Wuhan General Hospital of PLA

Wuhan, China

Wuhan General Hospital of PLA

Wuhan, China
SEARCH FILTERS
Time filter
Source Type

Lu Q.,Southern Medical University | Lu Q.,Wuhan General Hospital of PLA | Gong Z.,Southern Medical University | Gong Z.,Wuhan General Hospital of PLA | And 13 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2017

Acute myocardial infarction (AMI) often leads to myocardial ischemia reperfusion (MIRI), thereby causing myocardial remodeling. Percutaneous coronary intervention (PCI) is the primary treatment of AMI, but easily results in myocardial ischemia-reperfusion injury, leading to myocardial remodeling. It was showed that miR-24 plays a role in cardiac remodeling. However, miR-24 expression and effect in AMI after PCI treatment have not been fully elucidated. A total of 80 cases of AMI patients after PCI surgery were enrolled. Information about echocardiography ejection fraction (EF), left ventricular end systolic diameter (LVESD), left ventricular thickness, and left ventricular end diastolic diameter (LVEDD) were recorded. MiR-24 expression before and after PCI treatment was detected by real-time PCR and analyzed with cardiac function. Rat AMI model was established and transfected by miR-24 lentivirus. Cardiac function in rats was assessed by M-mode ultrasound. Type I collagen content was determined by ELISA. Bax and Bcl-2 protein expressions in rat myocardial cells were tested by Western blot. EF reduced, LVESD and LVEDD increased, left ventricular thickness decreased, and miR-24 downregulated significantly in AMI patients after PCI compared with the preoperative group (P < 0.05). MiR-24 was positively correlated with left ventricular thickness and EF, and negatively correlated with LVESD and LVEDD (P < 0.05). Overexpression of MiR-24 in AMI rats obviously improved heart function index, reduced type I collagen content, downregulated Bax level, and enhanced Bcl-2 expression compared with AMI group (P < 0.05). MiR-24 downregulated in AMI and increased after PCI treatment. MiR-24 overexpression improved cardiac function through reducing type I collagen, regulating apoptosis balance, and alleviating MIRI.


Song J.,Wuhan General Hospital of PLA | Song J.,The Occurrence and Intervention of Central Nervous System Tumors Key Laboratory of Hubei Province | Lu W.,Wuhan General Hospital of PLA | Lu W.,The Occurrence and Intervention of Central Nervous System Tumors Key Laboratory of Hubei Province | And 12 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2017

Objective: To study the interaction between glucose-regulated protein 78 (GRP78) and heat shock protein 70 (HSP70) in lipopolysaccharide (LPS) treated mouse microglial cells, and explore its mechanism. Methods: mouse microglia (BV2) was the research object, bacterial lipopolysaccharide (LPS) infected BV2 cells were used to observe the active status which were stimulated by LPS. We analyzed TLR2, TLR4 expression level of the infected cells. We also investigated LPS stimulated BV2 cell. Expression level of IL-1β, TNF-α, IFN-β and other cytokines were observed. When GRP78 and HSP70 were injected into BV2 LPS-stimulated cells, changes of nitric oxide synthase (iNOS) and reactive oxygen species (ROS) were observed. Results: Immunofluorescence staining showed that surface of normal BV2 cell appeared red fluorescent particles, with some activation state. After LPS, GRP, HSP70 protein and LPS treatment, microglia activation state had different degrees of incensement. Expression results of TLR2 and TLR4 showed that after LPS stimulated TLR2 expression showed significant difference (P>0.05) compared with the normal cells, while expression of GRP78 and HSP70 injected LPS stimulated TLR2 showed significant difference compared with the normal group and the LPS-treated group with significant difference (P<0.05); expression of TLR4 in LPS stimulated group, GRP78 + LPS group and HSP70 + LPS group showed statistical difference (P<0.05) compared with the normal cells. ELISA results showed that the IL-1β had significant difference between five experimental groups (P<0.05), while it was increased significantly in HSP70 + LPS treatment group, and LPS treatment group was followed; TNF-α in normal cells group showed statistical significance (P<0.05) compared with the rest four experimental groups; IFN-β in normal cells and LPS-treated group showed statistical significance compared with GRP78 + LPS group and HSP70 + LPS group (P<0.05), but there was no difference when compared with LPS stimulated neurons. Expression of iNOS, compared with the five experimental groups, had significant difference (P<0.05), while HSP70 + LPS treatment group showed the most obvious incensement. The results of ROS had significant difference (P<0.05) compared with the results of five experimental groups, while HSP70 + LPS treatment group also showed the most obvious incensement. Conclusion: LPS stimulation can cause microglial activation in mice. Through TLR4 pathway, IL-1β, TNF-α and other cytokines can be secreted extensively, leading iNOS and reactive oxygen species (ROS) increased. Meanwhile, GRP78 protein may play a more important role in the inhibition of LPS-stimulated microglia inflammation and other stress. © 2017, E-Century Publishing Corporation. All rights reserved.


