• The korean journal of orthodontics
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• v.28 no.3 s.68
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• pp.441-452
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• 1998

The c-fos is known as neuronal marker of second neurons which is activated by noxious peripheral stimulation. To investigate the changes of c-fos el(pression in the trigeminal nucleus complex during tooth movement, immunohistochemical study was performed. Experimental rats(9 weeks old, 210 gm 21 rats) were divided into seven groups(normal, 1 hour group, 3 hour group, 6 hour group, 12 hour group, 1 day group,3 day group). Rats in the normal group were anesthesized without orthodontic force. Rats in the experimental groups were applied orthodontic force (approximately 30 gm) to upper right maxillary molar. Frozen sections of brain stem were immunostained using rabbit antisera. The changes of c-fos expression were observed with respect to rostrocaudal distribution, laminar organization, md duration of orthodontic force application. The study results were as follows $\cdot$The c-fos nuclei in the dorsal part were observed from ipsilateral transition zone of subnucleus interpolaris and subnucleus caudalis to $C_1$ cervical dorsal horn rostrocaudally. The maximal peak point was the rostral part of subnucleus caudalis. The greatest proportion of c-fos cells were located within lamina I and II. $\cdot$The c-fos nuclei in the dorsal Part were observed from the most caudal part of subnucleus interpolaris to the middle part of the subnucleus caudalis. $\cdot$The number of c-fos immunoreactive dot increased at 1 hour group, reached its maximum at the 3 and 6 hour groups, and showed a decreasing trend after 12 hours. These results imply that nociceptive stimulation caused by continuous orthodontic force might be modulated by transition zone of subnucleus interpolaris and subnucleus caudalis, subnucleus caudalis, $C_1$ spinal dorsal hem.

• Tuberculosis and Respiratory Diseases
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• v.43 no.3
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• pp.420-433
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• 1996

Background : There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitirc oxide synthase(NOS) activity in the neurogenic inflammation of airways. Method : To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, $N^{\omega}$-nitro-L-arginine (L-NNA) on plasma extravastion were evaluated in four groups of Sprague-Dawley rats ; sham operation group(sham NANC group), electrical vagal stimulation group(NANC2 group), intravenous pretreatment groups with FK224 (1mg/kg ; FK224 group), and L-NNA(1mg/kg ; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells(iNOS), brain(bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results : The results are that plasma extravsation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment(P<0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224(P<0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea(p<0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion : These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.

• Progress in Medical Physics
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• v.20 no.4
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• pp.277-289
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• 2009

Recently, functional MRI has been used to investigate the neurobiological mechanisms of acupuncture and the specificity of acupoint. The group data tend to be regarded as more important than the individual data in the most of previous studies. This study was designed to investigate the effect of the variability of individual data on the group results. A functional MRI (fMRI) of the whole brain was performed in fifteen healthy subjects during placebo and acupuncture stimulations at the ST36 acupoint. After remaining at rest for 30 seconds, the acupuncture was inserted and twisted at the rate of 2 Hz for 45 seconds and then the acupuncture was removed immediately. This process was repeated three times. Individual and group analyses were performed by voxel-based analyses using SPM2 software. Visual inspections of the activation and deactivation maps from individual sessions have shown the large variability across fifteen subjects. This means that the group data reflected the brain activation responses of only a few subjects. We suggest that the individual data should be presented to demonstrate the effect of acupuncture.

• Clinical and Experimental Pediatrics
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• v.46 no.7
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• pp.695-701
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• 2003

