• The Journal of Korean Medicine
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• v.24 no.3
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• pp.108-117
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• 2003

Objective : The central opioid mechanism of acupuncture analgesia has been fairly well documented in acute behavioral experiments, but little electrophysiological study has been performed on the peripheral mechanism and subtypes of opioid receptors responsible for acupuncture-induced antinociception in chronic animal models. In the present electrophysiological experiment, we studied the peripheral mechanism and opioid receptor subtypes which Were implicated in electroacupuncture-induced antinociception in the rat with chronic inflammatory and neurogenic pain. Methods : In the rat with complete Freund's adjuvant-induced inflammation and spinal nerve injury, dorsal horn cell responses to afferent C fiber stimulation were recorded before and after electroacupuncture (EA) stimulation applied to the contralateral Zusanli point for 30 minutes. Also studied Were the effects of specific opioid receptor antagonists and naloxone methiodide, which can not cross the blood-brain barrier, on EA-induced inhibitory action. Results : EA-induced inhibitory action was significantly attenuated by naloxone methiodide, suggesting that EA-induced inhibition was mediated through peripheral mechanism. Pretreatment, but not posttreatment of naltrexone and spinal application significantly blocked EA-induced inhibitory actions. In inflammatory and neurogenic pain models, ${\mu}-$ and ${\delta}-opioid$ receptor antagonists (${\beta}-funaltrexamine$ & naltrindole) significantly reduced EA-induced inhibitory action, but ${\kappa}-opioid$ receptor antagonist had weak inhibitory effect on EA-induced antinociception. Conclusion : These results suggest that 2Hz EA-stimulation induced antinoeiceptive action is mediated through peripheral as well as central mechanism, and mainly through ${\mu}-$ and ${\delta}-opioid$ receptors.

• The Journal of Korean Medicine
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• v.41 no.4
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• pp.88-99
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• 2020

Objectives: The purpose of this study is to investigate the mechanism of acupuncture for treating chemotherapy-induced peripheral neuropathy. Methods: Based on domestic and international papers reported until October 2020, experimental papers on "chemotherapy induced peripheral neuropathy", "mechanism", and "acupuncture" were set up to identify the mechanisms of chemotherapy induced peripheral neuropathy. A total of seven papers were selected and searched: one pilot paper for people and six experimental papers for rats. Results: In the pilot paper studied by Bao, T., the effect of EA was demonstrated but no significant results were produced for the mechanism. Moon et al. derived the association between EA and plasma 𝛽-endorphin in rat experimental studies on oxalilatin-induced cold hypersensitivity. Meng et al. found relevance to 𝜇, 𝛿, and 𝛿 opioid through EA stimulation in paclitaxel-induced peripheral neuropathy. Lee et al. studied the relationship between EA and muscarin and 5-HT in rat experiments on oxaliplatin-induced coldness, associated with 5-HT and EA, especially with 5-HT3 receptors. Choi et al. revealed the association of adrenaline and opioid acting on 𝛼2- and 𝛽 adrenaline receptors with EA in rat experiments on paclitaxel-induced neuralgia. In rat experiments on oxaliplatin-induced neuralgia reported by Lee, 𝛽-endorphin and encephalin were studied to be mediated by EA. Zhang, T. et al. revealed in the paclitaxel induced rat experiment that EA activates 5-HT. Conclusion: It is inferred that peripheral neuropathy caused by anticancer drugs can be reduced by activating the action of 5-HT, 𝛽-endorphin, and encephalin through the descending inhibitory pathways. cell differentiation, herbal medicine, Pongamia, stem cells

• Journal of Hospice and Palliative Care
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• v.1 no.1
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• pp.65-68
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• 1998

The neuropathic pains are not well controlled by common analgesics and opioid drugs in terminal cancer patients. The types of these pains are divided within the two cages, one is due to continuous central sensitization and the other is due to paroxymal peripheral sensitization. The mechanism of continuous central sensitization is the activity of dorsal horn neurones that are activated by C-fiber input. The tricyclic antidepressants, non-tricyclic antidepressants, and oral local anaesthesia probably produce analgesic effects in neuropathic pains through suppression of this activity. The mechanism of paroxymal peripheral sensitization is the hyper-excitability of peripheral neurones. The neuropathic pains due to peripheral sensitization respond relatively the anticonvulsants and baclofen that stabilize membranes and suppress paroxymal electrical discharge. The patients was a 38-year-old female who complained of hyperthemia on upper right extremity. The symptom of this patient was improved with anticonvulsant(dilantin 600mg).

