Xiamen, China
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Ren G.,First Peoples Hospital of Huzhou | Ren G.,Huzhou Teachers College | Zhao D.-A.,174th Hospital of PLA | Xu J.,First Peoples Hospital of Huzhou | Li B.-A.,Xiamen University
Tumori | Year: 2015

Aims and Background: Chibby (CBY), a β-catenin binding partner, inhibits Wnt/β-catenin-mediated transcriptional activation by competing with Tcf/Lef factors for β-catenin binding and promoting the export of β-catenin from nucleus to cytoplasm. The regulatory effect of CBY in this signaling pathway suggests its biological importance as a potential tumor suppressor gene. The purposes of this study were to determine whether the expression of CBY was downregulated in human laryngeal squamous cell carcinoma (LSCC) samples, the CpG sites of CBY at the promoter region were methylated in these tumor samples, and reduced expression of CBY was induced by methylation of CBY promoters. Methods: CBY expression was investigated by quantitative real-time PCR and immunohistochemistry in samples from 36 LSCC patients. The methylation status of the CBY promoter was detected by methylation-specific PCR. Results: Compared with normal laryngeal mucosa, the expression of CBY was downregulated in LSCC samples. The reduced CBY expression rate was 58.33% (21/36) at the mRNA and 66.67% (24/36) at the protein level. The promoters of CBY were methylated in 12/36 tumor samples, partially methylated in 5, and unmethylated in 19 samples. The methylation rate including incomplete methylation was 47.22% (17/36) in tumor samples, while no methylation was detected in normal laryngeal squamous epithelium. Compared with the unmethylated group, the expression of CBY was significantly different in the methylated group (p≤0.05) but similar in the partially methylated group (p>0.05). Conclusions: Our data indicate that CBY expression was downregulated in LSCC, which may be partially caused by methylation of CBY promoters. © 2015 INTM, Italy.


Li P.,174th Hospital of PLA | Li P.,Xiamen University | Zhong Y.,Xiamen University | Jiang X.,174th Hospital of PLA | And 3 more authors.
Biological Trace Element Research | Year: 2012

The aim of the current study was to assess relationships between multiple metals burden in human seminal plasma and semen quality parameters. Levels of five metals (lead, manganese, copper, arsenic, and selenium) in human seminal plasma were determined by inductively coupled plasma mass spectrometry (ICP-MS), and the correlations between the metal concentrations and semen parameters (sperm concentration, sperm motility rate, and sperm morphology) were analyzed. The activities of acid phosphatase (ACP) and of α-glucosidase in human seminal plasma were also determined. Of the 100 subjects, 21 had fertility problems according to the World Health Organization criteria and were designated as "abnormal group." Significant inverse correlations were found between the concentrations of Cu, As, Pb, and the sperm concentrations (r Cu∈=∈-0.312, P Cu∈=∈0.029; r As∈=∈-0.328, P As∈=∈0.021; r Pb∈=∈-0.377, P Pb∈=∈0.008). Moreover, the Cu, Mn, and Se concentrations were significantly higher in the abnormal group than that in the normal group (P Cu∈=∈0.024, P Mn∈=∈0.002, P Se∈=∈0.002). The ACP activity was significantly higher in the normal group than that in the abnormal group (P∈=∈0.021). We also found a significantly negative correlation between α-glucosidase activity and the levels of As (r∈=∈-0.367, P∈=∈0.023). These findings provide evidence for relationships between human semen quality and metal exposures. These relationships are consistent with animal data, but additional human and mechanistic studies are needed. © 2012 Springer Science+Business Media, LLC.


Xu J.,Zhejiang University | Ren G.,Zhejiang University | Zhao D.-A.,174th Hospital of PLA | Li B.-A.,Xiamen University | And 3 more authors.
Oncology Reports | Year: 2014

