The Experts below are selected from a list of 195 Experts worldwide ranked by ideXlab platform

Hongmin Xiao - One of the best experts on this subject based on the ideXlab platform.

  • oxidative stress disturbs energy metabolism of mitochondria in ethanol induced Gastric Mucosa injury
    World Journal of Gastroenterology, 2008
    Co-Authors: Shaozhen He, Hongzhi Xu, Xiaojuan Zhan, Xiaoning Yang, Hongmin Xiao
    Abstract:

    AIM: To study the role of mitochondrial energy disorder in the pathogenesis of ethanol-induced Gastric Mucosa injury. METHODS: Wistar rats were used in this study. A Gastric Mucosal injury model was established by giving the rats alcohol. Gross and microscopic appearance of Gastric Mucosa and ultrastructure of mitochondria were evaluated. Malondiadehyde (MDA) in Gastric Mucosa was measured with thiobarbituric acid. Expression of ATP synthase (ATPase) subunits 6 and 8 in mitochondrial DNA (mtDNA) was determined by reverse transcription polymerase chain reaction (RTPCR). RESULTS: The Gastric Mucosal lesion index was correlated with the MDA content in Gastric Mucosa. As the concentration of ethanol was elevated and the exposure time to ethanol was extended, the content of MDA in Gastric Mucosa increased and the extent of damage aggravated. The ultrastructure of mitochondria was positively related to the ethanol concentration and exposure time. The expression of mtDNA ATPase subunits 6 and 8 mRNA declined with the increasing MDA content in Gastric Mucosa after gavage with ethanol. CONCLUSION: Ethanol-induced Gastric Mucosa injury is related to oxidative stress, which disturbs energy metabolism of mitochondria and plays a critical role in the pathogenesis of ethanol-induced Gastric Mucosa injury.

Thomas Kirchner - One of the best experts on this subject based on the ideXlab platform.

  • Immunological and morphogenic basis of Gastric Mucosa atrophy and metaplasia
    Virchows Archiv, 2005
    Co-Authors: Gerhard Faller, Thomas Kirchner
    Abstract:

    Chronic gastritis with Gastric Mucosa atrophy, intestinal metaplasia and endocrine cell hyperplasia are alterations with an increased risk for the development of Gastric neoplasias. Immunological studies in autoimmune gastritis, in atrophic Helicobacter pylori gastritis and in studies with transgenic mice point to a central role of the parietal cell in the development of Gastric Mucosa atrophy. Destruction of Gastric epithelial cells alone might not be sufficient for the loss of complete Gastric glands. Gastric atrophy, endocrine cell hyperplasia and intestinal and pancreatic metaplasia can be regarded as the result of altered morphogenesis within the Gastric Mucosa. Impaired expression of the Gastric morphogenic factor Sonic Hedgehog by parietal cells and increased expression of the transcriptional activators of intestinal and pancreatic differentiation, namely CDX2 and PDX1, seem to be crucial for the development of Gastric atrophy and for intestinal, endocrine and pancreatic transdifferentiation processes. Altered expression of these morphogenic factors is partly caused by changes in the Gastric milieu. Further studies concerning the normal and pathological morphogenesis of the Gastric Mucosa and related tissues might give new insight into the pathogenesis of Gastric atrophy and metaplasia.

Shaozhen He - One of the best experts on this subject based on the ideXlab platform.

  • oxidative stress disturbs energy metabolism of mitochondria in ethanol induced Gastric Mucosa injury
    World Journal of Gastroenterology, 2008
    Co-Authors: Shaozhen He, Hongzhi Xu, Xiaojuan Zhan, Xiaoning Yang, Hongmin Xiao
    Abstract:

    AIM: To study the role of mitochondrial energy disorder in the pathogenesis of ethanol-induced Gastric Mucosa injury. METHODS: Wistar rats were used in this study. A Gastric Mucosal injury model was established by giving the rats alcohol. Gross and microscopic appearance of Gastric Mucosa and ultrastructure of mitochondria were evaluated. Malondiadehyde (MDA) in Gastric Mucosa was measured with thiobarbituric acid. Expression of ATP synthase (ATPase) subunits 6 and 8 in mitochondrial DNA (mtDNA) was determined by reverse transcription polymerase chain reaction (RTPCR). RESULTS: The Gastric Mucosal lesion index was correlated with the MDA content in Gastric Mucosa. As the concentration of ethanol was elevated and the exposure time to ethanol was extended, the content of MDA in Gastric Mucosa increased and the extent of damage aggravated. The ultrastructure of mitochondria was positively related to the ethanol concentration and exposure time. The expression of mtDNA ATPase subunits 6 and 8 mRNA declined with the increasing MDA content in Gastric Mucosa after gavage with ethanol. CONCLUSION: Ethanol-induced Gastric Mucosa injury is related to oxidative stress, which disturbs energy metabolism of mitochondria and plays a critical role in the pathogenesis of ethanol-induced Gastric Mucosa injury.

Gerhard Faller - One of the best experts on this subject based on the ideXlab platform.

  • Immunological and morphogenic basis of Gastric Mucosa atrophy and metaplasia
    Virchows Archiv, 2005
    Co-Authors: Gerhard Faller, Thomas Kirchner
    Abstract:

    Chronic gastritis with Gastric Mucosa atrophy, intestinal metaplasia and endocrine cell hyperplasia are alterations with an increased risk for the development of Gastric neoplasias. Immunological studies in autoimmune gastritis, in atrophic Helicobacter pylori gastritis and in studies with transgenic mice point to a central role of the parietal cell in the development of Gastric Mucosa atrophy. Destruction of Gastric epithelial cells alone might not be sufficient for the loss of complete Gastric glands. Gastric atrophy, endocrine cell hyperplasia and intestinal and pancreatic metaplasia can be regarded as the result of altered morphogenesis within the Gastric Mucosa. Impaired expression of the Gastric morphogenic factor Sonic Hedgehog by parietal cells and increased expression of the transcriptional activators of intestinal and pancreatic differentiation, namely CDX2 and PDX1, seem to be crucial for the development of Gastric atrophy and for intestinal, endocrine and pancreatic transdifferentiation processes. Altered expression of these morphogenic factors is partly caused by changes in the Gastric milieu. Further studies concerning the normal and pathological morphogenesis of the Gastric Mucosa and related tissues might give new insight into the pathogenesis of Gastric atrophy and metaplasia.

A I Yemets - One of the best experts on this subject based on the ideXlab platform.