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The National Health Insurance Research Database (NHIRD)
Liang-Yu Lin,Charlotte Warren-Gash,Liam Smeeth,Pau-Chung Chen 한국역학회 2018 Epidemiology and Health Vol.40 No.-
Electronic health records (EHRs) can provide researchers with extraordinary opportunities for population based research. The National Health Insurance system of Taiwan was established in 1995 and covers more than 99.6% of the Taiwanese population; this system’s claims data are released as the National Health Insurance Research Database (NHIRD). All data from primary outpatient departments and inpatient hospital care settings are included in this database. After a change and update in 2016, the NHIRD is maintained and regulated by the Data Science Centre of the Ministry of Health and Welfare of Taiwan. Datasets for approved research are released in three forms: sampling datasets comprising two million subjects, disease-specific datasets, and full population datasets. These datasets are de-identified and contain basic demographic information, disease diagnoses, prescriptions, operations, and investigations. Data can be linked to governmental surveys or other research datasets. While only a small number of validation studies with small sample sizes have been undertaken, they generally report positive predictive values of over 70% across different diagnoses. Currently, patients cannot opt out of inclusion in the database, though this requirement is under review. In conclusion, the NHIRD is a large, powerful data source for biomedical research.
Trichloroethylene induces dopaminergic neurodegeneration in Fisher 344 rats
Liu, Mei,Choi, Dong-Young,Hunter, Randy L.,Pandya, Jignesh D.,Cass, Wayne A.,Sullivan, Patrick G.,Kim, Hyoung-Chun,Gash, Don M.,Bing, Guoying Blackwell Publishing Ltd 2010 Journal of Neurochemistry Vol.112 No.3
<P><I>J. Neurochem.</I> (2010) <B>112</B>, 773–783.</P><P>Abstract</P><P>Trichloroethylene, a chlorinated solvent widely used as a degreasing agent, is a common environmental contaminant. Emerging evidence suggests that chronic exposure to trichloroethylene may contribute to the development of Parkinson’s disease. The purpose of this study was to determine if selective loss of nigrostriatal dopaminergic neurons could be reproduced by systemic exposure of adult Fisher 344 rats to trichloroethylene. In our experiments, oral administration of trichloroethylene induced a significant loss of dopaminergic neurons in the substantia nigra pars compacta in a dose-dependent manner, whereas the number of both cholinergic and GABAergic neurons were not decreased in the striatum. There was a robust decline in striatal levels of 3, 4-dihydroxyphenylacetic acid without a significant depletion of striatal dopamine. Rats treated with trichloroethylene showed defects in rotarod behavior test. We also found a significantly reduced mitochondrial complex I activity with elevated oxidative stress markers and activated microglia in the nigral area. In addition, we observed intracellular &agr;-synuclein accumulation in the dorsal motor nucleus of the vagus nerve, with some in nigral neurons, but little in neurons of cerebral cortex. Overall, our animal model exhibits some important features of Parkinsonism, and further supports that trichloroethylene may be an environmental risk factors for Parkinson’s disease.</P>