Chibby (Cby) inhibits Wnt/β-catenin-mediated transcriptional activation by competing with Lef-1 (the transcription factor and target of β-catenin) to bind to β-catenin. This suggests that Cby could be a tumor suppressor protein. In the present study, we examined Cby expression in laryngeal squamous cell carcinoma (LSCC) and its function and mechanism in laryngeal carcinoma cell lines. Cby expression levels were investigated by immunohistochemistry in a panel of 36 LSCC patient cases. The expression of β-catenin, c-myc and cyclin D1 in Hep-2 were determined through RT-PCR and western blot analysis. Activity of Wnt/β-catenin signaling pathway after overexpression of Cby was measured by TCF/LEF luciferase reporter gene assay. Proliferation, clone forming ability, cell cycle distribution and cell apoptosis of Hep-2 cells were detected by MTT assay, plate colony forming assay, flow cytometry and TUNEL assay, respectively. This study showed that expression of Cby protein was strongly downregulated in LSCC tumor tissues in comparison to normal laryngeal mucosa samples. No significant correlation was found between the expression of Cby in tumor tissue and gender, age, clinical stage and tumor differentiation of laryngeal cancer patients. When Cby was overexpressed in Hep-2 cells, the expression of cyclin D1 was reduced and β-catenin activity was inhibited. Proliferation and plate colony forming assays revealed a significant inhibitory effect of Cby on growth and colony formation ability of Hep-2 cells after Cby overexpression in comparison to control and mock-infected cells. In addition, we also found that upregulated expression of Cby resulted in accumulation of numbers of cells in G0/G1 phase with concomitant decrease in S phase by cell cycle assay. TUNEL staining demonstrated that, compared with the control group, the rate of apoptosis in the plv-cs2.0-Cby group was significantly increased. Taken together, downregulation of Cby was observed in LSCC, but with no significant correlation to the clinicopathological features of LSCC patients. Overexpression of Cby effectively suppressed laryngeal carcinoma cell growth and promoted its apoptosis. A better understanding of the mechanisms of Cby gene activation in LSCC could provide potential novel therapeutic targets for human laryngeal carcinoma.


Chen S.,174th Hospital of PLA | Dong Y.,463rd Hospital of PLA | Xu C.,174th Hospital of PLA | Jiang L.,174th Hospital of PLA | And 4 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

The Fas/FasL signaling pathway, controlled by nuclear factor-κB (NFκB) at the transcriptional level, is critical for triggering germ cell apoptosis in response to mono-(2-ethylhexyl) phthalate (MEHP)-induced Sertoli cell (SC) injury, but the exact regulation mechanism remain unknown. Here, we discovered that expression level of Metastasis associated protein 1 (MTA1), a component of the Mi-2/nucleosome remodeling and deacetylase complex, was upregulated in SCs during the early recovery after MEHP exposure. This expression change was in line with the dynamic changes in germ cell apoptosis in response to MEHP treatment. Furthermore, a knockdown of MTA1 by RNAi in SCs was found to impair the MEHP-induced early activation of NFκB pathway and abolish the recruitment of NFκB onto FasL promoter, which consequently diminished the MEHP-triggered FasL induction. Considering that Fas/FasL is a well characterized apoptosis initiating signaling during SCs injury, our results point to a potential "switch on" effect of MTA1, which may govern the activation of NFκB/FasL cascade in MEHP-insulted SCs. Overall, the MTA1/NFκB/FasL circuit may serve as an important defensive/repairing mechanism to help to control the germ cell quality after SCs injury. © 2013 Elsevier Inc. All rights reserved.


Liu Y.,Southern Medical University | Zheng P.,Southern Medical University | Ji T.,174th Hospital of PLA | Liu X.,Southern Medical University | And 7 more authors.
Gut | Year: 2013

Objective: This study investigated the epigenetic role of PRL-3, a key metastasis gene in colorectal cancer (CRC), as a regulator of histone demethylation and the functions of Jumonji domain-containing protein 1B (JMJD1B) and JMJD2B in the progression of CRC. Methods: PRL-3-associated proteins were analysed using functional distribution and category enrichment analysis. Western blotting and immunofluorescence were used to detect nuclear PRL-3. The relationship between PRL-3 and JMJD1B or JMJD2B and the roles of JMJD1B, JMJD2B and PRL-3 in histone demethylation were determined after these proteins were knocked down using RNA interference. Case-control studies on JMJD1B and JMJD2B in patients with CRC were performed using immunohistochemical analysis. The in vitro functional effects of JMJD2B and JMJD1B were examined further. Results: JMJD1B and JMJD2B, two histone demethylases, were enriched among PRL-3-associated proteins. Nuclear PRL-3 was observed in CRC cells and clinical samples of CRC. The expression of nuclear PRL-3 was increased in patients with CRC at more advanced Dukes' stages. PRL-3 was involved in the regulation of histone methylation by affecting the activities of JMJD1B and JMJD2B. A low expression of the JMJD1B protein was positively correlated with the lymph node status (p=0.032), Dukes' classification (p=0.008) and TNM staging (p=0.022) of patients with CRC. A high expression of JMJD2B was positively correlated with the lymph node status (p=0.03), Dukes' classification (p=0.036) and tumour invasion (p=0.003) of patients with CRC. A loss-of-function analysis confirmed that JMJD2B promoted the proliferation, colony formation and migration of human CRC cells. Conclusion: Our data reveal a new role for PRL-3 as a key regulator of histone demethylation. JMJD1B seems to be a candidate tumour suppressor and JMJD2B seems to be a potential oncoprotein in the development and progression of CRC.


