The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform

K. S. Lau - One of the best experts on this subject based on the ideXlab platform.

  • The role of interferon-gamma in lymphocytic thyroiditis: its functional and Pathological Effect on human thyrocytes in culture.
    Clinical and experimental immunology, 2008
    Co-Authors: Awc Kung, K. S. Lau
    Abstract:

    Interferon-gamma (IFN-gamma) has been recognized to possess diverse non-immunological Effects on epithelial cells such as cellular growth and differentiation. We have previously demonstrated that IFN-gamma suppressed thyroid-stimulating hormone (TSH)-stimulated thyroglobulin (TG) synthesis in human thyrocytes through inhibition of TG gene transcription. To define the Pathological mechanism involved in the action of IFN-gamma, we studied the ultrastructural changes of human thyrocytes cultured in monolayer. Stimulation of the thyrocytes with TSH 10 mU/ml for 2 days resulted in marked increase in TG release into the medium. This was accompanied by elongation of microvilli, increase in follicles and acinar formation, increase in secretory granules and prominence of Golgi apparatus and rough-surfaced endoplasmic reticulum. Addition of IFN-gamma (500 U/ml) resulted in marked degeneration with shrinkage of the cell membrane, vacuolation of cytoplasm, swollen mitochondria and presence of lysosomal granules. Co-culturing the thyrocytes with the IFN-gamma and TSH resulted in suppression of the morphological responsiveness to TSH. There was also suppression of TSH-induced TG secretion. However, at 500 U/ml IFN-gamma did not cause lysis of the thyrocytes as estimated by the cellular DNA content. Furthermore, binucleated cells were frequently encountered in those wells that were treated with IFN-gamma for either 2 or 5 days. The findings suggest that IFN-gamma resulted in de-differentiation and degeneration of the thyrocytes, which subsequently regained the growth potential and showed attempts at regeneration. This may explain why most patients with lymphocytic thyroiditis recover from the acute injury and do not suffer from permanent hypothyroidism.

Zhao-hui Chen - One of the best experts on this subject based on the ideXlab platform.

  • Comparative proteome analysis of untreated and Helicobacter pylori-treated HepG2.
    World journal of gastroenterology, 2005
    Co-Authors: Yan Zhang, Xue-fei Tian, Xue-gong Fan, Ren Chen, Zhi-qiang Xiao, Xue-ping Feng, Zhao-hui Chen
    Abstract:

    AIM: To investigate the Pathological Effect of Helicobacter pylori (H pylori) on human hepatic cells, proteomic methods were used to find and to identify proteins that were overexpressed in HepG2 cells treated by H pylori. METHODS: H pylori was co-cultured with HepG2 for 6 h. Two-dimensional gel electrophoresis was used to gain the protein expression pattern of untreated and H pylori-treated HepG2. After staining and image analysis, spots of interest were isolated and subjected to mass spectrometry. RESULTS: Seven proteins, which were up-regulated in H pylori-treated HepG2 cells, were identified. These proteins included integrin beta-1, protein kinase C alpha, LIM/homeobox protein Lhx1, eIF-2-beta, MAP kinase kinase 3, PINCH protein and Ras-related protein Rab-37, which involved in transcription regulation, signal transduction, metabolism and so on. CONCLUSION: H pylori may exert the Pathological Effect on HepG2 cells by up-regulating the expression of some proteins.

Steven A. White - One of the best experts on this subject based on the ideXlab platform.

Xue-fei Tian - One of the best experts on this subject based on the ideXlab platform.

  • The Pathological Effect of Helicobacter pylori infection on liver tissues in mice
    Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases, 2009
    Co-Authors: Yan Huang, Xue-fei Tian, Xue-gong Fan, Cai Zhu
    Abstract:

