You L.-Y.,The First Peoples Hospital of Kunming |
Liang Y.-P.,First Peoples Hospital of Kunming |
Yang J.,Kunming Medical University |
Yang L.-H.,Kunming Medical University |
And 5 more authors.
World Chinese Journal of Digestology | Year: 2014
Methods: Seventy-six hospitalized patients with liver fibrosis treated at the Second Affiliated Hospital of Kunming Medical University from March 2011 to February 2012 were included. All patients underwent the liver biopsy, realtime tissue elastography to quantify the degree of liver fibrosis, and measurement of serological indexes including hyaluronic acid (HA), collagen type IV (C IV), type III procollagen (PC III), laminin (LN), transforming growth factor-β1 (TGF-β1), and platelet derived growth factor (PDGF). The diagnostic accuracy of real-time tissue elastography and serological indexes was compared with that of liver biopsy.Aim: To compare the significance of real-time tissue elastography and serological indexes with liver biopsy in liver fibrosis staging and diagnosis.Results: The LF value of real-time tissue elastography, serological indexes and liver biopsy had significant differences in the staging of hepatic fibrosis (P < 0.05). All the values gradually increased with the degree of liver fibrosis. Significant correlations were noted between different methods (P < 0.05). When LF was 3.1 or less, liver fibrosis stage was mainly S1; when LF was > 3.1, liver fibrosis stage was mainly S2, 3 and 4. When HA, LN, CIV, PC III, PDGF and TGF-β1 were equal to or lower than 66.5, 70.5, 59, 116.6, 28.3, and 665.4, respectively, liver fibrosis stage was mainly S1; when HA, LN, CIV, PC III, PDGF and TGF-β1 were > 66.5, 70.5, 59, 116.6, 28.3, and 665.4, respectively, liver fibrosis stage was mainly S2, 3 and 4. The area under the ROC curve was > 0.9 for LF, between 0.7 and 0.9 for HA and PC III, and between 0.5 and 0.7 for LN, CIV, PDGF and TGF-β1.Conclusion: Real-time tissue elastography findings are positively correlated with the degree of liver fibrosis. Serological indexes of HA, LN, CIV, PC III, PDGF and TGF-β1 increase with the increase of degree of hepatic fibrosis, and can be used to indirectly assess the degree of liver fibrosis. LF has high accuracy in the diagnosis of liver fibrosis, HA and PC III have medium accuracy, and LN, CIV, PDGF and TGF-β1 have low accuracy. Real-time tissue elastography findings are coincident with the pathological results and can be used to assess the degree of liver fibrosis. © 2014 Baishideng Publishing Group Inc. All rights reserved. Source
Sun X.,First Peoples Hospital of Kunming |
Liao N.-K.,Shanghai JiaoTong University |
Yu J.-J.,Shanghai JiaoTong University
Journal of International Medical Research | Year: 2012
Objective: To evaluate the utility of a mitochondrial functional score in predicting the progress of prostate cancer. Methods: This retrospective study included 72 patients (mean age 70.1 years) with prostate cancer who were treated by radical prostatectomy between October 2006 and March 2007. The epithelio - glandular mitochondrial functional scores were assessed according to the Flameng grading. Patients were divided into six groups (groups 1 - 6) according to their Gleason score (Gleason score 2 - 7, respectively). The correlation between Gleason score and mitochondrial functional score was examined using Pearson's correlation coefficient. Results: The mean mitochondrial functional score was significantly lower in group 6 compared with group 1. An inverse correlation was found between the Gleason and mitochondrial functional scores. At 1 year, significantly fewer patients in group 1 had died (0/15 patients) than in group 6 (2/10 patients); the deaths were cancerrelated. Conclusion: Mitochondrial dysfunction exists in patients with prostate cancer, particularly in cases with a higher degree of malignancy. The mitochondrial functional score, combined with the Gleason score, is beneficial for predicting the progress of prostate cancer. © 2012 Field House Publishing LLP. Source
Liu W.-H.,Yunnan University |
Zhao Y.-S.,Yunnan University |
Gao S.-Y.,Chuxiong Normal University |
Li S.-D.,Kunming Medical College |
And 3 more authors.
