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Lu J.-X.,Yancheng Health Vocational and Technical College | Lu Z.-Q.,People's Care | Zhang S.-L.,Yancheng Health Vocational and Technical College | Zhi J.,Yancheng Health Vocational and Technical College | And 2 more authors.
Balkan Medical Journal | Year: 2014

Background: Recent studies have reported contrasting results regarding the association of polymorphisms in two integrin genes, ITGA2 and ITGB3, with ischemic stroke. Aims: The present study aimed to investigate the correlation between the ITGA2 C807T and ITGB3 T176C polymorphic loci with ischemic stroke, as well as plasma lipid and lipoprotein levels. Study Design: Case control study. Methods: Human venous blood samples were collected from patients admitted for ischemic stroke (n=350, 'patients') and healthy individuals (n=300, 'controls'). Blood was genotyped at these loci by polymerase chain reaction-restriction fragment length polymorphism. Plasma lipid and lipoprotein levels were measured by routine enzymatic, masking, and turbidimetry methods. Results: As expected, total cholesterol, triglycerides, and low-density lipoprotein were all significantly higher in patients than in controls (p<0.05). Genotype and allele frequencies of ITGA2 C807T were significantly different between patients and controls (p<0.05), but no difference was detected in genotype or allele frequencies for ITGA3 T176C. For ITGA-2, the T allele conferred a 1.226 times higher relative risk of ischemic stroke than the C allele (odds ratio=1.226, 95% confidence interval=1.053-1.428). Similarly, total cholesterol was higher in T allele carriers than in non-carriers (p<0.05). Conclusion: ITGA2 C807T polymorphism is associated with ischemic stroke, with the T allele acting as a susceptibility allele that appears to confer increased cholesterol levels. © Trakya University Faculty of Medicine.


Wu J.,The First Peoples Hospital of Yancheng City | Lu W.-Y.,The Sixth Peoples Hospital of Yancheng City | Cui L.-L.,The First Peoples Hospital of Yancheng City
Asian Pacific Journal of Cancer Prevention | Year: 2015

Objective: To investigate the regulatory effect of curcumin on expression of signal transducer and activator of transcription 3 (STAT3) in skin squamous cell carcinoma tissues as well as possible mechanisms of curcumin in prevention and treatment of skin squamous cell carcinoma. Materials and Methods: Highly invasive A431 cells were treated with curcumin at various doses. The cytotoxic effects of treatment with 5, 10, 15, 20, 25, 30, 35, 40 and 50 umol/L curcumin for 24, 48 and 72 hours on A431 cells were measured by MTT assay. The invasion capacity of cells treated with 5, 10 and 15 umol/L curcumin was measured by Transwell test, while adhesive ability was assessed by cell adhesion assay. The effects of 5,10 and 15 umol/L curcumin on expression levels of STAT3 were determined by Western blotting and on transcription levels of STAT3 mRNA by RT-PCR. Results: Treatment with curcumin at a doses of more than 15 umol/L for more than 24 hour inhibited the growth of A431 cells in a time-and dose-dependent fashion (p<0.001). The doses of 15 umol/L and less for 24 hours showed no significant cytotoxic effects on the cells, survival rates being more than 85%.The invasion and adhesive abilities decreased gradually with the increasing curcumin concentration, 15 umol/L exerting the strongest inhibitory effects (p<0.05). Curcumin showed significant dose-dependent inhibitory effects on the transcription level of STAT3 mRNA (p<0.05). Conclusions: Curcumin may reduce the invasive ability of A431 cells by inhibiting the activation of STAT3 signal pathway and expression of STAT3 as a target gene in the pathway.


PubMed | The First Peoples Hospital of Yancheng City and The Sixth Peoples Hospital of Yancheng City
Type: Journal Article | Journal: Molecular medicine reports | Year: 2015

The present study aimed to investigate the significance of the phosphorylation of signal transducer and activator of transcription3 (STAT3) and mitogenactivated protein kinase (MAPK), and the protein expression of cyclinD1, in skin squamous cell carcinoma (SCC) tissues. SCC specimens from the skin were collected from 30patients, and normal skin tissues were collected from 10individuals as a control. Immunohistochemistry was used to assess the protein expression levels of phosphorylated (p)STAT3, pMAPK and cyclinD1 in the SCC tissues. The levels of pSTAT3 protein were abnormally increased in SCC (P<0.05); however, no significant differences in the protein expression of pMAPK were identified between the normal skin and the SCC specimens. The extent of the upregulation of the expression of pSTAT3 and cyclinD1 correlated with the depth of tumor invasion (P<0.05). A positive correlation existed between the expression of pSTAT3 and cyclinD1 in SCC. However, no association between the expression intensity of pMAPK and cyclinD1 was identified in SCC. It is postulated that the activation of STAT3 may induce the overexpression of cyclinD1, which results in the persistent proliferation of these tumor cells in SCC.


