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Yan H.,Harrison International Peace Hospital | Xi H.,Harrison International Peace Hospital | Wang H.,Harrison International Peace Hospital | Zhang F.,Harrison International Peace Hospital | Cao D.,Harrison International Peace Hospital
International Journal of Clinical and Experimental Medicine | Year: 2017

Purpose: This study aims to investigate the effect of butylphthalide on the prognosis of acute massive cerebral infarction (MCI). Methods: A total of 92 MCI patients, who received inpatient treatment in the Department of Neurology, Harrison International Peace Hospital from February 2011 to December 2013, were enrolled into this study. As a controlled study, patients were randomly divided into two groups: control group (n=46) and treatment group (n=46). Patients in the control group were administered with an intravenous drip of edaravone, while patients in the treatment group were given edaravone combined with butylphthalide capsules. Furthermore, patients in the two groups underwent continuous administration for two weeks as a course of treatment. Improvement of symptoms in the two groups was assessed based on the National Institutes of Health Stroke Scale (NIHSS). The effect of butylphthalide on collateral circulation in the ischemic infarct area was assessed according to the collateral vessel grading standard of susceptibility-weighted imaging (SWI), and these results were analyzed. Results: Symptoms and signs of patients in both the control and treatment groups improved to some extent. Improvement in patients in the treatment group was significantly better than patients in the control group (P<0.05). NIHSS scores of patients in the treatment group were better than that in the control group (P<0.05). Furthermore, SWI collateral vessel display grades of patients in both the control and treatment groups were upgraded, but the number of upgraded cases in treatment group was significantly larger than that in the control group (P<0.05). No obvious adverse reaction occurred in the two groups during the treatment. Conclusion: Butylphthalide exhibited good efficacy in the treatment of MCI, which could effectively improve nerve function defect and promote the re-formation of collateral circulation in the infarct area. © 2017, E-Century Publishing Corporation. All rights reserved.


Li Y.,Harrison International Peace Hospital | Liu X.,Hengshui Blood Center | Guo X.,Harrison International Peace Hospital | Liu X.,Harrison International Peace Hospital | Luo J.,Hebei Medical University
Leukemia Research | Year: 2017

Introduction Extensive studies on SHP-1 protein and SHP-1 mRNA revealed that the diminishment or abolishment of the expression of SHP-1 in leukemias/lymphomas was due to aberrant promoter methylation. Thus far, the mechanism of epigenetic silencing of the SHP-1 tyrosine phosphatase gene that occurs in chronic myelogenous leukemia cells remains poorly understood. Methods The expressions of the target molecules were determined by quantitative real time PCR and western blot, respectively. Bisulfite sequencing PCR was used to detect methylation status of DNA CpG. The lentiviral vectors were applied to modify gene expression. Results In the present study, we found that the promoter 2 of SHP-1 gene is located between positions from −577 bp to +300 bp, and 22 CpG sites contained in positions −353 bp ∼ +182 bp are aberrantly methylated in K562 cells. In vitro, we demonstrated that DNMT1 silencing induced demethylation of the 22 CpG sites located in the SHP-1 promoter and re-expression of SHP-1 gene in K562 cells. Moreover, we proved that the expression levels of DNMT1 and SHP-1 mRNA and protein were negatively correlated in K562 cells and BM aspirates mononuclear cells from CML patients. Conclusion Collectively, these results indicate that DNMT1 mediates aberrant methylation and silencing of SHP-1 gene in chronic myelogenous leukemia cells, and provide a novel therapeutic target for CML. © 2017 Elsevier Ltd


Zheng L.,Harrison International Peace Hospital | Zheng L.,University of Sichuan | Tan W.,Harrison International Peace Hospital | Tan W.,Shanghai JiaoTong University | And 4 more authors.
Cancer Immunology, Immunotherapy | Year: 2014

The anti-ErbB2 antibody trastuzumab has currently been approved for ErbB2-positive gastric cancer. Despite the effectiveness of trastuzumab, resistance is common. Thus, there is an urgent need to overcome trastuzumab resistance. Here, we obtain a trastuzumab-resistant cell line, which is derived from the human gastric cancer NCI-N87 cell line, by modeling the development of acquired resistance in patients. Our data show that combining trastuzumab and cetuximab leads to a significant decrease in EGFR/ErbB2 heterodimers and signaling compared with either antibody alone, and the combination results in greater antitumor activity against the trastuzumab-resistant NCI-N87 cell line, both in vitro and in vivo, suggesting that a combined EGFR/ErbB2 inhibition may overcome trastuzumab resistance. © 2014 Springer-Verlag Berlin Heidelberg.


