• Journal of Chest Surgery
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• v.27 no.1
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• pp.9-14
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• 1994

Substance P[SP] has been known to be a peptide which may be plays a role as a neurotransmitter in central nervous system as well as peripheral autonomic nervous system. It has been reported that SP was widely distributed in the nerve of the tracheal smooth muscle and induced the muscle contraction. However, definite action mechanism of SP in the tracheal smooth muscle was not clear, yet. Thus, present experiment was performed to elucidate an effect of substance P and an action mechanism on contraction of the smooth muscle in rabbits. In order to find a neural mechanism to the effect of SP on the tracheal smooth muscle contraction, atropine sulfate, tetrodotoxin, propranol and phentolamine were administered at 10 min before the addition of SP. Otherwise,to find effect of SP antagonists on the action of SP, [D-Pro2, D-Try7,9]SP, [D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP and [D-Pro4, D-Trp7,9]SP were administered as a same fashion. These following results were obtained. 1] SP induced contraction of the tracheal smooth muscle under resting condition and the contraction was increased dose-dependently. 2] Cholinergic blocker[atropine], neural blocker[tetrodotoxin] and adrenergic blocker[propranol and phentolamine] didn`t have an effect on the contractile response. 3] Three SP antagonists inhibited the contractile response. 4] Isoproterenol relaxed the contraction induced by SP. The above results suggested that SP induced contraction of the tracheal smooth muscle directly act to the smooth muscle in rabbits. The autonomic nervous system did not seem to participate in the SP action.

• International Journal of Oral Biology
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• v.46 no.1
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• pp.39-44
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• 2021

This study aimed to investigate whether neurotransmitter receptors in the nervous system were also expressed in oral keratinocytes. Expressions of various neurotransmitter receptor genes in immortalized mouse oral keratinocyte (IMOK) cells were examined by reverse transcriptase polymerase chain reaction. IMOK cells expressed calcitonin gene-related peptide (CGRP) receptor subunit genes Ramp1 and Ramp3 and glutamate receptor subunit genes Grina, Gria3, Grin1, Grin2a, and Grin2d. Moreover, IMOK cells expressed Adrb2 and Chrna5 that encode beta 2 adrenergic receptor and cholinergic receptor nicotinic alpha 5 for sympathetic and parasympathetic neurotransmitters, respectively. The expression of Bdkrb1 and Ptger4, which encode receptors for bradykinin and prostaglandin E2 involved in inflammatory responses, was also observed at low levels. Expressions of Ramp1 and Grina in the mouse gingival epithelium were also confirmed by immunohistochemistry. When the function of neurotransmitter receptors expressed on IMOK cells was tested by intracellular calcium response, CGRP, glutamate, and cholinergic receptors did not respond to their agonists, but the bradykinin receptor responded to bradykinin. Collectively, oral keratinocytes express several neurotransmitter receptors, suggesting the potential regulation of oral epithelial homeostasis by the nervous system.

• Journal of Acupuncture Research
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• v.22 no.1
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• pp.99-108
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• 2005

Objective : The aim of this study is to investigate the analgesic effect and its mechanism of bee venom acupuncture on collagen-induced arthritis(CIA) rats. Methods : Bee venom (1 mg/kg) was subcutaneously punctured into Choksamni (ST36) of CIA Analgesic effect was evaluated by using the tail flick latency (TFL). Opioid and ${\alpha}2$-adrenergic neurotransmitter system were examined by naloxone as an opioid receptor antagonist and yohimbine as ${\alpha}2$-adrenoceptor antagonist prior to bee venom cupuncture. Results : The results were as follows; 1. The TFL for the CIA rat was decreased as time went by. 2. The TFL in CIA rat was increased in bee venom acupuncture group compared with control group (no treatment). 3. Analgesic effect of bee venom acupuncture was not abolished by naloxone pre-treatment in the CIA rat. 4. Analgesic effect of bee venom aqua-acupuncture was abolished by yohimbine pre-treatment in the CIA rat. 5. Two weeks bee venom acupuncture had the continous analgesic effect for 4 weeks. Conclusions : Bee venom acupuncture has an analgesic effect on the CIA rat and has an antinociception mediated by ${\alpha}2$-adrenergic system.

