• Journal of Preventive Medicine and Public Health
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• 제26권4호
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• pp.565-573
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• 1993

Noise is not only affecting the ear and the auditory cortex locally, but its influence is widely spread throughout the brain structures, e. g., the reticular formation, the brain stem nuclei or the subcortical forebrain area. Hence, any of the organism's activities can be hindered or stimulated by noise. High noise is a stressor and the catecholamine level can be used both as a stress marker and as an indicator of modified sympathetic nervous system activity. Several recent studies have found that the urinary excretion of catecholamines is increased due to high noise intensity, especially unexpectedly high and long lasting noise. The present study was conducted in order to examine the effects of noise stress on urinary excretion of ctecholamines in rats and humans. Rats were exposed to 90 dB noise for 10, 30, and 60 minutes, 3 and 12 hours. 24 hour . urinary samples were collected and the catecholamones were extracted by alumina and analyzed by HPLC-ECD. Catecholamine levels increased with time of exposure up to 60 minutes : norepinephrine concentration at 60 min of noise=1.038 ng/ml, epinephrine=0.636 ng/ml. Urine catecholamines of blue collar workers exposed to 90 dB of noise at the work place were collected between 2 and 4 p.m. and compared to that of white collar workers exposed to 70 dB. Mean norepinephrine level of the blue collar workers was 0.89 ng/ml (${\pm}0.25$), epinephrine 0.24ng/m1 (${\pm}0.09$), and that of the white collar workers 0.48 ng/ml (${\pm}0.12$), epinephrine 0.19 ng/ml(${\pm}0.05$). It was concluded that noise acts as a stressor and increases the catecholamine levels in both rats and humans.

• Archives of Pharmacal Research
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• 제28권9호
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• pp.1092-1096
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• 2005

Huperzine A-loaded microspheres composed of poly(D,L-lactide-co-glycolide) were prepared by an O/w emulsion solvent evaporation method. The characterization of the microspheres such as drug loading, size, shape and release profile was described. The in vitro release in the initial 7 days was nearly linear with $10\%$ released per day. Thereafter drug release rate became slow gradually and about $90\%$ drug released at day 21. The in vitro release rate determined by dialysis bag method had a good correlation with the in vivo release rate. Huperzine A aqueous solution was intramuscularly injected (i.m.) at 0.4mg/kg and microspheres were intra­muscularly injected at 8.4 mg eq huperzine A/kg in rats. The maxium plasma concentration $(C_{max})$ after i.m. microspheres was only $32\%$ of that after i.m. solution. Drug in plasma could be detectd until day 14 and about $5\%$ of administered dose was residued at the injection site at day 14. The relative bioavailability of huperzine A microspheres over a period of 14 days was $94.7\%$. Inhibition of acyecholinesterase activity (AchE) in rat's cortex, hippocampus and striatum could sustain for about 14 days. In conclusion, huperzine A-loaded microspheres possessed a prolonged and complete drug release with significant inhibition of AchE for 2 weeks in rats.

• The Korean Journal of Physiology and Pharmacology
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• 제2권4호
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• pp.435-441
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• 1998

