323 Hospital of PLA

Fengcheng, China

323 Hospital of PLA

Fengcheng, China

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Lu X.,323 Hospital of PLA | Chen Z.,Shanghai University | Liang H.,PLA Fourth Military Medical University | Li Z.,323 Hospital of PLA | And 4 more authors.
Cellular Signalling | Year: 2013

The interactions between kidney and thyroid functions have been known for many years, but how the thyroid affects the kidney function is largely unknown. Here we analyzed the role of T3 on the tubular epithelial-to-mesenchymal transition (EMT), which is recognized to play pivotal roles in the process of renal fibrosis. T3 was found to significantly inhibit the TGFβ1 induced EMT in human proximal tubular epithelial cell line HK-2. Meanwhile, T3 induced the expression of miR34a. Molecularly, the T3 receptor could directly bind the T3R recognition motif at the -. 1505 to -. 1526. bp and -. 604 to -. 609. bp regions in the miR34a promoter and transcriptionally activate the expression of miR34a upon T3 treatment. Inhibition of the miR34a by miR34a knockdown nearly blocked the effects of T3 on EMT. Taken together, our study here revealed that thyroid hormone T3 could inhibit TGFβ1 induced renal tubular epithelial to mesenchymal transition by increasing miR34a expression. © 2013 Elsevier Inc.

Liu Q.-P.,323 Hospital of PLA | Zhou D.-X.,Xi'an Jiaotong University | Sun L.,Shaanxi Peoples Hospital | Ling L.,First Hospital of PLA | And 3 more authors.
Pathology Research International | Year: 2014

Seawater drowning can lead to acute lung injury (ALI). Several studies have shown that bone marrow mesenchymal stem cells (BMSC) treatment could attenuate ALI. However, the mechanisms underlying this phenomenon still remain elusive. Therefore, this study aimed to investigate whether BMSC treatment can ameliorate seawater-induced ALI and its underlying mechanisms in a rat model. In this study, arterial blood gas, lung weight coefficient, and TNF-α, and IL-8 in bronchoalveolar lavage fluid (BALF), as well as histopathology examination, were used to detect the lung injury of seawater exposure. Moreover, western blot and RT-PCR were used to explore autophagy in lung tissues. The results demonstrated that seawater exposure induced ALI including impaired arterial blood gas, pulmonary edema, histopathologic changes, and inflammatory response in lung tissues. What is more, these changes were partly ameliorated by BMSC treatment through inhibition of autophagy in lung tissues. The application of BMSC may be a potential effective treatment for seawater-induced ALI. Copyright © 2014 Qiu-ping Liu et al.

Liu Q.-P.,323 Hospital of PLA | Zhou D.-X.,Xi'an Jiaotong University | Zhou D.-X.,Key Laboratory of Environment and Genes Related to Diseases | Lin P.,Shaanxi Electrical Power Research Institute | And 3 more authors.
Experimental Lung Research | Year: 2013

Seawater drowning can lead to acute lung injury (ALI). However, the molecular and cellular mechanisms underlying this phenomenon remain elusive. The overall aim of this study is to clarify the role of autophagy in seawater-induced ALI, by which we can further understand the molecular mechanism and develop new methods for prevention and treatment of seawater-induced ALI. In this study, electron microscopy, western blot analysis, and RT-PCR were used to detect autophagy in lung tissues. Moreover, arterial blood gas analysis, lung weight coefficient, TNF-α, IL-8 in bronchoalveolar fluid (BALF), histopathology were used to detect the lung injury of seawater exposure. An inhibitor of autophagy (3-Methyladenine, 3-MA) was injected intraperitoneally before seawater exposure to further explore the role of autophagy in ALI. Electron microscopy revealed increasing autophagosomes in alveolar epithelial cell in seawater group compared with the control. The transcription and expression levels (mRNA and protein levels) of the LC3 II significantly increased in lung tissue of seawater group compared with those in control group. Furthermore, the alterations of autophage were basically consistent with the changes in arterial blood gas, lung weight coefficient, TNF-α, IL-8 in BALF and morphologic findings. In addition, inhibition of autophagy by 3-MA partly ameliorated seawater-induced ALI, as indicated by reduced lung weight coefficient and TNF-α in BALF, as well as increased PaO2. In conclusion, seawater aspiration triggered autophagy, and autophagy may be a scathing factor responsible for ALI induced by seawater. © 2013 Informa Healthcare USA, Inc.

