• Journal of the Korean Geosynthetics Society
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• v.19 no.1
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• pp.25-33
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• 2020

To improvement the swelling characteristics of the existing cutoff wall against the moisture, the permeability of the sand, calcium bentonite and solidifier mixture according to the contact with trichloroethylene (TCE) was evaluated. Characteristics analysis and the permeability test of the research materials were performed. The permeability was decreased as the mixing ratio of the calcium bentonite was increased and it was increased as the mixing ratio of the solidifier was increased. In conclusion, when mixing 15% of calcium bentonite and more than 30% of solidifier, the permeability coefficient in the underground water movement was analyzed as more than α × 10^-4 cm/sec showing that it does not block the underground water movement. In addition, as the permeability coefficient of mixtures after TCE reaction was analyzed as less than α ×10^-7 cm/sec, it satisfied the condition of blocking layer (less than 1.0 × 10^-6 cm/sec). Therefore, the calcium bentonite and solidifier can be utilized as barrier that showing the characteristic of percolation ability conversion in soil and underground water contaminated with TCE.

• Journal of Chest Surgery
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• v.37 no.3
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• pp.267-271
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• 2004

Compensatory sweating is the main cause of patient dissatisfaction after sympathetic surgery for craniofacial hyperhidrosis. Surgery that sympathetic nerve trunk preserved and extent of resection limited was introduced to decrease compensatory sweating. From Jan 2000 to July 2002, the vidio-assisted thoracoscopic T2 sympathetic clipping and rami comunicantes selective division were performed in 36 patients suffering from craniofacial hyperhidrosis. Twenty two patients underwent a T2 sympathetic nerve clipping (Group 1), and fourteen patients underwent division of the T2 ramicommunicates (Group 2). We retrospectively analysed the rate of satisfaction, dryness of face, the rate of compensatory sweating, grade of compensatory sweating. The dryness of face was that no statistical difference between group 1 and group 2 (p=0.387); group1: dry 22.7% (5/22), humid 77.3% (17/22) group 2: dry 14.3% (2/14), humid 78.5% (11/14), persist 7.2% (1/14). The rate of satisfaction was 77.3% in T2 clipping and 64.2% in T2 sympathicotomy with no significant in the statistic analysis (p=0.396). The rate of compensatory sweating on group 2 was lower than group 1 (p=0.042); 95.4% (21/22) in T1 sympathetic clipping and 71.4% in T2 ramicotomy. The rate of embarrassing and disabling compensatory sweating was 70.5% (embarassing 8 patients, disabling 9 patients) in T2 clipping and 42.9% (embarassing 8 patients, disabling 9 patients)in T2 ramicotomy with statistically significant difference (p=0.036). The sympathetic trunk preservation surgery for craniofacial hyperhidrosis (T2 ramicotomy) redueced the rate of compensatory sweating when compared to the blocking surgery of sypathetic trunk (T2 clipping).

• The Korean Journal of Nuclear Medicine
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• v.36 no.4
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• pp.261-270
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• 2002

Purpose: Nicotinic acetylcholine receptors (nAChRs), which mediate excitatory neurotransmission, are known to participate in various neurophysiological functions. Severe losses of nAChRs have been noted in Alzheimer's and Parkinson's diseases. Therefore, noninvasive and quantitative imaging of nAChRs would offer a better understanding on the function of these receptors. In this study, $2-[^{18}F]fluoro-A85380\;([^{18}F]1)$, an ${\alpha}_4{\beta}_2$ nAChRs radioligand, was prepared using one HPLC purification and evaluated in mouse brain, and the results were compared with those in the literature. Materials and Methods: $[^{18}F]1$ was prepared by $[^{18}F]$fluorination of the iodo precursor followed by acidic deprotection and then purified by HPLC. Tissue distribution studies were performed in mouse brain at the indicated time points and the result was expressed as %ID/g. Inhibition studies were also carried out with pretreatment of various ligands. Results: One HPLC purification method gave the desired product in 15-20% radiochemical yield and with high specific activity ($38-55GBq/{\mu}mol$). Tissue distribution studies showed that $[^{18}F]1$ specifically labeled nAChRs in mouse brain with a high thalamus to cerebellum uptake ratio (13.8 at 90 min). Inhibition studios demonstrated selective binding of $[^{18}F]1$ to nAChRs, blocking the uptake of the $[^{18}F]1$ in nAChR-rich legions by selective ligands such as cytisine and nicotine which are well-known nAChRs agonists. Conclusion: This study demonstrated that the $[^{18}F]1$ produced by the method using one HPLC purification gave the results similar to those reported in the literature. Therefore, this synthetic method can be readily applied to the routine preparation of $[^{18}F]1$, a PET radioligand for ${\alpha}_4{\beta}_2$ nAChRs imaging.

