The Peoples Hospital of Jilin Province

Changchun, China

The Peoples Hospital of Jilin Province

Changchun, China
SEARCH FILTERS
Time filter
Source Type

Cong X.-Q.,Jilin University | Li Y.,The Peoples Hospital Of Jilin Province | Zhao X.,Jilin University | Dai Y.-J.,The Friendship Hospital of Linjiang | Liu Y.,Jilin University
Journal of Cardiovascular Translational Research | Year: 2015

Bone marrow stem cells (BMSCs) have been used to treat patient with ST-segment elevation myocardial infarction (STEMI) via intracoronary route. We performed a meta-analysis to evaluate the short-term efficacy and safety of this modality. Seventeen randomized controlled trials (RCTs) of BMSC-based therapy for STEMI, delivered with 9 days of reperfusion and followed up shorter than 12 months, were identified by systematic review. Intracoronary BMSC therapy resulted in an overall significant improvement in left ventricular ejection fraction (LVEF) by 2.74 % (95 % confidence interval (CI) 2.09–3.39, P < 0.00001, I2 = 84 %) at 3–6-month follow-up and 5.1 % (95 % CI 4.16–6.03, P < 0.00001 and I2 = 85 %) at 12 months. The left ventricular end-systolic volume (LVESV) and wall motion score index (WMSI) were also reduced at 3–6 months. At 12 months, left ventricular end-diastolic volume (LVEDV), LVESV, and WMSI were significantly reduced in BMSC group. In conclusion, intracoronary BMSC therapy at post-STEMI is safe and effective in patient with acute STEMI. © 2015, Springer Science+Business Media New York.


Yang L.,The Peoples Hospital of Jilin Province | He J.-T.,Jilin University | Guan H.,The Peoples Hospital of Jilin Province | Sun Y.-D.,The Peoples Hospital of Jilin Province
Asian Pacific Journal of Cancer Prevention | Year: 2013

AKT1 is a member of the serine/threoine AGC protein kinase family involved in thyroid cancer metabolism, growth, proliferation and survival. It is overexpressed in thyroid tumors. In this study, we designed two AKT1 specific DNAzymes (DRz1 and DRz2) that target AKT1 mRNA. The results showed that DRz1 could decrease the expression of AKT1 by 58%. Furthermore, DRz1 significantly inhibited cell proliferation, induced apoptosis and inhibited invasion in SW597 cells. In addition, down-regulation of survivin expression was associated with decreased caspase-3, VEGF and MMP2 in SW597 cells after 24 h. In our study, the efficacy of DRz1 in decreasing AKT1 protein levels were better than DRz2. AKT1-DRz1 might have anti-tumorigenic activity and may provide the basis for a novel therapeutic intervention in thyroid cancer treatment.


Liu X.,Jilin University | Ye F.,Mount Sinai School of Medicine | Xiong H.,Mount Sinai School of Medicine | Hu D.,Tissue Culture Center | And 8 more authors.
Inflammation | Year: 2014

Diabetic retinopathy shares some similarity with chronic inflammation and Müller cells dysfunction may play an important role in its initiation and progression since these cells are thought to be a major source of inflammatory factors. The goal of this study was to examine the effect of cytokines on human retinal Müller cells and to understand the underlying signal transduction pathways regulating interleukin-8 (IL-8) expression. In this study, human MIO-M1 cells were treated with interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-8, vascular endothelial growth factor (VEGF), interferon-gamma (IFN-γ), glucose, or mannitol, followed by examination of their IL-8 protein and mRNA levels by Western blotting and PCR, respectively. After treatment with IL-1β, the levels of phosphorylated p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 3 (STAT3) were measured. IL-8 was also measured by Western blotting and ELISA following Müller cell culture with IL-1β and specific inhibitors of the p38 MAPK, ERK1/2, JNK, or JAK2 pathways. The results showed that IL-1β was a potent inducer of IL-8 expression in MIO-M1 cells, although a relatively small increase was induced by TNF-α. IL-6, IL-8, VEGF, and IFN-γ did not modify IL-8 expression. Increase of IL-8 expression was accompanied by a significant increased phosphorylation of p38 MAPK, ERK, and JNK, but not of JAK2 and STAT3. Furthermore, inhibitors of p38 MAPK and MEK1/2, but not for JNK and JAK2, significantly inhibited IL-8 expression. In conclusion, IL-1β potently stimulates IL-8 expression in Müller cells mainly through the p38 MAPK and ERK1/2 pathways. © 2014, Springer Science+Business Media New York.


