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is type Ⅰ alpha 2 collagen gene responsible for intracranial aneurysm in Northeast China?

Neural Regeneration Research 2013年第5期8卷 445-451页

作者： Pengfei Wu Bo Li Anhua Wu Yunjie Wang Department of Neurosurgery First Affiliated Hospital of China Medical University Department of Developmental Biology Key Laboratory of Cell Biology Ministry of Public Health of China China Medical University

in this study, we investigated whether a single nucleotide polymorphism （rs42524 G 〉 C） in the type i alpha 2 collagen gene was associated with sporadic ruptured intracranial aneurysm or its clinical characteristics in patients from Northeast China. Genotyping of the rs42524 G 〉 C polymorphism was carried out using a polymerase chain reaction-restriction fragment length polymorphism assay. The data showed that the frequency of the rs42524 GC ＋ CC genotype was significantly higher than the GG genotype among intracranial aneurysm patients whose Hunt and Hess grading scale was 〉 3. in addition, the rs42524 G 〉 C genotype was found to have a statistically significant association with intracranial aneurysm risk. These findings indicate that the type i alpha 2 collagen gene gene may be involved in a predisposition to intracranial aneurysm in the Northeast Chinese population. Crucially, the rs42524 C allele may be an important risk factor for increased severity of the condition in patients with ruptured intracranial aneurysms.

关键词： neural regeneration clinical practice intracranial aneurysm type i collagen gene single nucleotide polymorphism polymerase chain reaction-restriction fragment length polymorphism assay susceptibility risk factors neuroregeneration

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Role of ethanol in the regulation of hepatic stellate cell function

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World Journal of Gastroenterology 2006年第43期12卷 6926-6932页

作者： Jian-Hua Wang Robert G Batey Jacob George Storr Liver Unit Westmead Millennium Institute University of Sydney and WestmeadHospital Westmead New South Wales Australia Drug and Alcohol Clinical Services HunterNew England Area Health Service Locked Bag 119 WallsendNew South Wales 2287 Australia

Evidence has accumulated to suggest an important role of ethanol and/or its metabolites in the pathogenesis of alcohol-related liver disease. in this review, the fibrogenic effects of ethanol and its metabolites on hepatic stellate cells (HSCs) are discussed. in brief, ethanol interferes with retinoid metabolism and its signaling, induces the release of fibrogenic cytokines such as transforming growth factor β-1 (TGFβ-1) from HSCs, up-regulates the gene expression of collagen i and enhances type i collagen protein production by HSCs. Ethanol further perpetuates an activated HSC phenotype through extracellular matrix remodeling. The underlying pathophysiologic mechanisms by which ethanol exerts these pro-fibrogenic effects on HSCs are reviewed.

关键词： Ethanol Acetaldehyde Hepatic stellate cells liver fibrosis type i collagen gene Transcription factors Transforming growth factor β-1

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