PubMed | Hebei Medical University, Chongqing Three Gorges University, Cangzhou Peoples Hospital, Military General Hospital of Beijing and 7 more.
Type: Journal Article | Journal: Diabetes, obesity & metabolism | Year: 2016

To compare the efficacy and safety of liraglutide versus sitagliptin as add-on to metformin after 26 weeks of treatment in Chinese patients with type 2 diabetes mellitus (T2DM).This 26-week open-label, active comparator trial (NCT02008682) randomized patients (aged 18-80 years) with T2DM inadequately controlled with metformin [glycated haemoglobin (HbA1c) 7.0-10.0% (53-86 mmol/mol)] 1 : 1 to once-daily subcutaneously administered liraglutide 1.8 mg (n = 184) or once-daily oral sitagliptin 100 mg (n = 184), both as add-on to metformin. The primary endpoint was change in HbA1c from baseline to week 26.Liraglutide was superior to sitagliptin in reducing HbA1c from baseline [8.1% (65 mmol/mol)] to 26 weeks, as evidenced by estimated mean HbA1c change of -1.65% (-18.07 mmol/mol) versus -0.98% (-10.72 mmol/mol), respectively [estimated treatment difference for liraglutide vs sitagliptin of -0.67% (95% CI -0.86, -0.48) or -7.35 mmol/mol (95% CI -9.43; -5.26); p < 0.0001]. More patients receiving liraglutide (76.5%) than sitagliptin (52.6%) achieved the HbA1c target of <7.0% (53 mmol/mol) at week 26 [odds ratio 3.65 (95% CI 2.18, 6.12); p < 0.0001]. Reductions in fasting plasma glucose, 7-point self-measured plasma glucose and body weight were greater with liraglutide than with sitagliptin (p < 0.0001 for all). More patients experienced nausea (14.8% vs 0.5%), diarrhoea (8.2% vs 2.2%) and decreased appetite (10.9% vs 0.5%) with liraglutide than sitagliptin. Two hypoglycaemic episodes were confirmed for liraglutide and one for sitagliptin; none were severe or nocturnal.Liraglutide provided better glycaemic control and greater body weight reduction than sitagliptin when administered as add-on to metformin. More patients had nausea, diarrhoea and decreased appetite with liraglutide versus sitagliptin.


Tang S.-Y.,University of South China | Zhong M.-Z.,Central South University | Yuan G.-J.,Chinese People's Liberation Army | Hou S.-P.,Harrison International Peace Hospital | And 3 more authors.
Oncology Reports | Year: 2013

We investigated the effect of casticin on apoptosis induced by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). We found that casticin potentiated TRAIL-induced apoptosis in human colon cancer cells. Casticin downregulated cell survival proteins including Bcl-xL, Bcl-2, survivin, XIAP and cFLIP, and induced death receptor 5 (DR5), but had no effect on DR4 and decoy receptors (DcR1 or DcR2). Deletion of DR5 by siRNA significantly reduced the apoptosis induced by TRAIL and casticin. In addition, casticin induced reactive oxygen species (ROS) generation in a dose-dependent manner. Collectively, the present study showed that casticin potentiates TRAIL-induced apoptosis through downregulation of cell survival proteins and induction of DR5 mediated by ROS.


Yang B.,Harrison International Peace Hospital | Tan Z.,Jilin University | Song Y.,Jilin University
International Journal of Clinical and Experimental Medicine | Year: 2015