Purpose : It had been suggested that pain arising from deep somatic body regions influences neural activity within periaqueductal gray(PAG) of midbrain via distinct spinal pathways. Aspirin is one of the popular non-steroidal anti-inflammatory drugs used in the management of pain. Fos expression was used as a marker for neuronal activity throughout central neurons following painful peripheral stimulation. This study was prepared to investigate changes of c-Fos immunoreactivity in midbrain by deep pain and effects of aspirin. Methods : Male Sprague-Dawley rats were injected with 0.1 mL of 5% formalin in the plantar muscle of the right hindpaw. For experimental group II, aspirin was injected intravenously before injection of formalin. An aspirin-untreated group was utilized as group I. Rats were sacrificed at 0.5, 1, 2, 6 and 24 hours after formalin injection. Rat's brains were removed and sliced in rat brain matrix. Brain slices were coronally sectioned at interaural 1.00-1.36 mm. Serial sections were immunohistochemically reacted with polyclonal c-Fos antibody. The numbers of c-Fos protein immunoreactive neurons in ventrolateral periaqueductal gray(VLPAG) and dorsomedial periaqueductal gray(DMPAG) were counted and analyzed statistically with Mann-Whitney U tests. Results : Higher numbers of c-Fos protein immunoreactive neurons were found in VLPAG. In both VLPAG and DMPAG of formalin-treated group, the numbers of c-Fos protein immunoreactive neurons were significantly higher at all time points than the formalin-untreated group, which peaked at two hours. The numbers of c-Fos immunoreactive neuron of the aspirin-treated group were less compared to the aspirin-untreated group at each time point. Conclusion : These results provide some basic knowledge in understanding the mechanism of formalin-induced deep somatic pain and the effects of aspirin.

• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.299-311
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• 1995

Platelets resemble monoaminergic neurons in several respects, i.e. the uptake of 5-HT and its inhibition, the subcellular storage and release of 5-HT, and the metabolism of aromatic amines brought about by monoamine oxidase. And the 5-HT content of rabbit platelets is well known to be about 40 times higher than that of human platelets. Therefore, this study was carried out to investigate the influences of amitriptyline (AMT) and sertraline (SRT) on the aggregation, contents of signaling second messengers, and protein phosphorylations of rabbit platelets in response to thrombin, 0.25 unit/ml, comparing with those of chlorpromazine (CPZ). Thrombin-induced aggregation was inhibited by SRT $(IC50:4.37{\times}10^{-5}\;M)$, CPZ $(IC50:5.76{\times}10^{-5}\;M)$, and AMT $(IC50:1.15{\times}10^{-4}\;M)$, respectively, and the aggregation by A23187 $(1.0\;{\mu}M)$ or PMA (320 nM) was also inhibited by SRT, CPZ, and AMT. AMT, SRT, and CPZ had little affects on basal contents of platelet $TXB_2$ and $PGE_2$, but all of them inhibited the thrombin-induced increase of $TXB_2$. Thrombin did not change the platelet contents of cAMP and cGMP. CPZ, AMT, and SRT produced the slight decrease of basal cAMP content, and their effects were not affected by thrombin-treatment. But SRT and AMT moderately increased the basal cGMP content, and the cGMP content of thrombin-stimulated platelets was gradually increased by the pretreatment with SRT, AMT, and CPZ. Particularly, the SRT-dependent increase of the cGMP content was notable. Platelet $Ins(1,4,5)P_3$ content was rapidly increased up to a plateau within 10 sec after thrombin-stimulation, AMT, SRT, and CPZ increased the basal $Ins(1,4,5)P_3$ content, and the thrombin-dependent increase was enhanced by pretreatment with CPZ and AMT, but was blunted by SRT. Platelet $[Ca^{2+}]_i$, was rapidly increased up to a peak level within 20 sec after thrombin-stimulation. The increase of $[Ca^{2+}]_i$ was sisnificantly inhibited by AMT, SRT, and CPZ. Thrombin- or PMA-induced phosphorylations of platelet $41{\sim}43\;kDa$ and 20 kDa proteins were significantly inhibited by AMT, SRT, and CPZ. These results suggest that the antiplatelet activities of AMT and CPZ may be considerably attributed to the inhibition of protein kinase C activity, and the activity of SRT may be associated with the inhibitory effect on the thrombin-induced increase of $Ins(1,4,5)P_3$ and the increasing effect on the cGMP content of ptatelets. Therefore, it seems to be evident that AMT and SRT may produce their antidepressant activity, at least, partly through the inhibition of protein kinase C activity or the increase of resting $Ins(1,4,5)P_3$, content and in case of SRT, to a lesser extent, via the increase of cGMP in the brain.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.101-111
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• 1990