• Journal of environmental and Sanitary engineering
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• v.10 no.3
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• pp.45-55
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• 1995

This study was carried out to elucidate the toxic mechanism of cadmium in peripheral nerve. An animal model of cadmium neuropathy was induced by feeding diet containing cadmium to Sprague- Dawley rat (or two weeks. Four weeks aged Sprague- Dawley rats were divided into four groups : normal control group, 10ppm- cadmium treated group, 100ppm- cadmium treated group, 1000ppm- cadmium treated group, reference drug- treated group. All rats were sacrificed at the end of two weeks for assessing the development of cadmium neuropathy, These results obtained were summarized as follows : 1. Cadmium reduced peripheral flow of both acetylcholinesterase and cholinesterase in rat sciatic nerve. 2. The toxic mechanism of cadmium might be the result of an reduction of myo-inositol concentration in peripheral nervous system 3. Reduction in myo-inositol content of peripheral nerve resulted from the inhibition of sodium- Potassium ATPase activity, which is responsible for myo-inositol transport, by cadmium 4. Oral administration of myo-inositol improved the flow of both acetylcholinesterase and cholinesterasenerve in cadmium intoxicated rat. These results suggest that mild cadmium neuropathy might be diagnosed by checking nervous myo-inositol content and oral administraion of myo-inositol might prevent the development of severe cadmium neuropathy with special reference to detective axonal transport.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.4
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• pp.363-368
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• 2018

Hypotension is one of the potential causes of dizziness. In this review, we summarize the studies published in recent years about the electrophysiological and pharmacological mechanisms of hypotension-induced dizziness and the role of the vestibular system in the control of blood pressure in response to hypotension. It is postulated that ischemic excitation of the peripheral vestibular hair cells as a result of a reduction in blood flow to the inner ear following hypotension leads to excitation of the central vestibular nuclei, which in turn may produce dizziness after hypotension. In addition, excitation of the vestibular nuclei following hypotension elicits the vestibulosympathetic reflex, and the reflex then regulates blood pressure by a dualcontrol (neurogenic and humoral control) mechanism. In fact, recent studies have shown that peripheral vestibular receptors play a role in the control of blood pressure through neural reflex pathways. This review illustrates the dual-control mechanism of peripheral vestibular receptors in the regulation of blood pressure following hypotension.

• The Journal of the Korean dental association
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• v.49 no.6
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• pp.321-326
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• 2011

Neuropathic pain is caused by functional abnonnalities of structural lesions in the peripheral or central nervous system, and occurs without peripheral nociceptor stimulation. Trigeminal neuropathy always pose differential location difficulties as multiple diseases are capablc of producing them: they can be the result of traumatism, tumors, or diseases of the connective tissue, infectious or demyelinating diseases, or may be of idiopathic origin. There are a number of mechanisms described as causing neuropathy. They can be described as ectopic nerve activity, neuroma, ephatic trasmission, change of sodium channel expression, sympathetic activity, central sensitization, and alteration in central inhibition systems. More than I mechanism may be active to create individual clinical presentations. In order to provide better pain control, the mechanism-based approach in treating neuropathic pain should be familiar to physicians.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.6
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• pp.489-495
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• 2014