American Journal of Pathology | Year: 2010
Elevated homocysteine levels are defined as hyperhomocysteinemia (HHcy), a disorder that is associated with cardiovascular and neurodegenerative diseases as well as with hepatic fibrosis. Recent studies have shown that HHcy promotes hepatic injury by increasing oxidative stress. Although homocysteine induces cell cycle arrest in a variety of different cell types, it is not known whether HHcy has a definitive role in hepatocyte proliferation during liver regeneration. In this report, we investigated the effect of homocysteine on liver regeneration. Our results demonstrated that mice with HHcy exhibited an impairment in liver regeneration after partial hepatectomy, as measured by immunohistochemical staining of proliferation cell nuclear antigen and bromodeoxyuridine incorporation. Impaired proliferation was also correlated with reduced cyclin D1 induction and elevated expression levels of both p53 and p21Cip1. In addition, the phosphorylation of Akt, which plays an essential role in normal regeneration responses, was attenuated during the early phases of liver regeneration in HHcy mice. Our results also indicated that the cAMP/protein kinase A pathway mediated the inhibitory effect of homocysteine on liver regeneration. These findings provide evidence that impairment of liver regeneration by HHcy may result in delayed recovery from liver injury induced by homocysteine itself. Copyright © American Society for Investigative Pathology. Source
Hao X.-D.,CAS Kunming Institute of Zoology |
Hao X.-D.,Yunnan University |
Yang Y.,CAS Kunming Institute of Zoology |
Song X.,CAS Kunming Institute of Zoology |
And 14 more authors.
Oncology Reports | Year: 2013
Genomic instability caused by telomere erosion is an important mechanism of tumorigenesis. p53 plays a key role in cellular senescence and/or apoptosis associated with telomere erosion which positions p53 as a guard against tumorigenesis. The present study was undertaken to investigate the potential interactions between p53 functional mutations, polymorphisms, allelic loss and telomere erosion in 126 breast tumor patients and 68 esophageal cancer patients. Telomere length (TL) was measured by real-time quantitative PCR. Somatic mutations, polymorphisms and allelic loss in the TP53 gene were detected by direct sequencing of both tumor and normal tissue samples. Our results showed that telomeres were significantly shorter in tumors with somatic p53 mutations compared with tumors with wild-type p53 in both breast tumors (P=0.007) and esophageal cancer (P=0.001). Telomeres of patients with minor genotype CC of rs12951053 and GG of rs1042522 were significantly shorter compared to patients with other genotypes of this single nucleotide polymorphism in esophageal cancer tissue. Furthermore, TP53 allelic loss was detected and significantly associated with somatic mutations in both types of tumor tissues. These findings suggest that somatic p53 mutations, rs12951053 genotype CC and rs1042522 genotype GG contribute to erosion of telomeres, and TP53 allelic loss may be one of the representations of chromosomal instability caused by telomere erosion combined with somatic p53 mutations. These results support that the TP53 gene has a strong interaction with TL erosion in tumorigenesis. Source
Zhuang L.,Kunming Medical University |
Shen L.-D.,Kunming Medical University |
Li K.,Kunming Medical University |
Yang R.-X.,Kunming Medical University |
And 8 more authors.
Molecular Medicine Reports | Year: 2015
Livin is a novel member of the inhibitor of apoptosis protein family that has been reported to be overexpressed in various types of human malignancy. Although several studies have demonstrated that livin may be used as an effective target for tumor therapy, few studies have investigated its role in human lung adenocarcinoma. In the present study, two different methods were used in order to investigate the tumor-suppressing effect of livin in human lung adenocarcinoma cells. Firstly, small interfering (si)RNA technology was used to down regulate livin expression; siRNA-mediated knockdown of livin was confirmed using reverse transcription quantitative polymerase chain reaction and western blot analysis, and cell proliferations was assessed using an MTT assay in vitro. Secondly, inhibition of livin expression was induced through the synergistic inhibitory effect between flavopiridol and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Experimental results revealed that, following transfection of the livin gene-silencing vector, the gene expression of livin was markedly decreased, SPC-A1 cell proliferation was significantly reduced and the therapeutic effect of the chemotherapy drug cisplatin was markedly improved. This growth inhibitory effect was also observed in the flavopiridol and TRAIL combination treatment group. In the flavopiridol and TRAIL combination treatment group, the protein expression of livin was significantly reduced and the survival rate of SPC-A1 cells was significantly lower than the flavopiridol and TRAIL single operation group. In conclusion, the RNA silencing and the synergistic inhibitory effect between flavopiridol with TRAIL was able to effectively inhibit the expression of livin, significantly decrease SPC-A1 tumor cell proliferation and significantly enhance sensitivity to the chemotherapy drug cisplatin. These findings suggest that livin may be used as a novel target for tumor gene therapy. Source