Peoples Hospital of heNan Province

Zhengzhou, China

Peoples Hospital of heNan Province

Zhengzhou, China
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Xing Y.,Peoples Hospital of Henan Province | Song H.M.,Beijing Union Medical College | Wei M.,Beijing Union Medical College | Liu Y.,Peoples Hospital of Henan Province | And 2 more authors.
Journal of Immunotoxicology | Year: 2013

Pediatric patients were recruited to analyze differences in Epstein-Barr virus (EBV) copy numbers and adaptive immune reactions in children with chronic active vs acute EBV infection (CAEBVI vs AEBVI), as well as to examine the relationship between these parameters and the pathogenesis of CAEBVI. Fluorescent qPCR was used to assess EBV-DNA levels, while ELISA, antibody affinity, flow cytometry, and heterophil agglutination (HA) assays were used to evaluate patient EBV-adaptive humoral and cellular immunity. Lastly, ELISPOT was employed to assess interferon (IFN)-γ secretory functions of EBV-specific cytotoxic T-lymphocytes (CTL) as a marker of subject EBV-specific adaptive cellular immunity. The results indicated that, compared with AEBVI patients or normal children, there was a dramatic elevation in viral copy levels, viral capsid antigen (VCA)-IgA, early antigen (EA)-IgA, and EA-IgG, but a lack of EBV nuclear antigen (EBNA)-IgG and a negative HA in CAEBVI patients (p < 0.01). These subjects also had decreased CD4+, CD8+ (naïve), CD8+CD38+, and effective memory T-lymphocyte levels compared with AEBVI patients (p < 0.01), and decreased EBV-specific CTL function compared with normal children (p < 0.01). These results suggest that there is a disturbance in EBV antigen availability and in both the adaptive humoral and cellular immune responses in patients with CAEBVI, and that these outcomes may be associated with the chronic active re-infection process itself associated with CAEBVI. © 2013 Informa Healthcare USA, Inc.

Zhao S.J.,Peoples Hospital of Henan Province | Zhao H.W.,Peoples Hospital of Henan Province | Du S.,Peoples Hospital of Henan Province | Qin Y.H.,Peoples Hospital of Henan Province
Indian Journal of Pharmaceutical Sciences | Year: 2015

The study determined pharmacist support on patients receiving multi-drug therapy for coronary heart disease by evaluating patient self-care ability, quality of life, and drug therapy compliance. In this study, ninety patients were randomly assigned to an experimental group (n=45) and a control group (n=45). The control group received conventional clinical care. The experimental group received clinical care plus pharmacist support that included medication review, patient education, lifestyle management, discharge guidance, and telephone follow-up. Eighty-five patients completed the study. Self-care ability and quality of life were evaluated before hospital discharge. The experimental group understood their condition better than the control group (P<0.05), the differences between the groups in understanding treatment goals, drug regimens, lifestyle modifications, psychogenic disorders, and satisfaction evaluations were more pronounced (P<0.01). At six-month follow-up, the difference between the groups in drug therapy compliance was P<0.01, as was success rate by intention-to-treat (77.8% vs. 48.9%) and per-protocol (81.4% vs. 52.4%). Two adverse drug reactions occurred in the experimental group and three in the control group. Pharmacist support improved self-care ability, quality of life, drug therapy compliance, and treatment success rate in coronary heart disease patients.

Li T.,Peoples Hospital of Henan Province | Zhang W.W.,Louisiana State University Health Sciences Center | Bai W.,Peoples Hospital of Henan Province | Zhai S.,Peoples Hospital of Henan Province | Pang Z.,Zhengzhou University
Journal of Vascular Surgery | Year: 2010

Objectives: Pulmonary embolism (PE) is one of the major complications after percutaneous balloon angioplasty (PTBA) for Budd-Chiari's syndrome (BCS). The purpose of this study was to investigate the role of warfarin pre-treatment in the prevention of PE after PTBA in patients with large inferior vena cava (IVC) thrombus. Patients and Methods: From October 2002 to December 2009, 16 patients with symptomatic membranous or segmental IVC occlusion and large thrombus were treated with warfarin before PTBA. Eleven patients were men and 5 were women. The median age was 36 years, ranging from 21 to 52 years. The median duration of warfarin treatment before PTBA was 7 months, ranging from 3 to 12 months. Fourteen patients had membranous IVC occlusion and 2 had segmental occlusion. All 16 patients had significant thrombi underneath the obstructive lesions. PE diagnosis was based on clinical presentation and pulmonary computerized tomographic angiogram, if indicated. Results: In 14 of 16 patients, IVC thrombus was completely or near-completely resolved based on follow-up cavogram and PTBA was performed. In the other 2 patients, residual thrombus was demonstrated by cavogram at 12 months. PTBA and stent placement were carried out. IVC patency in the 16 patients was confirmed by completion cavogram. No major bleeding complication during warfarin pre-treatment aimed to keep international normalized ratio (INR) 2 to 3. There was no clinically significant PE or death in this group during follow-up, ranging from 6 to 40 months (median 21 months). Conclusion: Spontaneous fibrinolysis of IVC thrombus occurs within 1 year in the majority of the patients treated with warfarin. Pre-treatment with warfarin prevents PE after PTBA in the patients with BCS with IVC membranous or segmental occlusion and large thrombus. Copyright © 2010 by the Society for Vascular Surgery.

