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Gao H.-N.,Zhejiang University | Lu H.-Z.,Fudan University | Cao B.,Capital Medical University | Du B.,Peking Union Medical College | And 38 more authors.
New England Journal of Medicine | Year: 2013

BACKGROUND: During the spring of 2013, a novel avian-origin influenza A (H7N9) virus emerged and spread among humans in China. Data were lacking on the clinical characteristics of the infections caused by this virus. METHODS: Using medical charts, we collected data on 111 patients with laboratory-confirmed avian-origin influenza A (H7N9) infection through May 10, 2013. RESULTS: Of the 111 patients we studied, 76.6% were admitted to an intensive care unit (ICU), and 27.0% died. The median age was 61 years, and 42.3% were 65 years of age or older; 31.5% were female. A total of 61.3% of the patients had at least one underlying medical condition. Fever and cough were the most common presenting symptoms. On admission, 108 patients (97.3%) had findings consistent with pneumonia. Bilateral ground-glass opacities and consolidation were the typical radiologic findings. Lymphocytopenia was observed in 88.3% of patients, and thrombocytopenia in 73.0%. Treatment with antiviral drugs was initiated in 108 patients (97.3%) at a median of 7 days after the onset of illness. The median times from the onset of illness and from the initiation of antiviral therapy to a negative viral test result on real-time reverse-transcriptase-polymerase- chain-reaction assay were 11 days (interquartile range, 9 to 16) and 6 days (interquartile range, 4 to 7), respectively. Multivariate analysis revealed that the presence of a coexisting medical condition was the only independent risk factor for the acute respiratory distress syndrome (ARDS) (odds ratio, 3.42; 95% confidence interval, 1.21 to 9.70; P = 0.02). CONCLUSIONS: During the evaluation period, the novel H7N9 virus caused severe illness, including pneumonia and ARDS, with high rates of ICU admission and death. (Funded by the National Natural Science Foundation of China and others.) Copyright © 2013 Massachusetts Medical Society.


Chen Y.,Shanghai JiaoTong University | Zhou X.,Shanghai JiaoTong University | Rong L.,Peoples Hospital of Bozhou
Molecular Medicine Reports | Year: 2015

Gene expression profiles of samples taken from patients with acute lung injury (ALI) induced by mechanical ventilation (MV) and lipopolysaccharide (LPS) were analyzed in order to identify key genes, and explore the underlying mechanisms. The GSE2411 microarray data set was downloaded from the Gene Expression Omnibus. This data set contained microarray data from 24 mouse lung samples, which were equally divided into four groups: Control group, MV group, LPS group and MV+LPS group. Differentially expressed genes (DEGs) were identified in the MV, LPS and MV+LPS groups, as compared with the control group, using packages of R software. Hierarchical clustering and between-group comparisons were performed for each group of DEGs. Overrepresented biological processes were revealed by functional enrichment analysis using the Database for Annotation, Visualization and Integrated Discovery. Unique DEGs in the LPS and MV+LPS groups were selected, and pathway enrichment analyses were performed using the Kyoto Encyclopedia of Genes and Genomes Orthology Based Annotation system. A total of 32, 264 and 685 DEGs were identified in the MV, LPS and MV+LPS groups, respectively. The MV+LPS group had more DEGs, as compared with the other two treatment groups. Genes associated with the immune and inflammatory responses were significantly overrepresented in both the LPS and MV+LPS groups, suggesting that LPS dominated the progression of ALI. Unique DEGs in the LPS and MV+LPS groups were associated with cytokine-cytokine receptor interaction. The Janus kinase-signal transducer and activator of transcription signaling pathway was shown to be enriched in the LPS+MV-unique DEGs. The results of the present study demonstrated that MV could exaggerate the transcriptional response of the lungs to LPS. Numerous key genes were identified, which may advance knowledge regarding the pathogenesis of ALI.


Chai P.,Peoples Hospital of Bozhou | Tian J.,Peoples Hospital of Bozhou | Zhao D.,Hospital of Suzhou | Zhang H.,Peoples Hospital of Bozhou | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2016

Gse1 coiled-coil protein (GSE1), also known as KIAA0182, is a proline rich protein. However, the function of GSE1 is largely unknown. In this study, we reported that GSE1 is overexpression in breast cancer and silencing of GSE1 significantly suppressed breast cancer cells proliferation, migration and invasion. Furthermore, GSE1 was identified as a direct target of miR-489-5p, which is significantly reduced in breast cancer tissues. In addition, forced expression of miR-489-5p suppressed breast cancer cells proliferation, migration and invasion. Moreover, depletion of GSE1 by siRNAs significantly abrogated the enhanced proliferation, migration and invasion of breast cancer cells consequent to miR-489-5p depletion. Taken together, these findings suggest that GSE1 may function as a novel oncogene in breast cancer and it can be regulated by miR-489-5p. © 2016 Elsevier Inc. All rights reserved.