• Tuberculosis and Respiratory Diseases
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• v.57 no.5
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• pp.449-460
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• 2004

Background : PS-341 is a novel, highly selective and potent proteasome inhibitor, which showed cytotoxicity against some tumor cells. Its anti-tumor activity has been suggested to be associated with modulation of the expression of apoptosis-associated proteins, such as p53, $p21^{WAF/CIP1}$, $p27^{KIP1}$, NF-${\kappa}B$, Bax and Bcl-2. c-Jun N-terminal kinase (JNK) and glycogen synthase kinase-$3{\beta}$ (GSK-$3{\beta}$) are important modulators of apoptosis. However, their role in PS-341-induced apoptosis is unclear. This study was undertaken to elucidate the role of JNK and GSK-$3{\beta}$ in the PS-341-induced apoptosis in lung cancer cells. Method : NCI-H157 and A549 cells were used in the experiments. The cell viability was assayed using the MTT assay and apoptosis was evaluated by proteolysis of PARP. The JNK activity was measured by an in vitro immuno complex kinase assay and by phosphorylation of endogenous c-Jun. The protein expression was evaluated by Western blot analysis. Dominant negative JNK1 (DN-JNK1) and GSK-$3{\beta}$ were overexpressed using plasmid and adenovirus vectors, respectively. Result : PS-341 reduced the cell viability via apoptosis, activated JNK and increased the c-Jun expression. Blocking of the JNK activation by overexpression of DN-JNK1, or pretreatment with SP600125, suppressed the apoptosis induced by PS-341. The activation of caspase 3 was mediated by JNK activation. Blocking of the caspase 3 activation suppressed PS-341-induced apoptosis. PS-341 activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, but its blockade enhanced the PS-341-induced cell death via apoptosis. GSK-$3{\beta}$ was inactivated by PS-341 via the PI3K/Akt pathway. Overexpression of constitutively active GSK-$3{\beta}$ enhanced PS-341-induced apoptosis; in contrast, this was suppressed by dominant negative GSK-$3{\beta}$ (DN-GSK-$3{\beta}$). Inactivation of GSK-$3{\beta}$ by pretreatment with lithium chloride or the overexpression of DN-GSK-$3{\beta}$ suppressed both the JNK activation and c-Jun up-regulation induced by PS-341. Conclusion : The JNK/caspase pathway is involved in PS-341-induced apoptosis, which is negatively regulated by the PI3K/Akt-mediated inactivation of GSK-$3{\beta}$ in lung cancer cells.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.407-416
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• 1996

The reactive intermediates formed during the metabolism of therapeutic agents, toxicants and carcinogens by cytochromes P450 are frequently capable of covalently binding to tissue macromolecules and causing tissue damage. It has been shown that YH439, a congener of malotilate, is effective in suppressing hepatic P450 2E1 expression. The present study was designed to further establish the mechanistic basis of YH439 protection against toxicant by assessing its effects against chemical-mediated potentiated hepatotoxicity. Retinoyl palmitate (Vit-A) pretreatment of rats for 7 days substantially enhanced carbon tetrachloride hepatotoxicity, as supported by an ${\sim}5-fold$ increase in serum alanine aminotransferase (ALT) activity, as compared to $CCl_4$ treatment alone. The elevation of ALT activity due to Vit-A was completely blocked by the treatment of $GdCl_3$ a selective inhibitor of Kupffer cell activity. Concomitant pretreatment of rats with both YH439 and Vit-A resulted in a 94% decrease in Vit-A-potentiated $CCl_4$ hepatotoxicity. YH439 was also effective against propyl sulfide-potentiated $CCl_4-induced$ hepatotoxicity. Whereas propyl sulfide (50 mg/kg, 7d) enhanced $CCl_4-induced$ hepatotoxicity by >5-fold, relative to $CCl_4$ treatment alone, concomitant treatment of animals with both propyl sulfide and YH439 at the doses of 100 and 200 mg/kg prevented propyl sulfide-potentiated $CCl_4$ hepatotoxicity by 35% and 90%, respectively. Allyl sulfide, a suppressant of hepatic P450 2E1 expression, completely blocked the propyl sulfide-enhanced hepatotoxicity, indicating that propyl sulfide potentiation of $CCl_4$ hepatotoxicity was highly associated with the expression of P450 2E1 and that YH439 blocked the propyl sulfide-enhanced hepatotoxicity through modulation of P450 2E1 levels. Propyl sulfide- and $CCl_4-induced$ stimulation of lipid peroxidation was also suppressed by YH439 in a dose-related manner, as supported by decreases in malonedialdehyde production. The role of P450 2E1 induction in the potentiation of $CCl_4$ toxicity and the effects of YH439 were further evaluated using pyridine as a P450 2E1 inducer. Pyridine pretreatment substantially enhanced the $CCl_4$ hepatotoicity by 23-fold, relative to $CCl_4$ alone. YH439, however, failed to reduce the pyridine-potentiated toxicity, suggesting that the other form(s) of cytochroms P450 inducible by pyridine, but not suppressible by YH439 treatment, may play a role in potentiating $CCl_4-induced$ hepatotoxicity. YH439 was capable of blocking cadmium chloride-induced liver toxicity in mice. These results demonstrated that YH439 efficiently blocks Vit-A-enhanced hepatotoxiciy through Kupffer cell inactivation and that the suppression of P450 2E1 expression by YH439 is highly associated with blocking of propyl sulfide-mediated hepatotoxicity.

