The First hospital of Shijiazhuang City

Shijiazhuang, China

The First hospital of Shijiazhuang City

Shijiazhuang, China
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Chen Z.,Peking University | Li Y.,The First Hospital of Shijiazhuang City | Deng X.,Peking University | Wang X.,Peking University
Journal of Prosthodontics | Year: 2014

Purpose: Fiber-reinforced composite dowels have been widely used for their superior biomechanical properties; however, their preformed shape cannot fit irregularly shaped root canals. This study aimed to describe a novel computer-aided method to create a custom-made one-piece dowel-and-core based on the digitization of impressions and clinical standard crown preparations. Materials and Methods: A standard maxillary die stone model containing three prepared teeth each (maxillary lateral incisor, canine, premolar) requiring dowel restorations was made. It was then mounted on an average value articulator with the mandibular stone model to simulate natural occlusion. Impressions for each tooth were obtained using vinylpolysiloxane with a sectional dual-arch tray and digitized with an optical scanner. The dowel-and-core virtual model was created by slicing 3D dowel data from impression digitization with core data selected from a standard crown preparation database of 107 records collected from clinics and digitized. The position of the chosen digital core was manually regulated to coordinate with the adjacent teeth to fulfill the crown restorative requirements. Based on virtual models, one-piece custom dowel-and-cores for three experimental teeth were milled from a glass fiber block with computer-aided manufacturing techniques. Furthermore, two patients were treated to evaluate the practicality of this new method. Results: The one-piece glass fiber dowel-and-core made for experimental teeth fulfilled the clinical requirements for dowel restorations. Moreover, two patients were treated to validate the technique. Conclusion: This novel computer-aided method to create a custom one-piece glass fiber dowel-and-core proved to be practical and efficient. © 2013 by the American College of Prosthodontists.

Du Y.,Hebei Medical University | Du Y.,The First Hospital of Shijiazhuang City | Zhang X.,Hebei Medical University | Zhang X.,Hebei Institute of Cardio Cerebral Vascular Diseases | And 6 more authors.
Neuroscience Letters | Year: 2012

Inflammation and oxidative stress play an important role in cerebral ischemic pathogenesis. It has been well established that atorvastatin and probucol could elicit a variety of biological effects through its anti-inflammatory and anti-oxidant properties respectively. This study was to examine whether probucol and atorvastatin in combination had the enhanced protective effect against cerebral ischemia. Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO). Experiment 1 was used to evaluate the time course expression of Peroxiredoxin2 (Prx2) and Foxo3a after cerebral ischemia. Experiment 2 was used to detect neuroprotective effect of atorvastatin and probucol in cerebral ischemia. At 24. h or 72. h, neurologic deficit, brain water content and infarct size were measured. Immunohistochemistry, RT-PCR, Western blot and confocal microscope were used to analyze the expressions of Prx2, Foxo3a and nuclear factor erythroid 2-related factor 2 (Nrf2). Compared with the normal-control group, the expressions of Prx2 and Foxo3a were down-regulated in ischemic brain. Compared with the use of probucol or atorvastatin alone, the combined treatment dramatically reduced the brain water content and the infarct volume (P< 0.05). Meanwhile, the decrease of Prx2, Foxo3a and Nrf2 was significantly alleviated in combined treatment group. Probucol combined with atorvastatin can get the augmented neuroprotection from the damage caused by MCAO, this effect may be through up-regulation of Prx2, Foxo3a and Nrf2. © 2012 Elsevier Ireland Ltd.

Zhang Y.,The First Hospital of Shijiazhuang City | Du W.,Henan Province Hospital of TCM | Chen Z.,Binzhou City Center Hospital | Xiang C.,The First Hospital of Shijiazhuang City
Experimental Cell Research | Year: 2017

Tumor-associated macrophages (TAMs) polarization represents a key regulatory process of tumor progression. However, the underlying mechanisms are unclear. This study aimed to investigate the relationship between secreted phosphoprotein 1 (SPP1) and TAMs in lung adenocarcinoma cells. THP-1 monocytes were differentiated into macrophages using PMA. PMA-treated THP-1 cells were co-cultured with human A549 cells culture supernatant. SPP1 expression in TAMs isolated from lung adenocarcinoma tissues and PMA-treated THP-1 cells were measured. Macrophage polarization was identified by flow cytometric analysis. Cell migration and apoptosis were assessed by Transwell migration assays and flow cytometric analysis, respectively. SPP1 is highly expressed in tumor tissues and TAMs isolated from patients with an advanced TNM stage, and also in PMA-treated THP-1 cells. Co-culture with A549 cells strongly induced SPP-1 expression as well as M2 polarization of THP-1 cells, but it had little effect on short hairpin SPP1 (shSPP1)-transfected THP-1 cells. Interestingly, programmed death ligand 1 (PD-L1), a critical regulator of M2 polarization, was downregulated in SPP1 knockdown THP-1 cells. Inhibition of PD-L1 induced a greater decline of the M2 markers IL-10 and Arg-1 but an increase in the M1 markers IL-12 and TNF-α. In addition, SPP1 knockdown in THP-1 cells can mitigate migration but promote apoptosis of A549 cells, and PD-L1 inhibition can further enhance this effect. THP-1 cells co-cultured with A549 cells attenuated CD4+ T-cell activation, whereas SPP1 inhibition restored T-cell activation. These results highlight the importance of SPP1 in mediating macrophage polarization and lung cancer evasion, suggesting a potential therapeutic target for lung cancer. © 2017 Elsevier Inc.

