First Hospital of xiAn

Fengcheng, China

First Hospital of xiAn

Fengcheng, China
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Ren B.,First Hospital of Xian | Li W.,First Hospital of Xian | Yang Y.,China Institute of Technology | Wu S.,First Hospital of Xian
World Journal of Surgical Oncology | Year: 2014

Background: To evaluate the relationship between cyclin D1 overexpression and bladder cancer prognosis. Methods: A systematic literature search up to July 27, 2013 was carried out in PubMed and Wanfang databases, and the references of retrieved articles were screened. The hazard ratios (HRs) and their 95% CIs were used to combine the data. Heterogeneity and publication bias were also evaluated. Results: A total of 15 studies containing 2,591 cases were included. We found that increased cyclin D1 levels were significantly correlated with progression-free survival with a pooled HR estimate of 0.54 (95% CI: 0.32-0.92). There was a significant degree of heterogeneity (I2 = 93.8%, P <0.001). Moreover, subgroup analysis indicated that elevated cyclin D1 levels were significantly associated with overall survival in muscle-invasive bladder patients (HR: 0.95, 95% CI: 0.91-0.99), without a significant heterogeneity in the data (I2 = 0.0%, P = 0.456). Conclusions: Increased cyclin D1 expression level detected by immunohistochemistry is associated with good progression-free survival for bladder cancer. Because of the limited number of studies, further well-designed prospective studies are warranted to confirm the findings from our study. © 2014 Ren et al.; licensee BioMed Central Ltd.

Zhao Z.,Xi'an Jiaotong University | Zhao Z.,First Hospital of Xian | Wu Y.,Xi'an Jiaotong University | Cheng M.,First Hospital of Xian | And 6 more authors.
Atherosclerosis | Year: 2011

Objective: Th1 activation and regulatory T (Treg) cell suppression have been observed in acute coronary syndrome (ACS), including unstable angina (UA) and acute myocardial infarction (AMI). However, the role of Th17 cell or IL-17A remains controversial in ACS patients, and little is known about the role of recently discovered Th17/Th1 cells, a subset of Th17 cells, in coronary artery disease (CAD). The purpose of this study is to investigate functional changes of Th17/Th1, Th17, Th1, Th2 and Treg cells in ACS patients. Methods: The contents of Th17/Th1, Th17, Th1, Th2 and Treg cells, related gene expression, and plasma cytokines from CAD and control patients with normal coronary arteries (NCA) were measured by flow cytometry, real-time quantitative PCR and ELISA. Results: Th17/Th1 and Th1 cell contents and related gene expression (T-bet, IFN-γ, STAT4, RORγt, STAT3 and IL-17) were significantly increased in ACS patients, whereas plasma IFN-γ only increased in CAD patients. In contrast, Treg cell population, Foxp3 levels, and plasma TGF-β1 were decreased in ACS patients compared with stable angina (SA) and NCA patients. Conclusion: The study showed activation of Th17/Th1 and Th1 cell in ACS patients, which may provide insight into the mechanisms underlying culprit plaque relevant T-cell activation in ACS patients. © 2011 Elsevier Ireland Ltd.

Wang Y.,Sichuan University | Wang Y.,First Hospital of Xian | Zhu X.,First Hospital of Xian | Yang Z.,Sichuan University | And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

Our previous report has shown that honokiol (HNK), a constituent of Magnolia officinalis, induces a novel form of non-apoptotic programmed cell death in human leukemia NB4 and K562 cells. In this study, we further explored the relationship between the cell death pathway and cytoplasmic vacuolization and studied the underlying mechanism of leukemia cell death mediated by honokiol. The results showed that low concentrations of honokiol activated an novel alternative cell death fitted the criteria of paraptosis, such as cytoplasmic vacuolization derived from endoplasmic reticulum swelling, lack of caspase activation, and lack of apoptotic morphology. Results further indicated that the cell death was time- and concentration-dependent. In addition, honokiol-induced paraptosis did not involve membrane blebbing, chromatin condensation and phosphatidylserine exposure at the outer of the plasma membrane. The mechanism of the cell death may be associated, at least in part, with the increased generation of reactive oxygen species. Further analysis showed that honokiol induces cell death predominantly via paraptosis and to a certain extent via apoptosis in NB4 cells, and predominantly via apoptosis and to a certain extent via paraptosis in K562 cells. These observations suggest that cell death occurs via more than one pathway in leukemia cells and targeting paraptosis may be an alternative and promising avenue for honokiol in leukemia therapy. © 2012 Elsevier Inc.

