Wei Fang Peoples Hospital

Weifang, China

Wei Fang Peoples Hospital

Weifang, China
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Zhang Y.-M.,Wei Fang Peoples Hospital | Wang J.,Wei Fang Peoples Hospital | Liu X.-G.,Weifang Medical University
Medicine (United States) | Year: 2017

Evidence from observational studies shows that hypertension may be a risk factor for knee osteoarthritis (OA). However, the relationship between hypertension and knee OA risk remains controversial. This study aimed to quantitatively assess the relationship between hypertension and risk of knee OA. Three electronic databases (PubMed, Embase, and Cochrane Library) were searched up to July 25, 2016. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were extracted from the included observational studies. Publication bias, heterogeneity test, and subgroup analyses were performed. Eight studies including 2 cohort studies and 6 cross-sectional studies with 9762 participants were finally included in this meta-Analysis. The results showed that hypertension was significantly associated with higher radiographic knee OA and symptomatic knee OA risks of 2.01 (95% CI, 1.28-3.15, I 2 =90.2%, P for heterogeneity <.001) and 1.49 (95% CI, 1.26-1.77, I 2 =0%, P for heterogeneity <.412), respectively. No publication bias was detected. The subgroup analysis showed that the study design did not influence the results (radiographic knee OA: OR=1.42, 95% CI, 1.19-1.71 for cross-sectional studies and OR=2.17, 95% CI, 1.30-3.63 for cohort studies; and symptomatic knee OA: OR=1.85, 95% CI, 1.10-3.13) for cross-sectional studies and OR=2.74, 95% CI, 1.81-4.16 for cohort studies). This meta-Analysis showed that there was a significant relationship between hypertension and knee OA (both radiographic and symptomatic). However, further original studies are needed that use a better design. Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc.


Wang M.,Weifang Center for Maternal | Zhang B.,Wei Fang Peoples Hospital | Dai X.,Weifang Center for Maternal | Zhang Y.,Weifang Center for Maternal | Lian W.,Weifang Center for Maternal
International Journal of Clinical and Experimental Pathology | Year: 2016

Background: MicroRNA-433 (miR-433), possessing tumor suppressive activity, has been found to be down-regulated in different types of cancer. However, its clinical significance in epithelial ovarian cancer (EOC) is still unclear. Therefore, the aim of this study was to detect the miR-433 expression and its prognostic value in patients suffering from EOC. Methods: The miR-433 expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) analysis in 115 EOC tissues and 45 normal tissues. Then, the associations of miR-433 expression with clinicopathologic characteristics as well as overall survival of EOC patients were determined by Chi-square test and Kaplan-Meier method respectively. Besides, the prognostic value of miR-433 was estimated via Cox regression analysis. Results: The expression of miR-433 in EOC tissues were significantly lower than that in normal tissues (P<0.05). In addition, low miR-433 expression was found to be closely correlated with tumor size (P=0.050), advanced FIGO stage (P=0.009), and recurrence (P=0.002). Moreover, the Kaplan-Meier analysis demonstrated that EOC patients with low miR-433 expression had a poorer overall survival than those with high miR-433 expression (P=0.000). Furthermore, the multivariate analysis identified miR-433 (P=0.013; HR=2.973; 95% CI=1.260-7.012) was an independent prognostic factor for EOC patients. Conclusion: For the first time, the current study offered convincing evidence that the expression of miR-433 was decreased in EOC and it might be associated with tumor progression of EOC. Therefore, miR-433 may be an independent prognostic marker for EOC patients.


Chen J.-L.,Shandong Academy of Sciences | Chen F.,Wei Fang Peoples Hospital | Zhang T.-T.,Shandong University | Liu N.-F.,Shandong University
International Journal of Molecular Medicine | Year: 2016

Epithelial ovarian cancer (EOC), the sixth most common cancer in women worldwide, is the most commonly fatal gynecologic malignancy in developed countries. One of the main reasons for this is that relatively little was known about the molecular events responsible for the development of this highly aggressive disease. In the present study, we demonstrated that salt inducible kinase 1 (SIK1; which is also known as MSK/SIK/SNF1LK) was downregulated in ovarian cancer tissue samples. Using HEY ovarian cancer cells, we noted that SIK1 overexpression inhibited proliferation as well as cancer stem cell-associated traits. Silencing SIK1 promoted the proliferation of the EG ovarian cancer cell line. We performed an analysis of potential microRNAs (miRNAs or miRs) target sites using three commonly used prediction algorithms: miRanda, TargetScan and PicTar. All three algorithms predicted that miR-141 targets the 3'UTR of SIK1. Subsequent experiments not only confirmed this prediction, but also showed that miR-141 was associated with the progression of this disease. Finally, we found that miR-141 promoted proliferation of EG cells, whereas silencing miR-141 restored SIK1 expression and inhibited the proliferation of the HEY cells. Elucidating the molecular mechanism of ovarian cancer not only enables us to further understand the pathogenesis and progression of the disease, but also provides new targets for effective therapies.


