Ningxia Peoples Hospital

Ningxia, China

Ningxia Peoples Hospital

Ningxia, China

Time filter

Source Type

Li J.,Nantong University | Song J.,Nantong University | Jiang M.-H.,Nantong University | Zheng J.-G.,People's Care | And 3 more authors.
Journal of Interferon and Cytokine Research | Year: 2012

There is an accumulating body of evidence indicating a strong association between inflammation and the pathogenesis of atrial fibrillation (AF). Interleukin-6 (IL-6) is a pleiotropic cytokine, functions as a mediator of inflammatory response, and has both proinflammatory and anti-inflammatory properties. The aim of the present study was to investigate the association of the -634C/G polymorphism of the IL-6 gene with AF in elderly Han Chinese patients with essential hypertension (EH). A total of 169 elderly patients with EH were eligible for this study. Patients with AF (n=75) were allocated to the AF group, and 94 subjects without AF to the control group. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique was used to assess the genotype frequencies. The distribution of the IL-6 -634C/G genotypes (CC, CG, and GG) was 67.02%, 30.85%, and 2.13% in the controls, and 50.67%, 40.00%, and 9.33% in AF subjects, respectively (P=0.0312). The frequency of the G allele in the AF group was significantly higher than that in the control group (29.33% vs. 17.55%, P=0.0103). Compared with the CC and CG genotypes, the GG homozygote had a 4.7353-fold increased risk of AF [95% confidence interval (CI)=0.9537-23.5116, P=0.0382]. These findings suggest that the IL-6 -634C/G polymorphism is associated with AF, and the G allele has increased risk of AF in elderly Han Chinese patients with EH. © Copyright 2012, Mary Ann Liebert, Inc. 2012.


Shukla V.,U.S. National Institutes of Health | Zheng Y.-L.,Ningxia Peoples Hospital | Mishra S.K.,U.S. National Institutes of Health | Amin N.D.,U.S. National Institutes of Health | And 4 more authors.
FASEB Journal | Year: 2013

Alzheimer's disease (AD), one of the leading neurodegenerative disorders of older adults, which causes major socioeconomic burdens globally, lacks effective therapeutics without significant side effects. Besides the hallmark pathology of amyloid plaques and neurofibrillary tangles (NFTs), it has been reported that cyclin-dependent kinase 5 (Cdk5), a critical neuronal kinase, is hyperactivated in AD brains and is, in part, responsible for the above pathology. Here we show that a modified truncated 24-aa peptide (TFP5), derived from the Cdk5 activator p35, penetrates the blood-brain barrier after intraperitoneal injections, inhibits abnormal Cdk5 hyperactivity, and significantly rescues AD pathology (up to 70-80%) in 5XFAD AD model mice. The mutant mice, injected with TFP5 exhibit behavioral rescue, whereas no rescue was observed in mutant mice injected with either saline or scrambled peptide. However, TFP5 does not inhibit cell cycle Cdks or normal Cdk5/p35 activity, and thereby has no toxic side effects (even at 200 mg/kg), a common problem in most current therapeutics for AD. In addition, treated mice displayed decreased inflammation, amyloid plaques, NFTs, cell death, and an extended life by 2 mo. These results suggest TFP5 as a potential therapeutic, toxicity-free candidate for AD. © FASEB.


Jiang H.,Zhejiang University | Deng M.,Zhejiang University | Zhang Y.,The Seventh Peoples Hospital of Hangzhou | Chen H.,Ningxia Peoples Hospital | And 4 more authors.
Clinical Gastroenterology and Hepatology | Year: 2014