Du B.,Jilin University | Liu S.,Jilin University | Cui C.,Changchun University of Chinese Medicine | Wang S.,The Peoples Hospital of Jilin Province | Cui W.,Jilin University
Journal of Diabetes | Year: 2013

Background: So far, studies on the association between the glucose transporter 1 (GLUT1) rs841853 polymorphism and type 2 diabetes mellitus (T2DM) risk have generated considerable controversy. The present study was performed to clarify the association of this genetic variation with T2DM. Methods: A comprehensive literature search of electronic databases was conducted to obtain articles focused on the relationship between the GLUT1 rs841853 polymorphism and T2DM, followed by a systemic meta-analysis. Results: Fourteen articles and 19 individual studies were included for analysis. Main analyses revealed extreme heterogeneity and random effect pooled odds ratios (OR) were weakly significant in allele contrast (OR 1.28; 95% confidence interval [CI] 1.01, 1.63; P=0.04) and dominant model (OR 1.52; 95% CI 1.19, 1.94; P=0.0008) for T allele. Subgroup analyses for Caucasians showed marginal positive results in the dominant model. However, analyses for Asians yielded an obvious relationship to T2DM risk in all genetic models. Interestingly, T allele even seemed to be a protective factor against the development of T2DM in Blacks in allele contrast. Sensitivity analyses did not alter materially for most comparisons and no publication bias was found in this meta-analysis. Conclusions: The results of the present meta-analysis provide evidence that the GLUT1 rs841853 polymorphism may confer increased susceptibility to T2DM in Asians. However, there is no currently available strong evidence supporting the association between this genetic variation and T2DM in Caucasians, Blacks, or the overall population. © 2013 Wiley Publishing Asia Pty Ltd and Ruijin Hospital, Shanghai Jiaotong University School of Medicine.


Liu X.,Jilin University | Ye F.,Mount Sinai School of Medicine | Xiong H.,Mount Sinai School of Medicine | Hu D.-N.,Tissue Culture Center | And 12 more authors.
Experimental Cell Research | Year: 2015

IL-6 plays an important role in various inflammatory ocular diseases, including diabetic retinopathy. Müller cells are the major source of inflammatory mediators, including IL-6, in the retina. However, the mechanism of regulating IL-6 production in these cells remains unclear. Examination of signaling pathways in human retinal Müller cells (MIO-M1 cell line) cultured with IL-1β, TNF-α, IL-6, IL-8, VEGF, IFN-γ, glucose or mannitol showed that IL-1β was the most potent stimulator of IL-6 production. In addition, IL-1 β also increased NF-κB p50 protein level and phosphorylation of p38 MAPK, ERK1/2 and c-Jun. Induction of IL-6 production by IL-1β was significantly reduced by addition of p38 MAPK (SB203580), MEK1/2 (U0126) or NF-κB (BAY11-7082) inhibitors, with the highest effect being observed with SB203580. To explore the specific elements in IL-6 promoter responsible for IL-1β-induction of IL-6 expression, a series of plasmids bearing various IL-6 promoter mutations were transiently expressed in MIO-MI cells cultured in the presence or absence of IL-1β (10. ng/ml) and/or SB203580 (10. μM). Results showed that IL-6 promoter activity of the parent pIL-6-Luc651 was significantly enhanced by IL-1β, but the level was significantly attenuated by SB203580. Furthermore, the IL-6 promoter activity was also reduced upon deletion of NF-κB, AP-1 or C/EBP binding sites, with NF-κB deletion being the greatest. These results are the first demonstration that IL-1β induces IL-6 production in Müller cells by activation of IL-6 promoter activity predominantly through the p38 MAPK/NF-κB pathway. © 2014 Elsevier Inc.