Yu C.-Y.,Anhui Medical University | Yu C.-Y.,Nanjing Medical University | Gui W.,Anhui Medical University | Gui W.,Peoples Hospital of Bozhou | And 7 more authors.
NeuroMolecular Medicine | Year: 2014

To address the role of the transforming growth factor beta (TGFβ)-Smad3 signaling pathway in dendrite growth and associated synaptogenesis, we used small inhibitory RNA to knockdown the Smad3 gene in either cultured neurons and or primary astrocytes. We found that TGFβ1 treatment of primary neurons increased dendrite extensions and the number of synapsin-1-positive synapses. When Smad3 was knockdown in primary neurons, dendrite growth was inhibited and the number of synapsin-1-positive synapses reduced even with TGFβ1 treatment. When astrocyte-conditioned medium (ACM), collected from TGFβ1-treated astrocytes (TGFβ1-stimulated ACM), was added to cultured neurons, dendritic growth was inhibited and the number of synapsin-1-positive puncta reduced. When TGFβ1-stimulated ACM was collected from astrocytes with Smad3 knocked down, this conditioned media promoted the growth of dendrites and the number of synapsin-1-positive puncta in cultured neurons. We further found that TGFβ1 signaling through Smad3 increased the expression of chondroitin sulfate proteoglycans, neurocan, and phosphacan in ACM. Application of chondroitinase ABC to the TGFβ1-stimulated ACM reversed its inhibitory effects on the dendrite growth and the number of synapsin-1-positive puncta. On the other hand, we found that TGFβ1 treatment caused a facilitation of Smad3 phosphorylation and translocation to the nucleus induced by status epilepticus (SE) in wild-type (Smad3 +/+) mice, and this treatment also caused a promotion of γ-aminobutyric acid-ergic synaptogenesis impaired by SE in Smad3 +/+ as well as in Smad3-/- mice, but more dramatic promotion in Smad3+/+ mice. Thus, we provide evidence for the first time that TGFβ-Smad3 signaling pathways within neuron and astrocyte differentially regulate dendrite growth and synaptogenesis, and this pathway may be involved in the pathogenesis of some central nervous system diseases, such as epilepsy. © 2014 Springer Science+Business Media New York.


Tang J.,Nanjing Medical University | Zhu Y.,Nanjing Medical University | Xie K.,Nanjing Medical University | Xie K.,Peoples Hospital of Bozhou | And 10 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2016

Background: MUC4 is a high molecular weight membrane protein that is overexpressed in pancreatic cancer (PC) and is associated with the development and progression of this disease. However, the exact mechanisms through which MUC4 domains promote these biological processes have rarely been studied, partly because of its high molecular weight, difficulty to overexpress it. Here, we use MUC4/Y, one of the MUC4 transcript variants, as a model molecule to investigate the AMOP-domain of MUC4(MUC/Y). Methods: We used cell proliferation, migration, invasion and tube formation assays in vitro to explore the abilities of AMOP domain in PC. In vivo, the matrigel plug assay, orthotopic implantation and Kaplan-Meier survival curves were used to check the results we observed in vitro. Finally, we discovered the underlying mechanism through western blot and immunofluorescence. Results: We found that MUC4/Y overexpression could enhance the angiogenic and metastatic properties of PC cells, both in vitro and in vivo. However, the deletion of AMOP domain could cutback these phenomena. Additionally, Kaplan-Meier survival curves showed that mice injected with MUC4/Y overexpressed cells had shorter survival time, compared with empty-vector-transfected cells (MUC4/Y-EV), or cells expressing MUC4/Y without the AMOP domain (MUC4/Y-AMOP). Our data also showed that overexpression of MUC4/Y could activate NOTCH3 signaling, increasing the expression of downstream genes: VEGF-A, MMP-9 and ANG-2. Conclusions: The AMOP domain had an important role in MUC4/Y (MUC4)-mediated tumour angiogenesis and metastasis of PC cells; and the NOTCH3 signaling was involved. These findings provided new insights into PC therapies. Our study also supplies a new method to study other high molecular membrane proteins. © 2016 The Author(s).


