• The Korean Journal of Physiology and Pharmacology
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• 제4권1호
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• pp.73-79
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• 2000

This study investigated whether propofol, an intravenous, non-barbiturate anesthetic, could reduce brain damage following global forebrain ischemia. Transient global ischemia was induced in gerbils by occlusion of bilateral carotid arteries for 3 min. Propofol (50 mg/kg) was administered intraperitoneally 30 min before, immediately after, and at 1 h, 2 h, 6 h after occlusion. Thereafter, propofol was administered twice daily for three days. Treated animals were processed in parallel with ischemic animals receiving 10% intralipid as a vehicle or with sham-operated controls. In histologic findings, counts of viable neurons were made in the pyramidal cell layer of the hippocampal CA1 area 4 days after ischemia. The number of viable neurons in the pyramidal cell layer of CA1 area was similar in animals treated with a vehicle or a subanesthetic dose of propofol. In terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, semiquantitative analysis of dark-brown neuronal cells was made in the hippocampal CA1 area. There was no significant difference in the degree of TUNEL staining in the hippocampal CA1 area between vehicle-treated and propofol-treated animals. These results show that subanesthetic dose of propofol does not reduce delayed neuronal cell death following transient global ischemia in Mongolian gerbils.

• 대한전자공학회논문지SP
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• 제41권3호
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• pp.139-146
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• 2004

본 논문에서는 솔더페이스트의 이차원 및 삼차원 자동검사를 함께 할 수 있는 복합 검사 광학계와 그 구동유닛을 단일 프로브 시스템으로 구현하고, 그를 위한 효과적인 비젼검사 알고리즘을 제안하였다. 솔더페이스트의 이차원 검사에는 One-pass Run Length 레이블링 알고리즘을 제안하여 입력 영상으로부터 솔더 페이스트 형상을 효과적으로 추출하도록 하였고, 고속 검사를 위한 프로브의 최적 이동 경로도 구하였으며, 삼차원 검사에는 기존의 레이져 슬릿빔(slit-beam) 방식 대신 격자 투영식 모아레 간섭계에 기반한 위상이동 알고리즘을 도입하여 고정밀 검사가 가능토록 하였다. 전체 소프트웨어 구현에는 MMX 병렬처리기법도 적용함으로써 더욱 고속화 하였다. 10㎜×10㎜의 단위 측정영역(field of view: FOV)에 대하여 x, y 축으로 10㎛ Z축으로 l ㎛의 분해능을 가지는 이차원 및 삼차원 복합 광학 검사 시스템을 제작하여 실험한 결과, 한 FOV에 대한 솔더페이스트의 이차원 및 삼차원 검사를 영상포착 후 각각 평균 11msec와 15msec의 짧은 시간에 처리할 수 있었고, ±1㎛의 두께 측정 정밀도를 얻을 수 있었다.

• Journal of Korean Neurosurgical Society
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• 제30권4호
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• pp.430-436
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• 2001

Objective : The proliferative potential of intracranial glioma affects the histological malignancy and prognosis of patients with these tumors. In this study, we present the relationship between MIB-1 labeling index(LI) and clinical variables which might play the major role in determining the prognosis of patient with astrocytic tumors. Patients and Methods : Excised tumor specimens from a total of 52 patients were stained to detect monoclonal MIB-1-Ki-67 antibody by avidin-biotin complex immunohistochemistry. The MIB-1 LI was evaluated with histological grades, demograpghic data, and survival time. The statistical significance of their correlation was analyzed by Pearson correlation test. Results : The 52 patients included 30 male patients and 22 female patients. The tumors according to the criteria of the World Health Organization(WHO) classification were verified as pleomorphic xanthoastrocytoma in one, pilocytic astrocytomas 4, astrocytomas 1, anaplastic astrocytomas 3, and glioblastomas 31. MIB-1 LI in astrocytic ttumors showed no correlation with age and gender. However, the patients under 10 years had the longest survival time, whereas short survival time was observed in the older patients. The mean MIB-1 LI of different tumor grades were as follows : pleomorphic xanthoastrocytoma, $4.40{\pm}0.00$ ; pilocytic astrocytoma, $4.53{\pm}3.09$ ; astrocytoma, $5.50{\pm}6.03$ ; anaplastic astrocytoma, $12.68{\pm}12.50$ ; Glioblastoma, $21.31{\pm}19.63$. Although the levels of MIB-1 LI were varied in individual tumors, the MIB-1 LI was increased in parallel with the histological grades. Glioblstomas showed significantly higher MIB-1 LI compared with that of anaplastic astrocytomas and low grade astrocytomas (p = 0.001). The mean survival time of entire group of patients was also well correlated with MIB-1 LI in astrocytic tumors(p = 0.015). Moreover, the mean survival time of the entire group of patients with Lis < 10 was $125.33{\pm}113.57weeks$, and the mean survival of those with $Lis{\geq}10$ was $60.71{\pm}62.58weeks$. This difference was also statistically significant(p = 0.004). Conclusion : The results of this study suggest that MIB-1 LI correlates with histological grades and might play a significant role in predicting the survival of patients with astrocytic tumors.

