Affiliated Hospital of xiAn Medical College

Xi’an, China

Affiliated Hospital of xiAn Medical College

Xi’an, China
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Sun F.,Xi'an Jiaotong University | Sun F.,Affiliated Hospital of Xian Medical College | Qu J.-N.,Xi'an Jiaotong University | Qu J.-N.,Hong Hui Hospital | Zhang Y.-G.,Xi'an Jiaotong University
Pain Physician | Year: 2013

The establishment of a reliable animal model of lumbar disc degeneration (AMDD) is important for studying pathogenesis and evaluating treatment effectiveness. However, an ideal AMDD for use in laboratory studies has not yet been produced. This retrospective study reviews and compares several common AMDD and discusses their strengths and weaknesses. We also suggest a new method for establishing future AMDD. The identified genes associated with disc degeneration are susceptibility genes, which elevate risk but do not necessarily lead to disease occurrence. We propose to identify families with hereditary disc degeneration, find major casual genes with exome sequencing, and establish transgenic animal models. This approach may help us to build an improved AMDD.


Lin Y.,306 Hospital of PLA | Xu J.,XiAn No1 Hospital | Liao H.,Affiliated Hospital of xiAn Medical College | Li L.,306 Hospital of PLA | Pan L.,PLA Fourth Military Medical University
Tumor Biology | Year: 2014

The aim of this study was to evaluate the cytotoxic and apoptotic effects of piperine on human lung cancer A549 cells and to explore its mechanisms. Piperine was found to exert the greatest cytotoxic effect against A549 cells in a dose-dependent manner, whereas it showed no effect on WI38 human lung fibroblasts. This cell growth-inhibitory effect might be attributed to cell DNA damage and cytotoxic effects. Besides, piperine had the ability to cause cell cycle arrest in G2/M phase and to activate caspase-3 and caspase-9 cascades in A549 cells. Furthermore, piperine-induced apoptosis could be blocked by the broad caspase inhibitor z-VAD-fmk in majority. In addition, piperine treatment decreased Bcl-2 protein expression, but increased Bax protein expression in A549 cells, which were positively correlated with an elevated expression of p53 compared to control. Taken together, these results suggested that piperine could induce p53-mediated cell cycle arrest and apoptosis via activation of caspase-3 and caspase-9 cascades, as well as increasing the Bax/Bcl-2 ratio. Thus, piperine could be developed as an effective antitumor agent in the prevention and treatment of lung cancer without toxicity to the host. © 2013 International Society of Oncology and BioMarkers (ISOBM).


Wang L.,Shanxi Medical University | Wang L.,Affiliated Hospital of xiAn Medical College | Liu X.-Y.,PLA Fourth Military Medical University | Li Z.-W.,Affiliated Hospital of xiAn Medical College | Zhang S.-Y.,PLA Fourth Military Medical University
Acta Crystallographica Section E: Structure Reports Online | Year: 2013

In the title compound, C13H13NO3, the isoxazole ring is approximately coplanar with the phenyl ring, the dihedral angle between their planes being 7.37 (19)°. In the crystal, centrosymmetrically related molecules are linked into dimers by pairs of C - H⋯O hydrogen bonds, generating a ring of graph-set motif R 2 2(10).


Wang R.S.,XiAn Fourth Hospital | Lv P.L.,XiAn First Hospital | Wang W.J.,XiAn Fourth Hospital | Wang X.D.,Affiliated Hospital of xiAn Medical College | And 4 more authors.
Visual Neuroscience | Year: 2011

Numerous methods and drugs have been used to treat anterior ischemic optic neuropathy (AION); however, further investigations to determine the value of treatments for AION have been impeded by the lack of appropriate animal models of AION, significantly impacting on in-depth study of the disease. A rat model of AION was established, and corresponding functional changes of the fundus were observed using fundus fluorescein angiography (FFA), optical coherence tomography (OCT), and flash visual-evoked potential (F-VEP) in order to confirm the reliability of the AION model histopathologically. One day after model establishment, histopathology demonstrated that portions of the optic disc were highly edematous, with edema of nerve fibers and loose tissue, accompanied by displacement of the surrounding retina. At 23 days, the optic disc and surrounding nerve fiber layers had become thinner. None of the above-mentioned changes was observed in the laser, hematoporphyrin derivative (HPD), or naive groups. The results of fundus, FFA, F-VEP, and OCT'within 90 days after model establishment'confirmed that krypton red laser irradiation (647 nm), applied 2 h after HPD injection, can establish an ideal animal model of AION. © 2011 Cambridge University Press.