Zhang G.-H.,Chinese People's Liberation Army | Qin R.,Peoples Hospital of Bozhou | Zhang S.-H.,Harbin Medical University | Zhu H.,Harbin Medical University
Molecular Biology Reports | Year: 2014

Vascular endothelial growth factor B (VEGF-B) was reported to be angiogenic, and it was considered as a neuroprotective agent in mouse retinal ganglion cells following optic nerve crush. Thus, it was necessary to investigate whether VEGF-B contributes to the process of retinal and choroidal neovascularization. We aimed to investigate the effects of VEGF-B on proliferation and migration in EA.Hy926 cells. The proliferation of cells was analyzed by cell counting kit 8 assay, and the migration of cells was evaluated by a modified Boyden chamber assay. The levels of phospho-ERK1/2 (P-ERK1/2), ERK1/2, phospho-p38 and p38 were detected by western blotting. The results showed that VEGF-B induced proliferation and migration of EA.Hy926 cells (P < 0.01 and P < 0.05, respectively), and ERK1/2 and p38 phosphorylation were significantly activated. Our study suggested that VEGF-B was an angiogenesis factor in vitro and that ERK1/2 and p38-related signaling pathways were involved in these VEGF-B activities. © Springer Science+Business Media 2013.


Rong L.,Anhui University of Science and Technology | Rong L.,Peoples Hospital of Bozhou | Wu J.,Anhui University of Science and Technology | Wang W.,Anhui University of Science and Technology | And 3 more authors.
European Review for Medical and Pharmacological Sciences | Year: 2016

OBJECTIVE: The aim of this study was to investigate the effect of resveratrol on the idiopathic bleomycin (BLM)-induced pulmonary fibrosis, which is increasingly recognized as an epithelial-To-mesenchymal transition (EMT)-Associated disease. MATERIALS AND METHODS: We evaluated the effect of resveratrol on the BLM-induced fibrosis in a mouse model, via monitoring the pathological chance in mice lung, the mice body weight change and the mice death. And we also explored the regulation by BLM on (and) resveratrol on the expression and activity of Sirt 1 and on the expression of epithelial-To-mesenchymal transition (EMT)-Associated markers in mice lung. RESULTS: It was demonstrated that resveratrol ameliorated the BLM-induced fibrosis-like pathological change in mice lung, inhibited BLM-induced mice body weight loss and death. Moreover, resveratrol also inhibited the BLMinduced EMT-Associated molecular events, such as reduced E-cadherin and elevated collagen I and α-SMA. We also confirmed the amelioration by resveratrol on the BLM-mediated inhibition of Sirt 1 in expression and activity in mice lung. CONCLUSIONS: Our study confirmed the inhibitory role of resveratrol in the BLM-induced pulmonary fibrosis in a mouse model. Resveratrol ameliorated the BLM-induced pathological change of fibrosis, mice body weight loss and death. And such amelioration might be associated with the activation of Sirt 1 in mice lung. The present study implied that resveratrol might be a promising agent for effective control the pulmonary fibrosis.


Wu S.,Peoples Hospital Of Bozhou | Su J.,Peoples Hospital Of Bozhou | Qian H.,Peoples Hospital Of Bozhou | Qian H.,Anhui Medical University | And 2 more authors.
Tumor Biology | Year: 2015

Autophagy is a highly conserved self-digestion process to promote cell survival in response to nutrient starvation and other metabolic stresses in eukaryotic cells. Dysregulation of this system is linked with numerous human diseases, including cancers. ATG4B, a cysteine protease required for autophagy, cleaves the C-terminal amino acid of ATG8 family proteins to reveal a C-terminal glycine which is necessary for ATG8 proteins conjugation to phosphatidylethanolamine (PE) and insertion to autophagosome precursor membranes. However, the mechanism governing the protein stability of ATG4B in human cancer cells is not fully understood. In this study, tandem affinity purification/mass spectrometry (TAP/MS) were applied to the investigation of the interaction between ATG4B and potential candidate proteins. Then, co-immunoprecipitation (Co-IP) and GST-pull down assays indicated that the candidate protein-SLC27A4 directly interacts with ATG4B in lung cancer cell lines. Intriguingly, we also found that ATG4B protein expression was increased in parallel with SLC27A4 in lung cancer cell lines as well as lung tumor tissues. However, relevant functional research of SLC27A4 in autophagy or oncotherapy has not been investigated before. In this study, we hypothesized that SLC27A4 might act as a mediator of ATG4B, in some respects, through the protein binding directly. Further, we found that the high expression level of SLC7A4 increased the ATG4B stability and was conducive to rapid reaction to everolimus (RAD001)-induced autophagy in human lung cancer cells. As expected, the results showed that SLC27A4 could help to maintain the protein stability and intracellular concentration of ATG4B, thereby triggering rapid autophagy through releasing ATG4B to cytoplasm under conditions of reduced nutrient availability or during stress of chemotherapy in lung cancer cells. Reduced SLC27A4 by si-RNA also showed the enhanced therapeutic efficiency of everolimus, doxorubicin, and cisplatin in human lung cancer cell lines. Collectively, this study may help researchers better understand the mechanism of autophagy vitality in human cancers and SLC27A4/ATG4B complex might act as a new potential therapeutic target of lung tumor chemotherapy. © 2015 International Society of Oncology and BioMarkers (ISOBM)