PubMed | Jilin University and The Peoples Hospital of Jilin Province
Type: Journal Article | Journal: Journal of biomaterials science. Polymer edition | Year: 2016

The application of Doxorubicin (DOX) in the chemotherapy for lymphoma is seriously hampered by the side effects of DOX, especially the cardiotoxicity and nephrotoxicity. Nanoscale micelle as a promising drug delivery system has gained more and more interest in malignancy chemotherapy. In this study, we successfully fabricated DOX-loaded stereocomplex micelle (SCM/DOX) from the equimolar mixture of the enantiomeric four-armed poly(ethylene glycol)-polylactide (PDM and PLM) copolymers. The SCM/DOX showed proper hydrodynamic size of ~90nm and slow DOX release in phosphate-buffered saline at pH 7.4. The antitumor activities of DOX, PDM/DOX, PLM/DOX, and SCM/DOX toward lymphoma cells were tested in vitro and in vivo. Our data demonstrated that the SCM/DOX more effectively inhibited the cell proliferation than PDM/DOX, PLM/DOX, and free DOX in vitro. In the in vivo antitumor test, the SCM/DOX more effectively inhibited the growth of EL4 lymphoma, too. In addition, the body weight loss caused by SCM/DOX was alleviated than DOX. More importantly, the cardiotoxicity, nephrotoxicity, and hepatotoxicity caused by DOX in mice were obviously attenuated compared to the free DOX treatment group. Taken together, all the results indicated that the SCM/DOX could inhibit the growth of EL4 lymphoma cells and attenuate the toxicity of DOX more efficiently, which suggested SCM/DOX was promising for the prevention and treatment of lymphoma.


PubMed | Jilin University, Chinese People's Liberation Army and The Peoples Hospital of Jilin Province
Type: Journal Article | Journal: BMC pulmonary medicine | Year: 2016

No systemic evaluation of asthma control in Jilin Province has been reported. Asthma control might provide the basis for asthma management in this region. A multicenter hospital-based cross-sectional study was performed to investigate the asthma control and related factors for severe asthma exacerbations in patients with moderate or severe asthma in Jilin Province, China.The study enrolled 1546 patients in five grade one general hospitals from January to December 2013. Asthma medication, patient self-management, asthma control test (ACT) scores and frequency of severe asthma exacerbations during the follow-up (12months) were collected via a follow-up questionnaire.In the study, 889 patients provided a complete follow-up questionnaire. Severe asthma exacerbations occurred in 54.89% of patients. ACT score 15, asthma medication3months, severe asthma, income level lower than average Per Capita Disposable Income (PCDI) and a lower educational level were risk factors of a severe exacerbation.Poor adherence to asthma medication, poor asthma symptom control, lower income, a low educational level might be possible reasons for the high incidence of severe asthma exacerbations and poor asthma control in Jilin Province of China.


PubMed | Jilin University, Jilin Medical College and The Peoples Hospital of Jilin Province
Type: Journal Article | Journal: International journal of oncology | Year: 2014

The mechanisms underlying cisplatin resistance in tumors are not fully understood. Previous studies have reported that cellular resistance to oxidative stress is accompanied by resistance to cisplatin. However, the relationship between the resistance to oxidative stress and cisplatin drug resistance in human ovarian cancer cells (HOCCs) is not clear. Here, we reveal a critical role for the multifunctional protein p62/SQSTM1 in cisplatin resistance in human ovarian cancer cells (HOCCs). p62/SQSTM1 (sequestosome1) plays important roles in cell differentiation, proliferation and as an antiapoptotic molecule. We found that cisplatin-resistant SKOV3/DDP cells express much higher levels of p62 than do cisplatin-sensitive SKOV3 cells. The protein p62 can activate the Keap1-Nrf2-ARE signaling pathway and induce the expression of antioxidant genes in SKOV3/DDP cells. Knockdown of p62 resensitizes SKOV3/DDP cells to cisplatin. Collectively, our data indicate that cisplatin resistance in HOCCs is partially attributable to their high expression of p62, which plays an important role in preventing ROS stress-induced apoptosis by regulating the Keap1-Nrf2-ARE signaling pathway.


