• Restorative Dentistry and Endodontics
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• v.30 no.6
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• pp.470-476
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• 2005

The purpose of this Study was to invest)gate the function or calcitonin gene-related peptide (CGRP) in regulatory mechanism of pulpal microcirculation with the aim of elucidating neurogenic inflammation. Experiments were performed on twelve cats under general anesthesia. CGRP was administered through the femoral vein to see the systemic Influence and through the external carotid artery to see the local effect. Sympathetic nerve to the dental pulp was stimulated electrically and pulpal blood flow (PBF) was measured with a laser Doppler flowmeter on the canine teeth to the drug administration. The paired variables of control and experimental data were compared by paired t-test and differences with p < 0.05 were considered statistically significant. Systemic administration of CGRP $(0.3{\mu}g/ka)$ exerted decreases in systemic blood pressure and caused changes in PBF with an initial increase i311owed by decrease and a move marked second increase and decrease. Close intra-arterial (i.a.) injection of CCRP $(0.03{\mu}g/kg)$ resulted in slight PBF increase. The effect of CGRP resulted in no significant increase in PBF in the presence of $CGRP_{8-37}$. The electrical stimulation of the sympathetic nerve alone resulted in PBF decreases. The j.a. administration of CGRP following the electrical stimulation of the sympathetic nerve compensated the decreased PBF. Therefore, CGRP effectively blocked the sympathetic nerve stimulation-induced PBF decrease. Results of the present study have provided evidences that even though the local vasodilatory function of CGRP are weak, CCRP is effectively involved in blocking the vasoconstriction caused by sympathetic nerve stimulation in the feline dental pulp.

• Journal of the Society of Disaster Information
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• v.14 no.2
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• pp.219-229
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• 2018

Purpose: This research proposes an optimization model for effective evacuation routing and scheduling of civilians near the border area when full-scale war threats heighten. Method: To reflect the reality, administrative unit network is created using Kruscal's Algorithm, Harmony Search, CCRP based on the geographical features, population, and traffic data of real cities, and then, optimal civilian evacuation routes are found. Results: Optimal evacuation routes and schedules are computed by repetitive experiments, and it is found that the scenario that minimizes the average civilian evacuation time is effective for the civilian evacuation plan. Conclusion: By using the civilian evacuation plan this research proposes, at the time of establishing the actual civilian evacuation plan, quantitative analysis is used for the effective plan making rather than only depending.

• Restorative Dentistry and Endodontics
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• v.26 no.5
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• pp.436-442
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• 2001

Neuropeptide such as calcitonin gene-related peptide and substance P may mediate neurogenic inflammation, but little is known about the regulation of neuropeptide release from rat spinal cord. Eugenol has been reported to reduce odontogenic pain and is known to have a structure similar to capsaicin, a potent stimulant of certain nociceptors. This study was done to examine the effect of capsaicin and eugenol on immunoreactive calcitonin gene-related peptide (iCGRP) release from rat spinal cord and whether eugenol regulates capsaicin-sensitive release of iCCRP or it evokes capsaicin-sensitive release of iCGRP. The dor-sal half of rat lumbar spinal cord was chopped into 200$\mu$m slices. They were superfused (500$\mu$l/min) in vitro with an oxygenated Kreb's buffer. The EC$_{50}$ of capsaicin on iCGRP release was measured. Eugenol (600$\mu$M and 1.2mM) and vehicle (0.02% 2-hydroxyl-$\beta$-cyclodextrin) were administered prior to stimulation of rat lumbar spinal cord with capsaicin. The amount of iCGRP release from rat lumbar spinal cord was measured by radioimmunoassay. The results were as follows : 1. iCGRP release from rat lumbar spinal cord was dependent on concentration of capsaicin. The EC$_{50}$ of capsaicin on iCGRP release was 3$\mu$M. 2. In the vehicle treated group, capsaicin (3$\mu$M) evoked a 14-fold increase over basal iCGRP level. 3. Administration of 600$\mu$M and 1.2mM eugenol evoked a 2.2-fold increase and a 2.3-fold increase over basal iCGRP level respectively. 4. Administration of 600$\mu$M and 1.2mM eugenol increased capsaicin evoked release of iCGRP by more than 50%. These results indicate that eugenol evoke CGRP release from central nervous system and potentiate the pain-inducing action of capsaicin on it.