Yan Y.,Wuhan General Hospital of PLA | Song J.,Wuhan General Hospital of PLA | Xu G.,Wuhan General Hospital of PLA | Yao S.,Wuhan General Hospital of PLA | And 4 more authors.
Journal of Clinical Neuroscience | Year: 2017

This study investigated the characteristics of the small-world brain network architecture of patients with mild traumatic brain injury (MTBI), and a correlation between brain functional connectivity network properties in the resting-state fMRI and Standardized Assessment of Concussion (SAC) parameters. The neurological conditions of 22 MTBI patients and 17 normal control individuals were evaluated according to the SAC. Resting-state fMRI was performed in all subjects 3 and 7. days after injury respectively. After preprocessing the fMRI data, cortex functional regions were marked using AAL90 and Dosenbach160 templates. The small-world network parameters and areas under the integral curves were computed in the range of sparsity from 0.01 to 0.5. Independent-sample t-tests were used to compare these parameters between the MTBI and control group. Significantly different parameters were investigated for correlations with SAC scores; those that correlated were chosen for further curve fitting. The clustering coefficient, the communication efficiency across in local networks, and the strength of connectivity were all higher in MTBI patients relative to control individuals. Parameters in 160 brain regions of the MTBI group significantly correlated with total SAC score and score for attention; the network parameters may be a quadratic function of attention scores of SAC and a cubic function of SAC scores. MTBI patients were characterized by elevated communication efficiency across global brain regions, and in local networks, and strength of mean connectivity. These features may be associated with brain function compensation. The network parameters significantly correlated with SAC total and attention scores. © 2017 Elsevier Ltd.


Song J.,Wuhan General Hospital of PLA | Liu M.,No 457 Hospital of PLA | Yao S.,Wuhan General Hospital of PLA | Yan Y.,Wuhan General Hospital of PLA | And 4 more authors.
Frontiers in Behavioral Neuroscience | Year: 2017

It has been shown that emotionally positive facial expressions are recognized substantially faster than emotionally negative facial expressions, the positive classification advantage (PCA). In this experiment we explored the involvement of configural computations while processing positive and negative faces in an expression categorization task using artificial faces. Analyzing the reaction times (RTs), we found that happy faces were categorized more quickly than sad faces (PCA) and this effect disappeared for inverted faces. Event-related potentials (ERPs) data showed that the face-sensitive N170 component was larger for sad than for happy faces only at upright condition and that face inversion significantly enhanced N170 amplitudes only for happy faces. Moreover, the happy faces elicited shorter N170 latency than did the sad faces, whereas for inverted condition the N170 latency did not differ between happy and sad faces. Finally, the significant positive correlation between the RTs and the latency of the N170 was not found for N170 amplitudes. Because the configural computation was task-irrelevant in the present study, these behavioral and ERP data indicated that one of the sources of PCA is the configural analysis applied by default while categorizing facial emotions. © 2017 Song, Liu, Yao, Yan, Ding, Yan, Zhao and Xu.