Background & Aims: Interferon-α (IFN-α)-induced depression is a major complication to treatment of chronic hepatitis C virus (HCV) infection. Specific serotonin reuptake inhibitors (SSRIs) can be used to treat depression, but it is not clear whether they can prevent depression in patients receiving IFN therapy for chronic HCV infection. Methods: We performed a meta-analysis by searching the Cochrane Library, PubMed, and EMBASE databases through 2013 for published results from randomized, placebo-controlled trials evaluating the utility of SSRIs in preventing IFN-induced depression in HCV patients. We analyzed data from 7 studies with a total of 662 patients. The incidence of IFN-induced major depression and depression severity were defined as primary outcomes. Sustained virologic response, completion of antiviral therapy, and tolerability were considered secondary outcomes. Results: A meta-analysis of IFN-induced major depression revealed that prophylactic SSRIs reduced the risk of depression, compared with placebo (relative risk [RR], 0.56; 95% confidence interval [CI], 0.37-0.84; P=.005). Proportions of patients achieving a sustained virologic response (RR, 1.02; 95% CI, 0.79-1.32; P=.87) and completing antiviral therapy (RR, 0.98; 95% CI, 0.66-1.44; P=.91) were similar between patients given SSRIs and controls. Prophylactic SSRIs were tolerated in patients with HCV during treatment. Conclusions: On the basis of a meta-analysis of 7 randomized controlled trials, prophylactic administration of SSRIs to patients with HCV significantly lowered the incidence of IFN-induced major depression, compared with placebo, and the SSRIs were well tolerated. © 2014 AGA Institute.


Yang W.,Xi'an Jiaotong University | Lv S.,Xi'an Jiaotong University | Liu X.,Guangzhou Medical College | Liu H.,Central South University | And 2 more authors.
Japanese Journal of Clinical Oncology | Year: 2010

Objective: T-cell lymphoma invasion and metastasis 1 (Tiam1) specifically activates Rho-like GTPases (e.g. Rac1) and Tiam1-Rac1 pathway affects the migration and invasion of many tumors, such as nasopharyngeal carcinoma, breast cancer and retinoblastoma. However, no studies have yet comprehensively examined the involvement of Tiam1-Rac1 pathway in hepatocellular carcinoma. In this study, we examined the relationship of the up-regulation of Tiam1 and Rac1 with clinicopathological features in patients with hepatocellular carcinoma. Methods: Expression of Tiam1 and Rac1 was assessed in 242 hepatocellular carcinoma tissues and their adjacent normal hepatic tissues by performing immunohistochemistry and was gauged regarding stage, grade and survival. Results: Immunohistochemistry showed that patients with a high clinical stage hepatocellular carcinoma (III-IV) and α-fetoprotein levels had a higher tendency to express Tiam1 and Rac1 on tumor cells than the patients with low pathologic grade hepatocellular carcinoma (I-II) (P = 0.008 and 0.01, respectively) and low α-fetoprotein levels (P = 0.006 and 0.002, respectively). In addition, Tiam1 and Rac1 up-regulation was also significantly associated with vascular invasion status (both P = 0.02), intrahepatic metastasis status (P = 0.009 and 0.01, respectively) and histological differentiation (P = 0.008 and 0.009, respectively) of patients with hepatocellular carcinoma. Moreover, post-operative survival analysis indicated that hepatocellular carcinoma patients with strong Tiam1 (P = 0.01) and Rac1 (P = 0.02) expression had shorter disease-specific survival than those with weak expression. Multivariate analysis also showed that Tiam1 and Rac1 overexpression could be two predictors of poor prognosis (P = 0.02 and 0.03, respectively). Conclusions: The current study demonstrated for the first time that the Tiam1-Rac1 pathway may play a critical role in tumor progression of hepatocellular carcinoma. The expression of Tiam1 and Rac1 can be considered as the two useful indicators for predicting the prognosis of hepatocellular carcinoma. © The Author (2010). Published by Oxford University Press. All rights reserved.


Piao W.,Ningxia Peoples Hospital | Wang H.,Shenyang Northern Hospital | Inoue M.,DNAVEC Research Corporation | Hasegawa M.,DNAVEC Research Corporation | And 3 more authors.
Angiogenesis | Year: 2010

Sendai viral vector (SeV) is emerging as a promising vector for gene therapy. However, little information is available regarding the combination of SeV-mediated gene and mesenchymal stem cell (MSC) therapy in dealing with ischemic diseases. In this study, we infected SeV to the MSCs in vitro; and injected MSCs modified with SeV harboring human angiopoietin-1 gene (SeVhAng-1) into the ischemic limb of rats in vivo. We found SeV had high transductive efficiency to the MSCs. Both MSCs and SeVhAng-1-modified MSCs improved the blood flow recovery and increased the capillary density of the ischemic limb, compared with the control. However, in contrast to MSCs, SeVhAng-1-modified MSCs had a better improvement of blood flow recovery in the ischemic limb. We further found the ischemic limb injected with SeVhAng-1-modified MSCs had strong expression of p-Akt, which improved survival of MSCs injected into the ischemic limb. This indicated SeVhAng-1 modification enhanced angiogenetic effect of MSCs by both angiogenesis and cell protection. We conclude that SeVhAng-1-modified MSCs may serve as a more effective tool in dealing with ischemic limb disease. © 2010 Springer Science+Business Media B.V.