Tan Y.,Jiangsu University | Pan T.,Peoples Hospital of Bozhou | Ye Y.,Jiangsu University | Ge G.,Jiangsu University | And 3 more authors.
PLoS ONE | Year: 2014

Background: Circulating microRNAs (miRNAs), which are extremely stable and protected from RNAse-mediated degradation in body fluids, have emerged as candidate biomarkers for many diseases. The present study aimed to identify a serum microRNA (miRNA) expression profile that could serve as a novel diagnostic biomarker for primary biliary cirrhosis (PBC).Methods: Serum miRNA expression was investigated using four cohorts comprising 380 participants (healthy controls and patients with PBC) recruited between August 2010 and June 2013. miRNA expression was initially analyzed by Illumina sequencing using serum samples pooled from 3 patients and 3 controls. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was then used to evaluate the expression of selected miRNAs in a screening set (n= 40). A logistic regression model was then constructed using a training cohort (n= 192) and validated using another cohort (n =142). The area under the receiver operating characteristic curve (AUC) was used to evaluate diagnostic accuracy.Results: We identified a miRNA panel (hsa-miR-122-5p, hsa-miR-141-3p, and hsa-miR-26b-5p) with a high diagnostic accuracy for PBC (AUC = 0.905, 95% confidence interval (CI) = 0.857 to 0.953; sensitivity = 80.5%, specificity = 88.3%). There was a significant difference between AUC values of the miRNA panel and those of alkaline phosphatase (ALP) (AUC= 0.537, difference between areas= 0.314, 95% CI=0.195 to 0.434, P<0.001), and those of antinuclear antibody (ANA) (AUC=0.739, difference between areas=0.112, 95% CI=0.012 to 0.213, P=0.0282).Conclusion: We identified a serum microRNA panel with considerable clinical value in PBC diagnosis. The results indicate that the miRNA panel is a more sensitive and specific biomarker for PBC than ALP and ANA. © 2014 Tan et al.


PubMed | Peoples Hospital of Bozhou
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Autophagy is a highly conserved self-digestion process to promote cell survival in response to nutrient starvation and other metabolic stresses in eukaryotic cells. Dysregulation of this system is linked with numerous human diseases, including cancers. ATG4B, a cysteine protease required for autophagy, cleaves the C-terminal amino acid of ATG8 family proteins to reveal a C-terminal glycine which is necessary for ATG8 proteins conjugation to phosphatidylethanolamine (PE) and insertion to autophagosome precursor membranes. However, the mechanism governing the protein stability of ATG4B in human cancer cells is not fully understood. In this study, tandem affinity purification/mass spectrometry (TAP/MS) were applied to the investigation of the interaction between ATG4B and potential candidate proteins. Then, co-immunoprecipitation (Co-IP) and GST-pull down assays indicated that the candidate protein-SLC27A4 directly interacts with ATG4B in lung cancer cell lines. Intriguingly, we also found that ATG4B protein expression was increased in parallel with SLC27A4 in lung cancer cell lines as well as lung tumor tissues. However, relevant functional research of SLC27A4 in autophagy or oncotherapy has not been investigated before. In this study, we hypothesized that SLC27A4 might act as a mediator of ATG4B, in some respects, through the protein binding directly. Further, we found that the high expression level of SLC7A4 increased the ATG4B stability and was conducive to rapid reaction to everolimus (RAD001)-induced autophagy in human lung cancer cells. As expected, the results showed that SLC27A4 could help to maintain the protein stability and intracellular concentration of ATG4B, thereby triggering rapid autophagy through releasing ATG4B to cytoplasm under conditions of reduced nutrient availability or during stress of chemotherapy in lung cancer cells. Reduced SLC27A4 by si-RNA also showed the enhanced therapeutic efficiency of everolimus, doxorubicin, and cisplatin in human lung cancer cell lines. Collectively, this study may help researchers better understand the mechanism of autophagy vitality in human cancers and SLC27A4/ATG4B complex might act as a new potential therapeutic target of lung tumor chemotherapy.

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