The effect of physostigmine (PS), which has been shown to act on the muscarinic receptors in the brains of the rat, dog and cat, on the arterial blood pressure (BP) was investigated in urethane-anesthetized rabbits. Intravenous (iv) PS, $25{\sim}300\;{\mu}g/kg$, caused little change in BP. However, after treatment of rabbits with either of chlorisondamine (CS), hexamethonium, intracerebroventricular (icv) clonidine, icv xylazine and icy reserpine iv PS produced a pressor response. Spinalization of the rabbit also caused iv PS to increase BP. The pressor effect of iv PS in CS-treated rabbits was markedly reduced after prazosin or pirenzepine. Iv PS inhibited the pressor response to McN-A-343 in CS-treated and in spinal rabbits; alternately during the infusion of McN-A-343 iv PS failed to produce the pressor response. The pressor response to DMPP was not affected by iv PS. Icv PS, $12{\sim}200\;{\mu}g/kg$, produced a pressor response which was accentuated after CS-treatment. This pressor effect was inhibited, though not complete, by prazosin or by pirenzepine. A simultaneous treatment of rabbits with both $[Sar^{1},\;Ala^{8}]-angiotensin$ II, an angiotensin II antagonist, and prazosin or pirenzepine almost completely abolished the pressor effect of icv PS, whereas the angiotensin II antagonist did not enhance the inhibitory effect of pirenzepine and prazosin on the pressor response to iv PS . Icv pirenzepine blocked the pressor response to icv PS without affecting that to iv PS. The present results show that the pressor response to iv PS in CS-treated and in spinal rabbits arises from stimulation of the muscarinic receptors in the sympathetic ganglia, whereas the pressor response by icv PS via activation of the muscarinic receptors in the brain which causes an enhancement in the outflow of sympathetic discharge and angiotensin. The results also suggest that iv PS is unable to produce a pressor response in the rabbit unless the sensitivity of the gangionic muscarinic receptors is altered by ganglionic nicotinic blockade, by the decrease of central sympathetic outflow on the sympathetic ganglia or by spinalization.

• Journal of Food Hygiene and Safety
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• v.21 no.2
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• pp.118-128
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• 2006

This study was conducted to determination of the endocrine distruptor function of 'Parabens' by dosing ethyl paraben, propyl paraben, isopropyl paraben, butyl paraben and isobutyl paraben to the immature SD rats. 18 groups were given vehicle control group, negative control group (Dibutyl phthalate), postive control group ($1'7-{\alpha}$ Ethynylestrdiol) and each paraben groups involved 3 dose level. Rats were injected with 62.5, 250 and 1,000mg/kg from postnatal day 19 till 21 once a day in subcutaneous and a total 3, times. There was no treatment related death. but, subcutaneous nodule, edema, alopecia and scrub formation on injection site was observed. These signs was become worse in high dose level. these signs was cause from physical stimulation by test substance which parabens were mix with com oil as vehicle. In the analysis of organ weights, absolute and relative weights of brain, spleen, liver, thymus, heart, kidneys, adrenals, ovaries and vagina were no difference with control group. but, wet and blotted weight of uterus was increased in every high dose parabens treat group. Especially, all dose level of isobutyl paraben was showed increment of uterus weight. uterus dilatation of parabens treated group was observed in gross anatomic pathology and these result was agree with wet and blotted weight of uterus. In the result of this study, estrogenic effect as endocrine distruptor was observed in ethyl paraben, propyl paraben, isopropyl paraben, butyl paraben and isobutyl paraben. and it was considered isobutyl paraben has highest estrogrnic effect under the condition of this study.

• The Journal of Korea Institute of Information, Electronics, and Communication Technology
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• v.12 no.6
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• pp.657-665
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• 2019