Xu J.,Capital Medical University | Yao Q.,Capital Medical University | Hou Y.,Capital Medical University | Liu S.,Tongji University | And 3 more authors.
Biomedicine and Pharmacotherapy | Year: 2013

Osteosarcoma is one of the most common tumors. The mechanisms of formation and development of osteosarcoma have been studied for a long time. Recently, more and more evidence showed that miRNAs play important roles in regulating tumor growth. In this study we found that miRNA-223 was downregulated in both osteosarcoma patients' tumor tissues and osteosarcoma cell lines. Overexpression of miRNA-233 greatly inhibited the proliferation of Saos-2 cells. Cell cycle analysis by flow cytometry showed the arrest of cell cycle progression at the G1 phase. Further mechanistic study indicated that Ect2 was directly targeted by miR-223. Downregulation of Ect2 by miR-223 induces the expression of p21, p27 and the phospharylation of retinoblastoma, which are involved in the G1 block. We concluded that miR-223 functions as a tumor suppresser in osteosarcoma and miR-223/Ect2/p21 signaling is an important pathway that regulates the osteosarcoma cell cycle progression and proliferaion. © 2013 Elsevier Masson SAS.

Fan C.,XuZhou Childrens Hospital | Liu S.,Tongji University | Zhao Y.,Tongji University | Han Y.,Shandong University | And 4 more authors.
Biomedicine and Pharmacotherapy | Year: 2013

FOXO1 is downregulated in a number of cancers. However, the underlying mechanisms are poorly understood. In this study, we report that the expression of miR-370 was upregulated in gastric cancer cell lines and gastric cancer tissues. Overexpression of miR-370 in gastric cancer cells promoted the cell proliferation and anchorage-independent growth, while silencing of miR-370 showed opposite effects. miR-370-induced proliferation was correlated with the downregulation of cyclin-dependent kinase inhibitors, p27Kip1 and p21Cip1, and the upregulation of the cell cycle regulator cyclin D1. Furthermore, we identified that FOXO1 is the functional target of miR-370. Restored expression of FOXO1 together with miR-370 strongly abrogated miR-370-induced cell proliferation. Taken together, our results revealed a novel mechanism of FOXO1 suppression mediated by miR-370 in gastric cancer. © 2013 Elsevier Masson SAS.

Liu Y.,The First Hospital of Shijiazhuang City | Liu K.,Hebei Medical University
Experimental and Therapeutic Medicine | Year: 2014

The aim of the present study was to investigate the effects of spironolactone and losartan on the early healing stage of acute myocardial infarction (AMI) in rats. An AMI rat model was established and the rats were randomly divided into four groups: AMI (n=12), AMI + spironolactone (AMI + S; n=12), AMI + losartan (AMI + L; n=12) and AMI + spironolactone combined with losartan (AMI + S + L; n=12). Sham-operated rats served as a control group (n=12). The expression levels of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) in the non-infarcted myocardium surrounding the AMI area were determined using immunohistochemistry. In addition, the capillary density in the non-infarcted myocardium surrounding the AMI area was detected. The capillary densities around the infarcted area in the AMI and treatment groups at day 7 and 14 following AMI surgery were significantly higher compared with the sham-operated rats. Compared with the AMI group, the capillary densities around the infarcted area and the ratio of MMPs/TIMP-1 were increased in the treatment groups following AMI surgery; however, the increased ratio of MMPs/TIMP-1 was reduced at day 14 following AMI surgery. Therefore, these results indicated that spironolactone and losartan may promote the formation of collateral circulation in the non-infarcted tissue surrounding the infarcted area by regulating the production of MMPs.

PubMed | The Infectious Disease Hospital of Handan City, The First Hospital of Shijiazhuang City and Hebei Medical University
Type: | Journal: Scientific reports | Year: 2017

Noninvasive serum markers for assessment of liver fibrosis in chronic hepatitis B (CHB) patients have not been well-studied. The present study was to evaluate the predictive value of serum interferon gamma-inducible protein-10 (IP-10/CXCL10) and the interferon (IFN)-/interleukin (IL)-4 ratio for liver fibrosis progression in CHB patients. A total of 180 CHB patients were categorized into four groups: no fibrosis, mild fibrosis, moderate fibrosis, and severe fibrosis. Serum and intrahepatic levels of IP-10, IFN-, and IL-4 were examined, from which the IFN-/IL-4 ratio was calculated. We found that the serum IP-10 levels were positively correlated with the severity of liver fibrosis, whereas the IFN-/IL-4 ratio was negatively associated with the progression of hepatic fibrosis. Multivariate logistic regression analysis revealed that the serum IP-10 was an independent predictor for significant fibrosis. For predicting significant fibrosis, the IP-10 cut-off value of 300ng/mL had a sensitivity of 92.7% and a specificity of 68.6%. When the IP-10 level was combined with the IFN-/IL-4 ratio, the specificity and positive predictive value were 93.8% and 94.6%, respectively; thus, the discriminatory ability was much improved. In conclusion, the serum IP-10 level and the IFN-/IL-4 ratio have great potential to predict significant fibrosis among CHB patients.