PubMed | Wei Fang Peoples Hospital, Shandong Academy of Sciences and Shandong University
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2016

Epithelial ovarian cancer(EOC), the sixth most common cancer in women worldwide, is the most commonly fatal gynecologic malignancy in developed countries. One of the main reasons for this is that relatively little was known about the molecular events responsible for the development of this highly aggressive disease. In the present study, we demonstrated that saltinducible kinase1(SIK1; which is also known as MSK/SIK/SNF1LK) was downregulated in ovarian cancer tissue samples. Using HEY ovarian cancer cells, we noted that SIK1 overexpression inhibited proliferation as well as cancer stem cell-associated traits. Silencing SIK1 promoted the proliferation of the EG ovarian cancer cell line. We performed an analysis of potential microRNAs(miRNAs or miRs) target sites using threecommonly used prediction algorithms: miRanda, TargetScan and PicTar. All three algorithms predicted that miR-141 targets the 3UTR of SIK1. Subsequent experiments not only confirmed this prediction, but also showed that miR-141 was associated with the progression of this disease. Finally, we found that miR-141 promoted proliferation of EG cells, whereas silencing miR-141 restored SIK1 expression and inhibited the proliferation of the HEY cells. Elucidating the molecular mechanism of ovarian cancer not only enables us to further understand the pathogenesis and progression of the disease, but also provides new targets for effective therapies.


PubMed | Weifang Medical University, Wei Fang Peoples Hospital, Shandong University and Shantou University
Type: | Journal: European journal of pharmacology | Year: 2015

Leucine aminopeptidase 3 (LAP3) is a cell surface aminopeptidase that catalyzes the hydrolysis of leucine residues from the amino termini of protein or peptide substrates. The over-expression of LAP3 correlates with prognosis and malignant development of several human cell carcinomas. However, the molecular mechanism remains unknown. In this study, we used ES-2 ovarian cancer cell line as a model system to explore the role of LAP3 in regulation of cancer cell invasion by employing a natural LAP3 inhibitor bestatin and LAP3 siRNA. Bestatin inhibited tumor cell migration and invasion in a dose-dependent manner. More interestingly, bestatin down-regulated expression of fascin protein and inhibited activity of fascin promoter luciferase reporter. Both proteome profiler array and Western blot assay showed that bestatin up-regulated the phosphorylation of Hsp27. Furthermore, LAP3 siRNA could up-regulate the phosphorylation of Hsp27 and down-regulate the expression of fascin. Meanwhile, LAP3 siRNA could also down-regulate the phosphorylation of Akt and the expression of MMP-2/9. Taken together, LAP3 could affect the expression of fascin and MMP-2/9 and may act as a potential anti-metastasis therapeutic target.


PubMed | Wei Fang Peoples Hospital and Qingdao University
Type: Journal Article | Journal: Archives of medical science : AMS | Year: 2016

The aim of the study was to investigate the significance of factors associated with minimal hepatic encephalopathy (MHE) in cirrhotic patients.Between September 2012 and August 2013, 60 cirrhotic patients, including MHE and non-MHE (NMHE) patients, were included in the study. Associated factors and clinical factors were analyzed to see if they were significantly different between MHE and non-MHE patients. Upon identifying the factors showing differences, we applied multivariate regression analysis to further decide which were the most significant ones to differentiate MHE from NMHE patients.There were 26 patients diagnosed with MHE and 34 with NMHE. Our results demonstrated that the prevalence rate of small intestinal bacterial overgrowth (SIBO) was highly associated with patients with MHE (65.4%, 17 out of 26), in contrast to the rate in NMHE patients (8.8%, 3 out of 34). We also found that factors including age, education level, intelligent test results, plasma albumin level and plasma ammonia levels were significantly different between MHE and NMHE patients. Ultimately, with logistic regression analysis, we found that SIBO was the most significant factor differentiating MHE patients from NMHE patients (p < 0.05).In cirrhotic patients, SIBO was highly associated with MHE. This may further our understanding of the mechanisms of MHE and help to develop potential therapeutic interventions to treat cirrhotic patients with MHE.