Zhou Y.,Yancheng Health Vocational and Technical College | Jiang Y.-Q.,The First Peoples Hospital of Yancheng City | Wang W.-X.,The First Peoples Hospital of Yancheng City | Zhou Z.-X.,The First Peoples Hospital of Yancheng City | And 3 more authors.
Human Immunology | Year: 2012

Previous work indicated that high mobility group box-1 (HMGB1) protein may be involved in neutrophilic asthma. Here, we sought to investigate the correlation between HMGB1 and one of its receptors, receptor for advanced glycosylation end products (RAGE), with the severity of bronchial asthma. Compared to the control group (30 healthy individuals), patients in the asthma group (n=72) exhibited a higher percentage of neutrophils and higher HMGB1 and RAGE levels in induced sputum samples (P<0.05). Concurrently, FEV1% was significantly lower in the asthma group (P<0.05). Further, compared to mild and moderate asthma, in patients with severe asthma ACQ scores, the percentage of neutrophils, and HMGB1 levels were significantly higher, while FEV1% was significantly lower (P<0.05). The percentage of neutrophils and HMGB1 and RAGE levels were lower after treatment than before treatment (P<0.05). Finally, negative correlations were observed between HMGB1 or RAGE levels and FEV1% (r=-0.777 and r=-0.291, P<0.05), and positive correlations were detected between HMGB1 or RAGE levels and percentage of neutrophils (r=0.803 and r=0.326, P<0.05). Additionally, positive correlations were observed between HMGB1 and RAGE levels within the asthma group (r=0.306, P<0.05). Therefore, HMGB1 protein levels correlate with the severity of asthma, and HMGB1 may contribute to the inflammatory process of asthma. © 2012 .


Cui Y.,Shanghai Punan Hospital | Cui Y.,Yancheng Health Vocational and Technical College | Jiang Y.,The First Peoples Hospital Of Yancheng City | Ji Y.,The First Peoples Hospital Of Yancheng City | And 5 more authors.
American Journal of Translational Research | Year: 2014

Domestic mite species like Dermatophagoides farinae induce allergies in people worldwide. Here, the cDNA coding for group 21 allergen of Dermatophagoides farinae (Hughes; Acari: Pyroglyphidae) from China was cloned, sequenced, and expressed in E. coli to aid in the development of diagnostic and treatment options for domestic mite hypersensitivity. First, the Der f 21 cDNA fragment was synthesized by RT-PCR; the confirmed full-length sequence comprised 411 nucleotides. The cDNA was ligated to the vector pCold-TF to construct an expression plas-mid, pCold-TF-Der f 21. pCold-Tf-Der f 21 was transformed into E. coli BL21 cells, and its expression was induced by IPTG treatment. SDS-PAGE showed a specific band at the predicted molecular weight of Der f 21, demonstrating its successful expression. The recombinant fusion protein was obtained and its structure and molecular weight were confirmed by MALDI-TOF/TOF. Bioinformatics analysis revealed that the protein contained a signal peptide of 17 amino acids. The molecular weight of the mature Der f 21 allergen was approximately 14.16 kDa with a theoretical pI of 4.87. Its predicted secondary structure comprises a-helix (84.03%), extension chain (1.68%), and random coil (14.29%). The successful cloning of Der f 21 and a basic bioinformatics analysis of the protein provide a foundation for further study of this allergen in diagnosis and treatment of domestic mite hypersensitivity. © 2014, E-Century Publishing Corporation. All rights reserved.


