• Journal of Korean Neurosurgical Society
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• 제30권3호
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• pp.272-277
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• 2001

Polymethylmethacrylate(PMMA)는 척추 전적출술후에 척추를 재건하기 위해 사용되지만 액체 형태의 PMMA가 응고하면서 발생되는 열은 척수 신경의 열 손상 가능성을 가지고 있다. 이 연구의 목적은 이미 응고된 PMMA sheet가 척수 신경을 보호하는 방어 벽으로서의 열 차단 역할을 할 수 있는지 또한 열손상으로부터 신경을 보호하기 위해 필요한 방어벽의 최소한의 두께를 탐구하는 데 있다. 실험실에서 제 12번째 흉추체 전 적출후의 상태와 동일한 크기와 모양의 정육면체의 용기를 제작하였다. 60ml의 액체형 PMMA를 용기 안에 주입하여 응고하는 PMMA중심부와 세 가지 다른 두께의(제 1 군 : 0mm, 제 2 군 : 5mm, 제 3 군 : 8mm) 이미 응고된 PMMA sheet의 하부(척수의 전면을 의미)에서 온도를 측정하였다. 또한 이 결과에 대한 위의 세 가지 군에 대해 열역학적 분석도 시행하였다. 응고하는 PMMA 덩이의 중심부에서의 온도는 18회의 실험 동안 매우 일정하여($106.8{\pm}3.9^{\circ}C$)이 실험 모델의 재현성을 보여주고 있었다. 방어 벽이 없는 군(제 1 군)에서 척수 신경 전면의 최고 온도가 $60.3^{\circ}C$이었으나 5mm군 (제 2 군)과 8mm군(제 3 군)에서는 각각 $47.3^{\circ}C$와 $43.3^{\circ}C$로 이미 응고된 PMMA는 통계적으로 유의한(p<0.00005) 온도 차단 효과를 보였다. 최고 온도에 도달하기까지의 계산된 시간은 실제 실험치 보다 35%이내의 오차를 보였으나 최고 온도에 대한 열역학적인 계산치는 실제 실험에서 나타난 수치의 1%이내의 오차를 보였다. 이상의 열역학적인 자료를 토대로 볼 때, PMMA를 이용한 척추의 재건술에서 PMMA 방어벽은 척수의 열손상을 방지하는 효과가 있으며, 이 실험에서 가정한 척수의 열손상 역치인 $39^{\circ}C$이하로 척수 온도를 유지하기 위해 필요한 PMMA방어벽의 두께는 10mm정도로 계산되었다. PMMA 방어벽의 임상 적용에 대해서는 추가적인 임상 실험이 필요하다고 사료된다.

• The Journal of Korean Physical Therapy
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• 제22권1호
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• pp.67-73
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• 2010

Purpose: We tested whether repetitive transcranial magnetic stimulation (rTMS) improved recovery following spinal cord injury (SCI) in rats with transplantation of adipose tissue-derived stromal cells (ATSCs). Methods: Twenty Sprague-Dawley rats (200-250 g, female) were used. Moderate spinal cord injury was induced at the T9 level by a New York University (NYU) impactor. The rat ATSCs (approximately $5{\times}10^5$ cells) were injected into the perilesional area at 9 days after SCI. Starting four days after transplantation, rTMS (25 Hz, 0.1 Tesla, pulse width=$370{\mu}s$, on/off time=3 sec/3 sec) was applied daily for 7 weeks. Functional recovery was assessed using the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale as well as pain responses for thermal and cold stimuli. Results: Both groups showed similar, gradual improvement of locomotor function. rTMS stimulation decreased thermal and cold hyperalgesia after 7 weeks, but sham stimulation did not. Conclusion: rTMS after transplantation of ATSCs in an SCI model may reduce thermal hyperalgesia and cold allodynia, and may be an adjuvant therapeutic tool for pain control after stem cell therapy in SCI.

