• Journal of Biomedical Engineering Research
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• v.19 no.1
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• pp.59-68
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• 1998

Digital hearing aids offer many advantages over conventional analog hearing aids. With the advent of high speed digital signal processing chips, new digital techniques have been introduced to digital hearing aids. In addition, the evaluation of new ideas in hearing aids is necessarily accompanied by intensive subject-based clinical tests which requires much time and cost. In this paper, we present an objective method to evaluate and predict the performance of hearing aid systems without the help of such subject-based tests. In the hearing impairment simulation(HIS) algorithm, a sensorineural hearing impairment medel is established from auditory test data of the impaired subject being simulated. Also, the nonlinear behavior of the loudness recruitment is defined using hearing loss functions generated from the measurements. To transform the natural input sound into the impaired one, a frequency sampling filter is designed. The filter is continuously refreshed with the level-dependent frequency response function provided by the impairment model. To assess the performance, the HIS algorithm was implemented in real-time using a floating-point DSP. Signals processed with the real-time system were presented to normal subjects and their auditory data modified by the system was measured. The sensorineural hearing impairment was simulated and tested. The threshold of hearing and the speech discrimination tests exhibited the efficiency of the system in its use for the hearing impairment simulation. Using the HIS system we evaluated three typical hearing aid algorithms.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.2
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• pp.244-251
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• 2009

Extraction characteristics of dried jujube and functional properties of corresponding extract were monitored by response surface methodology. Maximum extraction yield of 53.69% was obtained at extraction temperature of $50.35^{\circ}C$, extraction time of 16.69 hr, and ethanol concentration of 72.88%. At extraction temperature, extraction time, and ethanol concentration of $45.80^{\circ}C$, 15.47 hr, and 73.12%, respectively, maximum cyclic adenosine monophosphate content was 8.20 mg/100 g. Maximum total polyphenol content was 18.85 mg/g at extraction temperature, extraction time, and ethanol concentration of $64.91^{\circ}C$, 20.84 hr, and 66.91%, respectively. Maximum total flavonoid content was 0.48 mg/g at extraction temperature, extraction time, and ethanol concentration of $57.36^{\circ}C$, 15.14 hr, and 71.08%, respectively. $IC_{50}$ value of electron donating ability showed maximum level of 32.34 mg/mL at extraction temperature of $48.46^{\circ}C$, extraction time of 19.25 hr, and ethanol concentration of 65.36%. Maximum ascorbic acid equivalent antioxidant capacity was 3.58 mg ascorbic acid equivalent per gram sample at extraction temperature, extraction time, and ethanol concentration of $56.09^{\circ}C$, 21.86 hr, and 65.36%, respectively.

• Development and Reproduction
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• v.10 no.2
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• pp.105-113
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• 2006

Reactive oxygen species(ROS) generated in cellular metabolism have an effect on cell maturation and development. In human reproductive tract, oxidative injury by ROS may induce female infertility. Also, oxidative injury may be responsible for developmental retardation and arrest of mammalian preimplantation embryos. Activating transcription factor 4(ATF4) is a member of the cyclic-AMP response element-binding(CREB) familiy of basic region- leucine zipper(bZip). ATF4 is known to regulate stress response to protect cell from various stress factors and inducer of apoptisis. The purpose of this study was to investigate whether ATF4 is involved in the defensive mechanism in oxidative stress condition during the development of mouse preimplantation embryos. To verify the expression of ATF4 in oxidative stress condition, 2-cell stage embryos were cultured in HTF media containing 0.1mM, 0.5mM or 1mM hydrogen peroxide($H_2O_2$) for 1hr(2-cell), 8hr(4-cell), 17hr(8-cell), 24hr(morula), 48hr(early blastocyst) or 64hr(late blastocyst). The developmental rate decreased in the 0.1mM $H_2O_2$ treated group compared with control group. In embryos treated with 0.5mM and 1mM $H_2O_2$ showed 2-cell block. As a results of the semi-quantitative RT-PCR analysis of SOD1, ATF4 and Bax gene expression, SOD1, ATF4 and Bax genes were increased in 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. In 2-cell embryos, expression of SOD1, ATF4 and Bax genes were notably increased in 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. Immunofluorescence analysis showed that ATF4 protein was localized at the cytoplasm of preimplantation embryos. The increase in ATF4 immunoreactivety was observed in the 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. It suggests that oxidative stress by $H_2O_2$ induces expression of ATF4 and may be involved in protection mechanism in preimplantation embryos from oxidative injury.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.39-49
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• 1996

In the present study, we observed change in intracellular $Ca^{2+}$$([Ca^{2+}]_i)$ as measured with the fluorescent $Ca^{2+}-indicator$ fura-2 in association with force development of the rat basilar arteries during activation by$K^+$ depolarizing solution and U46619, a thromboxane analogue, in the absence and the presence of calcitonin-gent related peptide (CGRP). CGRP (30 and 100 nM) caused a concentration-dependent inhibition of U46619-induced contraction with decrease in $[Ca^{2+}]_i$, whereas it did not exert any effect on the $K^+$ (90 mM)-induced contraction and increase in $[Ca^{2+}]_i$, Further, $[Ca^{2+}]_i-force$ relationships were determined by plotting the ratio of $F_{340}/F_{380}$ $([Ca^{2+}]_i)$ as a function of the force induced by U46619, and the results were compared with those obtained in the presence of CGRP. The curves obtained in the presence of CGRP (30 and 100 nM) were significantly moved to downward without right shift of the curves suggesting that CGRP inhibited the U46619-induced contraction only by mediation of reduction in $[Ca^{2+}]_i$ with out any change in the sensitivity of contractile apparatus to $Ca^{2+}$. The CGRP-induced attenuation of $[Ca^{2+}]_i$ and force development was significantly inhibited under pretreatment with CGRP $(8{\sim}37)$ fragment (100 nM), a CGRP1 receptor antagonist. Both the reduced contraction and reduction in $[Ca^{2+}]_i$ caused by CGRP were fully reversed by pretreatment with charybdotoxin (100 nM) and iberiotoxin (100 nM), large conductance $Ca^{2+}-activated$ $K^+$ channel blockers, but not by apamin (300 nM), a small conductance $Ca^{2+}-activated$ $K^+$ channel blocker, and glibenclamide ( 1 ${\mu}M$), an ATP-sensitive $K^+$ channel blocker. In conclusion, it is suggested that the CGRP1 receptor, upon activation by CGRP, are coupled to opening of $Ca^{2+}-activated$ $K^+$ channel and cause to decrease in $[Ca^{2+}]_i$, thereby leading to vasodilation of the rat basilar artery. However, it is not defined that the mechanism underlying vasodilation whether the $K^+$ channel blockers, charybdotoxin and iberiotoxin directly block the CGRP receptors and that CGRP-evoked relaxation is dependent on the cyclic AMP or $K^+$ channel opening or both actions.