Ningbo, China
Ningbo, China

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Lu Y.,Fudan University | Sun Q.,Cixi Peoples Hospital | Zheng Y.,Fudan University | Liu X.,Fudan University | And 2 more authors.
Frontiers in Bioscience - Elite | Year: 2011

p50 is a member of the NF-kappaB family known to be involved in endometriosis. To gain insight into the roles of p50 in the development of endometriosis, we crosstransplanted endometrial fragments from p50 knockout mice to wild-type mice and vice versa, and also autotransplanted the fragments within the knockout and wild-type mice, inducing endometriosis. We then evaluated the size of the endometrial implants, and immunoreactivity to phosphorylated p65 (p-p65), PKCepsilon and TRPV1 in ectopic and eutopic endometrium as well as in vagina. We found that p50 deletion significantly reduces the size of endometrial implants. The immunoreactivity to p-p65 and PKCepsilon, but not TRPV1, was reduced in endometrial implants in p50 knockout mice. Deletion of p50 significantly reduced p-p65 and PKCepsilon, but not TRPV1, expression in eutopic endometrium and vagina. It also disrupts NF-kappaB activation and PKCepsilon expression in eutopic and vagina, suggesting the role of NF-kappaB in regulating PKCepsilon, which plays an important role in nociception. These data show that p50 is involved in the development of endometriosis and may be a promising therapeutic target.


PubMed | Cixi Peoples Hospital, Zhejiang Agriculture And forestry University and Zhejiang University
Type: | Journal: Virus research | Year: 2014

Inflammatory mediators (i.e. cytokines) play a pivotal role in the regulation of pathophysiological processes during EV71-induced hand, foot and mouth disease (HFMD). Different T cell subsets have distinct cytokine secretion profiles, and alteration in the T cell subsets frequency (imbalance) during infection leads to changed cytokine patterns. However, the effects of EV71 infection on T cell subsets were not clear. The objective of this study was to determine whether EV71-induced HFMD can be explained by the emergence of particular T-cell subsets (Th1, Th2, Tc1, Tc2, Th17, Tc17 and Treg cells) and the cytokine they produced (IFN-, IL-4, IL-17A and TGF-1), as well as distinct responses to EV71 infection. We found that when compared to the control group, the percentage of Th1 and Tc1 cells was significantly higher in mild and severe HFMD group. Similar results were found in the Th1/Th2 ratio and IFN- levels. On the other hand, the percentage of Th17 cells and IL-17A levels were the highest in severe HFMD cases, and lowest in controls. Similar trend was also found for the Th17/Treg cell ratio. An optimal cutoff value of 2.15% for Th17 cell and 6.72 pg/ml for IL-17A provided a discriminatory value for differentiating the severity of HFMD cases by receiver operating characteristic curve analyses. These findings reveal that the Th1/Th2 and Th17/Treg imbalance exist in HFMD patients, suggesting their involvement in the pathogenesis of EV71 infection, which may have potential value as biomarkers.


Chen X.-H.,Cixi Peoples Hospital | Wu W.-G.,Shanghai JiaoTong University | Ding J.,Hangzhou Normal University
Tumor Biology | Year: 2014

Recently, it has been reported that tazarotene-induced gene 1 (TIG1) methylation was frequently detected in a variety of human cancers. However, the relationship between the TIG1 methylation and the characteristics of hepatocellular carcinoma (HCC) remains unknown. The aim of present study was to observe the promoter methylation of TIG1 in HCC tissues and assess its prognostic significance for HCC. Real-time quantitative polymerase chain reaction and methylation-specific polymerase chain reaction were used, respectively, to examine the mRNA expression and methylation status of TIG1 in 91 pairs of HCC and adjacent noncancerous tissues. The mRNA expression level of TIG1 was significantly lower in HCC tissues than in adjacent noncancerous tissues. The rate of TIG1 promoter methylation was significantly higher in HCC tissues than in adjacent noncancerous tissues (P<0.001). A strong correlation between downregulation and promoter methylation was found in these tumors (P<0.001). More importantly, TIG1 methylation status was related to tumor size (P=0.015), histological differentiation (P=0.004), and tumor stage (P<0.001). Kaplan-Meier survival analysis showed that TIG1 promoter hypermethylation was associated with a worse outcome in patients with HCC. Further, Cox multivariate analysis indicated that TIG1 methylation status was an independent prognostic factor for the overall survival rate of HCC patients. In conclusion, our data suggested that epigenetic silencing of TIG1 gene expression by promoter hypermethylation may play an important role in HCC. © International Society of Oncology and BioMarkers (ISOBM) 2013.