Li P.,Academy of Military Medical science | Yang C.,Academy of Military Medical science | Xie J.,Academy of Military Medical science | Liu N.,Academy of Military Medical science | And 6 more authors.
BMC Infectious Diseases | Year: 2015

We have recovered one bla NDM-1-harboring bacterial strain, designated as XM1570, from a sputum sample obtained from a fatal case of pneumonia in China. Methods: Biochemical profiling, 16S rRNA sequencing and antimicrobial susceptibility testing were performed. Conjugation experiments were conducted to determine transmissibility of resistance. Pulsed-field gel electrophoresis and whole genome sequencing were performed to identify strain-specific features. Results: The isolate XM1570 was identified as Acinetobacter calcoaceticus. Whole genome sequencing identified two plasmids, pXM1 and pXM2. Comparative analysis showed >99% similarity between XM1570 and A. calcoaceticus PHEA-2. Plasmid pXM1 carried the carbapenemase gene bla NDM-1 and displayed high homology with previously described plasmids isolated from different Acinetobacter spp., which were collected from human or livestock distributed in China and worldwide. The bla NDM-1 gene was located on this conjugative plasmid in a transposon-like region flanked by two copies of the insertion sequence ISAba125; and resistance to all tested β -lactams was observed. Transferability of resistance from pXM1 to the transconjugants was identified. Plasmid pXM2 had an insertion sequence ISAba125 and a -35 region of the bla NDM-1 gene promoter but the bla NDM-1 gene was not present. A chromosomally located carbapenemase-encoding gene bla OXA-75 was detected; however, this gene was interrupted by an insertion sequence ISAba22 belonging to IS3 family. Conclusions: Location of bla NDM-1 on different self-transmissible plasmids could facilitate geographically broad dissemination and host range expansion of the bla NDM-1 gene via horizontal gene transfer. Our findings of this normally environmental species A. calcoaceticus XM1570 further underline the significant clinical challenge and the essential need for surveillance including molecular methods and plasmid analyses. © Li et al.; licensee BioMed Central.


Peng J.,Nanjing General Hospital | Peng J.,174th Hospital of PLA | Zhang L.-J.,Nanjing General Hospital | Luo S.,Nanjing General Hospital | And 3 more authors.
Chinese Journal of Radiology | Year: 2011

Objective: To investigate the feasibility and accuracy of dual energy CT (DECT) in detecting acute myocardial ischemic reperfusion injury in a swine model. Methods: Acute myocardial ischemic reperfusion injury model was made by ligaturing the left anterior descending coronary artery (LAD) or the first diagonal artery (D1) of swine heart, the first-pass contrast enhanced DECT was performed. And then pigs were sacrificed, and the hearts were removed, triphenyltetrazolium chloride staining was performed. The CT numbers of non-ischemic and ischemic regions were measured. In the short axis of the left ventricle, the ventricular wall was divided into 17 segments for analysis, segments with myocardial perfusion defect in DECT myocardial iodine maps, DECT (140, 100 kV, weighted average 120 kV) were determined and compared with histopathology. The sensitivity, specificity and inter-modality agreement of DECT in detecting myocardial injury were calculated. One-way ANOVA test was used to analyze the differences between the CT number and weight of infracted myocardium measured on DECT at 140, 100 kV, weighted average 120 kV in ischemic and normal regions. Results: Partial sparse or defective perfusion in the apical anterior and septal wall were demonstrated in DECT myocardial iodine maps. The CT number of injured myocardium was significantly lower than that of normal myocardium at 140, 100 kV, weighted average 120 kV. The sensitivity, specificity of DECT myocardial iodine maps were 85.2% (23/27), 86.2% (94/109), and Kappa value was 0.62, the sensitivity, specificity at 140 kV were 88.9% (24/27), 92.7% (101/109), and Kappa value was 0.76, the sensitivity, specificity at 100 kV were 85.2% (23/27), 89.0% (97/109), and Kappa value was 0.67, the sensitivity, specificity at weighted average 120 kV were 88.9% (24/27), 91.7% (100/109), and Kappa value was 0.74. There were no significant differences between the weight of infracted myocardium measured on DECT at 140, 100 kV, weighted average 120 kV and histopathological results (F = 0.419, P = 0.741). Conclusion: DECT myocardial iodine maps can detect acute myocardial ischemic reperfusion injury in a swine model and have a good correlation with histopathology.