Li F.,University of Kansas Medical Center | Miao Y.,Peoples Hospital of Henan Province | Zhang L.,Zhengzhou University | Neuenswander S.A.,University of Kansas | And 2 more authors.
Drug Metabolism and Pharmacokinetics | Year: 2011

Isoniazid (INH) is a first-line drug for tuberculosis control; the side effects of INH are thought to be associated with its metabolism, and this study was designed to globally characterize isoniazid metabolism. Metabolomic strategies were used to profile isoniazid metabolism in humans. Eight known and seven novel INH metabolites and hydrazones were identified in human urine. The novel products included two hydroxylated INH metabolites and five hydrazones. The two novel metabolites were determined as 2-oxo-1,2-dihydro-pyridine-4-carbohydrazide and isoniazid N-oxide. Five novel hydrazones were produced by condensation of isoniazid with keto acids that are intermediates in the metabolism of essential amino acids, namely, leucine and/or isoleucine, lysine, tyrosine, tryptophan, and phenylalanine. This study enhances our knowledge of isoniazid metabolism and disposition and may offer new avenues for investigating INHinduced toxicity. © 2011 by the Japanese Society for the Study of Xenobiotics (JSSX).

Li Z.,Zhengzhou University | Tian T.,Zhengzhou University | Lv F.,Peoples Hospital of Henan Province | Chang Y.,Zhengzhou University | And 7 more authors.
PLoS ONE | Year: 2013

Six1 is one of the transcription factors that act as master regulators of development and are frequently dysregulated in cancers. However, the role of Six1 in pancreatic cancer is not clear. Here we show that the relative expression of Six1 mRNA is increased in pancreatic cancer and correlated with advanced tumor stage. In vitro functional assays demonstrate that forced overexpression of Six1 significantly enhances the growth rate and proliferation ability of pancreatic cancer cells. Knockdown of endogenous Six1 decreases the proliferation of these cells dramatically. Furthermore, Six1 promotes the growth of pancreatic cancer cells in a xenograft assay. We also show that the gene encoding cyclin D1 is a direct transcriptional target of Six1 in pancreatic cancer cells. Overexpression of Six1 upregulates cyclin D1 mRNA and protein, and significantly enhances the activity of the cyclin D1 promoter in PANC-1 cells. We demonstrate that Six1 promotes cell cycle progression and proliferation by upregulation of cyclin D1. These data suggest that Six1 is overexpressed in pancreatic cancer and may contribute to the increased cell proliferation through upregulation of cyclin D1. © 2013 Li et al.

Li Z.,Zhengzhou University | Tian T.,Zhengzhou University | Hu X.,Huazhong University of Science and Technology | Zhang X.,Zhengzhou University | And 4 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

Paclitaxel resistance remains a major challenge in the treatment of breast cancer. Six1 is a homeodomain-containing transcription factor invloved in the initiation, progression and metastasis of breast cancer. We herein investigate the relationship between Six1 and resistance of paclitaxel in this study. The results indicate that six1 is a mediator of the paclitaxel resistance in breast cancer. The expression level of Six1 in breast cancer cells correlates with their resistance to paclitaxel. On the one hand, forced overexpression of Six1 in Six1-low/paclitaxel-sensitive MCF-7 or HS578T breast cancer cells induce their resistance to paclitaxel treatment directly; On the other hand, knockdown of endogenous Six1 in Six1-high/drug-resistant BT-474 breast cancer cells sensitized these cells to paclitaxel treatment. Besides, Six1 overexpression confers resistance to paclitaxel-mediated apoptosis in breast cancer cells. Furthermore, clinical data and the publicly available breast cancer gene expression datasets display that the association of Six1 expression with paclitaxel sensitivity is clinically relevant. In conclusion, these data suggest that Six1 may function as an important modifier of the paclitaxel response in breast cancer cells, and serve as a potential target for overcoming paclitaxel resistance in breast cancer. © 2013 Elsevier Inc.