We examined effects of interleukin $1{\alpha}$ ($IL1{\alpha}$) and phorbol 12, 13 dibutyrate (PDB), an activator of protein kinase C, on mRNA for Prostaglandin H synthase (PGHS) and prostanoid production in cultured ovine meningeal fibroblasts. Immuno- and morphologically-identified fibroblasts were derived from cerebral cortex and white matter from fetal lambs (approximately 120 days gestation) and grown to confluence on glass coverslips in 12 well plates. Levels of prostaglandin $F_{2{\alpha}}$ and the stable hydrolysis product of prostacyclin (i.e., $6-keto-PGF_{1{\alpha}}$) were determined using enzyme immunoassay. Relative amounts of mRNA were determined by in situ hybridization using ovine cDNA for PGHS1. $IL1{\alpha}$ (10 ng/ml) increased mRNA levels over baseline by $62{\pm}19%$ (p＜0.05) at 60 min., $37{\pm}12%$ (NS) at 120 min., and $36{\pm}18%$ (NS) at 240 min (n=12). Levels of $6-keto-PGF_{1{\alpha}}$ were $148{\pm}18%$ pg/ml during baseline, $246{\pm}41%$ pg/ml at 60 min., $248{\pm}40%$ pg/ml at 120 min., and $259{\pm}62%$ pg/ml at 240 min (all p＜0.05) (n=12). $PGF_{2{\alpha}}$ was increased although it wasn't statistically significant. However, $IL1{\alpha}$ decreased $PGE_2$ level significantly (all p＜0.05). PDB $(10^{-6}M)$ increased mRNA levels over baseline by $25{\pm}6%$ after 30 min., $40{\pm}6%$ after 60 min., and $20{\pm}8%$ after 90 min. (n=9) (all p＜0.05). Levels of $6-keto-PGF_{1{\alpha}}$ were $200{\pm}43%$ pg/ml during baseline, $202{\pm}43%$ pg/ml after 30 min. (NS), $268{\pm}58%$ pg/ml after 60 min. (p＜0.05), and $296{\pm}60%$ pg/ml after 90 min. (p＜0.05) (n=9). Levels of $PGF_{2{\alpha}}$ were $178{\pm}26%$ pg/ml during baseline, $300{\pm}30%$ pg/ml after 30 min., $299{\pm}35%$ pg/ml after 60 min., and $355{\pm}32%$ pg/ml after 90 min (all p＜0.05) (n=6). Actinomycin-D (1 mg/ml) prevented increases in mRNA, $6-keto-PGF_{1{\alpha}}$, and $PGF_{2{\alpha}}$ at 60 min. for both $IL1{\alpha}$ and PDB. We conclude that cerebral fibroblasts are avid producers of prostanoids, and that enhanced production of PGHS is responsible for augmented $PGF_{2{\alpha}}$ and prostacyclin production in the presence of an activator of protein kinase C and for decreased $PGE_2$ and increased prostacyclin production in the presence of $IL1{\alpha}$.

• 한국산업정보학회논문지
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• 제18권5호
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• pp.33-37
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• 2013

본 논문은 FPGA를 이용한 SDRAM Controller 설계 방법에 관하여 기술한다. 임베디드 시스템의 성능 향상과 함께, 대용량의 메모리를 지원하기 위하여 SDRAM이 사용되고 있으며, 이를 위해서는 SDRAM 컨트롤러의 설계가 요구된다. 본 논문에서는 FPGA에서 SDRAM 제어기를 구현함으로써 SDRAM을 사용할 수 있도록 하며 ARM코어로부터 제어되는 AHB-Lite 버스에서 SDRAM이 동작하는 결과를 보여준다.

• Journal of information and communication convergence engineering
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• 제19권3호
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• pp.175-179
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• 2021

Enhancing the reliability of the system is important for recent system-on-chip (SoC) designs. This importance has led to studies on fault diagnosis and tolerance. Fault-injection (FI) techniques are widely used to measure the fault-tolerance capabilities of resilient systems. FI techniques suffer from limitations in relation to environmental conditions and system features. Moreover, a hardware-based FI can cause permanent damage to the target system, because the actual circuit cannot be restored. Accordingly, we propose a simulation-based FI framework based on the Verilog Procedural Interface for measuring the failure rates of SoCs caused by soft errors. We execute five benchmark programs using an ARM Cortex M0 processor and inject soft errors using the proposed framework. The experiment has a 95% confidence level with a ±2.53% error, and confirms the reliability and feasibility of using proposed framework for fault analysis in SoCs.

• Korean Journal of Acupuncture
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• 제17권1호
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• pp.179-190
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• 2000

This study was undertaken to determine whether Juglandis semen extract solution (JLS solution) exerts protective effect against oxidant-induced inhibition of glutamate uptake by synaptosomes. Synaptosome was prepared from rabbit brain cortex. Glutamate uptake increased by incubation time during 10 minutes, which was significantly inhibited by 1mM t-buthylhydroperoxide(t-BHP). JLS solution prevented t-BHP-induced inhibition of glutamate uptake in a dose-dependent manner. t-BHP reduced glutamate uptake in dose-dependent fashion, which was significantly prevented by 2% JLS solution. t-BHP(1mM) and $ascorbate/Fe^{2+}(50/1{\mu}M)$ increased lipid peroxidation in synaptosomes by 5-fold, and it was significantly prevented by 2% JLS solution. $HgCl_2(0.1mM)$ inhibited glutamate uptake and increased lipid peroxidation. These changes were prevented by 2% JLS solution. Synaptosomal Na-K-ATPase activity was inhibited by t-BHP(1mM) and $H_2O_2(50mM)$, which was prevented by 2% JLS solution. The results indicate that JLS solution prevents oxidant-induced inhibition of glutamate by synaptosomes, and this may result from inhibition of lipid peroxidation induced by oxidants.