Wu J.,The First Peoples Hospital of Yancheng City | Zhang J.-R.,The Peoples Hospital of Dafeng City | Qin J.,The First Peoples Hospital of Yancheng City
International Journal of Clinical and Experimental Medicine | Year: 2014

Epigenetic regulation of genes by DNA methylation contributes to cancer. The present study sought to identify methylation changes in the promoters of E-cadherin and p14ARF, two genes with potential cancer roles promoting in skin squamous cell carcinoma. Skin squamous cell carcinoma specimens were collected from 40 patients and normal skin tissues were collected from 30 individuals as controls. Promoter methylation was detected for E-cadherin and p14ARFby methylation-specific PCR. Correlations between E-cadherinor p14ARF methylation and clinicopathological parameters were analyzed by the Spearman rank test. Methylation of E-cadherin(37.5%) and p14ARF(60.0%) was significantly more common in skin squamous cell carcinoma than in normal skin tissue (10.0 and 6.7%, respectively; P < 0.05). Additionally, E-cadherin and p14ARF methylation were positively correlated within skin squamous cell carcinoma (r = 0.422, P = 0.007). Furthermore, methylation of these gene promoters in skin squamous cell carcinoma was correlated with differentiation, lymph node metastasis, and clinical stage (P < 0.05). Aberrant methylation in promoters of E-cadherin and p14ARFmay promote occurrence and progression of skin squamous cell carcinoma.


Yang W.,The First Peoples Hospital Of Yancheng City | Mu X.-M.,The First Peoples Hospital Of Yancheng City | Li X.-Q.,Suzhou University
Journal of Biomaterials and Tissue Engineering | Year: 2015

Vascular smooth muscle cells (VSMCs) have been considered the core of vascular remodeling, which contributes to the development and complications of hypertension. XAV939 is a potent inhibitor of Wnt/β-catenin signaling, which is crucial for the regulation of VSMCs behavior. But the effects of XAV939 in vascular remodeling are unclear. Our results showed that the treatment with XAV939 (0.1 mg/kg body weight, i.p.) reduced the systolic blood pressure from 215±5 in 2-kidney, 2 clip rats to 117±9 mmHg (P <0.05). The levels of α smooth muscle actin, fibronectin and ki67, one of the proliferation markers, are decreased in the basilar artery on XAV939 treatment group. In vitro, the basilar artery smooth muscle cells (BASMCs) proliferation was induced by angiotensin II (Ang II). The BASMCs exposed to Ang II displayed higher cell viability and increased expression of β-catenin, p-GSK3β and its downstream target protein cyclin D1. In contrast, the expression of Axin2, a negative Wnt regulator, was decreased compared to the vehicle-control group. XAV939 treatment significantly reversed the cell proliferation and protein expression in Ang II-induced BASMCs. Our results demonstrate that XAV939 inhibits vascular remodeling by reducing BASMCs proliferation through Wnt/β-catenin pathway on hypertensive rats. © 2015 American Scientific Publishers.


PubMed | Fudan University, University of California at San Diego and The First Peoples Hospital of Yancheng City
Type: Journal Article | Journal: Medical physics | Year: 2014

The purpose of this study was to investigate the effect of excitation, fat saturation, long T2 saturation, and adiabatic inversion pulses on ultrashort echo time (UTE) imaging with bicomponent analysis of bound and free water in cortical bone for potential applications in osteoporosis.Six bovine cortical bones and six human tibial midshaft samples were harvested for this study. Each bone sample was imaged with eight sequences using 2D UTE imaging at 3T with half and hard excitation pulses, without and with fat saturation, long T2 saturation, and adiabatic inversion recovery (IR) preparation pulses. Single- and bicomponent signal models were utilized to calculate the T2(*)s and/or relative fractions of short and long T2(*)s.For all bone samples UTE T2(*) signal decay showed bicomponent behavior. A higher short T2(*) fraction was observed on UTE images with hard pulse excitation compared with half pulse excitation (75.6% vs 68.8% in bovine bone, 79.9% vs 73.2% in human bone). Fat saturation pulses slightly reduced the short T2(*) fraction relative to regular UTE sequences (5.0% and 2.0% reduction, respectively, with half and hard excitation pulses for bovine bone, 6.3% and 8.2% reduction, respectively, with half and hard excitation pulses for human bone). Long T2 saturation pulses significantly reduced the long T2(*) fraction relative to regular UTE sequence (18.9% and 17.2% reduction, respectively, with half and hard excitation pulses for bovine bone, 26.4% and 27.7% reduction, respectively, with half and hard excitation pulses for human bone). With IR-UTE preparation the long T2(*) components were significantly reduced relative to regular UTE sequence (75.3% and 66.4% reduction, respectively, with half and hard excitation pulses for bovine bone, 87.7% and 90.3% reduction, respectively, with half and hard excitation pulses for human bone).Bound and free water T2(*)s and relative fractions can be assessed using UTE bicomponent analysis. Long T2(*) components are affected more by long T2 saturation and IR pulses, and short T2(*) components are affected more by fat saturation pulses.


