcinoma (ccRCC) is one of the most common urological cancers with poor prognosis. In this study, we examined the functional role of the lncRNA, nuclear enriched abundant transcript 1 (NEAT1) in ccRCC progression. METHODS: We performed quantitative real time PCR and western blotting assays to measure mRNA and protein expression levels, respectively. CCK-8 assay, cell invasion and migration assays were used to determine the cell proliferative, cell invasive and migratory ability. Flow cytometric analysis was performed to examine cell apoptosis. RESULTS: The expression levels of NEAT1 was up-regulated in ccRCC tissues and up-regulation of NETA1 was positively correlated with tumor size, higher Fuhrman grade, and lymph node metastasis, and also predicts worse 5-year survival rate of patients with ccRCC. NEAT1 knock-down by NEAT siRNAs transfection suppressed cell proliferation and induced cell apoptosis in ccRCC cell lines. In addition, NEAT1 knock-down suppressed cell invasion and migration and inhibited the mRNA and protein expression levels of epithelial-mesenchymal transition-related markers in ccRCC cell lines. CONCLUSIONS: In conclusion, NEAT1 may be an important mediator in the regulation of ccRCC progression and predicts the poor prognosis in patients with ccRCC. © 2017 - IOS Press and the authors. All rights reserved.

Shu Y.,Xi'an Jiaotong University | Shu Y.,First Affiliated Hospital of Xian Medical University | Yang Y.,Xian Central Hospital | Zhang P.,Xi'an Jiaotong University
Brain Research Bulletin | Year: 2016

Various reports have suggested that penehyclidine hydrochloride (PHC), a new cholinergic antagonist, exhibits a variety of biological actions such as anti-tumor and cardioprotective effects. This study aimed to investigate the effects of PHC on cerebral ischemia/reperfusion (I/R) injury and evaluate whether the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (p38MAPK) pathway is involved in the protective effects of PHC. Male C57BL/6 mice were randomly assigned to Sham group, ischemia/reperfusion (I/R) group, I/R + PHC (0.1 mg/kg) group, and I/R + PHC (1 mg/kg) group. Mice were subjected to 2 h of transient middle cerebral artery occlusion, followed by 24 h of reperfusion except the mice in the sham group. Neurological deficits, infarct volume, brain water content, blood-brain barrier (BBB) integrity, and neuronal apoptosis were evaluated. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), superoxide production, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were measured. The expressions of the key proteins in the JNK/p38MAPK pathway were detected using the Western blot. The results suggested that compared to the I/R group, the PHC-treated group showed improved neurological deficits and BBB integrity, and reduced infarction volume, brain water content, and apoptosis. In addition, PHC significantly suppressed the levels of TNF-α, IL-1β, superoxide production, and MDA, and increased the levels of SOD and GSH-Px. Finally, PHC significantly downregulated the phosphorylation of JNK, p38MAPK, and c-Jun, indicating PHC protects against cerebral I/R injury by downregulating the JNK/p38MAPK signaling pathway. © 2016 Elsevier Inc.

Wang F.,First Affiliated Hospital of Xian Medical University | Luo D.,Yihe Hospital | Liu X.,Shaanxi Normal University
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2016

Objective To explore the relationship between signal transducers and activators of transcription 3 (STAT3) and nuclear factor κB (NF-κB) signaling pathway in papillary thyroid carcinoma. Methods The study enrolled 69 patients with thyroid cancer and 58 control individuals. Real-time fluorescence quantitative PCR, ELISA and immunohistochemistry were separately used to detect mRNA and protein expressions of NF-κB and STAT3 in normal thyroid and thyroid carcinoma tissues. Results Compared with normal thyroid tissues, both mRNA and protein expressions of NF-κB and STAT3 increased significantly in thyroid carcinoma tissues. Immunohistochemistry showed that the positive rate of STAT3 in all patients with thyroid cancer (89.3%) was significantly higher than that in the patients with normal thyroid tissue (10.2%). Conclusion The function of NF-κB pathway mediated by STAT3 is activated in patients with thyroid cancer.