• Toxicological Research
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• 제23권3호
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• pp.279-287
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• 2007

Copper (Cu) is an essential trace element indispensable for brain development and function; either excess or deficiency in Cu can cause brain malfunction. While it is known that Cu and Fe homeostasis are strictly regulated in the brain, the question as to how systemic Fe status may influence brain Cu distribution was poorly understood. This study was designed to test the hypothesis that dietary Fe condition affects Cu transport into the brain, leading to an altered brain distribution of Cu. Rats were divided into 3 groups; an Fe-deficient (Fe-D) group which received an Fe-D diet ($3{\sim}5 mg$ Fe/kg), a control group that was fed with normal diet (35mg Fe/kg), and an Fe-overload group whose diet contained an Fe-O diet (20g carbonyl Fe/kg). Following a 4-week treatment, the concentration of Cu/Fe in serum, CSF (cerebrospinal fluid) and brain were determined by AAS, and the uptake rates of Cu into choroids plexus (CP), CSF, brain capillary and parenchyma were determined by an in situ brain perfusion, followed by capillary depletion. In Fe-D and Fe-O, serum Fe level decreased by 91% (p<0.01) and increased by 131% (p<0.01), respectively, in comparison to controls. Fe concentrations in all brain regions tested (frontal cortex, striatum, hippocampus, mid brain, and cerebellum) were lower than those of controls in Fe-D rats (p<0.05), but not changed in Fe-O rats. In Fe-D animals, serum and CSF Cu were not affected, while brain Cu levels in all tested regions (frontal cortex, striatum, hippocampus, mid brain, and cerebellum) were significantly increased (p<0.05). Likewise, the unidirectional transport rate constants $(K_{in})$ of Cu in CP, CSF, brain capillary and parenchyma were significantly increased (p<0.05) in the Fe-D rats. In contrast, with Fe-O, serum, CSF and brain Cu concentrations were significantly decreased as compared to controls (p<0.05). Cu transport was no significant change of Cu transport of serum in Fe-O rats. The mRNA levels of five Cu-related transporters were not affected by Fe status except DMT1 in the CP, which was increased in Fe-D and decreased in Fe-O. Our data suggest that Cu transport into brain and ensuing brain Cu levels are regulated by systemic Fe status. Fe deficiency appears to augment Cu transport by brain barriers, leading to an accumulation of Cu in brain parenchyma.

• 대한핵의학회지
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• 제32권5호
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• pp.397-402
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• 1998

목적: 대뇌피질의 구조적 병변이 없는 기저핵 혈종환자에 있어서, 대뇌와 소뇌의 해리 현상에 관해 알아보고자하였다. 대상 및 방법 : CT와 MRI상 혈종이 기저핵에 국한되고, 대뇌 피질의 구조적 병변이 없는 12명의 환자를 대상으로 하였다. Tc-99m ECD PECT검사가 전 예에서 시행되었고, 대조군으로 MRI상 구조적 병변이 없고 SPECT 검사상 육안적으로 정상 소견을 보인 20명의 정신과 환자가 선택되었다. 해리 현상에 의한 rCBF의 변화를 육안적으로 확인하였고, 반정량적 분석을 위해 asymmetric index (AI)를 이용하였다. AI가 기저핵, 시상, 소뇌와 대뇌 피질 (전두엽, 측두엽, 두정엽)에서 측정되었고, 대조군 AI의 (평균+2X표준편차)보다 큰 AI를 가지는 경우를 저혈류로 정의하였다. 결과: 환자군에서 측정된 소뇌와 대뇌 피질의 평균 AI는 대조군과 비교하여 통계학적으로 의미 있게 큰 수치를 보였다 (p<0.05): 소뇌 ($18.68{\pm}8.94$ vs $4.35{\pm}0.94$, 평균 표준표차), 시상 ($31.91{\pm}10.61$ vs $2.51{\pm}1.45$), 기저핵 ($35.94{\pm}16.15$ vs $4.34{\pm}2.08$), 두정엽 ($18.94{\pm}10.69$ vs $3.24{\pm}0.87$), 전두엽 ($13.60{\pm}10.8$ vs $4.02{\pm}2.04$), 측두엽 ($18.92{\pm}11.95$ vs $5.13{\pm}1.69$). 12명의 환자 중 혈종의 반대측 소뇌(10명), 동측 시상 (12명) 동측 두정엽 (12명), 전두엽 (6명), 측두엽 (10명)에서 육안적으로 또한 AI를 이용한 반정량적 분석상 의미 있는 저혈류를 보였다. 결론: 교차소뇌해리 현상과 피질 해리 현상은 기저핵 혈종 환자에서 빈번하게 관찰되었다. 이는 교차 소뇌해리 현상이 기존에 알려진 피질 뇌교 소뇌로 (corticopontocerebellar tract)의 장애가 없이도 발생할 수 있다는 것을 시사한다.