• Journal of Life Science
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• v.30 no.2
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• pp.211-220
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• 2020

The activity of CAR can be regulated not only by ligand binding but also by phosphorylation of regulatory factors involved in extracellular signaling pathways, cross-talk interactions with transcription factors, and the recruitment, degradation, and expression of coactivators and corepressors. This regulation of CAR activity can in turn have effects on the control of diverse physiological homeostasis, including xenobiotic and energy metabolism, cellular proliferation, and apoptosis. CAR is phosphorylated by the ERK1/2 signaling pathway, which causes formation of a complex with Hsp-90 and CCRP, leading to its cytoplasmic retention, whereas phenobarbital inhibits ERK1/2, which causes dephosphorylation of the downstream signaling molecules, leading to the recruitment to CAR of the activated RACK-1/PP2A components for the dephosphorylation, nuclear translocation, and the transcriptional activation of CAR. Activated CAR cross-talks with FoxO1 to induce inhibition of its transcriptional activity and with PGC-1α to induce protein degradation by ubiquitination, resulting in the transcriptional suppression of PEPCK and G6Pase involved in gluconeogenesis. Regulation by CAR of lipid synthesis and oxidation is achieved by its functional cross-talks, respectively, with PPARγ through the degradation of PGC-1α to inhibit expression of the lipogenic genes and with PPARα through either the suppression of CPT-1 expression or the interaction with PGC-1α each to induce tissue-specific inhibition or stimulation of β-oxidation. Whereas CAR stimulates cellular proliferation by suppressing p21 expression through the inhibition of FoxO1 transcriptional activity and inducing cyclin D1 expression, it suppresses apoptosis by inhibiting the activities of MKK7 and JNK-1 through the expression of GADD45B. In conclusion, CAR is involved in the maintenance of homeostasis by regulating not only xenobiotic metabolism but also energy metabolism, cellular proliferation, and apoptosis through diverse cross-talk interactions with extracellular signaling pathways and intracellular regulatory factors.

• The korean journal of orthodontics
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• v.27 no.4 s.63
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• pp.607-621
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• 1997

GRP was known as the modulator of Pain transmission in central nervous system and local effector to peripheral tissue causing vasodilation, increased blood flow, modulation of immune sysem, stimulation of endothelial cell proliferation, and stimulation of bone formation. Numerous study, therefore, were done to elucidate involvement of CGRP to tooth movement. To investgate the response of CGRP immunoreactive nerve cells according to cell size in trigeminal ganglion during tooth movement, immunohistochemical study was performed using rat. Experimental rats(9 weeks old, 210 gm) were divided as six groups(normal(n=6), 3 hour group(n=5), 12 hour group(n=4), 1 day group(n=5), 3 day group(n=5), 7 day group(n=5)), and were applied orthodontic force (approximately 30 gm) to upper right maxillary molar. After frozen sections of trigeminal ganglions were immunostained using rabbit antisera, the changes of CGRP immunoreactive cells in regard to cell size distribution(small cell(upto $20{\mu}m$), medium cell($20-35{\mu}m$), large cell(above $35{\mu}m$)) were observed. The results were as follows 1. The percentage of CGRP immunoreactive cells to all nerve cells in trigeminal ganglion was 33.0% in normal control group, was decreased to 24.5% in 1 day group, and was increased to 41.8% in 7 day group. 2. The percentage of small, medium, and large cells expressing CGRP immunoreactivity in normal trigeminal ganglion to all CGRP immunoreactive cells were 51.3%, 44.0%, 4.7%, respectively. 3. The percentage of small cells with CGRP immunoreactivity to all CGRP immunopositive cells was increased in 3 hour and 12 hour groups. 4. The percentage of medium cells with CGRP immunoreactivity was increaed in 3 day and 7 day groups. 5. The percentage of large cells with CGRP immunoreactivity was increaed in 7 day group. Conclusively, the small cells with CGRP immunoreactivity in trigeminal ganglion respond to orthodontic force during initial phase of tooth movement, and later the medium and large cells with CGRP immunoreactivity respond