• The Korean Journal of Pain
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• 제35권3호
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• pp.271-279
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• 2022

Background: Inflammation is known to underlie the pathogenesis in neuropathic pain. This study investigated the anti-inflammatory and neuroprotective mechanisms involved in antinociceptive effects of co-administration of acetaminophen and L-carnosine in chronic constriction injury (CCI)-induced peripheral neuropathy in male Wistar rats. Methods: Fifty-six male Wistar rats were randomly divided into seven experimental groups (n = 8) treated with normal saline/acetaminophen/acetaminophen + L-carnosine. CCI was used to induce neuropathic pain in rats. Hyperalgesia and allodynia were assessed using hotplate and von Frey tests, respectively. Investigation of spinal proinflammatory cytokines and antioxidant system were carried out after twenty-one days of treatment. Results: The results showed that the co-administration of acetaminophen and L-carnosine significantly (P < 0.001) increased the paw withdrawal threshold to thermal and mechanical stimuli in ligated rats compared to the ligated naïve group. There was a significant (P < 0.001) decrease in the levels of nuclear factor kappa light chain enhancer B cell inhibitor, calcium ion, interleukin-1-beta, and tumour necrotic factor-alpha in the spinal cord of the group coadministered with acetaminophen and L-carnosine compared to the ligated control group. Co-administration with acetaminophen and L-carnosine increased the antioxidant enzymatic activities and reduced the lipid peroxidation in the spinal cord. Conclusions: Co-administration of acetaminophen and L-carnosine has anti-inflammatory effects as a mechanism that mediate its antinociceptive effects in CCI-induced peripheral neuropathy in Wistar rat.

• 정신신체의학
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• 제3권1호
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• pp.91-97
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• 1995

Pain is a complex symptom consisting of a sensation underlying potenial disease and associated emotional state. Acute pain is a reflex biological response to injury, in contrast, chronic pain consists of pain of a mininum of 6 months duration and associates with physical, emotional past experience, economic resources of the patient, family and society. Moreover, chronic pain is characterized by physiological affective and behavioral responses that are quite different than those of acute pain. The different type of stimuli exciting pain receptor are mechanical, thermal and chemical stimli and chronic pain are concerned with three of all stimli. The major three components of pain central(Analgesia) system in the brain and spinal cord are 'periaqueductal gray area of the mesencephalon', 'the raphe magnus nucleus' and 'pain inhibitory complex located in the dorsal horns of the spinal cord'. But unfortunately, the central biochemical mechanisms of chronic pain are not clearly defined. To proper management of chronic pain, comprehensive urderstanding as a psychosomatic aspect and multidisciplinary therapeuti-team approach must be emphasized.

• 한국전문물리치료학회지
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• 제2권1호
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• pp.14-20
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• 1995

The purpose of this study was to measure and compare the skin temperature over the exercised muscle and corresponding non-exercised muscle after unilateral isokinetic exercise using digital thermography. Thirty-two young healthy volunteers with no history of knee injury were tested. After isokinetic exercise at 60 degree per second angular velocity using the right leg in a climatic chamber at ambient temperature of $23-26^{\circ}C$, skin temperature of the anterior thigh was tested. After exercise, the skin temperature of both the right and left leg had fallen significantly. The skin temperature of the exercised leg fell less than that of the non-exercised leg. The fall in skin temperature after work was not due to increased evaporative cooling, but was the result of segmental vasoconstriction probably caused reflexly in the spinal cord by non-thermal afferents from exercising muscle or moving tissues. The effect of thermoregulatory vasodilation was reduced by reflex vasoconstriction caused by non-thermal factors such as catecholamine.

• The Korean Journal of Pain
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• 제36권4호
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• pp.425-440
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• 2023

Background: Muscimol's quick onset and GABAergic properties make it a promising candidate for the treatment of pain. This systematic review and meta-analysis of preclinical studies aimed at summarizing the evidence regarding the efficacy of muscimol administration in the amelioration of nerve injury-related neuropathic pain. Methods: Two independent researchers performed the screening process in Medline, Embase, Scopus and Web of Science extracting data were extracted into a checklist designed according to the PRISMA guideline. A standardized mean difference (SMD [95% confidence interval]) was calculated for each. To assess the heterogeneity between studies, ² and chi-square tests were utilized. In the case of heterogeneity, meta-regression and subgroup analyses were performed to identify the potential source. Results: Twenty-two articles met the inclusion criteria. Pooled data analysis showed that the administration of muscimol during the peak effect causes a significant reduction in mechanical allodynia (SMD = 1.78 [1.45-2.11]; P < 0.0001; I² = 72.70%), mechanical hyperalgesia (SMD = 1.62 [1.28-1.96]; P < 0.0001; I² = 40.66%), and thermal hyperalgesia (SMD = 2.59 [1.79-3.39]; P < 0.0001; I² = 80.33%). This significant amendment of pain was observed at a declining rate from 15 minutes to at least 180 minutes post-treatment in mechanical allodynia and mechanical hyperalgesia, and up to 30 minutes in thermal hyperalgesia (P < 0 .0001). Conclusions: Muscimol is effective in the amelioration of mechanical allodynia, mechanical hyperalgesia, and thermal hyperalgesia, exerting its analgesic effects 15 minutes after administration for up to at least 3 hours.