Objective: This study aims to identify the target gene of hsa-miR-195 and to research the molecular mechanism of hsa-miR-195 which is through its target genes in the colorectal cancer invasion and metastasis. Methods: We used biological informatics (RNAhybrid and Target Scan analysis database) to predict the target genes of hsa-miR-195. Collected colon cancer tissues from clinical colorectal cancer patients by surgical removal of the carcinoma and control tissues, and researched the expression of Bcl-2 in tissues by immunohistochemical. Next, Real-time PCR was used to research the expression of hsa-miR-195 in Caco-2 and NCM460 cell line. hsa -miR-195 Mimics was transient transfered to Caco-2 cells, western blot was used to analysis the expression changes of Bcl-2. To analysis the possibility that hsa-miR-195 can affect the invasive ability of tumor cells by Bcl-2, we transferred hsa-miR-195 Mimics and Bcl-2 expression plasmid, and used the cell invasion experiment to discusses hsa-miR-195 effect on the ability of tumor cell invasion. Results: the immunohistochemical results showed that, the semi-quantitative parameters for the Bcl-2: control by 0.89 ± 0.51, 6 colon cancer by 31 ± 0.79. The expression of has-miR-195 in Caco-2 is 0.39 ± 1.5 while the value in control is2.01 ± 0.2, **P < 0.01. Conclusion: In colorectal cancer, has-miR-195 can promote cell apoptosis and inhibit the invasion and metastasis by inhibiting the expression of Bcl-2. © 2015, Int J Clin Exp Med. All rights reserved.


Li M.,Harrison International Peace Hospital | Dong F.,Hebei Medical University | Zhang F.,Hebei Medical University
International Journal of Clinical and Experimental Medicine | Year: 2016

Physical exercise could exert neuroprotection in both human and animals. However, the exact mechanism of the neuroprotective effect is still not very clear. This study was to explore the possible signal pathway related to the neuroprotective effect of pre-ischemic exercise for ischemic stroke. Thirty-six rats were randomly divided into three groups (n = 12/group): middle cerebral artery occlusion (MCAO) group, exercise with MCAO group and sham surgery group. After treadmill training for three weeks, the MCA was occluded for 1.5 hours so as to induce ischemic stroke, followed by reperfusion. Forty-eight hours after reperfusion, six rats in each group were estimated for neurological deficits and then decapitated to calculate the infarct volume. The rest rats in each group were sacrificed to detect the expression level of phosphor-MEK1/2, MEK1/2 and PI3K (n = 6). The results in our study demonstrated that pre-ischemic treadmill training reduced brain infarct volume and neurological deficits, also alleviated the over expression of phosphor-MEK1/2 after ischemic stroke. The expression level of PI3K was up-regulated by exercise preconditioning. In summary, pre-ischemic exercise mitigated brain damage in the rat brain after ischemic stroke, involving in the regulation of MEK1/2 and PI3K. © 2016, E-Century Publishing Corporation. All rights reserved.


Li Y.,Hebei Medical University | Li Y.,Harrison International Peace Hospital | Yang L.,Hebei Medical University | Pan Y.,Hebei Medical University | And 3 more authors.
Oncology Reports | Year: 2014

Despite the unprecedented success of tyrosine kinase inhibitors (TKIs) in treating chronic myelogenous leukemia (CML), some patients nevertheless progress to advanced stages of the disease. Thus far, the biological basis leading to CML progression remains poorly understood. SH2-containing tyrosine phosphatase 1 (SHP-1) is reported to bind to p210BCR.ABL1 and to function as a tumor suppressor. Furthermore, its substrates have been found to be essential for p210BCR-ABL1 leukemogenesis or CML progression. In the present study, we found that SHP-1 mRNA and protein levels were markedly decreased in patients in the accelerated and blastic phases of CML (AP-CML and BP-CML) compared to those in the chronic phase (CP-CML). In.vitro, we demonstrated that overexpression of SHP-1 reduced p210BCR-ABL1 protein expression and activity in the K562 CML cell line and negatively regulated the AKT, MAPK, MYC and JAK2/STAT5 signaling pathways. Moreover, using a methylation-specific polymerase chain reaction (MSP) assay, abnormal methylation of the SHP-1 gene promoter region was found both in K562 cells and bone marrow (BM) or peripheral blood (PB) cells from AP-CML and BP-CML patients. In conclusion, our findings suggest that decreased expression levels of SHP-1 caused by aberrant promoter hypermethylation may play a key role in the progression of CML by dysregulating BCR-ABL1, AKT, MAPK, MYC and JAK2/STAT5 signaling.