• Toxicological Research
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• 제17권2호
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• pp.73-82
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• 2001

The incidence and distribution of necrotic and apoptotic neural cells, and activated astrocytes in the brain of rats intoxicated intra peritoneally with diisopropylfluorophosphate were investigated. Pyridostigmine bromide (0.1 mg/kg) and atropine methylnitrate (20 mg/kg) were pretreated intramuscularly 30 min and 10 min, respectively, prior to diisopropylfluorophosphate (4-10 mg/kg) administration. Diisopropylfluorophosphate induced severe limbic seizures, early necrotic and delayed apoptotic brain injuries, and rapid astrocytic responses. The necrosis, which was closely related to seizure intensity, was observed as early as 1 hr after intoxication predominently in hippocampal pyramidal cells, cerebellar Purkinje cells and neurons in pyriform/entorhinal cortices, showing malacia of neurophils. In contrast, apoptosis started to appear 12 hr after intoxication in neurons in thalamus, amygdala and neocortex, and ephendymal cells surrounding the 4th ventricle. Since marked apoptosis was induced in rats exhibiting relatively-low seizure intensity, the degree of necrosis and apoptosis was shifted to each type of injury according to the seizure intensity. Activated astrocytes, observed within 1 hr along the limbic system, were suggested to affect the neural injury patterns by producing high level of nitric oxide. However, the distribution of activated astrocytes was not in parallel with those of necrotic or apoptotic injuries, implying that the astrocytic responses resulted from seizure activity rather than neural injuries. Furthermore, astrocytes in malacic tissues disappeared during the severe limbic seizures. Therefore, it would be one of the cautionary notes on the expression of glial fibrillary acidic protein in astrocytes as a biochemical marker of brain injuries following acute exposure to organophosphates.

• 대한약리학회지
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• 제26권1호
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• pp.35-49
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• 1990

A highly purified $(Na^+,\;K^+)-ATPase$ from the rectal gland of Squalus acanthias and from the electric organ of Electrophorus electricus has been used to raise antibodies in rabbits. The 97,000 dalton catalytic subunit and glycoprotein derived from the rectal gland of spiny shark were also used as antigens. The two $(Na^+,\;K^+)-ATPase$ holoenzymes and the two shark subunits were antigenic. In Ouchterlony double diffusion experiments, these antibodies formed precipitation bands with their antigens. Antibodies prepared against the two subunits of shark holoenzyme also formed precipitation bands with their antigens and shark holoenzyme, but not with eel holoenzyme. These observations are in good agreement with inhibitory effect of these antibodies on the catalytic activity of $(Na^+,\;K^+)-ATPase$ both from the shark and the eel, since there is very little cross-reaction between the shark anticatalytic subunit antibodies and the eel holoenzyme. The maximum antibodies titer of the anticatalytic subunit antibodies is found to be 6 weeks after the initial single exposure to this antigen. Multiple injections of the antigen increased the antibody titer. However, the time required to produce the maximum antibody titer was approximately the same. These antibodies also inhibit catalytic activity of $(Na^+,\;K^+)-ATPase$ vesicles reconstituted by a slow dialysis of cholate after solubilization of the enzyme in a presonicated mixture of cholate and phospholipid. In these reconstituted $(Na^+,\;K^+)-ATPase$ vesicles, effects of these antibodies on the fluxes of $Na^+$, $Rb^+$, and $K^+$ were investigated. Control or preimmune serum had no effect on the influx of $^{22}Na^+$ or the efflux of $^{86}Rb^+$. Immunized sera against the shark $(Na^+,\;K^+)-ATPase$ holoenzyme, its glycoprotein or catalytic subunit did inhibit the influx of $^{22}Na^+$ and the efflux of $^{86}Rb^+$. It was also demonstrated that these antibodies inhibit the coupled counter-transport of $Na^+$ and $K^+$ as studied by means of dual labeling experiments. However, this inhibitory effect of the antibodies on transport of ions in the $(Na^+,\;K^+)-ATPase$ vesicles is manifested only on the portion of energy and temperature dependent alkali metal fluxes, not on the portion of ATP and ouabain insensitive ion movement. Simultaneous determination of effects of the antibodies on ion fluxes and vesicular catalytic activity indicates that an inhibition of active ion transport in reconstituted $(Na^+,\;K^+)-ATPase$ vesicles appears to be due to the inhibitory action of the antibodies on the enzymatic activity of $(Na^+,\;K^+)-ATPase$ molecules incorporated in the vesicles. These findings that the inhibitory effects of the antibodies specific to $(Na^+,\;K^+)-ATPase$ or to its subunits on ATP and temperature sensitive monovalent cation transport in parallel with the inhibitory effect of vesicular catalytic activity by these antibodies provide direct evidence that $(Na^+,\;K^+)-ATPase$ is the molecular machinery of active cation transport in this reconstituted $(Na^+,\;K^+)-ATPase$ vesicular system.