• 한방재활의학과학회지
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• 제25권1호
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• pp.27-44
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• 2015

Objectives This study was carried out to find the effects of Gami-cheongyulsaseub-tang (hereinafter referred to GCST) on the inhibition of zymosan-induced pain in rats and collagen II-induced arthritis (CIA) in DBA/1J mouse. Methods As an acute inflammatory pain model, peripheral inflammation was induced by intraplantar injection of zymosan into the right hind paw in rats and then the hyperalgesia and pain regulating factors in spinal cord were analyzed. As a chronic inflammation model, the mixture of collagen II and complete Freund's adjuvant was treated into mice to establish rheumatoid arthritis and then body weight, thickness of hind paw, pathological change of spleen, immunological rheumatoid factor (IgG1, IgG2a, IgG2b, IgM and anti-collagen II), pro-inflammatory cytokines, and bone injury were analyzed. Results In the acute inflammatory pain model, GCST significantly inhibited the thermal and mechanical hyperalgesia and the pain regulating factors, including Fos, CD11b, PKA and PKC, in the spinal cord with a dose-dependent manner. In the chronic rheumatoid arthritis model, GCST administration decreased arthritic index and paw edema as compared with CIA control group. In particular, GCST reduced significantly the serum levels of total IgG2a, IgG2b, IgM, and specific anti-collagen II, but not total IgG1. GCST also resulted in the attenuation of bone injury and spleen enlargement/adhesion in CIA mice. Moreover, the secretion of pro-inflammatory cytokines TNF-${\alpha}$ and IL-$1{\beta}$ in CIA mice was significantly reduced by GCST in a dose-dependent manner. Conclusions Comparison of the results in this study showed that GCST had anti-nociceptive and immunomodulatory effects. These data imply that GCST can be used as an effective drug for not only rheumatoid arthritic pain but also other auto-immune diseases.

• The Korean Journal of Physiology and Pharmacology
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• 제1권6호
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• pp.625-637
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• 1997

Calcium ions are implicated in a variety of physiological functions, including enzyme activity, membrane excitability, neurotransmitter release, and synaptic transmission, etc. Calcium antagonists have been known to be effective for the treatment of exertional angina and essential hypertension. Selective and nonselective voltage-dependent calcium channel blockers also have inhibitory action on the acute and tonic pain behaviors resulting from thermal stimulation, subcutaneous formalin injection and nerve injury. This study was undertaken to investigate the effects of iontophoretically applied $Ca^{++}$ and its antagonists on the responses of WDR (wide dynamic range) cells to sensory inputs. The responses of WDR cells to graded electrical stimulation of the afferent nerve and also to thermal stimulation of the receptive field were recorded before and after iontophoretical application of $Ca^{++}$, EGTA, $Mn^{++}$, verapamil, ${\omega}-conotoxin$ GVIA, ${\omega}-conotoxin$ MVIIC and ${\omega}-agatoxin$ IVA. Also studied were the effects of a few calcium antagonists on the C-fiber responses of WDR cells sensitized by subcutaneous injection of mustard oil (10%). Calcium ions and calcium channel antagonists ($Mn^{++}$, verapamil, ${\omega}-conotoxin$ GVIA & ${\omega}-agatoxin$ IVA) current-dependently suppressed the C-fiber responses of WDR cells without any significant effects on the A-fiber responses. But ${\omega}-conotoxin$ MVIIC did not have any inhibitory actions on the responses of WDR cell to A-fiber, C-fiber and thermal stimulation. Iontophoretically applied EGTA augmented the WDR cell responses to C-fiber and thermal stimulations while spinal application of EGTA for about $20{\sim}30\;min$ strongly inhibited the C-fiber responses. The augmenting and the inhibitory actions of EGTA were blocked by calcium ions. The WDR cell responses to thermal stimulation of the receptive field were reduced by iontophoretical application of $Ca^{++}$, verapamil, ${\omega}-agatoxin$ IVA, and ${\omega}-conotoxin$ GVIA but not by ${\omega}-conotoxin$ MVIIC. The responses of WDR cells to C-fiber stimulation were augmented after subcutaneous injection of mustard oil (10%, 0.15 ml) into the receptive field and these sensitized C-fiber responses were strongly suppressed by iontophoretically applied $Ca^{++}$, verapamil, ${\omega}-conotoxin$ GVIA and ${\omega}-agatoxin$ IVA. These experimental findings suggest that in the rat spinal cord, L-, N-, and P-type, but not Q-type, voltage-sensitive calcium channels are implicated in the calcium antagonist-induced inhibition of the normal and the sensitized responses of WDR cells to C-fiber and thermal stimulation, and that the suppressive effect of calcium and augmenting action of EGTA on WDR cell responses are due to changes in excitability of the cell.