Lv M.-M.,PLA Fourth Military Medical University | Lv M.-M.,323 Hospital of PLA | Cheng Y.-C.,Third Hospital of PLA | Xiao Z.-B.,323 Hospital of PLA | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2014

The molecular basis for group I metabotropic glutamate receptors (mGluR1 and 5) coupling to membrane ion channels and intracellular calcium pools is not fully understood. Homer is a family of post synaptic density proteins functionally and physically attached to target proteins at proline-rich sequences. In the present study, we demonstrate that Homer1b/c is constitutively expressed in PC12 cells, whereas Homer1a, the immediate early gene product, can be up-regulated by brain derived neurotrophic factor (BDNF) and glutamate. Knockdown of Homer1b/c using specific target small interfering RNA (siRNA) did not interfere the expression of mGluR1, mGluR5 and their downstream effectors, including inositol-1,4,5-trisphosphate receptors (IP3R), phospholipase C (PLC) and Gq proteins. By analyzing Ca2+ imaging in PC12 cells, we demonstrated that Homer1b/c is an essential regulator of the Ca2+ release from the endoplasmic reticulum (ER) induced by the activation of group I mGluRs, IP3R and ryanodine receptors (RyR). Furthermore, the group I mGluRs activation-dependent refilling of the Ca 2+ stores in both resting and depolarizing conditions were strongly attenuated in the absence of Homer1b/c. Together, our results demonstrate that in PC12 cells Homer1b/c is a regulator of group I mGluRs related Ca2+ homeostasis that is essential for the maintenance of normal Ca2+ levels in the ER. © 2014 Elsevier Inc. All rights reserved.

Bi L.,PLA Fourth Military Medical University | Li D.-C.,Ninth Hospital of Xian | Huang Z.-S.,323 Hospital of PLA | Yuan Z.,PLA Fourth Military Medical University
Artificial Organs | Year: 2013

Processed xenegeneic cancellous bone represents an alternative to bone autograft. In order to observe the effects of present prion inactivation treatments on the natural properties of xenogeneic cancellous bones, we treated bovine bone granules with sodium hydroxide (NaOH), sodium hypochlorite (NaOCl), and gaseous hydrogen peroxide (gH2O2) respectively in this study. The microstructure, composition, and mineral content of the granules were evaluated by scanning electron micrograph, energy dispersive X-ray spectroscopy, ash analysis, and micro-computed tomography. The biomechanical property was analyzed by a materials testing machine. The cytocompatibility was evaluated by using a mouse fibroblast cell line (3T3). The microstructure, organic content, and mechanical strength were dramatically altered at the surface of bone in both NaOH- and NaOCl-treated groups, but not in the gH2O2-treated group. Compared with the gH2O2-treated group, attachment and proliferation of 3T3 were reduced in either NaOH- or NaOCl-treated groups. As the consequence, gH2O2 treatment may be a useful approach of disinfection for the preparation of natural cancellous bone with well-preserved structural, mechanical, and biological properties. © 2013, International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.

Yang G.,PLA Fourth Military Medical University | Lu X.,323 Hospital of PLA | Yuan L.,PLA Fourth Military Medical University
Biochimica et Biophysica Acta - Gene Regulatory Mechanisms | Year: 2014

Unraveling the gene expression networks governing cancer initiation and development is essential while remains largely uncompleted. With the innovations in RNA-seq technologies and computational biology, long noncoding RNAs (lncRNAs) are being identified and characterized at a rapid pace. Recent findings reveal that lncRNAs are implicated in serial steps of cancer development. These lncRNAs interact with DNA, RNA, protein molecules and/or their combinations, acting as an essential regulator in chromatin organization, and transcriptional and post-transcriptional regulation. Their misexpression confers the cancer cell capacities for tumor initiation, growth, and metastasis. The review here will emphasize their aberrant expression and function in cancer, and the roles in cancer diagnosis and therapy will be also discussed. © 2014 Published by Elsevier B.V.