    Helicobacter pylori infection is associated with chronic gastritis, peptic ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Some reports also suggest that it causes extragastric disease, including hepatitis. In this study, the Pathological changes in the liver and gall bladder in H. pylori-colonized C57BL/6 mice were investigated. Twenty mice were inoculated orally with H. pylori strain SS1, and ten controls were injected with phosphate-buffered saline. Gastric colonization with H. pylori was assessed at 2 months after inoculation. Mice were examined at 8 months by histopathology, culture for H. pylori, and PCR for specific H. pylori genes. All C57BL/6 mice infected with H. pylori for 8 months developed severe gastric mucosal inflammation. Three mice showed mild-to-moderate multifocal hepatitis. The gall bladder mucosa of one H. pylori-infected mouse showed thickening of the mucous membrane with mild submucosal lymphocytic infiltration. H. pylori was observed morphologically in four liver specimens and six gall bladders from infected mice by immunohistochemistry. Specific H. pylori genes were also detected in six liver samples from infected mice, six samples of bile, and two blood samples by nested PCR. Thus, H. pylori inoculated orally may reach the hepatobiliary system and cause inflammation as an independent aetiological factor. The pathway to the liver may be via the blood or the biliary system.

  • Comparative proteome analysis of untreated and Helicobacter pylori-treated HepG2.
    World journal of gastroenterology, 2005
    Co-Authors: Yan Zhang, Xue-fei Tian, Xue-gong Fan, Ren Chen, Zhi-qiang Xiao, Xue-ping Feng, Zhao-hui Chen
    Abstract:

    AIM: To investigate the Pathological Effect of Helicobacter pylori (H pylori) on human hepatic cells, proteomic methods were used to find and to identify proteins that were overexpressed in HepG2 cells treated by H pylori. METHODS: H pylori was co-cultured with HepG2 for 6 h. Two-dimensional gel electrophoresis was used to gain the protein expression pattern of untreated and H pylori-treated HepG2. After staining and image analysis, spots of interest were isolated and subjected to mass spectrometry. RESULTS: Seven proteins, which were up-regulated in H pylori-treated HepG2 cells, were identified. These proteins included integrin beta-1, protein kinase C alpha, LIM/homeobox protein Lhx1, eIF-2-beta, MAP kinase kinase 3, PINCH protein and Ras-related protein Rab-37, which involved in transcription regulation, signal transduction, metabolism and so on. CONCLUSION: H pylori may exert the Pathological Effect on HepG2 cells by up-regulating the expression of some proteins.

  • Experimental study on the Pathological Effect of Helicobacter pylori on liver tissues
    Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology, 2005
    Co-Authors: Xue-fei Tian, Yan Huang, Xue-gong Fan, Cai Zhu
    Abstract:

    OBJECTIVE To observe whether H. pylori inoculated by oral route could arrive in livers and cause liver inflammation as an independent etiological factor. METHODS C57BL/6 mice were orally inoculated with H. pylori SS1 strains and fed for 8 months. H. pylori colonization and pathologic consequences were studied in the liver and gallbladder tissues of the mice; the blood, liver tissue and gastric mucosa were obtained and cultured for H. pylori growth; The bacterial DNA extracted from the liver, bile and blood was examined by nested PCR for H. pylori genes. 16S rRNA PCR amplicons were sequenced and compared with the sequencing results of 16S rRNA PCR amplicons of the bacteria cultured from gastric mucosa and the inoculated H. pylori SS1. RESULTS The bacterial DNA extracted from the liver, bile and blood of the infected mice was detected for H. pylori genes by nested PCR. Six of the 15 samples were positive (40%) in the liver, 6 of 10 samples in the bile (60%), and 2 of 10 samples in the blood (20%). Sequencing results of 16S rRNA PCR products of the livers showed 100% homogeneity when compared with the cultured H. pylori from gastric mucosa and inoculated H. pylori SS1. H. pylori was found in 4 liver tissues of the 15 infected mice (26.7%) and 6 in the gallbladders (40%). Infiltrations of lymphocyte cells along hepatic sinusoids and a lower degree infiltration around interlobular arteries and veins were observed; ballooning degeneration was also observed in some hepatocytes. CONCLUSION H. pylori inoculated by oral route could arrive in the liver and cause inflammation as an independent etiological factor. The routes which the microorganisms took to reach the livers may involve hematogenous and/or biliary system dissemination.

Xue-gong Fan - One of the best experts on this subject based on the ideXlab platform.