Objective To evaluate the clinical value of tube-sealing with norvancomycin and heparin saline mixture for prevention of central venous catheter- related infection (CRI). Methods A prospective randomized controlled trial was performed. 120 patients who were admitted to department of critical care medicine from January 2012 to January 2014 were included, with their subclavian vein catheterization installation time longer than 48 hours, age over 18 years and younger than 80 years, and acute physiology and chronic health evaluation II (APACHE II) score reaching 10-29. The patients were divided into two groups using a random number table, and finally 116 patients were enrolled. Norvancomycin and heparin saline mixture were used for tube sealing in the intervention group (n=56), while only heparin saline was used in the control group (n=60). The incidence of CRI, catheter correlated spectrum of pathogens, adverse events, mortality, hospital day, catheter retention time, and hospital costs were compared between two groups. Results 1 There was no significant difference in the incidence of CRI between intervention group and control group [7.14% (4/56) vs. 8.33% (5/60), x;2=0.058, P=1.000]. There was no catheter pathogenic colonization in the intervention group, but there were 2 cases of catheter pathogenic colonization in control group. 2 A total of 7 pathogens were found in two groups. Three cases with pathogenic bacteria was found in the intervention group, with 1 case of Pseudomonas aeruginosa, 1 case Acinetobacter baumannii, and 1 case fungi. Staphylococcus aureus, Staphylococcus epidermidis, fungi, and Acinetobacter baumannii was found in the control group, with 1 case of each. There was no significantly statistical difference between two groups (all P>0.05), but there was a decreasing trend of Gram-positive cocci infection in the intervention group. 3 There was no significant difference in the catheter thrombosis, local bleeding or hematoma, catheter dislocation and other adverse events between intervention group and control group [21.43% (12/56) vs. 23.33% (14/60), x2=0.060, P=0.806]. 4 There were no significant differences in mortality [7.14% (4/56) vs. 8.33% (5/60), x2=0.058, P=1.000], hospital day (days: 35.9±15.2 vs. 34.1±16.3, t=16.330, P=0.620), catheter retention time (days: 25.0±4.5 vs. 24.5±5.1, t=26.427, P=2.560) and cost of hospitalization (10 thousand Yuan: 3.42±1.22 vs. 3.72±1.30, t=13.215, P=1.560) between intervention group and control group. Conclusions For patients with central venous catheter, application norvancomycin with heparin saline mixture for tube sealing did not reduce the incidence of CRI, the incidence of adverse events and mortality, does not reduce hospitalization time, catheter retention time and hospital costs, but may reduce the catheter colonization and infection of Gram-positive bacteria.


Li P.,Harrison International Peace Hospital
Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery | Year: 2013

To investigate the clinical significance of applicating posterior internal fixation for regulating spinal curvature in thoracolumbar compression fractures. Between May 2006 and May 2009, 63 patients with thoracolumbar compression fractures were treated, and the clinical data were retrospectively analyzed. Among them, 33 patients received traditional posterior internal fixation in control group; 30 patients underwent posterior internal fixation with spinal curvature correction under C-arm X-ray device in trial group. There was no significant difference in age, gender, cause of injury, injured segment, grade of fracture, and time from injury to operation between 2 groups (P > 0.05). The Cobb angle, height of injured vertebral body, and disc height were measured by X-ray examination; loosening and breakage of internal fixation were observed and compared between 2 groups. The recovery rate was calculated according to pre- and post-operative visual analogue scale (VAS) and Oswestry disability index (ODI) scores for each patient. All cases were followed up 20-45 months (mean, 31 months). The postoperative VAS score, ODI, Cobb angle, height of injured vertebral body, and disc height were improved significantly when compared with preoperative values in 2 groups (P < 0.05). At last follow-up, VAS and ODI scores of trial group were significantly better than those of control group (P < 0.05); loss of Cobb angle was (2.1 +/- 1.7) degrees in trial group and (4.2 +/- 3.2) degrees in control group, showing significant difference (t=1.457, P=0.000); loss of disc height was (1.4 +/- 1.2) mm in trial group and (3.4 +/- 2.3) mm in control group, showing significant difference (t=9.336, P= 0.000); loss of height of injured vertebral body was 1.8% +/- 0.6% in trial group and 5.4% +/- 2.1% in control group, showing significant difference (t=3.435, P=0.000). Broken screw and loosening screw occurred in 1 case of control group, respectively (6.1%), but no broken or loosening screw in trial group, showing significant difference (P=0.000). Application of posterior internal fixation for regulating spinal curvature has a good clinical effectiveness. The postoperative spinal curvature, the height of injured vertebral body, and disc height can be improved significantly and low back pain can be recovered satisfactorily. The modified technique is also effective in reducing broken and loosening incidence of the fixation system.

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