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N D Kim

Publications and source records attributed to N D Kim.

97 records · Page 6Linked to original sources

Spatial variation of refractive index in a pane of float glass.

In the statistical interpretation of forensic glass evidence it is standard practice to make the assumption of homogeneity of the refractive index (RI) of the source glass, or of localized homogeneity. However, the work of Locke and Hayes showed that, for toughened windscreen glass, this assumption might not be true. This work is well cited, but there appears to have been little follow-on published research. Furthermore, the toughening process is something known to affect the refractive index, and is a process that float glass does not undergo. Float glass is a major component of casework in New Zealand and for that reason it would be interesting to know whether the findings of Locke and Hayes apply when dealing with float glass. In this paper we describe an experiment similar to that of Locke and Hayes, systematically examining the variation of RI in a pane of float window glass. It was found that, although there were no systematic differences in refractive index, there were observable differences across the pane.

Journal Article↗

Analysis of six anticonvulsant drugs using solid-phase extraction, deuterated internal standards, and gas chromatography-mass spectrometry.

A rapid method for simultaneously determining the anticonvulsant drugs carbamazepine, ethosuximide, phenobarbitone, phenytoin, primidone, and valproic acid is described. Blank plus single-point calibration gives reliable quantitation from therapeutic to high fatal concentrations, except for ethosuximide, for which it gives semiquantitative results. Whole blood and liver tissue samples containing deuterated internal standards were extracted using Bond Elut Certify columns. Butyl derivatives were formed using n-iodobutane and TMAH under mild conditions and were extracted into ethyl acetate as a cleanup step. Recoveries were greater than 50%, except for valproic acid (42%). Sample preparation time was less than 2 h, and the GC run time was less than 20 min per injection. At least two ion pairs formed by electron impact ionization were monitored for each drug. Intraday CVs were less than 6.28% (4.20%) and interday CVs less than 14.1% (for midtherapeutic concentrations in blood [liver], except for ethosuximide). Linearity was observed from subtherapeutic to high fatal levels for all drugs. This method has been applied to forensic cases and has significantly reduced analytical time while improving case-work quality. Results of a case study involving anticonvulsant drugs are given.

Anticonvulsants↗

2-(allylthio)pyrazine suppresses the growth and proliferation of human promyelocytic leukemia (HL-60) cells via induction of apoptosis.

Apoptosis or programmed cell death is a highly organized physiologic process of not only maintaining homeostasis but also selectively eliminating damaged or abnormal cells. Apoptotic destruction of predisposed cells may reduce the proportion of cells available for malignant progression. Thus, pharmacologic manipulation of apoptotic pathway is regarded as a novel strategy in cancer chemoprevention as well as therapy. 2-(Allylthio)pyrazine (2-AP), a pyrazine derivative of allylsulfide synthesized for use as a chemoprotective agent, has been shown to protect against experimental carcinogenesis and mutagenesis. The present study examined the capability of 2-AP to induce apoptosis in cultured human promyelocytic leukemia (HL-60) cells. Treatment of HL-60 cells with 2-AP led to suppression of viability and proliferation in a concentration-dependent manner. Microscopic examination of the treated cells revealed typical morphological features of apoptosis, such as nuclear fragmentation and chromatin condensation. Furthermore, cells treated with 2-AP exhibited internucleosomal DNA fragmentation. Flow cytometric analysis of HL-60 cells exposed to 2-AP showed appearance of a distinct peak representing the subdiploid cell population. 2-AP treatment decreased the ratio of anti-apoptotic Bcl-2 to the death stimulating protein Bax, which may account for the molecular basis of apoptosis-inducing activity of this chemopreventive organosulfur derivative.

Apoptosis↗