Gao Y.,First Affiliated Hospital Of Xian Jiaotong University | Gao F.,First Affiliated Hospital Of Xian Medical University | Chen K.,Zhejiang Sci-Tech University | Tian M.-L.,First Affiliated Hospital Of Xian Jiaotong University | Zhao D.-L.,First Affiliated Hospital Of Xian Jiaotong University
Drug Design, Development and Therapy | Year: 2015

The development of chemotherapeutic resistance is a major challenge in oncology. Elevated sphingosine kinase 1 (SK1) levels is predictive of a poor prognosis, and SK1 overexpression may confer resistance to chemotherapeutics. The SK/sphingosine-1-phosphate (S1P)/sphingosine-1-phosphate receptor (S1PR) signaling pathway has been implicated in the progression of various cancers and in chemotherapeutic drug resistance. Therefore, SK1 may represent an important target for cancer therapy. Targeting the SK/S1P/S1PR signaling pathway may be an effective anticancer therapeutic strategy, particularly in the context of overcoming drug resistance. This review summarizes our current understanding of the role of SK/S1P/S1PR signaling in cancer and development of SK1 inhibitors. © 2015 Gao et al.

Gao F.,PLA Fourth Military Medical University | Gao F.,First Affiliated Hospital of Xian Medical University | Liu Z.,Shaanxi Normal University | Ren W.,Shaanxi Normal University | Jiang W.,PLA Fourth Military Medical University
Neuropsychiatric Disease and Treatment | Year: 2014

Growing evidence indicates brain inflammation has been involved in the genesis of seizures. However, the direct effect of acute inflammation on neuronal circuits is not well known. Lipopolysaccharide (LPS) has been used extensively to stimulate brain inflammatory responses both in vivo and in vitro. Here, we observed the contribution of inflammation induced by 10 μg/mL LPS to the excitability of neuronal circuits in acute hippocampal slices. When slices were incubated with LPS for 30 minutes, significant increased concentration of tumor necrosis factor α and interleukin 1β were detected by enzyme-linked immunosorbent assay. In electrophysiological recordings, we found that frequency of epileptiform discharges and spikes per burst increased 30 minutes after LPS application. LPS enhanced evoked excitatory postsynaptic currents but did not modify evoked inhibitory postsynaptic currents. In addition, exposure to LPS enhanced the excitability of CA1 pyramidal neurons, as demonstrated by a decrease in rheobase and an increase in action potential frequency elicited by depolarizing current injection. Our observations suggest that acute inflammation induced by LPS facilitates epileptiform activity in vitro and that enhancement of excitatory synaptic transmission and neuronal excitability may contribute to this facilitation. These results may provide new clues for treating seizures associated with brain inflammatory disease. © 2014 Gao et al. This work is published by Dove Medical Press Limited.

Zhang M.,Xi'an Jiaotong University | Li. W.,First Affiliated Hospital of Xian Medical University | Yu L.,Xi'an Jiaotong University | Wu S.,Xi'an Jiaotong University
PLoS ONE | Year: 2014

Background: Hypoxia-inducible factor-1a (HIF-1α) is overexpressed in many human tumors and their metastases, and is closely associated with a more aggressive tumor phenotype. The aim of the present study was to investigate the effect of resveratrol (RES) on the expression of ischemic-induced HIF-1α and vascular endothelial growth factor (VEGF) in rat liver.Methods: Twenty-four rats were randomized into Sham, ischemia/reperfusion (I/R), and RES preconditioning groups. I/R was induced by portal pedicle clamping for 60 minutes followed by reperfusion for 60 minutes. The rats in RES group underwent the same surgical procedure as I/R group, and received 20 mg/kg resveratrol intravenously 30 min prior to ischemia. Blood and liver tissue samples were collected and subjected to biochemical assays, RT-PCR, and Western blot assays.Results: I/R resulted in a significant (P,0.05) increase in liver HIF-1α and VEGF at both mRNA and protein levels 60 minutes after reperfusion. The mRNA and protein expressions of HIF-1α and VEGF decreased significantly in RES group when compared to I/R group (P,0.05).Conclusion: The inhibiting effect of RES on the expressions of HIF-1α and VEGF induced by I/R in rat liver suggested that HIF-1α/VEGF could be a promising drug target for RES in the development of an effective anticancer therapy for the prevention of hepatic tumor growth and metastasis. © 2014 Zhang et al.

