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Wang J.,Academy of Military Medical Science | Yi X.,Academy of Military Medical Science | Liu M.,Academy of Military Medical Science | Zhou Q.,Red Cross | And 5 more authors.
PLoS ONE | Year: 2015

It has been hypothesized that the cytosolic esterase-induced fluorescence intensity (CEIFI) from carboxy dimethyl fluorescein diacetate (CMFDA) in platelets may related to platelet functions. In the present study, we measured the change of CEIFI in platelets during storage, and examined the correlations of CEIFI with the in vitro functionality of stored platelets, including the ADP-induced aggregation activity, hypotonic shock response, expression of CD62P as well as platelet apoptosis. The CEIFI of fresh platelets, when tested at 10 ìM CMFDA, the mean fluorescence intensity index (MFI) was 305.9 ± 49.9 (N = 80). After 1-day storage, it was 203.8 ± 34.4, the CEIFI of the stored platelets started to decline significantly, and reduced to 112.7 ±27.7 after 7-day storage. The change in CEIFI is highly correlated to all four functional parameters measured, with the correlation coefficients being 0.9813, 0.9848, -0.9945 and -0.9847 for the ADP-induced aggregation activity, hypotonic shock response (HSR), expression of CD62P and platelet apoptosis respectively. The above results show that the CEIFI measurement of platelets represents well the viability and functional state of in vitro stored platelets. This may be used as a convenient new method for quality evaluation for stored platelets if this result can be further validated by the following clinical trials. Copyright: © 2015 Wang et al.

Lu H.,Navy General Hospital | Xu M.,Second Artillery General Hospital PLA | Wang F.,Navy General Hospital | Liu S.,Navy General Hospital | And 3 more authors.
Experimental and Molecular Medicine | Year: 2016

Periodontitis is a common chronic inflammatory disease. Recent studies have shown that chronic stress (CS) might modulate periodontal disease, but there are few models of CS-induced periodontitis, and the underlying mechanisms are unclear. The present study established a rat model of periodontitis associated with CS induced by nylon thread ligatures. The severity of periodontitis was evaluated in this model by radiographic and pathological examination. The inflammatory reaction indicated by the elevated serum levels of interleukin (IL)-1β, IL-6 and IL-8 was assessed by enzyme-linked immunosorbent assay. Toll-like receptor-4 (TLR4) and glucocorticoid receptor (GR) expressions were detected by reverse transcriptase-PCR and western blotting. Open-field tests and serum corticosterone were used to evaluate CS. The results showed that CS induced behavioral changes and increased corticosterone levels of the animals with periodontitis. CS stimulation markedly increased alveolar bone loss, periodontal pocket depth and the number of plaques. It also enhanced the inflammatory reaction. These results suggest that CS accelerated the ligature-induced pathological changes associated with periodontitis. Further analysis of the mechanisms involved showed that GR expression was significantly downregulated in periodontal tissues of the animals undergoing CS. Blocking GR signaling in lipopolysaccharide and corticosteroid-treated human periodontal ligament fibroblast cells in vitro significantly upregulated the expression of p-Akt (protein kinase B) and TLR4, promoted nuclear factor-κB activity and increased levels of IL-1β, IL-6 and IL-8. This research suggests that CS might accelerate the pathological progression of periodontitis by a GR signaling-mediated inflammatory response and that this may be a potential therapeutic target for the treatment of periodontal disease, particularly in patients with CS. © 2016 KSBMB.

Liu M.,Shanghai University | Zhang H.,Second Artillery General Hospital PLA | Zhang Q.,Shanghai University | Huang C.,Shanghai University | And 2 more authors.
American Journal of Translational Research | Year: 2015

Preconditioning with ischemia/hypoxia (IPC/HPC) or clinically available volatile anesthetics such as isoflurane (Iso-PC) could activate cardioprotective signaling pathways, thereby reducing myocardial ischemia/reperfusion (IR) injury. However, their molecular targets remain elusive. We herein investigated the roles of syntaxin 1A (Stx-1A) in cardiomyocyte protection induced by HPC and Iso-PC. Both in vivo myocardial IR model and in vitro cardiomyocyte hypoxia/reoxygenation (HR) model were used to test the effects of IR/HR, IPC/HPC and Iso-PC on Stx-1A protein expression. Stx-1A knockdown and overexpression in cardiomyocytes were achieved by adenovirus infection to define the relationship between Stx-1A levels and IPC/Iso-PC-induced cardioprotection. Cardiac troponin T (cTnT), cell apoptosis rate, and cell viability were introduced as indicators for cardiomyocyte HR injury. Changes of cardioprotective signaling pathways activities including PI3K/AKT/GSK3β, ERK1/2, STAT3 and PKC were also detected using Western blot. Rat cardiomyocyte Stx-1A was upregulated 4 hours after IR or HR. IPC/HPC as well as Iso-PC further increased Stx-1A expression compared with IR/HR. Stx-1A knockdown was accompanied with more cell apoptosis and decreased cell viability while overexpression of Stx-1A seemed cardioprotective. Iso-PC induced decrease in cell apoptosis and increase in cell viability but not HPC-induced cardioprotection was reversed by Stx-1A shRNA transfection. No difference in cell apoptosis or cell viability was found before and after Stx-1A overexpression in each group. Moreover, Stx-1A knockdown were accompanied with increased PI3K/AKT/GSK3β activities irrespective of the treatments. Stx-1A is cardioprotective and a potential target of isoflurane induced cardioprotection. Further studies are needed to test whether stx-1A is regulated by AKT/GSK3β signaling. © 2015, E-Century Publishing Corporation. All rights reserved.