Jin H.,Capital Medical University | Li C.,The First Hospital of Shijiazhuang City | Ge H.,Capital Medical University | Jiang Y.,Capital Medical University | Li Y.,Capital Medical University
Journal of Translational Medicine | Year: 2013

Objective: To investigate warning effect of serum miRNA for intracranial aneurysm rupture through microarray hybridization.Methods: 24 were selected from 560 patients in our department and divided into group A, B, C and D. They are aneurysms with daughter aneurysms group, aneurysm without daughter aneurysms group, ruptured aneurysms group and angiography negative group. Then a microarray study was carried out using serum miRNA. Differentially expressed miRNAs were identified. Cluster analysis was performed in order to make the results looks more intuitive and potential gene targets were retrieved from miRNA target prediction databases.Results: Microarray study identified 86 miRNAs with significantly different (p < 0.05) expression levels between three experimental groups and control group. Among them 69 are up-regulated and 17 are down-regulated. All miRNAs in group A are up-regulated, while there are up and down-regulated in group B and C. A total of 8291 predicted target genes are related to these miRNAs. Bioinformatic analysis revealed that several target genes are involved in apoptosis and activation of cells associated with function of vascular wall.Conclusion: Our gene level approach reveals several different serum miRNAs between normal people and aneurysm patients, as well as among different phases of aneurysm, suggesting that miRNA may participate in the regulation of the occurrence and development of intracranial aneurysm, and also have warning effect for intracranial aneurysm rupture. All differently expressed miRNA in group A are up-regulated, which may suggesting protective function of miRNA for intracranial vascular wall. © 2013 Jin et al.; licensee BioMed Central Ltd.

Yang T.,The First Hospital of Shijiazhuang City | Zhang X.-B.,The First Hospital of Shijiazhuang City | Zheng Z.-M.,The First Hospital of Shijiazhuang City
Cancer Science | Year: 2013

The mitotic kinesin superfamily protein KIF14 is essential for cytokinesis and chromosome segregation and increased KIF14 expression is related to a variety of human cancers. In this study, we investigate KIF14 expression in association with clinical variables and the role of KIF14 during tumorigenesis. We found that KIF14 is overexpressed in most primary hepatocellular carcinoma (HCC) tissues compared with the adjacent normal liver tissues and KIF14 overexpression is associated with tumor grade (P = 0.002), stage (P = 0.013) and poor survival (P < 0.001). Downregulation of KIF14 decreased the capacity of proliferation both in vitro and in vivo. Furthermore, suppression of KIF14 not only decreases cancer cell migration but also induces apoptosis of cells with inactivation of the phosphatidylinositol 3-kinase-Akt signaling pathway. Therefore, our current study indicates that KIF14 promotes HCC carcinogenesis and may serve as a potential therapeutic target for human HCC. © 2013 Japanese Cancer Association.

Yang Y.,The First Hospital of Shijiazhuang City | Yang C.,The First Hospital of Shijiazhuang City | Zhang J.,The First Hospital of Shijiazhuang City
Medical oncology (Northwood, London, England) | Year: 2015

In our previous study, the epithelial-to-mesenchymal transition (EMT) has been identified to be involved in gastric cancer progression. Notably, nuclear protein C23 and bone morphogenetic protein-2 (BMP2) have been linked into EMT. However, the specific mechanisms underlying BMP2 pathway-mediated EMT are not still unraveled. In this study, we adopted immunohistochemistry and immunoblotting to determine the expression of C23 and BMP2 receptor II (BMPR-II) in 90 gastric cancer samples and cell lines. Subsequently, relevant cell lines were selected to be treated with si-C23 or si-BMPRII and the detection of in vitro assay. Our results revealed that both C23 and BMPRII were aberrantly and constitutively expressed in gastric cancer specimens and cell lines, whose expression was positively associated with metastasis, stage and differentiation, and portended poor survival outcome of gastric cancer patients. In vitro assay validated the increased expression of p-Erk1/2, p-Akt, vimentin, N-cadherin, and MMP2 in BMP2-stimulated MGC803 cells, which was in a dose-dependent manner. By contrast, si-C23 treatment attenuated the BMP2-stimulated expression of p-Erk1/2, p-Akt, vimentin, N-cadherin, and MMP2. Also, the treatment of either si-C23 or si-BMPRII decreased the ability of migration and invasion of MGC803 cells. In conclusion, C23 mediates BMP2-induced EMT progression via the up-regulation of Erk1/2 and Akt signaling pathway in gastric cancer, which indicated both C23 and BMPRII pathway could be recommended as prospective targets or biomarkers to antagonize the progression of gastric cancer.

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