• 분석과학
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• 제14권2호
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• pp.191-195
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• 2001

Sorbaria sorbifolia의 다양한 추출 및 정제방법에 의하여 protostane계 triterpenoid인 cucurbitacin D, F를 분리하여 그를 표준품으로 하여 S. sorbifolia에 함유된 cucurbitacin D, F를 정량하였다. 표준품으로서 cucurbitacin D, F는 $^1H$-NMR, FAB-MS, UV 등 각종 물리화학적자료에 의하여 구조 동정하였으며 그들은 YMC-Pack ODS-AQ(303)[$250{\times}4.6mm$ I.D., $S-5{\mu}m$, 120A]을 칼럼으로 사용한 고속액체 크로마토그래피에 의하여 분리하였다. Cucurbitacin D, F의 액체크로마토그래피에 의한 정량 분석 결과 cucurbitacin F의 경우 S. sorbifolia 시료에 10.73mg/kg으로 존재하였으나 cucurbitacin D는 검출되지 않았다. 또한 각종 암세포주에서 평균 $ED_{50}$값이 $0.1{\mu}g/mL$ 이하로서 강한 세포독성을 보였으며 이 두 화합물을 생쥐의 복강에 투여하였을 때 $LD_{50}$값은 각각 4.7, 2.5mg/kg/day로서 심한 급성독성을 나타내었다.

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2003년도 학술발표대회 발표논문초록집
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• pp.80-80
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• 2003

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms, accompanied by marked cell death in the striatum and cortex. Stereotaxic injection of quinolinic acid (QA) into striatum results in a degeneration of GABAergic neurons and exhibits abnormal motor behaviors typical of the illness. The objective of this study was carried out to obtain basic information about whether parthenogenetic mouse embryonic stem (PmES) cells are suitable for cell replacement therapy of HD. To establish PmES cell lines, hybrid F1 (C57BL/6xCBA/N) mouse oocytes were treated with 7% ethanol for 5 min and cytochalasin-B for 4 hr to initiate spontaneous cleavage. Thus established PmES cells were induced to differentiate using bFGF (20ng/ml) followed by selection of neuronal precursor cells for 8 days in N2 medium. After selection, cells were expanded at the presence of bFGF (20 ng/ml) for another 6 days, then a final differentiation step in N2 medium for 7 days. To establish recipient animal models of HD, young adult mice (7 weeks age ICR mice) were lesioned unilaterally with a stereotaxic injection of QA (60 nM) into the striatum and the rotational behavior of the animals was tested using apomorphine (0.1mg/kg, IP) 7 days after the induction of lesion. Animals rotating more than 120 turns per hour were selected and the differentiated PmES cells (1$\times$10$^4$cells/ul) were implanted into striatum. Four weeks after the graft, immunohistochemical studies revealed the presence of cells reactive to anti-NeuN antibody. However, only a slight improvement of motor behavior was observed. By Nissl staining, cell mass resembling tumor was found at the graft site and near cortex which may explain the slight behavioral improvement. Detailed experiment on cell viability, differentiation and migration explanted in vivo is currently being studied.