• Korean Journal of Biological Psychiatry
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• v.6 no.2
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• pp.240-245
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• 1999

Object : This study was designed to evaluate the effects of olanzapine on the schedule-induced polydipsia(SIP) which is one of animal model of obsessive-compulsive disorder in rats. We administered olanzapine as a serotonin and dopamine blocking agent, fluoxetine as a selective serotonin reuptake inhibitor, and haloperidol for the dopamine antagonist to rats which showed schedule-induced polydipsic behavior. Methods : Spraque-Dawley rats weighing 200-250gm were individually housed and maintained and allowed free access to water. The rats were placed on a restricted diet. To induce polydipsia, rats were placed in the cage where a pellet dispenser automatically dispensed 90mg pellets on a fixed-time 60 seconds(FT-60s) feeding schedule over 150 minute test session per day. Water was available at all times in the cage. After 4 weeks of daily exposure to the FT 60s feeding schedule, experimental rats met a predetermined criterion for polydipsic behavior(greater than 3 times of water per session on average). 5 groups of rats were administered olanzapine(3mg/kg, i.p), olanzapine(10mg/kg, i.p), fluoxetine(5mg/kg, i.p.), haloperidol(0.1mg/kg, i.p.), and vehicle(1cc/kg, i.p.) for 3 weeks. The rats were tested once a week to access schedule induced polydipsic behavior. Water bottles were weighed before and after the 150-minute test session. The chronic effects of administration of experimental drugs on schedule induced polydipsic behavior were analyzed with ANOVA and Scheffe test as a posthoc comparison. In order to measure water consumption in non-polydipsic food-deprived rats, a separate group of rats(N=8) were individually housed and given a single bolus(14.5gm) of food per day which maintained them at their average body weight. Results and Conclusion : The results were as follows ; 1) After 4 weeks of scheduled feeding procedure, the experimental group showed significant differences than the bolus control in the amount of water consumption as compared with their average water intakes for 4 weeks. At the same periods, there were no differences between the experimental group and the bolus control in the body weight. 2) The fluoxetine group showed significant decrease in the amount of water intake over the 3 weeks of drug treatment as compared with their average amount of polydipsic water intakes. The olanzapine 3mg group showed significant decrease in the amount of water intake at 3rd weeks of drug treatment as compared with their average amount of polydipsic water intakes. The olanzapine 10mg group showed significant decrease in the amount of water intake at 2nd and 3rd weeks of drug treatment as compared with their average amount of polydipsic water intakes. However, the haloperidol group and the vehicle control group showed no changes of amounts of water intake for 3 weeks of treatment as compared with their average amount of polydipsic water intakes. 3) The fluoxetine group showed significantly lower amounts of water intake than the haloperidol group at 2nd weeks of drug treatment. And also the fluoxetine group showed significantly lower amounts of water intake than the haloperidol group and the vehicle control at 3rd weeks of drug treatment. The olanzapine 3mg group and the olanzapine 10mg group showed significantly lower amounts of water intake than the haloperidol group and the vehicle control at 3rd weeks of drug treatment. Above findings suggest that the fixed time feeding procedure for schedule-induced polydipsia as an animal model of obsessive compulsive disorder was effective to the evaluation of pharmacological challenge study. The authors assume that the serotonin hypothesis and the serotonin-dopamine interaction hypothesis are preferred to the dopamine hypothesis in the biological etiology of obsessive-compulsive disorder.

• Journal of KIISE:Databases
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• v.28 no.4
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• pp.742-757
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• 2001

Since database management systems(DBMSS) have limited lock resources, transactions requesting locks beyond the limit mutt be aborted. In the worst carte, if such transactions are aborted repeatedly, the DBMS can become paralyzed, i.e., transaction execute but cannot commit. Lock escalation is considered a solution to this problem. However, existing lock escalation methods do not provide a complete solution. In this paper, we prognose a new lock escalation method, adaptive lock escalation, that selves most of the problems. First, we propose a general model for lock escalation and present the concept of the unescalatable look, which is the major cause making the transactions to abort. Second, we propose the notions of semi lock escalation, lock blocking, and selective relief as the mechanisms to control the number of unescalatable locks. We then propose the adaptive lock escalation method using these notions. Adaptive lock escalation reduces needless aborts and guarantees that the DBMS is not paralyzed under excessive lock requests. It also allows graceful degradation of performance under those circumstances. Third, through extensive simulation, we show that adaptive lock escalation outperforms existing lock escalation methods. The results show that, compared to the existing methods, adaptive lock escalation reduces the number of aborts and the average response time, and increases the throughput to a great extent. Especially, it is shown that the number of concurrent transactions can be increased more than 16 ~256 fold. The contribution of this paper is significant in that it has formally analysed the role of lock escalation in lock resource management and identified the detailed underlying mechanisms. Existing lock escalation methods rely on users or system administrator to handle the problems of excessive lock requests. In contrast, adaptive lock escalation releases the users of this responsibility by providing graceful degradation and preventing system paralysis through automatic control of unescalatable locks Thus adaptive lock escalation can contribute to developing self-tuning: DBMSS that draw a lot of attention these days.