Bk B.,U.S. National Institutes of Health | Zheng Y.-L.,U.S. National Institutes of Health | Zheng Y.-L.,Ningxia Peoples Hospital | Shukla V.,U.S. National Institutes of Health | And 3 more authors.
Journal of Alzheimer's Disease | Year: 2014

Multiple lines of evidence link the incidence of diabetes to the development of Alzheimer's disease (AD). Patients with diabetes have a 50 to 75% increased risk of developing AD. Cyclin dependent kinase 5 (Cdk5) is a serine/threonine protein kinase, which forms active complexes with p35 or p39, found principally in neurons and in pancreatic β cells. Recent studies suggest that Cdk5 hyperactivity is a possible link between neuropathology seen in AD and diabetes. Previously, we identified P5, a truncated 24-aa peptide derived from the Cdk5 activator p35, later modified as TFP5, so as to penetrate the blood-brain barrier after intraperitoneal injections in AD model mice. This treatment inhibited abnormal Cdk5 hyperactivity and significantly rescued AD pathology in these mice. The present study explores the potential of TFP5 peptide to rescue high glucose (HG)-mediated toxicity in rat embryonic cortical neurons. HG exposure leads to Cdk5-p25 hyperactivity and oxidative stress marked by increased reactive oxygen species production, and decreased glutathione levels and superoxide dismutase activity. It also induces hyperphosphorylation of tau, neuroinflammation as evident from the increased expression of inflammatory cytokines like TNF-α, IL-1β, and IL-6, and apoptosis. Pretreatment of cortical neurons with TFP5 before HG exposure inhibited Cdk5-p25 hyperactivity and significantly attenuated oxidative stress by decreasing reactive oxygen species levels, while increasing superoxide dismutase activity and glutathione. Tau hyperphosphorylation, inflammation, and apoptosis induced by HG were also considerably reduced by pretreatment with TFP5. These results suggest that TFP5 peptide may be a novel candidate for type 2 diabetes therapy. © 2014-IOS Press and the authors. All rights reserved.


Pan M.,Nantong University | Gao S.-P.,Ningxia Peoples Hospital | Jiang M.-H.,Nantong University | Guo J.,Fourth Peoples Hospital of Wuxi | And 2 more authors.
Journal of Investigative Medicine | Year: 2011

Background: Interleukin 6 (IL-6) is a cytokine involved in different physiologic and pathophysiologic processes, and circulating levels of IL-6 differ greatly between individuals, but the results have not always been concordant among diverse populations. The aim of present study was to determine the prevalence of the 3 polymorphisms (j174G/C, j597G/A, and j634C/G) in the IL-6 gene promoter region and their effects on inflammatory markers in normal Han Chinese population. Methods: A total of 232 subjects (143 men and 89 women; mean age, 51.37 ± 17.63 years; range, 22-88 years) of unrelated healthy Han Chinese in Jinangsu area (south of China) were enrolled. Genotyping of the 3 polymorphisms were performed by polymerase chain reaction and restriction fragment length polymorphism combined with gel electrophoresis and then confirmed by direct sequencing. Results: Among the 232 individuals studied, 231 carried the GG wild type of -174G/C; only 1 carried the GC genotype. For -597G/A polymorphism, individuals all carried the GG wild type; the GA or AA genotypes were not detected. The frequencies of -634C/G genotypes CC, CG, and GG were found to be 59.48%, 37.07%, and 3.45%, respectively, the derived allele frequencies for the C and G alleles were 78.02% and 21.98%. There were no significant differences in age, sex, body mass index, or lipids parameters between the -634 CC and CG+GG genotypes. However, individuals with CC genotype showed lower levels of high-sensitivity C-reactive protein and IL-6 than those with CG+GG genotype. Conclusions: IL-6 -174G/C and -597G/A are rare, but -634C/G is common in Han Chinese population, and the -634G allele is associated with circulating levels of IL-6 and C-reactive protein. Copyright © 2011 by The American Federation for Medical Research.