Li M.,Union Hospital | Wang X.,Union Hospital | Fu W.,Wuhan General Hospital of PLA | He S.,Union Hospital | And 3 more authors.
Cellular Physiology and Biochemistry | Year: 2011

Objective: To investigate the regulation of CD4 +CD25 + Regulatory T cells (Tregs) on pro-inflammatory adhesion molecules, Krüppel-Like Factor-2 (KLF-2) and its downstream transcriptional targets in human umbilical vein endothelial cells (HUVECs) impaired by ox-LDL and the mechanisms of it. Methods and results: HUVECs were cultured in the continuous presence of ox-LDL(0 mg/L,25 mg/L,50 mg/L,100 mg/L) for 4, 6, 12 and 24 hours to allow identification of early-and late-induced genes, respectively, whereas non-stimulated controls were taken at 0 hours. The expression of pro-inflammatory adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), E-selectin, KLF-2 and its target genes eNOS, PAI-1 were determined by real time RT-PCR and/or western-blot analysis. Expression of pro-inflammatory adhesion molecules, KLF-2, eNOS and PAI-1 in HUVEC cultured alone or with anti-CD3 mAbs activated Tregs, followed by addition of ox-LDL (50 mg/L) for 6 hours, are compared to expression levels in control cultures. Ox-LDL treated HUVECs increased pro-inflammatory adhesion molecules expression, as well as increased PAI-1 but decreased eNOS expression accompanied with significant downregulating of KLF-2 at a dose and time dependent manner. Furthermore, ox-LDL increased pro-inflammatory adhesion molecules but inhibited KLF2 expression was reversed by addition of Tregs. Small interfering RNA reduced endogenous KLF-2 expression and partly reversed the suppressive effect of Tregs on HUVECs activation, which strongly implicate KLF-2 as a transcriptional regulator of the Tregs-mediated effects in endothelial cells. Mechanism studies reveal that Treg-mediated KLF2 expression in HUVECs impaired by ox-LDL requires cell contact as well as soluble factors. Conclusions: Tregs could protect endothelial function that is largely dependent on KLF2 and its downstream transcriptional targets regulation involving cell-to-cell contact and soluble factors. Copyright © 2011 S. Karger AG, Basel.


Wei S.-J.,Wuhan General Hospital of PLA | Cai X.-H.,Wuhan General Hospital of PLA | Chen X.,Shanghai Institute of Technology | Chen D.,Shanghai Institute of Technology | Chen J.-D.,Shanghai Institute of Technology
Gongneng Cailiao yu Qijian Xuebao/Journal of Functional Materials and Devices | Year: 2012

Magnetic based capture of CTCs in microchip provides specific selection and high recovery rates with high purity. However, conventional perpendicular capture mode, which applies the magnetic field perpendicular to the flow field, shows lower capture rate under high flow field. In this paper, we suggest that the cell be captured in magnetic microchip may experience two stages which are lateral displacement stage and immobilization stage. Simulation by COMSOL and experiments were used to investigate the hydrodynamic force and magnetic force during these two stages. The data showed that the cell capture is greatly influenced by hydrodynamic force under the perpendicular capture mode. We also proposed a novel parallel capture mode design for CTC microfluidic chip. Experiment showed that this new type of chip can operated at a flow rate up to 6ml/h.


Yin Z.-G.,Chongqing Medical University | Cui M.,Chongqing Medical University | Cui M.,Wuhan General Hospital of PLA | Zhou S.-M.,Chongqing Medical University | And 3 more authors.
European Journal of Neurology | Year: 2014

Background and purpose: Metabolic syndrome (MetS) has been reported to be associated with silent lacunar infarction, which is highly related to white matter lesions (WMLs). However, little is known about the relationship between MetS and the prevalence of WMLs. The association between MetS, its components and WMLs in middle-aged and elderly patients was investigated. Methods: Consecutive patients aged 50 years and older were prospectively enrolled in this study. All participants underwent magnetic resonance imaging scans to assess the presence and severity of WMLs. The MetS was defined according to the updated National Cholesterol Education Program's Adult Treatment Panel III criteria. Multivariate logistic regression analyses were performed to examine the relationship between MetS, its components and WMLs. Results: A total of 852 patients were enrolled in the study. MetS was present in 38.4%. MetS was associated with an increased risk of periventricular WMLs (PVWMLs) and deep WMLs (DWMLs) after multivariable adjustment (odds ratio 3.21, 95% confidence interval 2.26-4.55 for PVWMLs; odds ratio 2.93, 95% confidence interval 2.09-4.09 for DWMLs). Amongst MetS components, elevated blood pressure, elevated fasting blood glucose and low high density lipoprotein cholesterol were associated with PVWMLs, whilst elevated blood pressure and low high density lipoprotein cholesterol were related to DWMLs. Conclusions: Our findings demonstrate that MetS is associated with the prevalence of PVWMLs and DWMLs independent of other risk factors in middle-aged and elderly patients. The association between MetS as a cluster and WMLs was not driven by MetS components. © 2014 EAN.


