Liaoning Cancer Hospital Institute

Nomhon, China

Liaoning Cancer Hospital Institute

Nomhon, China
SEARCH FILTERS
Time filter
Source Type

Wang X.,China Medical University at Heping | Yu T.,Liaoning Cancer Hospital & Institute | Yan Q.,China Medical University at Heping | Wang W.,Liaoning Cancer Hospital & Institute | And 3 more authors.
Molecular Neurobiology | Year: 2016

Neuromyelitis optica (NMO) is an autoimmune disorder. In pathogenesis, NMO-immunoglobulin G (NMO-IgG) selectively binds to aquaporin-4 (AQP4) and resulted in neuritis, myelitis, and brain lesion. Fc receptor-like 3 (FCRL3) gene encodes a member of the immunoglobulin receptor superfamily, which plays an important part in regulating immune activities. This study aimed at investigating the association between FCRL3 polymorphisms and NMO susceptibility and, hopefully, to contribute to the development of novel methods for diagnosis and treatment of NMO. We selected 150 NMO patients and 300 healthy controls from the Chinese population. Tag single nucleotide polymorphisms (SNPs) were identified with reference to CBI-dbSNP and HapMap databases. DNA were extracted and amplified. Matrix-assisted laser desorption-ionization time-of-flight mass spectrometry (MALDI-TOF-MS) was applied to determine the polymorphisms. χ2, odds ratio (OR), and 95 % confidence interval (95 % CI) were presented to evaluate genotype distribution and association between SNPs and NMO susceptibility. Six out of 15 SNPs were selected according to the filter. No significant altered genotype distribution was observed concerning -11G>C, -166C>T, -219G>C, and -1629C>G polymorphisms. The G allele of -1901A>G variation was demonstrated to be more frequent in patients compared with controls (P < 0.001). The T allele of -658C>T polymorphism was significantly more prevalent in NMO patients than controls (P = 0.009). In summary, the study revealed that the G allele in -1901A>G polymorphism and T allele in -658C>T polymorphism are genetic risk factors for NMO in the Chinese population. Further research is needed to account for different ethnicities and clarify the mechanisms behind, which might contribute to the elucidation of novel diagnosis methods. © 2015, Springer Science+Business Media New York.


Wang X.-L.,China Medical University at Heping | Yu T.,Liaoning Cancer Hospital & Institute | Yan Q.-C.,China Medical University at Heping | Wang W.,Liaoning Cancer Hospital & Institute | And 3 more authors.
Journal of Molecular Neuroscience | Year: 2015

Advanced glycation end products (AGEs) are extremely accumulated in diabetes mellitus, particularly in retinal vascular and epithelium cells, and are confirmed to contribute to diabetic retinopathy (DR). In the present study, we determined the promotion by AGEs to the oxidative stress and mitochondrial dysfunction in retinal pigmented epithelium ARPE-19 cells and investigated the influence by the knockdown or the overexpression of receptor for AGEs (RAGE) on the AGE-promoted oxidative stress and mitochondrial dysfunction. Furthermore, we determined the induction by AGEs to the cell apoptosis and to the activation of B-cell lymphoma 2 (Bcl-2) families in the AGE-BSA-induced apoptosis, and examined the RAGE-dependence in such induction. Results demonstrated that AGE-BSA upregulated the hydrogen peroxide production and induced mitochondrial dysfunction in ARPE-19 cells, dose-dependently. And the further investigation indicated that the AGE-RAGE interaction was required for the induction of oxidative stress and mitochondrial dysfunction. Moreover, the AGE-BSA treatment promoted a significantly high level of apoptotic cells, and the Bcl-2 family was implicated in the AGE-BSA-induced apoptosis, there was a significant high level of Cyt c release, Bcl-2-associated X protein (Bax) induction, Bcl-2 reduction, and caspase 9 activation in the AGE-BSA-treated cells. In conclusion, the present study recognized the apoptosis induction by AGE-BSAs in the retinal epithelium ARPE-19 cells, RAGE-dependently. The mitochondrial dysfunction was induced, and the Bcl-2 family was deregulated during the AGE-BSA-induced ARPE-19 cell apoptosis. © 2015, Springer Science+Business Media New York.