In this study, we conducted a study on the transcranial magnetic electrode, a method for the study of dementia and muscle pain, a neurodegenerative disease caused by an aging society, which is becoming a problem worldwide. In particular, transcranial magnetic electrodes have been studied to improve their ability to be deteriorated by dementia symptoms such as speech, cognitive ability, and memory by outputting magnetism deep into the brain using coils on the head epidermis. In this study, simulation was performed using Maxwell 3D program for the design of coil, the core of transcranial magnetic electrode. As a result of the simulation comparison between the coil designed by the previous research and the coil through the research and development, the output was found to be superior to the conventional designed coil. The graphs of the coil outputs of B-Field and H-Field are found to be symmetrical, but the symmetry between each coil is pseudo-symmetrical and not accurate. Based on these results, an experiment was conducted to confirm whether the output of the head epidermis through both coils is possible. In the magnitude field of the reverse-coil 2-coil analysis, the maximum output was 3.3920e + 004 H [A_per_meter], and the vector field showed the strongest magnetic field around 35 to 165 degrees. It was confirmed that the magnetic output canceled due to the magnetic output. In the case of the forward 2-coil, a maximum of 3.2348e + 004H [A_per_meter] similar to the reverse coil was observed, but in the case of the vector field, the magnetic output regarding the forward output and the head skin output was confirmed. However, when the height change in the output coil, the magnetic output was reduced.

• Journal of Life Science
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• v.30 no.4
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• pp.331-342
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• 2020

The suppression of neuroinflammatory responses in microglial cells can be considered a key target for improving the progression of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Asparagus cochinchinensis has traditionally been used as a medicine to treat fever, cough, kidney disease, breast cancer, inflammatory diseases, and brain diseases. In this study, we investigated the neuroprotective mechanism of an aqueous extract from A. cochinchinensis root (AEAC), particularly its anti-inflammatory effects on lipopolysaccharide (LPS)-activated BV-2 microglial cells. BV-2 cells were treated with four different concentrations of AEAC. No significant toxicity was detected in BV-2 cells treated with AEAC. Nitric oxide (NO), cyclooxygenase-2 (COX-2) mRNA, and inducible nitric oxide synthase (iNOS) mRNA levels were 21% lower in the AEAC+LPS group than in the Vehicle+LPS group. Lower proinflammatory (TNF-α and IL-1β) and anti-inflammatory cytokine (IL-6 and IL-10) levels were also detected in the AEAC+LPS group than in the Vehicle+LPS group, albeit at varying rates. Moreover, the phosphorylation of mitogen-activated protein kinase (MAPK) members after LPS treatment was significantly recovered in the AEAC-pretreated group compared to the Vehicle+LPS group, enhancement of the phosphorylation of mitogen-activated protein kinase (MAPK) members after LPS treatment was significantly recovered in the AEAC-pretreated group, while cell cycle arrest at the G2/M phase caused by LPS treatment was less severe in the AEAC+LPS group. The increase in reactive oxygen species (ROS) generation induced by LPS treatment was also lower in the AEAC-pretreated group than in the Vehicle+LPS group. This is the first study to show that AEAC exerts anti-neuroinflammatory activity against LPS stimulation by regulating the MAPK signaling pathway, the cell cycle, and ROS production.

• Science of Emotion and Sensibility
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• v.26 no.3
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• pp.149-160
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• 2023

This study develops a time-varying system-based noncontact fabric sensor that can measure cerebral blood-flow signals to explore the possibility of brain blood-signal detection and emotional evaluation. The textile sensor was implemented as a coil-type sensor by combining 30 silver threads of 40 deniers and then embroidering it with the computer machine. For the cerebral blood-flow measurement experiment, subjects were asked to attach a coil-type sensor to the carotid artery area, wear an electrocardiogram (ECG) electrode and a respiration (RSP) measurement belt. In addition, Doppler ultrasonography was performed using an ultrasonic diagnostic device to measure the speed of blood flow. The subject was asked to wear Meta Quest 2, measure the blood-flow change signal when viewing the manipulated image visual stimulus, and fill out an emotional-evaluation questionnaire. The measurement results show that the textile-sensor-measured signal also changes with a change in the blood-flow rate signal measured using the Doppler ultrasonography. These findings verify that the cerebral blood-flow signal can be measured using a coil-type textile sensor. In addition, the HRV extracted from ECG and PLL signals (textile sensor signals) are calculated and compared for emotional evaluation. The comparison results show that for the change in the ratio because of the activation of the sympathetic and parasympathetic nervous systems due to visual stimulation, the values calculated using the textile sensor and ECG signals tend to be similar. In conclusion, a the proposed time-varying system-based coil-type textile sensor can be used to study changes in the cerebral blood flow and monitor emotions.