• Korean Journal of Agricultural Science
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• v.44 no.4
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• pp.574-585
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• 2017

This study was conducted to investigate effects of a potato byproduct on growth performance, blood metabolites, and carcass characteristics of Hanwoo steers. The palm oil coated potato byproduct was supplemented to the diet of Hanwoo steers to estimate the effect on growth performance, blood metabolites, and carcass characteristics during the late fattening period. Thirteen steers with initial body weight of control ($676.8{\pm}31.7kg$), treatment 1 ($671.8{\pm}46.2kg$) and treatment 2 ($672.8{\pm}31.1kg$) were used for 60 days, respectively. Average daily gain of steers in treatment 2 and control was greater than that in treastment 1 (p > 0.05). All steers in treatment 2 had a grade quality grading system than B in meat quantity and had a meat quality higher than the $1^{st}$ grade. According to the physicochemical analysis of longissimus muscle, treatment 2 had high brightness resulting from high meat quality (p > 0.05), and a decrease in redness and yellowness is seen as a dilution effect due to muscle hypertrophy (p > 0.05). The fatty acid composition showed low levels of linoleic acid (p = 0.039) and arachidonic acid (p = 0.008) in treatment 2. This resulted in lower polyunsaturated fatty acid (PUFA) levels (p = 0.034). On the other hand, high levels of oleic acid resulted in high levels of MUFA (p > 0.05). These results indicate that potato byproduct had similar effects with ${\beta}_2-adrenergic$ agonist (${\beta}_2-AA$). And there was no negative effect on the intramuscular fat. In conclusion, palm oil coated potato byproduct could be potentially used as an alternative growth enhancer.

• The Korean Journal of Pain
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• v.21 no.3
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• pp.179-186
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• 2008

Background: The adrenergic nervous system in the spinal cord contributes to the development of neuropathic pain after nerve injury. Brain derived neurotrophic factor may facilitate the sympathetic change in the spinal cord and influence the state of neuropathic pain. We probed the effect of chronic repetitive administration of systemic 4-methylcatechol, which is known to be a neurotrophic factor inducer, in a spinal nerve ligation model. Methods: We made the rat neuropathic pain model by the ligation of the L5 spinal nerve. Intraperitoneal 4-methylcatechol ($10{\mu}g/kg$) or the same volume of saline wasadministrated twice daily just after the operation for 7 days. The tactile allodynia was measured by using von Frey filaments and its change was followed up from 3 days after SNL. The lumbosacral enlargement of the spinal cord was taken out and the mRNA contents of the ${\alpha}_2-adrenoceptor$ subtypes were measured by real time polymerase chain reaction and this was then compared with the control groups. The antiallodynic effect of intrathecal clonidine (3, 10, $30{\mu}g$) was evaluated and compared in the 4-methylcatechol treated rats and the control rats. Results: The expression of the ${\alpha}_{2A}$ and ${\alpha}_{2C}$ adrenoceptor subtypes did not change after 4-methylcatechol treatment. Intrathecal clonidine showed an earlier and better effect at the highest dose ($30{\mu}g$ intrathecal), but not with any other doses. Conclusions: Chronic intraperitoneal administration of 4-methylcatechol may improve the effect of intrathecal clonidine, but we could not prove the increase of ${\alpha}_{2A}$ and ${\alpha}_{2C}$ adrenoceptors in the spinal cord of 4-methylcatechol treated rats.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.83-92
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• 1988

Although the release of lysosomal enzymes from activated PMN leukocyte can be regulated by intracellular cyclic nucleotide levels, other responses of PMN leukocyte according to the binding of neurotransmitters to either ${\beta}$-adrenergic or muscarinic receptors are still not clarified. In addition, the function of PMN leukocyte mediated by ${\alpha}$-adrenergic receptors is uncertain. Atropine, phentolamine and propranolol inhibited calcium uptake, superoxide generation, NADPH oxidase activity and phagocytic activity in activated PMN leukocyte, whereas carbachol and isoproterenol slightly further stimulated the responses of activated cells. Either carbachol or isoproterenol stimulated superoxide generation was inhibited by their antagonists, atropine and propranolol, respectively. The response of activated PMN leukocyte was inhibited by chlorpromazine, verapamil and dantrolene but slightly stimulated by lithium. On the other hand, chlorpromazine and dibucaine did not affect NADPH oxidase activity. Atropine, phentolamine and propranolol suppressed the calcium dependent phagocytic activity. Thus, the results suggest that atropine, phentolamine and propranolol may inhibit superoxide generation in activated PMN leukocyte by the inhibition of calcium influx and by their direct action on the NADPH oxidase system which is associated with autonomic receptors.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.24 no.1
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• pp.21-27
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• 2013