Zhang R.,Zhejiang University | Hu Y.-Y.,Zhejiang University | Yang X.-F.,Zhejiang University | Gu D.-X.,Zhejiang University | And 5 more authors.
European Journal of Clinical Microbiology and Infectious Diseases | Year: 2014

One hundred and thirty-six blaOXA-51-negative strains were identified from 1,067 Acinetobacter calcoaceticus-A. baumannii complex (ACB complex) isolates, which were collected during October 2010 to March 2013 from 15 general hospitals in 10 cities throughout Zhejiang Province, China. Seven of the 136 blaOXA-51-negative ACB complex isolates were New Delhi metallo-β-lactamase-1 (NDM-1)-positive, among which three were identified as A. nosocomialis and four were identified as A. pittii strains using 16S-23S rRNA gene intergenic spacer (ITS) sequencing and partial RNA polymerase β-subunit (rpoB) sequencing. Pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) analysis showed that the seven NDM-positive isolates belonged to three clonal strains with three novel sequence types (STs). Polymerase chain reaction (PCR) assays and DNA sequence analysis of the carbapenemase and other β-lactamase genes indicated that all the isolates harbored the blaNDM-1 gene, and that only one strain of A. nosocomialis isolates harbored both blaNDM-1 and bla OXA-23. All of them were positive for blaADC, from which three novel blaADC genes (designated as blaADC-69, blaADC-70, and blaADC-71) were detected for the first time. The presence of ISAba125 upstream of blaNDM-1 was identified through genetic environment analysis. Carbapenem resistance can be transferred from A. nosocomialis and A. pittii to Escherichia coli EC600 by the conjugation experiment. Plasmid analysis, DNA hybridization, and extraction experiments indicated that bla NDM-1 was located on a plasmid of approximately 50 kb. In conclusion, we characterized the dissemination of NDM-1-positive A. pittii strains in Zhejiang Province, China, and reported the NDM-producing A. nosocomialis for the first time. © 2013 Springer-Verlag.


Li S.,Zhejiang University | Cai C.,Zhejiang University | Cai C.,Hangzhou Childrens Hospital | Feng J.,Cixi Peoples Hospital | And 5 more authors.
Virus Research | Year: 2014

Inflammatory mediators (i.e. cytokines) play a pivotal role in the regulation of pathophysiological processes during EV71-induced hand, foot and mouth disease (HFMD). Different T cell subsets have distinct cytokine secretion profiles, and alteration in the T cell subsets frequency (imbalance) during infection leads to changed cytokine patterns. However, the effects of EV71 infection on T cell subsets were not clear. The objective of this study was to determine whether EV71-induced HFMD can be explained by the emergence of particular T-cell subsets (Th1, Th2, Tc1, Tc2, Th17, Tc17 and Treg cells) and the cytokine they produced (IFN-γ, IL-4, IL-17A and TGF-β1), as well as distinct responses to EV71 infection. We found that when compared to the control group, the percentage of Th1 and Tc1 cells was significantly higher in mild and severe HFMD group. Similar results were found in the Th1/Th2 ratio and IFN-γ levels. On the other hand, the percentage of Th17 cells and IL-17A levels were the highest in severe HFMD cases, and lowest in controls. Similar trend was also found for the Th17/Treg cell ratio. An optimal cutoff value of 2.15% for Th17 cell and 6.72. pg/ml for IL-17A provided a discriminatory value for differentiating the severity of HFMD cases by receiver operating characteristic curve analyses. These findings reveal that the Th1/Th2 and Th17/Treg imbalance exist in HFMD patients, suggesting their involvement in the pathogenesis of EV71 infection, which may have potential value as biomarkers. © 2013 Elsevier B.V.