Jiang Y.-Q.,The First Peoples Hospital Of Yancheng City | Zhou Z.-X.,The First Peoples Hospital Of Yancheng City | Ji Y.-L.,The First Peoples Hospital Of Yancheng City
International Journal of Clinical and Experimental Medicine | Year: 2014

Overactive epidermal growth factor receptor (EGFR) signaling often underlies the rapid expansion of cancerous tissue. EGFR signaling is mediated by transcription factor signal transducer and activator of transcription 3, or STAT3. This study sought to investigate the effects of altered EGFR/STAT3 signal transduction on lung cancer cells in vitro. Lung cancer cells from the cell line A549 were divided into test and control groups. Test group cells were treated with an EGFR monoclonal antibody, Nimotuzumab, while control cells received no treatment. EGFR and STAT3 protein expression, cell apoptosis rate, cell proliferation, cell invasion, and cell division were analyzed and compared. Compared to cells in the control group, lung cancer cells treated with Nimotuzumab showed slowed proliferation rates, accelerated apoptosis, decreased invasion, and arrested cell division (P < 0.05). In conclusion, altered EGFR/STAT3 signaling results in significant changes in the biology of lung cancer cells. © 2014, E-Century Publishing Corporation. All rights reserved.


Jiang Y.-Q.,The First Peoples Hospital Of Yancheng City | Xue J.-S.,The First Peoples Hospital Of Yancheng City | Xu J.,The First Peoples Hospital Of Yancheng City | Zhou Z.-X.,The First Peoples Hospital Of Yancheng City | Ji Y.-L.,The First Peoples Hospital Of Yancheng City
International Journal of Clinical and Experimental Medicine | Year: 2016

To observe and analyze the effects of continuous positive airway pressure (CPAP) ventilation on advanced glycation end products (AGEs) and oxidized low density lipoprotein (ox-LDL) levels in patients with obstructive sleep apnea hypopnea syndrome (OSAHS), 60 patients with OSAHS were selected as the case group, and 30 patients with simple snoring were selected as the control group. The patients were treated with CPAP for 4 weeks. The serum levels of AGEs and ox-LDL of patients in the control group and of OSAHS patients before and after CPAP treatment were compared. Other clinical indexes were observed and compared including age, body mass index (BMI), waist circumference, neck circumference, insulin level, homeostasis model assessment (HOMA) index, systolic blood pressure (SBP), diastolic blood pressure (DBP), apnea hypopnea index (AHI), and lowest observed oxygen saturation (LSaO2). The serum levels of AGEs and ox-LDL in the case group prior to treatment were significantly higher than those in the control group (t = 6.494, 30.128, P < .05). After CPAP treatment, the serum levels of AGEs and ox-LDL measured in OSAHS patients decreased significantly (t = 18.057, 58.556, P < .05) but were still higher than those in the control group (t = 2.176, 14.156, P < .05). After CPAP treatment, patients in the case group showed significant improvement in insulin (t = 5.198, P < 0.05), HOMA index (t = 6.631, P < 0.05), SBP (t=5.921, P < 0.05), DBP (t = 5.022, P < 0.05), AHI (t = 8.025, P < 0.05) and LSaO2 (t = -12.016, P < 0.05). The AHI level after CPAP treatment of the patients with OSAHS was positively correlated with the patients’ BMI (standardized regression coefficient = 0.457), neck circumference (standardized regression coefficient = 0.337), HOMA index after the treatment (standardized regression coefficient = 0.669), SBP level after the treatment (standardized regression coefficient = 0.492), the serum AGE level after the treatment (standardized regression coefficient = 0.651), and the serum ox-LDL level after the treatment (standardized regression coefficient = 0.613; P < .05). LSaO2 was negatively correlated with the patients’ BMI (standardized regression coefficient = -0.415), HOMA index after the treatment (standardized regression coefficient = -0.537), SBP level after the treatment (standardized regression coefficient = -0.336), the serum AGE level after the treatment (standardized regression coefficient = -0.528), and the serum ox-LDL level after the treatment (standardized regression coefficient = -0.611; P < .05). In sum, patients with OSAHS show higher serum levels of AGEs and ox-LDL, and the application of CPAP treatment can improve clinical symptoms and reduce the serum AGE and ox-LDL levels of the patients with OSAHS. This reduction may play a role in reducing oxidative stress and regulating metabolism, thereby reducing the risk of cardiovascular and cerebrovascular disease. © 2016, E-Century Publishing Corporation. All rights reserved.

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