Tu Y.-J.,Daping Hospital | Tu Y.-J.,174th Hospital of PLA | Fan X.,Daping Hospital | Yang X.,Daping Hospital | And 2 more authors.
Oncology Reports | Year: 2013

Autophagy is a self-defense mechanism that provides nutrition and energy for cell survival by recycling the cytoplasm and organelles. Hence, chemotherapy is rendered less effective against cancer cells. Evodiamine is a previously described biological agent that possesses a cytotoxic activity in multiple cancer cells. However, little is known about evodiamine-induced autophagy in Lewis lung carcinoma (LLC) cells. In this study, LLC cells and a xenograft model were used. By use of a panel of techniques such as MTT assay, flow cytometry, western blotting, immunocytochemistry and TUNEL assay, the effects on the induction of apoptosis and autophagy were evaluated. We demonstrated that evodiamine inhibited LLC cell growth and induced apoptosis through caspase-independent manner in vitro and caspase-dependent pathway in vivo. In addition, we showed for the first time that evodiamine promoted autophagosome formation by enhancing the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and upregulating the expression of autophagy-specific genes (Atgs). Moreover, 3-methyladenine (3-MA), an autophagy inhibitor, attenuated evodiamine-induced autophagy through decreasing the conversion of LC3-I to LC3-II. The inhibition of autophagy was found to increase cell death and enhance evodiamine-induced apoptosis in vitro in a caspase-independent manner and in vivo in a caspase-dependent manner. In conclusion, evodiamine promoted autophagy in LLC cells and autophagy inhibition enhanced evodiamine-induced apoptosis in vitro and in vivo. These results demonstrate that evodiamine-induced autophagy plays a cytoprotective role in LLC cells and evodiamine combined with autophagy inhibitor therapy could increase the chemosensitivity of LLC cells.


PubMed | 174th Hospital of PLA
Type: Journal Article | Journal: Biochemical and biophysical research communications | Year: 2013

The Fas/FasL signaling pathway, controlled by nuclear factor-B (NFB) at the transcriptional level, is critical for triggering germ cell apoptosis in response to mono-(2-ethylhexyl) phthalate (MEHP)-induced Sertoli cell (SC) injury, but the exact regulation mechanism remain unknown. Here, we discovered that expression level of Metastasis associated protein 1 (MTA1), a component of the Mi-2/nucleosome remodeling and deacetylase complex, was upregulated in SCs during the early recovery after MEHP exposure. This expression change was in line with the dynamic changes in germ cell apoptosis in response to MEHP treatment. Furthermore, a knockdown of MTA1 by RNAi in SCs was found to impair the MEHP-induced early activation of NFB pathway and abolish the recruitment of NFB onto FasL promoter, which consequently diminished the MEHP-triggered FasL induction. Considering that Fas/FasL is a well characterized apoptosis initiating signaling during SCs injury, our results point to a potential switch on effect of MTA1, which may govern the activation of NFB/FasL cascade in MEHP-insulted SCs. Overall, the MTA1/NFB/FasL circuit may serve as an important defensive/repairing mechanism to help to control the germ cell quality after SCs injury.


PubMed | 174th Hospital of PLA and Academy of Military Medical science
Type: | Journal: BMC infectious diseases | Year: 2015

We have recovered one bla(NDM-1)-harboring bacterial strain, designated as XM1570, from a sputum sample obtained from a fatal case of pneumonia in China.Biochemical profiling, 16S rRNA sequencing and antimicrobial susceptibility testing were performed. Conjugation experiments were conducted to determine transmissibility of resistance. Pulsed-field gel electrophoresis and whole genome sequencing were performed to identify strain-specific features.The isolate XM1570 was identified as Acinetobacter calcoaceticus. Whole genome sequencing identified two plasmids, pXM1 and pXM2. Comparative analysis showed >99% similarity between XM1570 and A. calcoaceticus PHEA-2. Plasmid pXM1 carried the carbapenemase gene bla(NDM-1) and displayed high homology with previously described plasmids isolated from different Acinetobacter spp., which were collected from human or livestock distributed in China and worldwide. The bla(NDM-1) gene was located on this conjugative plasmid in a transposon-like region flanked by two copies of the insertion sequence ISAba125; and resistance to all tested -lactams was observed. Transferability of resistance from pXM1 to the transconjugants was identified. Plasmid pXM2 had an insertion sequence ISAba125 and a -35 region of the bla NDM-1 gene promoter but the bla NDM-1 gene was not present. A chromosomally located carbapenemase-encoding gene bla OXA-75 was detected; however, this gene was interrupted by an insertion sequence ISAba22 belonging to IS3 family.Location of bla(NDM-1) on different self-transmissible plasmids could facilitate geographically broad dissemination and host range expansion of the bla(NDM-1) gene via horizontal gene transfer. Our findings of this normally environmental species A. calcoaceticus XM1570 further underline the significant clinical challenge and the essential need for surveillance including molecular methods and plasmid analyses.

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