PubMed | First Hospital of Xian, Shaanxi Normal University and PLA Fourth Military Medical University
Type: Journal Article | Journal: The Analyst | Year: 2016

A novel method for sensitive detection of liver cancer cells using anti-CD155 and anti-CD112 monoclonal antibodies conjugated to ultrabright fluorescent mesoporous silica nanoparticles (FMSNs) encapsulating Rhodamine 6G and fluorescein was developed. The diameter of the obtained nanoparticles was 90 nm, and the quantum yield was 69%. Because the emission of fluorescein has a high degree of overlap with the excitation of Rhodamine 6G, and these two dyes were sufficiently close to each other on the nanoparticles, fluorescence resonance energy transfer can occur between these two dyes. This transfer not only maintains the original feature of the nanochannels and the skeletal network of the silica weakening the inner filtering of the dye, but also makes the excitation peak of the nanoparticles wider and increases the useful load amount of the dye. Because the wider Stokes shifts weaken the interference of excitation, the detection sensitivity is enhanced at the same time. The NaIO4 oxidation method does not use a cross-linker but rather uses covalent immobilization of the monoclonal antibodies on the FMSNs. This method can maintain the activity of the monoclonal antibodies more easily than the glutaraldehyde method. These advantages ensure that the nanosensor has high sensitivity and specificity for detecting liver cancer SMMC-7721 and HHCC cells. The in vivo imaging experiment also ensured that the biosensor can target tumor tissue in mice.

Wang Y.,Xiamen University | Wang Y.,First Hospital of xian | Xu K.,First Hospital of xian | Zhang H.,First Hospital of xian | And 3 more authors.
Molecular Medicine Reports | Year: 2014

Accumulative evidence has indicated that apoptosis is the common pathway for retinal ganglion cell (RGC) death and that autophagy promotes survival of RGCs in glaucoma. In the present review, it was hypothesized that the progressive death of RGCs in glaucoma involves another novel non-apoptotic programmed cell death, known as 'paraptosis', in the early stages of glaucoma. Paraptosis may be accompanied by apoptosis and/or autophagy in the moderate and severe stages. The secondary hypothesis suggests that paraptosis in glaucomatous RGCs may be triggered by damage to cellular mitochondria, and is associated with mitochondria-derived reactive oxygen species (ROS). Our preliminary laboratory studies, using transmission electron microscopy, provided evidence that supports the primary hypothesis. The secondary hypothesis is currently under investigation. These two hypotheses provide a novel way to investigate the mechanisms of cell death in glaucomatous RGCs and targeting paraptosis may be a promising strategy for RGC-protecting drug discovery.

Wang Y.,Xiamen University | Wang Y.,First Hospital of Xian | Huang C.,Xiamen University | Zhang H.,First Hospital of Xian | Wu R.,Xiamen University
Brain Research Bulletin | Year: 2015

Glaucoma is characterized by elevated intraocular pressure that causes progressive loss of retinal ganglion cells (RGCs). Autophagy is a lysosomal degradative process that updates the cellular components and plays an important role in cellular homeostasis. Recent studies have shown that autophagy is involved in the pathophysiological process of glaucoma. The role played by autophagy in glaucoma is complex, and conflicting evidence shows that autophagy promotes both RGC survival and death. The understanding of the major pattern of RGC loss and the crosstalk between autophagy and apoptosis remains limited in glaucoma. This review focuses on the relationship between autophagy and glaucoma, particularly on the influence of autophagy on apoptosis in glaucoma. Further research on autophagy in glaucoma may provide a novel understanding of the glaucoma pathology and novel treatment targets for glaucoma in the future. © 2015 Elsevier Inc.

Li M.,Xi'an Jiaotong University | Ji Y.,First Hospital of xiAn | Dong Y.,Xi'an Jiaotong University | Zhou Y.,Xi'an Jiaotong University | And 2 more authors.
Inflammation | Year: 2013

Hemorrhagic fever with renal syndrome (HFRS) is an acute infectious disease characterized by endothelial cell dysfunction, which results in plasma exosmosis, hyperpermeability, and sometimes hemorrhages. As one of the vascular permeability cytokines, vascular endothelial growth factor (VEGF) might mediate the hyperpermeability caused by HFRS. In the present study, the levels of serum VEGF were measured by competitive inhibition ELISA. We found variable but persistently elevated levels of VEGF throughout the various stages and types of HFRS disease, which suggested that the levels of VEGF were closely correlated to the progression of HFRS. Moreover, elevated levels of VEGF have correlation with the severity and degree of kidney damage. Therefore, to study the relationship between levels of VEGF and disease severity of patients with HFRS is helpful to clarify the pathogenesis of HFRS. © 2013 Springer Science+Business Media New York.