Mao J.,Xi'an Jiaotong University | Mao J.,Affiliated Hospital of Xian Medical College | Liu J.,Xi'an Jiaotong University | Pang X.,Xi'an Jiaotong University | And 5 more authors.
Molecules and Cells | Year: 2012

Atherosclerosis is an inflammatory disease in the vessel wall. Nicotine, a major component of cigarette smoke, is an independent risk factor for cardiovascular diseases including atherosclerosis. As an inflammatory molecule, C- reactive protein (CRP) participates in atherogenesis. Although it has been confirmed that CRP level in smoking patient is significantly higher than non-smokers and cigarette withdrawal,it is unknown whether nicotine induces CRP expression in macrophages. The present study was to observe effect of nicotine on CRP production and the related signal pathway in U937 macrophages. The results showed that nicotine significantly increased mRNA and protein expression of CRP in U937 macrophages in timeand concentration-dependent ways. Nicotinic acetylcholine receptor (nAChR) blocker hexamethonium, MEK1/2 inhibitor PD98059, p38 MAPK inhibitor SB203580 and NF- ?B inhibitor PDTC almost completely abolished nicotineinduced CRP expression in mRNA and protein levels in U937 macrophages. The further study indicated that hexamethonium, PD98059, and SB203580 significantly inhibited ERK1/2 and p38 MAPK phosphorylation. These demonstrate that nicotine has ability to induce CRP expression in macrophages through nAChR-ERK1/2/p38 MAPK-NF-kB signal pathway, which contributes to better understanding of the pro-inflammatory and pro-atherosclerotic effects of nicotine in cigarette smokers. © The Korean Society for Molecular and Cellular Biology.


Ma J.-L.,Xi'an Jiaotong University | Jin L.,Xi'an Jiaotong University | Li Y.-D.,Affiliated Hospital of xiAn Medical College | He C.-C.,Xi'an Jiaotong University | And 4 more authors.
Journal of Immunology Research | Year: 2014

Radiation therapy is one of the standard therapeutic modalities for esophageal cancer, achieving its main antitumor efficacy through DNA damage. However, accumulating evidence shows that radiotherapy can substantially alter the tumor microenvironment, particularly with respect to its effects on immune cells. We hypothesized that the immune response elicited by radiotherapy may be as important as the radiation itself for successful treatment. More specifically, immunomodulatory cytokines may enhance the effectiveness of radiotherapy. To investigate this hypothesis, we measured changes in the serum interferon-gamma (IFN-γ) and interleukin-2 (IL-2) concentrations during radiotherapy and compared these modifications with outcomes. We found that serum concentrations of IL-2 and IFN-γ were positively associated with local response to radiotherapy in esophageal cancer. More generally, the intensity of the radiotherapy-elicited immune response was positively associated with local response to radiotherapy in esophageal cancer. Changes in serum IL-2 and IFN-γ concentrations were further associated with increased risks of acute hematologic toxicity and acute organ toxicity of the esophagus, lung, and skin. These results suggest that deciphering the mechanisms of radiotherapy-elicited immune response may help in the development of therapeutic interventions that would enhance the efficacy of radiotherapy and convert some ineffective responses to effective responses. © 2014 Jin-lu Ma et al.


Lu T.,Shaoxing University | Yang C.,Affiliated Hospital of Xian Medical College | Sun H.,Shaoxing University | Lv J.,Shaoxing University | And 3 more authors.
Genetics and Molecular Research | Year: 2014

Our research demonstrated the potential for mouse bone marrow mesenchymal stem cells (mBMMSCs) to differentiate into hepatocytes in vitro and in vivo. However, the exact mechanism of this process remains unknown. In this study, we investigated the role of the mitogen-activated protein kinase (MAPK) cell-signaling pathway in the differentiation of mBMMSCs into hepatocytes. mBMMSCs were isolated from femurs and tibias, and hepatic differentiation was induced in Isove's modified Eagle's medium supplemented with 10% fetal bovine serum, containing human growth factor and fibroblast growth factor 4. After seven days of induction, morphological characteristics were examined. For inhibition of signaling molecular activities, the inhibitors p38 (SB203580), ERK1/2 (U0126), and MSK1 (H89) were added to the differentiation medium. Real-time polymerase chain reaction and Western blot analysis were used to evaluate the gene expression profiles and protein expression of several markers, including the early specific markers of hepatocytes (AFP and FOXa2), phosphorylated-p38 (p-p38), phosphorylated-ERK1/2 (p-ERK1/2), and phosphorylated-MSK1 (p-MSK1). Expressions of p-p38, p-ERK1/2, and p-MSK1 were effectively inhibited by their respective inhibitors. Expressions of early specific markers, AFP and FOXa2, in the p38, ERK1/2, and MSK1 inhibitor-treated groups were significantly decreased compared to those of the cytokine-induced control. Notably, the expressions of AFP and FOXa2 in the p38 inhibitor group were more obviously reduced than those in the ERK1/2 inhibitor group. The MAPK signaling pathway, especially p38, is sufficient to drive differentiation of mBMMSCs into hepatocytes. This could increase the efficiency of hepatocyte differentiation, which would benefit clinical applications. © FUNPEC-RP.