Pu J.,PLA Fourth Military Medical University | Bai D.,323 Hospital of PLA | Yang X.,PLA Fourth Military Medical University | Lu X.,The 323 Hospital of PLA | And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2012

Recently, catecholamines have been described as being involved in the regulation of cancer genesis and progression. Here, we reported that adrenaline increased the cell proliferation and decreased the cisplatin induced apoptosis in HT29 cells. Further study found that adrenaline increased miR-155 expression in an NFκB dependent manner. HT29 cells overexpressing miR-155 had a higher cell growth rate and more resistance to cisplatin induced apoptosis. In contrast, HT29 cells overexpressing miR-155 inhibitor displayed decreased cell proliferation and sensitivity to cisplatin induced cell death. In summary, our study here revealed that adrenaline-NFκB-miR-155 pathway at least partially contributes to the psychological stress induced proliferation and chemoresistance in HT29 cells, shedding light on increasing the therapeutic strategies of cancer chemotherapy. © 2012 Elsevier Inc.

Bai D.,PLA Fourth Military Medical University | Bai D.,323 Hospital of PLA | Gao Q.,PLA Fourth Military Medical University | Gao Q.,323 Hospital of PLA | And 4 more authors.
Cellular Signalling | Year: 2012

Persistent fibroblast activation in wound repair is believed to be the key reason for fibrosis and transforming growth factor (TGF)β is considered as one of the key mediators for the fibrogenic response, with the detailed mechanism largely unknown. Here we found that TGFβ1 treatment could induce a significant increase of endogenous TGFβ1 expression by enhancing the mRNA stability in cardiac fibroblasts. Further study revealed that TGFβ1 treatment translocated the nuclear HuR into cytoplasm, which in turn bound the ARE in the 3'UTR of TGFβ1 and increased the mRNA stability as seen from the RNA-IP and reporter assay. Knockdown of HuR decreased the endogenous expression of TGFβ1 under exogenous TGFβ1 treatment, simultaneously with the decrease of Col1a, Col3a and fibronectin expression. Our study here established a TGFβ1/HuR feedback circuit regulating the fibrogenic response in fibroblasts, and targeting this feedback loop is of great potential to control fibrosis. © 2012 Elsevier Inc..

PubMed | PLA Fourth Military Medical University and 323 Hospital of PLA
Type: | Journal: Scientific reports | Year: 2016

The leading cause of death in diabetic patients is diabetic cardiomyopathy, in which alteration of Akt signal plays an important role. Inpp5f is recently found to be a negative regulator of Akt signaling, while its expression and function in diabetic heart is largely unknown. In this study, we found that in both the streptozotocin (STZ) and high fat diet (HFD) induced diabetic mouse models, Inpp5f expression was coordinately regulated by insulin, blood glucose and lipid levels. Increased Inpp5f was inversely correlated with the cardiac function. Further studies revealed that Insulin transcriptionally activated Inpp5f in an Sp1 dependent manner, and increased Inpp5f in turn reduced the phosphorylation of Akt, forming a negative feedback loop. The negative feedback plays a protective role under diabetic condition. However, high blood glucose and lipid, which are characteristics of uncontrolled diabetes and type 2 diabetes, increased Inpp5f expression through activation of NF-B, blunts the protective feedback. Thus, our study has revealed that Inpp5f provides as a negative feedback regulator of insulin signaling and downregulation of Inpp5f in diabetes is cardioprotective. Increased Inpp5f by hyperglycemia and hyperlipidemia is an important mediator of diabetic cardiomyopathy and is a promising therapeutic target for the disease.

Jin Y.B.,Xi'an University of Architecture and Technology | Zhang C.Q.,323 Hospital of PLA
Advanced Materials Research | Year: 2012

The article is based on the circumstances of urbanization in process in Northwest China. The problems in the construction of village houses are analyzed and the rational strategy regarding the urbanization and its influence on constructing houses, so that the problems once harassed the developed area can be avoided. After through investigation and analysis, we propose that the local construction in the context of urbanization should conform to the following principles: First, house construction should go with the resource and technological condition. Second, the construction should accord with the climate and environment. Third, the reasonable principle uses the land. Last, Integration of architecture and green ecological technology. The synthesis of the four principles above is the apt choice of constructing residence in Northwest China, which is expected to lead the local village living environment onto a sustainable path. © (2012) Trans Tech Publications, Switzerland.

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