PubMed | New York University, The Peoples Hospital of Jilin Province, Jilin University, Mount Sinai School of Medicine and 2 more.
Type: Journal Article | Journal: Experimental cell research | Year: 2015

IL-6 plays an important role in various inflammatory ocular diseases, including diabetic retinopathy. Mller cells are the major source of inflammatory mediators, including IL-6, in the retina. However, the mechanism of regulating IL-6 production in these cells remains unclear. Examination of signaling pathways in human retinal Mller cells (MIO-M1 cell line) cultured with IL-1, TNF-, IL-6, IL-8, VEGF, IFN-, glucose or mannitol showed that IL-1 was the most potent stimulator of IL-6 production. In addition, IL-1 also increased NF-B p50 protein level and phosphorylation of p38 MAPK, ERK1/2 and c-Jun. Induction of IL-6 production by IL-1 was significantly reduced by addition of p38 MAPK (SB203580), MEK1/2 (U0126) or NF-B (BAY11-7082) inhibitors, with the highest effect being observed with SB203580. To explore the specific elements in IL-6 promoter responsible for IL-1-induction of IL-6 expression, a series of plasmids bearing various IL-6 promoter mutations were transiently expressed in MIO-MI cells cultured in the presence or absence of IL-1 (10ng/ml) and/or SB203580 (10M). Results showed that IL-6 promoter activity of the parent pIL-6-Luc651 was significantly enhanced by IL-1, but the level was significantly attenuated by SB203580. Furthermore, the IL-6 promoter activity was also reduced upon deletion of NF-B, AP-1 or C/EBP binding sites, with NF-B deletion being the greatest. These results are the first demonstration that IL-1 induces IL-6 production in Mller cells by activation of IL-6 promoter activity predominantly through the p38 MAPK/NF-B pathway.


PubMed | Jilin University and The Peoples Hospital of Jilin Province
Type: Journal Article | Journal: Biological trace element research | Year: 2016

Endoplasmic reticulum stress (ERS)-induced unfolded protein response (UPR) and the subsequent cell deaths are essential steps in the pathogenesis of diabetic cardiomyopathy (DCM), a main cause of diabetics morbidity and mortalities. The bis(maltolato)oxovanadium(IV) (BMOV), a potent oral vanadium complex with anti-diabetic properties and insulin-mimicking effects, was shown to improve cardiac dysfunctions in diabetic models. Here, we examined the effects of BMOV on UPR pathway protein expression and apoptotic cell deaths in both high glucose-treated cardiac H9C2 cells and in the hearts of diabetic rats. We show that in both the high glucose-treated cardiac cells and in the hearts of streptozotocin (STZ) diabetic rats, there was an overall activation of the UPR signaling, including both apoptotic (e.g., the cascades of PERK/EIf2/ATF4/CHOP and of IRE1/caspase 12/caspase 3) and pro-survival (GRP78 and XBP1) signaling. A high amount of apoptotic cell deaths was also detected in both diabetic conditions. The administration of BMOV suppressed both the apoptotic and pro-survival UPR signaling and significantly attenuated apoptotic cell deaths in both conditions. The overall suppression of UPR signaling by BMOV suggests that the drug protects diabetic cardiomyopathy by counteracting reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress. Our findings lend support to promote the use of BMOV in the treatment of diabetic heart diseases.

Loading The Peoples Hospital of Jilin Province collaborators
Loading The Peoples Hospital of Jilin Province collaborators