Gao Y.,Xi'an Jiaotong University | Gao F.,First Affiliated Hospital of Xian Medical University | Ma J.-L.,Xi'an Jiaotong University | Sun W.-Z.,Xi'an Jiaotong University | Song L.-P.,Xi'an Jiaotong University
OncoTargets and Therapy | Year: 2014

Lung cancer is the major cause of cancer deaths worldwide due to its late diagnosis and poor outcome. Understanding genomic medicine may widen our vision into the oncogenesis of lung cancer and may open the door to improvements in the clinical management of lung cancer. It is well known that almost half of all genes are regulated by microRNAs (miRNAs). This review focuses on the role of miRNAs in lung cancer and also touches on the value of miRNA-based novel therapies for lung cancers. © 2014 Gao et al. This work is published by Dove Medical Press Limited.

Gao Y.,Xi'an Jiaotong University | Chen K.,Zhejiang Sci-Tech University | Ma J.-L.,Xi'an Jiaotong University | Gao F.,First Affiliated Hospital of Xian Medical University
OncoTargets and Therapy | Year: 2014

With the development of many nanomedicines designed for tumor therapy, the diverse abilities of cerium oxide nanoparticles (CONPs) have encouraged researchers to pursue CONPs as a therapeutic agent to treat cancer. Research data have shown CONPs to be toxic to cancer cells, to inhibit invasion, and to sensitize cancer cells to radiation therapy and chemotherapy. CONPs also display minimal toxicity to normal tissues and provide protection from various forms of reactive oxygen species generation. Differential cytotoxicity is important for anticancer drugs to distinguish effectively between tumor cells and normal cells. The antioxidant capabili- ties of CONPs, which enable cancer therapy protection, have also resulted in the exploration of these particles as a potential anticancer treatment. Taken together, CONPs might be a potential nanomedicine for cancer therapy and this review highlights the current research into CONPs as a novel therapeutic for the treatment of cancer. © 2014 Gao et al.

Wang S.,First Affiliated Hospital Of Xian Medical University | Gong W.,First Affiliated Hospital Of Xian Medical University | Tian Y.,First Affiliated Hospital Of Xian Medical University | Zhou J.,First Affiliated Hospital Of Xian Medical University
Respiratory Care | Year: 2016

BACKGROUND: FEV6 can be used as a convenient alternative to FVC. The aim of this study was to determine an alternative to the fixed cutoff points of FEV1/FVC <0.70 suitable for FEV1/FEV6 in primary care. METHODS: Pulmonary function testing was conducted on volunteers recruited from 4 community centers in Xi’an, China, between July and August 2012. Participants underwent 3 FVC maneuvers. The maneuver with the best FEV1 was retained. FVC, FEV1, and FEV6 were measured by portable spirometer. The receiver operating characteristic curves that corresponded to the optimal combination of sensitivity and specificity for FEV1/FEV6 were determined. A kappa test was used to compare the agreement between FEV1/FVC and FEV1/FEV6. The positive predictive value and negative predictive value were also calculated. RESULTS: A total of 767 volunteers participated in this study, of whom 297 were male and 470 were female. Considering FEV1/FVC <0.70 as the accepted standard for COPD, the area under the curve was 98% (P <.001), and the FEV1/FEV6 cutoff, corresponding to the greatest sum of sensitivity and specificity, was 0.72. For the total population, the FEV1/FEV6 sensitivity, specificity, positive predictive value, and negative predictive value were 96.9, 98.8, 95.8, and 99.2%, respectively. The agreement between the 2 cutoff points was excellent, and the kappa value was 0.954. CONCLUSIONS: FEV1/FEV6 <0.72 can be used in primary care as a valid alternative to FEV1/FVC <0.70 as a fixed cutoff point for the detection of COPD in adults. This study suggests that FEV1/FEV6 is an effective and well validated option that should be used in primary care to detect COPD, which is a rampant problem. © 2016, Daedalus Enterprises. All right reserved.

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