Liu Q.,Second Artillery General Hospital PLA | Song Y.,Chinese PLA General Hospital | Xu X.,Second Artillery General Hospital PLA | Jin Z.,Interventional Radiology | And 2 more authors.
Digestive Diseases and Sciences | Year: 2014

Background and Aim: Sinistral portal hypertension (SPH) is a rare cause of upper gastrointestinal hemorrhage. Besides splenectomy, there is no consensus on the role of sclerotherapy and splenic embolization for bleeding gastric varices (GVs). This retrospective study summarizes our experience in managing GV bleeding from SPH in patients with pancreatic diseases. Methods: Patients with pancreatic diseases who had bleeding GVs from SPH in two tertiary hospitals were reviewed from January 2001 to December 2011. The etiology, clinical manifestations, diagnostic and therapeutic modalities were analyzed. Results: Twenty-one patients (15.2 %) complicating bleeding GVs among 139 patients with SPH secondary to pancreatic diseases were enrolled. The etiologies were acute pancreatitis in one patient, chronic pancreatitis in seven patients, and pancreatic tumors in 13 patients. Emergent endoscopic sclerotherapy was initially performed in five patients, and succeeded in two patients, while one patient died of massive hemorrhage. Initial transcatheter artery embolization using Gianturco coils was successfully performed in six patients. Splenectomy combined with other surgical procedures was undertaken for 15 patients. The patients undergoing artery embolization or splencetomy achieved hemostasis. The survivors had no recurrent bleeding during a median 72-month follow-up period. Conclusions: The incidence of bleeding GVs from SPH is relatively rare. Splenic artery embolization could be selected as a first-line choice for bleeding SPH, especially for patients in poor conditions, and sclerotherapy may not be preferentially recommended. Further studies are required to evaluate the optimum treatment algorithm for bleeding GVs from SPH. © 2014 Springer Science+Business Media.

Yu H.-J.,Second Artillery General Hospital PLA | Wu Y.,Chinese PLA General Hospital | Li F.-S.,Second Artillery General Hospital PLA | Li W.,Second Artillery General Hospital PLA | Jiang Q.-S.,Second Artillery General Hospital PLA
Chinese Journal of Cancer Prevention and Treatment | Year: 2015

OBJECTIVE: To investigate the role of Polo-like Kinase 1(Plk1) in migration of human hepatocellular carcinoma tumor-derived endothelial cells (TEC). METHODS: TEC cell line was cultured in RPMI1640 with 20% fetal bovine serum. siRNA segments targeting Plkl and negative control siRNA were synthesized. The Plk1siRNA group and siRNA negative control group were set in this experiment. siRNA segments targeting Plk1 and negative control siRNA were transfected into TEC cells. Effect of Plk1siRNA on the downregulation of Plk1 protein expression in TEC was evaluated by Western blot. After transfection, the changes in migration of TEC were measured by wound healing and Transwell migration assay. RESULTS: Successful transfection was confirmed using Western blot. Plk1 expression at the protein level in TEC was reduced by the Plk1siRNA segments. In transwell migration assay, the number of TEC crossing through chambers in Plk1siRNA group (130.9±23.0) was lower than that in the siRNA control group(184.9± 26.6), t=-5.943, P<0.001.In wound healing assay, the migration distance of Plk1siRNA group was (17.5±7.0) Pixel in 12 h, which was lower than that in the siRNA control group(72.6±12.4), t=-6.698, P=0.006; and the migration distance of Plk1 siRNA group was (70.9±6.9) Pixel in 24 h, which was lower than that in the siRNA control group(137.9±18.9), t=-5.761, P=0.016. CONCLUSION: Plk1 knocking down by siRNA may inhibit the migration of TEC, suggests that Plk1 might play an important role in the metastasis of human hepatocellular carcinoma tumor-derived endothelial cells. ©, 2015, The Editorial Board of Chinese Journal of Cancer Prevention and Treatment. All right reserved.

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