Bai J.-W.,Capital Medical University | Wang Z.,Capital Medical University | Wang Z.,Wei Fang Peoples Hospital | Gui S.-B.,Beijing Tiantan Hospital | Zhang Y.-Z.,Capital Medical University
Oncology Reports | Year: 2012

15-Hydroxyprostaglandin dehydrogenase (15-PGDH) may function as a tumor suppressor that antagonizes the action of the cyclooxygenase-2 (COX-2) oncogene in several types of tumors. However, it is unknown if it has a role in the pituitary. Recently, our group found that 15-PGDH expression was low in prolactin (PRL) secreting adenomas (prolactinomas) and growth hormone (GH) secreting adenomas (GHomas) using fiber-optic BeadArray technology. In this study, we examined the relative expression of 15-PGDH and COX-2 mRNA in clinical specimens and examined the effects of 15-PGDH on GH3 rat pituitary tumor cell proliferation, apoptosis and hormone secretion. 15-PGDH expression was lower and COX-2 expression was higher in prolactinomas and GHomas compared with normal controls. Overexpressed 15-PGDH inhibited tumor cell proliferation and induced apoptosis. It had a significant suppressive effect on mRNA levels and on the secretion of PRL and GH in GH3 cells. The inhibition of cell proliferation was accompanied by the decreased expression of COX-2, matrix metalloproteinase-9 (MMP-9) and B cell leukemia/lymphoma-2 (Bcl-2). These data are suggestive of a previously unrecognized pathway in pituitary tumorigenesis, and this novel observation may shed light on therapeutic strategies for pituitary tumors.


PubMed | Wei Fang Peoples Hospital
Type: Journal Article | Journal: Chinese medical journal | Year: 2013

Multiple epiphysis dysplasia (MED) is a common skeletal dysplasia with a significant locus heterogeneity. In the majority of clinically defined cases, mutations have been identified in the gene encoding cartilage algometric matrix protein (COMP).Five patients were included in the study. Linkage analysis and mutation analysis of the COMP gene were conducted in the patients and their family members.We have identified a novel mutation in axon 14 of COMP gene in the family.This mutation produced a severe MED phenotype with marked short stature, early onset osteoarthritis, and remarkable radiographic changes. Our results extended the range of disease-causing mutations in COMP gene and contributed more information about relationship between mutations and phenotype.


Cytotoxic T-lymphocyte antigen (CTLA-4) plays an important role in downregulating T cell activation and proliferation. The CTLA-4+49G>A polymorphism is one of the most commonly studied polymorphisms in this gene due to its association with many cancer types, but the association between CTLA-4+49G>A polymorphism and digestive system cancer risks remain inconclusive. An updated meta-analysis based on 17 independent case-control studies consisting of 5176 cancer patients and 6747 controls was performed to address this association. Overall, there was no statistically increased risk of digestive system cancers in every genetic comparison. In subgroup analysis, this polymorphism was significantly linked to higher risks for pancreatic cancer (GG vs. AA, OR=1.976, 95% CI=1.496-2.611; GA vs. AA, OR=1.433, 95% CI =1.093-1.879; GG/GA vs. AA, OR=1.668, 95% CI =1.286-2.164; GG vs. GA/AA, OR=1.502, 95% CI=1.098-2.054; G vs. A, OR=1.394, 95% CI=1.098-1.770). We also observed increased susceptibility of hepatocellular cell carcinoma in homozygote comparison (OR=1.433, 95% CI=1.100-1.866) and dominant model (OR=1.360, 95% CI=1.059-1.746). According to the source of controls, significant effects were only observed in hospital-based studies (GA/AA vs. GG, OR=1.257, 95% CI=1.129-1.399). In the stratified analysis by ethnicity, no significantly increased risks were found in either Asian or Caucasian. Our findings suggest that the CTLA-4+49G>A polymorphism may be associated with the risk of pancreatic cancer and hepatocellular cell carcinoma.


PubMed | Wei Fang Peoples Hospital and Shandong University
Type: Journal Article | Journal: Genetics and molecular research : GMR | Year: 2016

A previous study has revealed that miR-29c functions as a tumor suppressor in hepatocellular carcinoma (HCC), but the clinical significance and prognostic value of miR-29c in HCC have not been investigated. Paired human HCC tissues and adjacent noncancerous tissues were obtained from 91 patients, between 2008 to 2014. Quantitative real-time PCR (qRT-PCR) was used to analyze miR-29c expression. Kaplan-Meier survival plots and log-rank tests were used to assess differences in the overall survival of different subgroups of HCC patients. It was observed that miR-29c expression was remarkably decreased in HCC tissues relative to that in normal hepatic tissues (P < 0.001). The low miR-29c level was significantly associated with histologic grade (P = 0.001), microvascular invasion (P = 0.005), and tumor stage (P < 0.001). Kaplan-Meier analysis showed that decreased miR-29c expression correlated with shorter overall survival (P = 0.002). Multivariate Cox regression analysis showed that decreased miR-29c expression (hazard ratio = 2.19, 95%CI = 1.361-6.779, P = 0.025) was independently associated with poor survival in HCC. Our findings demonstrate that miR-29c expression is significantly downregulated in HCC patients and that miR-29c can act as an independent predictor of unfavorable clinical outcome.

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