PubMed | Xi'an Jiaotong University, PLA Fourth Military Medical University and First Hospital of Xian
Type: Journal Article | Journal: International journal of molecular sciences | Year: 2016

Panax ginseng is a famous herbal medicine widely used in Asia. Ginsenosides have been identified as the principle active ingredients for Panax ginsengs biological activity, among which ginsenoside Rd (Rd) attracts extensive attention for its obvious neuroprotective activities. Here we investigated the effect of Rd on neurite outgrowth, a crucial process associated with neuronal repair. PC12 cells, which respond to nerve growth factor (NGF) and serve as a model for neuronal cells, were treated with different concentrations of Rd, and then their neurite outgrowth was evaluated. Our results showed that 10 M Rd significantly increased the percentages of long neurite- and branching neurite-bearing cells, compared with respective controls. The length of the longest neurites and the total length of neurites in Rd-treated PC12 cells were much longer than that of respective controls. We also showed that Rd activated ERK1/2 and AKT but not PKC signalings, and inhibition of ERK1/2 by PD98059 or/and AKT by LY294002 effectively attenuated Rd-induced neurite outgrowth. Moreover, Rd upregulated the expression of GAP-43, a neuron-specific protein involved in neurite outgrowth, while PD98059 or/and LY294002 decreased Rd-induced increased GAP-43 expression. Taken together, our results provided the first evidence that Rd may promote the neurite outgrowth of PC12 cells by upregulating GAP-43 expression via ERK- and ARK-dependent signaling pathways.

Zhang L.-T.,Central Hospital of Zaozhuang Coal Mining Group | Zhang S.-X.,Central Hospital of Zaozhuang Coal Mining Group | Wu S.-D.,First Hospital of Xian
Clinical EEG and Neuroscience | Year: 2014

Cerebral hemorrhage may cause cognitive dysfunction. Electroencephalogram (EEG) is a noninvasive diagnostic tool for assessment of cerebral function. A total of 174 patients (including cognitively impaired and cognitively normal) with cerebral hemorrhage, and 120 healthy persons (CN), were recruited between August 2008 and July 2012 at the Department of Neurology. EEG was used to analyze cerebral function of patients and normal persons. Correlation, clustering and concordance analyses were performed to analyze the relationship between EEG power and Montreal Cognitive Assessment (MoCA) scores. Cognitively impaired patients had a significantly decreased EEG beta power (0.793 ± 0.176 μV2) compared with cognitively normal patients (1.589 ± 0.205 μV2, P <.01) or healthy persons (1.651 ± 0.185 μV2, P <.01). Significantly negative correlations between beta power and hemorrhage region, size, amount, and patients' age were apparent (r = -0.91888, -0.78569, -0.84961, and -0.80365, respectively, all Ps <.001). There was good concordance between the K-means clustering algorithm calculating beta power and MoCA scoring ( =.904, P <.001). In conclusion, the analysis method of EEG (beta power) abnormalities holds considerable promise to assess cognitive impairment after cerebral hemorrhage. Cognitive impairment was negatively correlated to hemorrhage region, size, amount, and age. © EEG and Clinical Neuroscience Society (ECNS) 2013.

Ji Y.,First Hospital of Xian | Zhao Z.,First Hospital of Xian | Cai T.,Xian Medical University | Yang P.,First Hospital of Xian | Cheng M.,First Hospital of Xian
Molecular Medicine Reports | Year: 2014

Clinically, diabetes mellitus is closely associated with and induces certain cardiovascular diseases. The aim of this study was to investigate endoplasmic reticulum (ER) stress-associated apoptosis of diabetic cardiomyopathy (DCM), and explore the protective mechanism of liraglutide. The DCM model was established with a high-fat diet and streptozotocin (STZ). Cardiac function was detected by echocardiogram examination and hematoxylin-eosin staining. ER stress unfolded protein response (UPR) hallmarks [inositol-requiring enzyme-α (IRE-α), p-Perk and ATF6] and transcription factors were detected with western blotting. Apoptosis inducers CHOP, c-Jun amino terminal kinase (JNK) and casapse-12 were also examined with western blotting. The results indicated that liraglutide is capable of improving cardiac function in DCM rats (P<0.05). IRE-α expression was significantly increased in the DCM group compared with the control group (P<0.05), and liraglutide is capable of decreasing IRE-α expression. X-box transcription factor-1 (XBP-1) was significantly spliced in the model group, and downregulated in the liraglutide-treated group. CHOP protein was upregulated in the DCM group, but inactivated by liraglutide treatment. In conclusion, liraglutide is capable of protecting DCM and blocking CHOP-mediated ER stress by inhibiting the IRE-α UPR pathway.

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