Zhang Z.-Y.,Huazhong University of Science and Technology | Chen X.-P.,Huazhong University of Science and Technology | Lu Q.-P.,Wuhan General Hospital of PLA
Frontiers of Medicine in China | Year: 2010

The inhibitory effect of different reperfusion periods 45 min following hepatic ischemia on the expression of cholecystokinin (CCK) and vasoactive intestinal peptide (VIP) in the jejunum and the effect of salvia miltiorrhiza pretreatment were investigated, and the possible mechanism and implications were explored. Eighty rats were randomly divided into four groups: normal control group (CO group), sham-operated group (SO group), ischemia/reperfusion (I/R) injury group (IR group) and salvia miltiorrhiza pretreatment group (SM group). The rat model of I/R was established by using a non-invasive artery clamp to clip (45 min) or relax the hepatic pedicle. In the SM group, saline (40 mL/kg) and salvia miltiorrhiza injection (6 g/kg) were injected via the tail vein 30 min before clipping the hepatic pedicle. In the SO group only the porta hepatis was dissected after laparotomy without clamping the hepatic pedicle. At 0, 3, 12, 24 and 72 h post-reperfusion, respectively, upper jejunum samples were taken for immunohistochemistry of CCK and VIP. It was found that 0 h after I/R, the expression of CCK and VIP in the upper jejunum was upregulated. With prolongation of the reperfusion period, the expression of CCK and VIP was also increased, reached the peak at the 24th h, and gradually returned to the normal level at the 72nd h after reperfusion. The levels of both CCK and VIP in the SM group were lower than those in the IR group. It is suggested that the digestive tract congestion injury caused by liver ischemia can upregulate the expression of CCK and VIP in the jejunum following reperfusion. Salviae pretreatment can partly reduce the increased expression of CCK and VIP in the jejunum in the same period, which might contribute to the early recovery of gastrointestinal motility. © 2010 Higher Education Press and Springer-Verlag Berlin Heidelberg.


Yin Z.-G.,Chongqing Medical University | Li L.,Chongqing Medical University | Cui M.,Wuhan General Hospital of PLA | Zhou S.-M.,Chongqing Medical University | And 2 more authors.
PLoS ONE | Year: 2014

Background: Apolipoprotein A-I (apoA-I), the major protein for high density lipoprotein, is essential for reverse cholesterol transport. Decreased serum levels of apoA-I have been reported to correlate with subcortical infarction and dementia, both of which are highly related to white matter lesions (WMLs). However, the association between apoA-I and WMLs has never been investigated. In this study, we sought to investigate the association between apoA-I and the presence of WMLs in middle-aged and elderly subjects. Methods: Consecutive patients aged 50 years and older of our department were prospectively enrolled in this study (n = 1282, 606 men and 676 women, 65.9±9.4 years). All participants underwent MRI scans to assess the presence and severity of WMLs. Multivariate logistic regression analyses were performed to examine the association of apoA-I with WMLs. Results: Patients with WMLs were older and showed significantly higher proportion of male sex, hypertension, diabetes mellitus, previous stroke, and coronary heart disease whereas levels of total cholesterol, high density lipoprotein cholesterol, and apoA-I were lower. After adjustment for potential confounders, the lowest apoA-I quartile was independently associated with an increased risk of WMLs (odds ratio: 1.87, 95% confidence interval: 1.29-2.72). In sex-specific analyses, this relationship was observed only in women. Conclusions: Our findings demonstrated that apoA-I was inversely associated with the presence of WMLs in middle-aged and elderly subjects. This results suggest that therapies which increase apoA-I concentration may be beneficial to reduce the risk of WMLs, dementia and stroke. © 2014 Yin et al.

Loading Wuhan General Hospital of PLA collaborators
Loading Wuhan General Hospital of PLA collaborators