  • The Pathological Effect of Helicobacter pylori infection on liver tissues in mice
    Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases, 2009
    Co-Authors: Yan Huang, Xue-fei Tian, Xue-gong Fan, Cai Zhu
    Abstract:

    Helicobacter pylori infection is associated with chronic gastritis, peptic ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Some reports also suggest that it causes extragastric disease, including hepatitis. In this study, the Pathological changes in the liver and gall bladder in H. pylori-colonized C57BL/6 mice were investigated. Twenty mice were inoculated orally with H. pylori strain SS1, and ten controls were injected with phosphate-buffered saline. Gastric colonization with H. pylori was assessed at 2 months after inoculation. Mice were examined at 8 months by histopathology, culture for H. pylori, and PCR for specific H. pylori genes. All C57BL/6 mice infected with H. pylori for 8 months developed severe gastric mucosal inflammation. Three mice showed mild-to-moderate multifocal hepatitis. The gall bladder mucosa of one H. pylori-infected mouse showed thickening of the mucous membrane with mild submucosal lymphocytic infiltration. H. pylori was observed morphologically in four liver specimens and six gall bladders from infected mice by immunohistochemistry. Specific H. pylori genes were also detected in six liver samples from infected mice, six samples of bile, and two blood samples by nested PCR. Thus, H. pylori inoculated orally may reach the hepatobiliary system and cause inflammation as an independent aetiological factor. The pathway to the liver may be via the blood or the biliary system.

  • Comparative proteome analysis of untreated and Helicobacter pylori-treated HepG2.
    World journal of gastroenterology, 2005
    Co-Authors: Yan Zhang, Xue-fei Tian, Xue-gong Fan, Ren Chen, Zhi-qiang Xiao, Xue-ping Feng, Zhao-hui Chen
    Abstract:

    AIM: To investigate the Pathological Effect of Helicobacter pylori (H pylori) on human hepatic cells, proteomic methods were used to find and to identify proteins that were overexpressed in HepG2 cells treated by H pylori. METHODS: H pylori was co-cultured with HepG2 for 6 h. Two-dimensional gel electrophoresis was used to gain the protein expression pattern of untreated and H pylori-treated HepG2. After staining and image analysis, spots of interest were isolated and subjected to mass spectrometry. RESULTS: Seven proteins, which were up-regulated in H pylori-treated HepG2 cells, were identified. These proteins included integrin beta-1, protein kinase C alpha, LIM/homeobox protein Lhx1, eIF-2-beta, MAP kinase kinase 3, PINCH protein and Ras-related protein Rab-37, which involved in transcription regulation, signal transduction, metabolism and so on. CONCLUSION: H pylori may exert the Pathological Effect on HepG2 cells by up-regulating the expression of some proteins.

  • Experimental study on the Pathological Effect of Helicobacter pylori on liver tissues
    Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology, 2005
    Co-Authors: Xue-fei Tian, Yan Huang, Xue-gong Fan, Cai Zhu
    Abstract:

    OBJECTIVE To observe whether H. pylori inoculated by oral route could arrive in livers and cause liver inflammation as an independent etiological factor. METHODS C57BL/6 mice were orally inoculated with H. pylori SS1 strains and fed for 8 months. H. pylori colonization and pathologic consequences were studied in the liver and gallbladder tissues of the mice; the blood, liver tissue and gastric mucosa were obtained and cultured for H. pylori growth; The bacterial DNA extracted from the liver, bile and blood was examined by nested PCR for H. pylori genes. 16S rRNA PCR amplicons were sequenced and compared with the sequencing results of 16S rRNA PCR amplicons of the bacteria cultured from gastric mucosa and the inoculated H. pylori SS1. RESULTS The bacterial DNA extracted from the liver, bile and blood of the infected mice was detected for H. pylori genes by nested PCR. Six of the 15 samples were positive (40%) in the liver, 6 of 10 samples in the bile (60%), and 2 of 10 samples in the blood (20%). Sequencing results of 16S rRNA PCR products of the livers showed 100% homogeneity when compared with the cultured H. pylori from gastric mucosa and inoculated H. pylori SS1. H. pylori was found in 4 liver tissues of the 15 infected mice (26.7%) and 6 in the gallbladders (40%). Infiltrations of lymphocyte cells along hepatic sinusoids and a lower degree infiltration around interlobular arteries and veins were observed; ballooning degeneration was also observed in some hepatocytes. CONCLUSION H. pylori inoculated by oral route could arrive in the liver and cause inflammation as an independent etiological factor. The routes which the microorganisms took to reach the livers may involve hematogenous and/or biliary system dissemination.