Lu F.,Peoples Hospital of Henan Province | Li X.,Tumor Hospital of Henan Province | Suo A.-Q.,Peoples Hospital of Henan Province | Zhang J.-W.,Peoples Hospital of Henan Province
Chinese Medical Journal | Year: 2010

Background Alzheimer's disease (AD) is a neurodegenerative disorder and the leading cause of dementia in the elderly. The two hallmark lesions in AD brain are deposition of amyloid plaques and neurofibrillary tangles (NFTs). Hypercholesteremia is one of the risk factors of AD. But its role in the pathogenesis of AD is largely unknown. The aim of this study was to investigate the relationship between hypercholesteremia and tau phosphorylation or β-amyloid (Aβ), and evaluate the effect of atorvastatin on the level of tau phosphorylation and Aβ in the brains of rats fed with high cholesterol diet. Methods Sprague-Dawley (SD) rats were randomly divided into normal diet control group, high cholesterol diet group, and high cholesterol diet plus atorvastatin (Lipitor, 15 mg·kg-1·d-1) treated group. Blood from caudal vein was collected to measure total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL) and high-density lipoprotein (HDL) at the end of the 3th and the 6th months by an enzymatic method. The animals were sacrificed 6 months later and brains were removed. All left brain hemispheres were fixed for immunohistochemistry. Hippocampus and cerebral cortex were separated from right hemispheres and homogenized separately. Tau phosphorylation and Aβ in the brain tissue were determined by Western blotting (using antibodies PHF-1 and Tau-1) and anti-Aβ40/anti-Aβ42, respectively. Results We found that high cholesterol diet led to hypercholesteremia of rats as well as hyperphosphorylation of tau and increased Aβ level in the brains. Treatment of the high cholesterol diet fed rats with atorvastatin prevented the changes of both tau phosphorylation and Aβ level induced by high cholesterol diet. Conclusions Hypercholesteremia could induce tau hyperphosphorylation and Aβ production in rat brain. Atorvastatin could inhibit tau hyperphosphorylation and decrease Aβ generation. It may play a protective role in the patho-process of hypercholesteremia-induced neurodegeneration in the brain.

Chen X.,Zhengzhou University | Wei L.,Peoples Hospital of Henan Province | Zhao S.,Zhengzhou University
Oncology Reports | Year: 2016

miR-338 as an intronic miRNA from apoptosis-associated tyrosine kinase (AATK) is involved in tumor proliferation and apoptosis, but its function and regulatory mechanism in lung cancer is still obscure. In the present study, we found that miR-338 was strikingly downregulated in 115 lung cancer tissues and 5 lung cancer cell lines. Besides, low level of miR-338 was associated with tumor emboli, TNM stage, tumor recurrence and poor survival. Regaining the expression of miR-338 in lung cancer cell lines significantly impaired cellular adhesion, migration, invasion and lung tumor formation in nude mice. Furthermore, we also identified a metastasis related protein, integrin β3 (ITGB3), as a novel target gene of miR-338. Our results reveal a new regulatory mechanism of miR-338 which may help us better understand the metastasis of lung cancer.

Hou G.,Zhengzhou University | Lu Z.,Zhengzhou University | Liu M.,Peoples Hospital of Henan Province | Liu H.,Zhengzhou University | Xue L.,Zhengzhou University
Digestive Diseases and Sciences | Year: 2011

Background: Esophageal squamous cell carcinoma (ESCC) is one of the most frequently diagnosed cancers in China, but the etiology and mode of carcinogenesis of this disease remain poorly understood. The phosphatase and tensin homolog deleted from chromosome 10 (PTEN) with putative tumor suppressing is frequently mutated in many cancers. Aims: The aim of this study was to investigate whether there exists a mutation in the PTEN gene of the ESCC cells, and the effects of the wild type and mutated PTEN genes on the proliferation and apoptosis of the ESCC cells. Methods: The wild type and mutated PTEN genes were cloned from human placenta and ESCC cells, respectively, and their effects on the proliferation and apoptosis of the ESCC cells were investigated. Also, the relationship between the PTEN gene status and sensitivity of the EC9706 cells to cisplatin was determined in the xenografts of nude mice. Results: There were mutations in the PTEN gene from ESCC cells. The proliferation of the EC9706 cells was clearly inhibited by the wild type PTEN gene, but not by the mutated PTEN gene in vitro. Furthermore, the wild type PTEN gene inhibited the growth of transplantable tumor, induced cell apoptosis, and improved the sensitivity of the EC9706 cells to cisplatin in vivo. Conclusion: The findings of the present study demonstrate that there are mutations in the PTEN gene of the ESCC cells and that the wild type PTEN gene has important effects on the ESCC cells in vitro and in vivo. © 2011 Springer Science+Business Media, LLC.

Hou G.,Zhengzhou University | Zhang Q.,Zhengzhou University | Wang L.,Zhengzhou University | Liu M.,Peoples Hospital of Henan Province | And 2 more authors.
Cancer Letters | Year: 2010

Accumulating evidences have demonstrated that mTOR pathway has a central role not only in cell growth but also in invasion and metastasis of cancers. Here we reported that rapamycin or cisplatin alone inhibited significantly the tumor growth and their combination had the strongest anticancer effect on transplantable tumor growth of human ESCC cell line EC9706 in nude mice. Furthermore, western blots, RT-PCR and TUNEL assay revealed that rapamycin specifically blocked mTOR pathway and induced apoptosis of ESCC cells in vivo. These findings indicate a rationale for using mTOR inhibitors as a mechanism-based therapeutic approach to patients with ESCC. © 2009 Elsevier Ireland Ltd. All rights reserved.

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