ABSTRACT
BACKGROUND: Recently developed full-range C-reactive protein (CRP) tests, which are based on the immunoturbidimetric method, have wider analytical measurement ranges (AMR) than previously used tests. We evaluated the AMR of 3 full-range CRP tests-2 new and 1 previously used test. METHODS: We analyzed the precision and AMR of 2 full-range CRP tests (Sekisui, Nanopia CRP, N-CRP and Iatron, IATRO CRP-EX, I-CRP) and compared the values obtained for these tests with those obtained for the conventional full-range CRP test (Sekisui, PureAuto S CRP, P-CRP). We evaluated the tests for the limit of quantification and for linearity. We also compared these results of these tests by using the comparative test (Dade Behring, cCRP) for cardiovascular risk assessment. RESULTS: Coefficients of variation (CVs) of all the full-range CRP tests were less than 10% for concentrations greater than 0.6 mg/L, and CVs of N-CRP and I-CRP were lower than those of P-CRP for concentrations less than 1 mg/L. N-CRP (0.1-467 mg/L) and I-CRP (0.1-280 mg/L) had wider AMR than P-CRP (3-233 mg/L). All the full-range CRP tests showed more than 90% agreement with the cCRP values for the assessment of cardiovascular risk. CONCLUSIONS: The 3 full-range CRP tests, by virtue of their wide AMR, may be used for the detection of acute inflammation as well as for the assessment of cardiovascular risk. N-CRP and I-CRP may be more useful than P-CRP for determining the CRP concentration, especially for the detection of concentrations close to the lower or upper limit of the analytical range, without the need for repetition of the test.
Subject(s)
Humans , C-Reactive Protein/analysis , Cardiovascular Diseases/diagnosis , Immunoassay/methods , Limit of Detection , Nephelometry and Turbidimetry/methods , Reproducibility of Results , Risk AssessmentABSTRACT
PURPOSE: Our study was an experimental model for the mechanism of cortical dysplasia. We examined the changes of neuronal cells and glial cells by intrauterine irradiation. This paper will elucidate the effect of these changes on the development of cortical dysplasia. METHODS: The cytotoxic effect of irradiation was examined by viability and numbers in cerebral cortical neurons and glial cells, which were derived from a mouse exposed to 225 cGy of gamma-irradiation on embryonic day 17. In addition, the protective effect of an inhibitor of intracellular calcium release, dantrolene sodium(DS), on irradiation-induced neurotoxicity was examined after DS(10 mg/kg) was administrated via intraperitoneal injection after intrauterine irradiation. RESULTS: 1) Irradiation induced the decrement of the cell number and cell viability of cerebral cortical neurons in the developing stages. 2) The number of glial cells in the mouse treated with intrauterine irradiation was increased in E20-P4 stages compared with the control group, but there was no difference in cell viability. 3) The glial fibrillary acidic protein(GFAP)-positive cells were seen in developing stages (E20-P4). 4) In the protective effect from neuronal cell death by intrauterine irradiation, DS attenuated cell death by an increase of neuronal cells. CONCLUSION: From these results, it is suggested that intrauterine irradiation has the neurotoxic effect as neuronal cell death and induced glial cell proliferation. A selective inhibitor of intracellular calcium release such as DS is effective in protecting neuronal cell death induced by irradiation of the intrauterine period. Cortical dysplasia induced by intrauterine irradiation may be involved in neuronal cell death and the hyperproliferation of glial cells. Intracellular calcium influx may contribute to the pathogenesis of irradiation-induced neuronal cell death.