PubMed | the Peoples Hospital of Liaoning Province, Hong Kong Baptist University, Shandong Academy of Sciences and Liaoning Cancer Hospital & Institute
Type: | Journal: Journal of pharmaceutical and biomedical analysis | Year: 2016

A sensitive UPLC-MS/MS method was developed and validated for the determination of brusatol in rat plasma. Chromatographic separation was carried out on a C18 column using methanol and 10mM ammonium acetate containing 0.1% (v/v) formic acid (55:45, v/v). The lower limit of quantification (LLOQ) was 1.0 ng/mL for brusatol in plasma. The intra- and inter-day precision for the analyte ranged from 3.2% to 9.2% and 1.3% to 7.8%, and the accuracy was between 97.3% and 108.5%. The method was successfully applied in a pharmacokinetic study of brusatol following intravenous injection (0.5, 1.0, and 2.0mg/kg) of brusatol.


PubMed | Shanghai Zhoupu Hospital of Pudong New Area, Xi'an Jiaotong University, Dalian No3 Peoples Hospital, Dalian Medical University and Liaoning Cancer Hospital & Institute
Type: Journal Article | Journal: Journal of orthopaedic surgery and research | Year: 2017

This study aimed to retrospectively review the clinical efficacy of open reduction and internal fixation (ORIF) for treatment of high-energy transsyndesmotic ankle fracture dislocation-the Logsplitter injury.Between December 2006 and December 2014, 41 patients (29 males and 12 females; mean age, 41.4613.42years) with Logsplitter injury were treated by ORIF procedure. Patients were grouped as typical injury (mainly vertical axial stress) and untypical injury (mainly rotational stress) according to the injury mechanism and the degree of the talus wedged into the distal tibiofibular joint.After the follow-up of 32.4824.18weeks, average American Orthopedic Foot and Ankle Society (AOFAS) score at final follow-up was 78.5410.66 and the excellent and good rate of 82.9%. Three patients in typical group developed nonunion, and other three cases had infection vs. none in untypical group (both P=0.053). Burwell-Charnely scoring system revealed anatomic reduction of fracture was achieved in 22 cases, fair reduction in 16 cases, and poor in only 3 cases. Patients in untypical group had better fracture reduction (P=0.015) and lower incidence rate of posttraumatic ankle arthritis (P=0.042) than typical cases as well as the range of motion (P<0.01).The ORIF may be an optimal approach to treat Logsplitter injuries. Patients with untypical injury had better fracture reduction, range of motion, and low incidence rate of posttraumatic ankle arthritis than those typical ones, and the postoperative outcome was affected by the injury and treatment characteristics.


Yu A.-S.,Dalian Medical University | Zhao L.,Liaoning Cancer Hospital & Institute | Zhao L.,Dalian Medical University
Tumor Biology | Year: 2015

Ovarian cancer (OC) is a deadly disease, and despite improvements in treatment, overall 5-year survival is low. Glycogen synthase kinase (GSK)-3β is a multifunctional serine/threonine kinase. We wished to ascertain if the GSK-3β inhibitor (2Z,3E)-6-bromoindirubin-3′-oxime, known as “BIO,” can suppress OC development. The OC cell lines A2780 and OVCAR3 were exposed to BIO. At different time points, cell proliferation, apoptosis, cell cycle, and cell invasion/cell migration assays were carried out. Phalloidin staining was undertaken to observe lamellipodia formation. Real-time reverse transcription-polymerase chain reaction and western blotting were used to assess expression of messenger RNA (mRNA) and protein of GSK-3β, cyclin D1, matrix metalloproteinase (MMP)-9, and p21. BIO suppressed the proliferation, invasion, and migration of OC cells; reduced lamellipodia formation; and induced G1 arrest of the cell cycle. BIO exposure led to a significant downregulation of mRNA and protein expression of cyclin D1 and MMP9 in comparison with untreated control cells. In contrast, BIO exposure upregulated mRNA and protein expression of p21 in comparison with untreated control cells. Besides, GSK-3β small interfering RNA (siRNA) transfection in ovarian cancer cells also downregulated GSK-3β, cyclin D1, and MMP9 protein expression while upregulated p21 expression. These data suggest that BIO, as an inhibitor of GSK-3β, can suppress OC development. Therefore, BIO could be a candidate drug for the treatment of OC. © 2015 International Society of Oncology and BioMarkers (ISOBM)