Lin Q.,Cixi Peoples Hospital | Shi J.,Cixi Peoples Hospital
Shanghai kou qiang yi xue = Shanghai journal of stomatology | Year: 2013

PURPOSE: With literatures review, this retrospective study was aimed to analyze the clinic characteristics and treatment of intraparotid facial nerve schwannoma (IFNS) treated in our department.METHODS: All cases treated in the Department of Oral and Maxillofacial Surgery and diagnosed as IFNS pathologically, from 2000-2007, were reviewed. The data of clinical symptoms, preoperative radio graphic imagings, preoperative diagnosis, tumor size and treatment method were collected and analyzed.RESULTS: Totally, 19 cases of IFNS were collected and reviewed. 3 of 19 (15.8%) were diagnosed as IFNS preoperatively, 2 cases were diagnosed by fine needle aspiration pathology, and 1 by physical examination. IFNS could occurred in any part of the facial nerve, 8 of 19 cases (43.1%) originated from the trunk of facial nerve in our cases. Nerve-sparing was applied in 12 cases, and the facial nerve was sectioned and anastomosed in 2 of these 12 cases; tumor resection with involved facial nerve were applied in 6 cases, and 5 of these 6 cases with facial nerve defect after tumor removal were repaired by auricular nerve transplantation, 1 case with nerve defect was not repaired; partial resection of the tumor was applied in 1 of the 19 cases. There was no tumor relapse in all 19 cases after 15-79 months of follow-up, while the function of the tumor-involved facial nerve were disturbed in all cases.CONCLUSIONS: Preoperative diagnosis of IFNS is difficult, and the diagnosis is based on preoperative fine needle aspiration or post operative pathology. Both nerve-sparing and nerve-resection approach can rarely keep the facial nerve function well after tumor removal.


Zhu H.,Zhejiang University | Yu D.,Zhejiang University | Zhou Y.,Zhejiang University | Wang C.,Wenzhou Medical College | And 3 more authors.
Journal of Biomedical Materials Research - Part B Applied Biomaterials | Year: 2013

This study reports the in vitro and in vivo biological activities of recombinant human bone morphogenetic protein 2 (rhBMP-2) released from the core-shell structure of a nanofibrous barrier membrane as a sustained delivery model for bone regeneration. RhBMP-2 incorporating poly(ethylene glycol) was used as the core, and poly(caprolactone) was used as the shell surrounding the core. To determine its release profiles, the release solution was collected and the amount of rhBMP-2 was measured by ELlSA at different time points. In vitro rhBMP-2, released from the delivery system over at least 24 days, reached a stable rate of 500 pg per day and guided bone marrow mesenchymal stem cells (BMMSCs) to express osteogenic genes. The distribution and proliferation of BMMSCs in the nanofibrous barrier membrane was measured by laser confocal scanning microscopy (LCSM) and scanning electron microscopy (SEM). The biological activity of rhBMP-2 was tested in BMMSC/membrane culture in vitro and in a rabbit calvarium defect model in vivo. Osteogenic genes osteonectin (ON) and core binding factor-α1 (Cbf-α1) expression of the BMMSCs cultured on the BMP-2-PEG/PCL membrane were significantly higher than those of cells on the PEG/PCL membrane at the late time points using realtime PCR (p > 0.05). The membranes containing the rhBMP-2 group exhibited the fastest and most bone formation compared to others in rabbit cranial defect models (p > 0.05). This study revealed that rhBMP-2 could be incorporated into a core-shell electrospun membrane, and preserve sustained release capability and biological activity. © 2012 Wiley Periodicals, Inc.