Zhang J.,Ningxia Peoples Hospital
Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi | Year: 2013

This paper is aimed to fulfill a prototype system used to classify and retrieve retinal image automatically. With the content-based image retrieval (CBIR) technology, a method to represent the retinal characteristics mixing the fundus image color (gray) histogram with bright, dark region features and other local comprehensive information was proposed. The method uses kernel principal component analysis (KPCA) to further extract nonlinear features and dimensionality reduced. It also puts forward a measurement method using support vector machine (SVM) on KPCA weighted distance in similarity measure aspect. Testing 300 samples with this prototype system randomly, we obtained the total image number of wrong retrieved 32, and the retrieval rate 89.33%. It showed that the identification rate of the system for retinal image was high.


Wang Z.,Ningxia Peoples Hospital | Wen P.,Ningxia Peoples Hospital | Luo X.,Ningxia Peoples Hospital | Fang X.,Ningxia Peoples Hospital | And 3 more authors.
Tumor Biology | Year: 2014

Osteosarcoma (OS) is the most common bone malignancy worldwide. The vascular endothelial growth factor (VEGF) gene plays an important role in the pathogenesis of OS. The objective of this study aimed to detect the potential association between VEGF genetic polymorphisms and OS susceptibility in Chinese Han population. We recruited 330 OS patients and 342 cancer-free controls in this case-control study. Three single-nucleotide polymorphisms (SNPs) (-634 G > C, +936 C > T, and +1612 G > A) of the VEGF gene were investigated by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and confirmed by direct DNA sequencing. Among these SNPs, we found that the genotypes/alleles of +936 C > T were statistically associated with the increased risk of OS (TT versus (vs.) CC: OR = 2.70, 95 % CI 1.34-5.45, χ2 = 8.2271, p = 0.0041; T vs. C: OR = 1.31, 95 % CI 1.02-1.68, χ2 = 4.3861, p = 0.0362). The T allele and TT genotype of +936 C > T could be factors that increase the risk for susceptibility to OS. The results from this study suggest that VEGF genetic variants are potentially related to OS susceptibility in Chinese Han population and might be used as molecular markers for assessing OS susceptibility. © 2013 International Society of Oncology and BioMarkers (ISOBM).


Fan Y.,Ningxia Peoples Hospital | Wang L.,Ningxia Medical University | Han X.,Ningxia Peoples Hospital | Liu X.,Ningxia Peoples Hospital | Ma H.,Ningxia Peoples Hospital
Molecular Medicine Reports | Year: 2015

Rab25, a member of the Rab family of small guanosine triphosphatase, was reported to have an essential role in the development of human epithelial ovarian cancer. The present study demonstrated that Rab25 mediated the sensitivity of ovarian cancer to cisplatin, a first-line chemotherapeutic agent for the treatment of ovarian cancer in the clinic. Overexpression of Rab25 and increased phosphoinositide 3-kinase (PI3K)/AKT signaling were detected in cisplatin-resistant SKOV-3 cells compared with those in cisplatin-sensitive ES-2 cells. The results of the present study indicated that cisplatin resistance was primarily due to reduced G1 cell cycle arrest following cisplatin treatment in SKOV-3 cells. By contrast, the corresponding phenomenon was not observed following treatment with a Rab25-specific small interfering RNA or treatment with the PI3K/AKT inhibitor LY294002. Of note, inhibition of the PI3K/AKT pathway reduced Rab25 gene expression and sensitized SKOV-3 cells to cisplatin. Furthermore, knockdown of Rab25 showed an effect comparable with blocking the PI3K/AKT pathway. In conclusion, the results of the present study demonstrated that PI3K/AKT and Rab25 significantly contributed to cisplatin resistance in human epithelial ovarian cancer; in addition, silencing Rab25 or inhibiting the PI3K/AKT pathway markedly increased the sensitivity of these cells to cisplatin.

Loading Ningxia Peoples Hospital collaborators
Loading Ningxia Peoples Hospital collaborators