PubMed | Dalian Medical University and Liaoning Cancer Hospital & Institute
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Ovarian cancer (OC) is a deadly disease, and despite improvements in treatment, overall 5-year survival is low. Glycogen synthase kinase (GSK)-3 is a multifunctional serine/threonine kinase. We wished to ascertain if the GSK-3 inhibitor (2Z,3E)-6-bromoindirubin-3-oxime, known as BIO, can suppress OC development. The OC cell lines A2780 and OVCAR3 were exposed to BIO. At different time points, cell proliferation, apoptosis, cell cycle, and cell invasion/cell migration assays were carried out. Phalloidin staining was undertaken to observe lamellipodia formation. Real-time reverse transcription-polymerase chain reaction and western blotting were used to assess expression of messenger RNA (mRNA) and protein of GSK-3, cyclin D1, matrix metalloproteinase (MMP)-9, and p21. BIO suppressed the proliferation, invasion, and migration of OC cells; reduced lamellipodia formation; and induced G1 arrest of the cell cycle. BIO exposure led to a significant downregulation of mRNA and protein expression of cyclin D1 and MMP9 in comparison with untreated control cells. In contrast, BIO exposure upregulated mRNA and protein expression of p21 in comparison with untreated control cells. Besides, GSK-3 small interfering RNA (siRNA) transfection in ovarian cancer cells also downregulated GSK-3, cyclin D1, and MMP9 protein expression while upregulated p21 expression. These data suggest that BIO, as an inhibitor of GSK-3, can suppress OC development. Therefore, BIO could be a candidate drug for the treatment of OC.


Tang Y.,Liaoning Cancer Hospital & Institute | Wang W.,Liaoning Cancer Hospital & Institute | Teng X.-Z.,Center Hospital of Liaoning Electrical Power | Shi L.,Liaoning Cancer Hospital & Institute
Tumor Biology | Year: 2014

For patients with advanced non-small cell lung adenocarcinoma that fail to respond to first-line chemotherapy and that do not involve epidermal growth factor receptor (EGFR) mutations, previous empirical analysis showed that a single second-line chemotherapy agent may be inadequate for the control of further tumor development. This study examines the combination of S-1 drugs and nedaplatin that has no cross-resistance to first-line treatments; 179 cases of IIIb-IV stage non-small-cell lung adenocarcinoma that failed to respond to first-line chemotherapy were included, and these subjects did not have mutated EGFRs. In the present study, S-1 plus nedaplatin chemotherapy was better than standard second-line chemotherapy options in the treatment of advanced lung adenocarcinoma that did not involve EGFR mutations and that failed to respond to first-line chemotherapy. Additionally, the combination of S-1 and nedaplatin seemed to be well tolerated, making this chemotherapy technique a potentially strong candidate for the treatment of advanced non-small-cell lung adenocarcinoma. © 2014, International Society of Oncology and BioMarkers (ISOBM).


Ma J.,Liaoning Cancer Hospital Institute | Bai J.,Liaoning Cancer Hospital Institute
International Journal of Clinical and Experimental Medicine | Year: 2015

Objective: This study aims to observe the protective effects of heparin on endothelial cells in sepsis and explore the involved signal pathway regulated by heparin. Methods Human vascular endothelial cells were treated by TNFα in vitro to simulate the inflammatory environment when sepsis occurred. They were intervened by heparin and the expression levels of soluble thrombomodulin (sTM) and serum activated protein C (APC) were detected by ELISA, the regulatory mechanism of heparin improving vascular endothelial cells injury induced by TNFα was detected by Western Blotting method, the methylation of histone in the gene promoter region of endothelial nitric oxide synthase (eNOS) and monocyte chemotactic protein-1 (MCP-1) were detected using chromatin immunoprecipitation method. Results Heparin could inhibit the secretion of sTM and APC protein and the expression of MCP-1 gene which involved in NF-κB signal pathway. Conclusions Heparin could protect vascular endothelial cells from injury induced by TNFα and sepsis, the mechanisms were related with the effects of heparin on the histone methylation of promoter region and the regulation of heparin on the MAPK and NF-κB signal pathways. These results provide a theoretical basis for the application of heparin in the prevention and treatment of vascular disease related with sepsis. © 2015, E-Century Publishing Corporation. All rights reserved.