Zhao G.,Zhejiang University | Hu Y.,Cixi Peoples Hospital | Chen P.,Zhejiang University | Shen Z.,Zhejiang University
Pakistan Journal of Zoology | Year: 2015

Chronic consumption of ethanol can alter brain morphology and function. The present study examined the effect of ethanol abuse on the number of neurons and astrocytes in the rat cerebral cortex. After 45 days of ethanol treatment (2 g/kg by intraperitoneal injection), tissue samples from the rat motor cortex were Nissl-stained and probed for glial fibrillary acidic protein (GFAP) expression. The number of neurons and GFAP-immunoreactive astrocytes in each cortical layer were counted per unit area. The results showed that ethanol-treated rats had fewer neurons (P < 0.01) but a greater number of GFAP-positive astrocytes in all cortical layers as compared to controltreated animals (P < 0.01). Neuronal loss was the most pronounced in layers III and V, the major output layers of the cortex, corresponding to increased astrocyte density in these layers. These results provide evidence that chronic ethanol exposure induces neuronal death but stimulates astrocyte hyperplasia in the cerebral cortex, especially in the output layers. Loss of neurons may lead to damage to neural circuitry, while astrocyte proliferation likely serves a protective function to compensate for the resultant dysfunction of the nervous system. Copyright © 2015 Zoological Society of Pakistan.


PubMed | Cixi Peoples Hospital
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2014

Recently, it has been reported that tazarotene-induced gene 1 (TIG1) methylation was frequently detected in a variety of human cancers. However, the relationship between the TIG1 methylation and the characteristics of hepatocellular carcinoma (HCC) remains unknown. The aim of present study was to observe the promoter methylation of TIG1 in HCC tissues and assess its prognostic significance for HCC. Real-time quantitative polymerase chain reaction and methylation-specific polymerase chain reaction were used, respectively, to examine the mRNA expression and methylation status of TIG1 in 91 pairs of HCC and adjacent noncancerous tissues. The mRNA expression level of TIG1 was significantly lower in HCC tissues than in adjacent noncancerous tissues. The rate of TIG1 promoter methylation was significantly higher in HCC tissues than in adjacent noncancerous tissues (P < 0.001). A strong correlation between downregulation and promoter methylation was found in these tumors (P < 0.001). More importantly, TIG1 methylation status was related to tumor size (P = 0.015), histological differentiation (P = 0.004), and tumor stage (P < 0.001). Kaplan-Meier survival analysis showed that TIG1 promoter hypermethylation was associated with a worse outcome in patients with HCC. Further, Cox multivariate analysis indicated that TIG1 methylation status was an independent prognostic factor for the overall survival rate of HCC patients. In conclusion, our data suggested that epigenetic silencing of TIG1 gene expression by promoter hypermethylation may play an important role in HCC.


PubMed | Cixi Peoples Hospital, Li Huili Hospital, Wenzhou University and Chinese PLA General Hospital
Type: Journal Article | Journal: Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics | Year: 2016

The blood-spinal cord barrier (BSCB) plays important roles in the recovery of spinal cord injury (SCI), and caveolin-1 is essential for the integrity and permeability of barriers. Basic fibroblast growth factor (bFGF) is an important neuroprotective protein and contributes to the survival of neuronal cells. This study was designed to investigate whether bFGF is beneficial for the maintenance of junction proteins and the integrity of the BSCB to identify the relations with caveolin-1 regulation. We examined the integrity of the BSCB with Evans blue dye and fluorescein isothiocyanate-dextran extravasation, measured the junction proteins and matrix metalloproteinases, and evaluated the locomotor function recovery. Our data indicated that bFGF treatment improved the recovery of BSCB and functional locomotion in contusive SCI model rats, reduced the expression and activation of matrix metalloproteinase-9, and increased the expressions of caveolin-1 and junction proteins, including occludin, claudin-5, p120-catenin, and -catenin. In the brain, in microvascular endothelial cells, bFGF treatment increased the levels of junction proteins, caveolin-1 small interfering RNA abolished the protective effect of bFGF under oxygen-glucose deprivation conditions, and the expression of fibroblast growth factor receptor 1 and co-localization with caveolin-1 decreased significantly, which could not be reversed by bFGF treatment. These findings provide a novel mechanism underlying the beneficial effects of bFGF on the BSCB and recovery of SCI, especially the regulation of caveolin-1.

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