• 대한한방내과학회지
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• 제27권1호
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• pp.288-293
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• 2006

Background : Monoplegia is the paralysis of a limb. It is commonly caused by an injury to the cerebral cortex, and rarely caused by injury to the internal capsule, brain stem, or spinal cord. Most problems with cerebral cortex is derived from the occlusion of a brain cortex blood vessel due to thrombus or embolus. Objectives : This study is to see if there is a significance in thermal differences of acupoints in diagnosis and treatment of monoplegia on an upper extremity to test the validity of acupuncture and herbal treatment for it. Methods : By using Digital Infrared Thermographic Imaging(DITI), thermal differences$({\Delta}T)$ of acupoints on the upper extremity in a patient with monoplegia on the right upper extremity were measured after an attack of the disease. By giving Mangeum-tang(萬金湯) and treating the patient with acupuncture. the temperature changes of the upper extremity were examined through DITI and improvement was observed. Results : Compared with the left arm which suffered no such injury, the right recovered about 80% of sensation, and the grade of monoplegia improved from Grade O to Grade V. Also, the temperatures of right palmar-dorsal hand and the region of Weiguan(外關, Waiguan, TE5) were $1^{\circ}C$ and $1.45^{\circ}C$ higher than the same left region on admission day, but the thermal differences$({\Delta}T)$ narrowed to $0.5^{\circ}C$ by the last day. Conclusions : Results suggest that DITI screening is a reliable method of prognosis and that the time required for treatment can be estimated through this method in cases of monoplegia to an upper extremity. Also, progress in treatment is reflected in thermal differences of acupoints of the monoplegic upper extremity in accordance with the theory of meridian. This supports a role for acupuncture and herbal treatment for monoplegia.

• Biomolecules & Therapeutics
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• 제27권4호
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• pp.414-422
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• 2019

There is accumulating evidence that microRNAs are emerging as pivotal regulators in the development and progression of neuropathic pain. MicroRNA-15a/16 (miR-15a/16) have been reported to play an important role in various diseases and inflammation response processes. However, whether miR-15a/16 participates in the regulation of neuroinflammation and neuropathic pain development remains unknown. In this study, we established a mouse model of neuropathic pain by chronic constriction injury (CCI) of the sciatic nerves. Our results showed that both miR-15a and miR-16 expression was significantly upregulated in the spinal cord of CCI rats. Downregulation of the expression of miR-15a and miR-16 by intrathecal injection of a specific inhibitor significantly attenuated the mechanical allodynia and thermal hyperalgesia of CCI rats. Furthermore, inhibition of miR-15a and miR-16 downregulated the expression of interleukin-$1{\beta}$ and tumor-necrosis factor-${\alpha}$ in the spinal cord of CCI rats. Bioinformatic analysis predicted that G protein-coupled receptor kinase 2 (GRK2), an important regulator in neuropathic pain and inflammation, was a potential target gene of miR-15a and miR-16. Inhibition of miR-15a and miR-16 markedly increased the expression of GRK2 while downregulating the activation of p38 mitogen-activated protein kinase and $NF-{\kappa}B$ in CCI rats. Notably, the silencing of GRK2 significantly reversed the inhibitory effects of miR-15a/16 inhibition in neuropathic pain. In conclusion, our results suggest that inhibition of miR-15a/16 expression alleviates neuropathic pain development by targeting GRK2. These findings provide novel insights into the molecular pathogenesis of neuropathic pain and suggest potential therapeutic targets for preventing neuropathic pain development.