Protease-activated receptor (PAR)-2 is expressed in endothelial cells and vascular smooth muscle cells. It plays a crucial role in regulating blood pressure via the modulation of peripheral vascular tone. Although some reports have suggested involvement of a neurogenic mechanism in PAR-2-induced hypotension, the accurate mechanism remains to be elucidated. To examine this possibility, we investigated the effect of PAR-2 activation on smooth muscle contraction evoked by electrical field stimulation (EFS) in the superior mesenteric artery. In the present study, PAR-2 agonists suppressed neurogenic contractions evoked by EFS in endothelium-denuded superior mesenteric arterial strips but did not affect contraction elicited by the external application of noradrenaline (NA). However, thrombin, a potent PAR-1 agonist, had no effect on EFS-evoked contraction. Additionally, ${\omega}$-conotoxin GVIA (CgTx), a selective N-type $Ca^{2+}$ channel ($I_{Ca-N}$) blocker, significantly inhibited EFS-evoked contraction, and this blockade almost completely occluded the suppression of EFS-evoked contraction by PAR-2 agonists. Finally, PAR-2 agonists suppressed the EFS-evoked overflow of NA in endothelium-denuded rat superior mesenteric arterial strips and this suppression was nearly completely occluded by ${\omega}$-CgTx. These results suggest that activation of PAR-2 may suppress peripheral sympathetic outflow by modulating activity of $I_{Ca-N}$ which are located in peripheral sympathetic nerve terminals, which results in PAR-2-induced hypotension.

• Fisheries and Aquatic Sciences
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• v.3 no.1
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• pp.23-25
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• 2000

To compare the respiratory burst activity potential of the phagocytes isolated from head kidney, spleen, and peripheral blood 1ll cultured rockfish (Sebastes schlegeli), chemiluminescent (CL) response analysis was performed. The phagocytes isolated from peripheral blood showed greater and faster CL response to the opsonized zymosan compared to that of the phagocytes isolated from kidney or spleen. This may imply a significant role of the blood phagocytes in defence mechanism of rockfish. The different responses found in the CL analysis among the phagocytes isolated from peripheral blood, kidney, and spleen may reflect differences in activation state or activity of phagocytes.

• The Journal of Internal Korean Medicine
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• v.31 no.2
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• pp.372-379
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• 2010

Objective : The purpose of this study was to report the effect of Bogijetong-tang on diabetic peripheral neuropathy. Methods : Nine patients who were diagnosed or suspected with diabetic peripheral neuropathy enrolled in this study. They took Bogijetong-tang 2 or 3 times a day and were given acupuncture therapy. To evaluate the therapeutic effect, Visual Analog Scale (VAS) or Total Symptom Score (TSS) were examined at intervals of about 7 days. Result : TSS score decreased an average of 2.74 points and VAS scores decreased an average of 3.67 points. As the pain decreased, accompanied gait disturbance also improved in some patients. Conclusion : Bogijetong-tang is effective in treating diabetic peripheral neuropathy, but study of the concrete mechanism and efficacy is needed.

• The Journal of Korea CHUNA Manual Medicine
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• v.3 no.1
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• pp.111-123
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• 2002

Objectives : There have been many studies of the effect of Bee Venom therapy about arthritis, but no one study was reported about its whole functional mechanism to musculo-skeletal system. This study was designed to investigate the effect, Indication, and side effect of Bee Venom therapy on musculo-skeletal disease by literature review of articles. Results : The effects of Bee Venom therapy to musculo-skeletal system are divided to Anti_inflammatory effect and Anti-nociceptive effect. Anti_inflammatory effect is achieved through competitive chemotaxis, immuno-regulation, increasing of cortisol secretion by stimulating hypothalamus-pituitary gland-adrenal cortex axis. Anti-nociceptive effect is achieved by Anti-inflammatory mechanism and it works similar to anti-nociceptive effect of the acupuncture acting on central and peripheral nociceptive transduction system. The Bee Venom therapy could cause severe side effect, for example, hypersensitivity and anaphylaxis, injury to central nerve system and cardiovascular system, peripheral blood system, and renal dysfunction. Conclusions : With its Anti-inflammatory and Anti-nociceptive mechanism, Bee Venom therapy is considered that has good effects to autoimmune disease, chronic inflammation of various musculo-skeletal disease and various pain syndrome. But the clinician must be careful for its side effects.