Ai F.,Liaoning Cancer Hospital & Institute | Hua X.,Liaoning Cancer Hospital & Institute | Liu Y.,Liaoning Cancer Hospital & Institute | Lin J.,Liaoning Cancer Hospital & Institute | Feng Z.,Liaoning Cancer Hospital & Institute
Cell Biochemistry and Biophysics | Year: 2014

Little is known about the relationship about Helicobacter pylori (H. pylori) infection and pancreatic, and this study was set to investigate how H. pylori infection is correlated with pancreatic cancer and provide references for the clinical prevention and treatment of pancreatic cancer. 56 cases of pancreatic cancer patients admitted to the hospital from August 2012 to August 2013 were collected as the observation group. The anti-Hp IgG (H. pylori-specific antibodies), Hp IgM (H. pylori antibodies), and CagA-Hp-IgG (H. pylori serotoxin-associated protein a antibody) in the serum were measured and compared with the related indicators of control group (60 cases of healthy subjects). The H. pylori infection rate was 64.29 % in the observation group, and that in the control group was 46.67 %. Our results showed that the H. pylori infection rate in the observation group was significantly higher than that in the control group, which was statistically different (P < 0.01). The positive rate of CagA-Hp in the observation group was 38.88, and 21.53 % in the control group, for which the observation group was significantly higher than the control group (P < 0.05). The occurrence of H. pylori infection in patients with pancreatic cancer was also positively correlated with the smoking history and the history of chronic pancreatitis (P < 0.05). Helicobacter pylori infection is one of the risk factors for pancreatic cancer, and the patients with positive CagA-Hp have the higher risk, so the prevention and treatment of H. pylori infection would be beneficial for the prevention and treatment of pancreatic cancer. © 2014, Springer Science+Business Media New York.


PubMed | Liaoning Cancer Hospital & Institute
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

The objective of this study was to evaluate the effects of dendritic cell and cytokine-induced killer (DC-CIK) cell-based immunotherapy combined with chemotherapy on the treatment of patients with advanced colorectal cancer. We prospectively included patients with advanced colorectal cancer and assessed the efficacy of DC-CIK cell-based immunotherapy combined with chemotherapy compared to treatment with chemotherapy alone. T cell subtypes, progression-free survival (PFS), overall survival (OS), and adverse events were evaluated in each group. In total, 134 patients were included in the DC-CIK group and 121 patients were included in the control group. No significant differences were observed in the percentages of CD3(+), CD3(+)CD4(+), CD3(+)CD8(+), and NK cells after DC-CIK cell-based immunotherapy compared to before chemotherapy in the DC-CIK group. The median PFS and OS in the DC-CIK treatment group were 8.8months (95% CI 8.4-9.1) and 14.7months (95% CI 13.9-15.5), respectively, which were significantly improved compared to the PFS and OS in the control group. The frequencies of grade III and IV leukopenia (8.2 vs. 19.0%, P=0.011), grade III and IV anemia (3.0 vs. 9.1%, P=0.039), and grade III and IV thrombocytopenia (3.7 vs. 10.7%, P=0.029) were significantly lower in the DC-CIK group compared to the control group. DC-CIK cell-based immunotherapy could induce an immune response against colorectal cancer and prolong PFS and OS. DC-CIK cell-based immunotherapy combined with chemotherapy had a significant benefit in terms of survival in patients with colorectal cancer compared to chemotherapy alone.

Loading Liaoning Cancer Hospital Institute collaborators
Loading Liaoning Cancer Hospital Institute collaborators