Chen Y.-L.,Affiliated Hospital Of Xian Medical College | Wang J.-L.,Childrens Hospital Of Xian | Li W.-Q.,Affiliated Hospital Of Xian Medical College
European Journal of Pediatrics | Year: 2014

Kawasaki disease (KD) is associated with the development of coronary arterial lesions (CALs) in children. We aimed to test the hypothesis that circulating 25-hydroxyvitamin D3 [25-(OH)D3] could be identified as a clinical parameter for predicting CALs secondary to KD in children. We enrolled 35 children with KD in the acute phase and measured serum 25-(OH)D3 levels in all of them, then followed up by echocardiography for CALs. Additionally, serum 25-(OH)D3 levels were obtained in 23 febrile children with respiratory tract infections and 30 healthy children. Of the 35 KD children, nine had CALs according to echocardiography and 26 did not (NCALs). Serum 25-(OH)D3 levels were not significantly different between NCALs and healthy children (49.2 ± 23.8 versus 44.1 ± 30.2 ng/ml; P = 0.49). Serum 25-(OH)D3 levels were significantly higher in children with CALs than those without CALs (83.9 ± 26.3 versus 49.2 ± 23.8 ng/ml; P = 0.001). The cutoff value of 65 ng/ml to predict subsequent CALs had a specificity of 0.73, sensitivity of 0.78, and diagnostic accuracy of 0.74. Conclusion: Serum 25-(OH)D3 levels were elevated dur-ing the acute phase in KD children who had subsequent CALs. Serum 25-(OH)D3 levels in the acute phase of KD may be used to predict subsequent CALs. © 2014, The Author(s).


Chen Y.,Affiliated Hospital of Xian Medical College | Li W.,Affiliated Hospital of Xian Medical College
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2014

OBJECTIVE: To explore the changes of serum 25-hydroxyvitamin D3 [25-(OH)D3] and interleukin-6 (IL-6) in children with Kawasaki disease (KD) after treatment with intravenous immunoglobulins (IVIG) and analyze their clinical implications.METHODS: Thirty-five children with KD (26 boys and 9 girls) were examined for serum 25-(OH)D3 and IL-6 levels before and after IVIG treatment using enzyme linked immunosorbent assay (ELISA), with 25 febrile children with respiratory tract infections and 25 healthy children as controls.RESULTS: Serum 25-(OH)D3 levels were significantly higher in healthy children than in febrile children (P=0.025), and was even higher in children with KD before IVIG treatment (P=0.023). Serum IL-6 levels were similar between healthy and febrile children (P=0.4), but significantly elevated in KD children (P=0.000). Serum 25-(OH)D3 level was positive correlated with serum IL-6 level in KD children before treatment (r=0.9, P=0.000). In KD children after IVIG treatment, serum 25-(OH)D3 level was significantly increased (P=0.012) and serum IL-6 levels slightly decreased (P=0.325) without showing any correlations (r=0.18, P=0.4).CONCLUSION: Serum 25-(OH)D3 level is positively correlated with serum IL-6 level in KD children before IVIG treatment but not after the treatment,. 25(OH)D3 may participate in the pathogenesis of KD and potentially serves as the therapeutic target for KD.


PubMed | Affiliated Hospital of Xian Medical College
Type: Journal Article | Journal: Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2014

To explore the changes of serum 25-hydroxyvitamin D3 [25-(OH)D3] and interleukin-6 (IL-6) in children with Kawasaki disease (KD) after treatment with intravenous immunoglobulins (IVIG) and analyze their clinical implications.Thirty-five children with KD (26 boys and 9 girls) were examined for serum 25-(OH)D3 and IL-6 levels before and after IVIG treatment using enzyme linked immunosorbent assay (ELISA), with 25 febrile children with respiratory tract infections and 25 healthy children as controls.Serum 25-(OH)D3 levels were significantly higher in healthy children than in febrile children (P=0.025), and was even higher in children with KD before IVIG treatment (P=0.023). Serum IL-6 levels were similar between healthy and febrile children (P=0.4), but significantly elevated in KD children (P=0.000). Serum 25-(OH)D3 level was positive correlated with serum IL-6 level in KD children before treatment (r=0.9, P=0.000). In KD children after IVIG treatment, serum 25-(OH)D3 level was significantly increased (P=0.012) and serum IL-6 levels slightly decreased (P=0.325) without showing any correlations (r=0.18, P=0.4).Serum 25-(OH)D3 level is positively correlated with serum IL-6 level in KD children before IVIG treatment but not after the treatment,. 25(OH)D3 may participate in the pathogenesis of KD and potentially serves as the therapeutic target for KD.

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