Objectives : Dysregulation of the central noradrenergic system may be involved in the pathophysiology of attention-deficit hyperactivity disorder (ADHD). The aim of this study was to examine the differences in pre- and post-treatment cerebral perfusion according to the MspI polymorphisms of the alpha-2A-adrenergic receptor gene (ADRA2A) in children with ADHD. Methods : Thirty seven drug-naive ADHD children (8.9+1.8 years old, M=32, F=5) were genotyped. Baseline single-photon emission computed tomography (SPECT) and clinical assessments were performed for ADHD children. After treatment with methylphenidate for eight weeks, SPECT and clinical assessment were repeated. Results : No differences in baseline clinical assessments or cerebral perfusion were observed according to the MspI genotype. However, after treatment, ADHD children with the G/G genotype at the MspI polymorphism showed hyperperfusion in the right cerebellar declive (p=.001, uncorrected) and hypoperfusion in the left lentiform nucleus and left cingulate gyrus (p<.001 and p=.001, uncorrected), compared to children without the G/G genotype. Conclusion : Although the results of this study should be interpreted cautiously, they suggest a possible role of the MspI polymorphisms of the ADRA2A gene in methylphenidate-induced changes in cerebral perfusion.

• The Korean Journal of Pharmacology
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• v.16 no.2 s.27
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• pp.31-38
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• 1980

Calvert et al. formulated the hypothesis that carbon tetrachloride ($CCl_4$) acted on the central nervous system to produce and intensify sympathetic discharge which resulted in anoxic necrosis of the liver. Recknagel suggested that the essential feature of $CCl_4$ hepatotoxicity depended on the cleavage of it to $CCl_3$(free radical) and the peroxidative decomposition of cytoplasmic membrane structural lipids. And there are many reports which show the increase of adrenergic activity in hyperthyroidism. In this paper, the influence of thyroxine on the hepatotexicity of carbon tetrachloride was investigated in mice. The results obtained were summarized as follows; 1) Hepatic total lipid and lipid peroxide contents were slightly decreased by L-sodium thyroxine injection(4mg/kg/day for 4days or 6days), but hepatic glycogen content was significantly decreased. 2) Hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were significantly increased by $CCl_4$ (4 ml/kg single dose or triple dose: 4ml/kg/day for 3days), but hepatic glycogen content was significantly decreased. 3) The increase of hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity induced by $CCl_4$ were significantly inhitited by the pretreatment of thyroxine. 4) The decrease of hepatic glycogen induced by $CCl_4$ was not affected by the pretreatment of thyroxine.

• The Korean Journal of Pharmacology
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• v.10 no.1 s.15
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• pp.47-52
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• 1974

The isolated rabbit gall bladder strips were prepared according to the technique described by Amer and Becvar (1969). The strips were placed in a bath containing 100 ml of Locke-Ringer solution maintained at $38^{\circ}C$. Oxygen was continuously bubbled through the solution. The tension of the muscle strip was initially adjusted to 0.7g. The contractile response was measured isometrically by a force-displacement transducer connected to a polygraph. The effect of a number of autonomic drugs were studied for their interaction with caerulein (Prof. V. Erspamer, F.I. 6934 Caerulein, Farmitalia, Italia), a gastrin or CCK.PZ like peptide, on isolated rabbit gall bladder strips. In this preparation caerulein produced contractions of CCK-PZ type, but the relative potency on a weight basis was 40 times that of CCK-PZ. The response of caerulein was not modified by either cholinergic or alpha or beta adrenergic blockade. However, the response of caerulein and of barium on the strips were prevented by papaverine or aminophylline. Isoproterenol, papaverine or aminophylline alone relaxed the preparation whereas caerulein, CCK-PZ, acetylcholine, serotonin, histamine or barium chloride contracted the preparation. In summary, it is concluded that caerulein on the gall bladder strip seems to act independently of the autonomic nervous system and mediated via mechanisms apparently similar to those involved in the action of barium chloride.

• Journal of the East Asian Society of Dietary Life
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• v.15 no.5
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• pp.606-612
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• 2005

This study was performed to provide basic data that predict the application of Saengmaegsan(SMS) as medicinal food. SMS has been used in oriental medicine for many years as a therapeutic agent for cerebral disease. We examined the effects of SMS on physiological function in isolated abdominal aorta and femoral artery from rabbit and measured the changes of regional cerebral hood flow(rCBF), which was continually monitored by laser-doppler flowmeter and pressure transducer in anesthetized adult Spargue-Dawley rats through the data acquisition system composed of MacLab and Macintosh computer. The contraction forces by injection of norephinephrine in isolated abdominal aorta and femoral artery were significantly decreased in each concentration of SMS treatment compared with control. rCBF was increased by SMS in a dose-dependent manner. These results suggest that SMS causes a diverse response of rCBF and arterial diameter. These mechanism in rCBF increase may be mediated by prostaglandis, cyclic GMP and adrenergic $\beta-receptor$. Also mechanism in artery contraction decrease is also mediated by prostaglandis and cyclic GMP. These results indicate that SMS can be nsed as a safe and clinically applicable as a supplementation of diet therapy for cerebral cardiovascular disease patients.