• Journal of Convergence for Information Technology
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• v.10 no.8
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• pp.203-212
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• 2020

The purpose of this study was to investigate the effects of cognitive rehabilitation programs using Virtual Reality(VR) content on the daily living abilities such as cognitive abilities, depression, and upper extremity functions of the elderly. The study group analyzed the effectiveness by separating the experimental group, which is the virtual reality cognitive rehabilitation application group, and the control group, the universal cognitive stimulation program application group. As a result of the study, the MMSE-K score improved by 13.0% in the experimental group and 2.3% in the control group. The improvement in each area of the experimental group was found to be 3.1% MBI, 7.1% MFT(Rt.), 3.5% MFT(Lt.), and 25.4% K-GDS. As a result of comparing the pre-post score change between each group, there was a significant difference between groups in daily living ability (p<.001) and MFT(Rt.)(p<.01). In addition, as a result of comparing the changes in absolute alpha waves to confirm the degree of depression through brain waves, there was no statistically significant difference. However, in the experimental group, it was confirmed that the average value increased to a positive value. This study is an experiment to verify the effectiveness of the cognitive rehabilitation program using virtual reality contents, and suggests a new intervention method to maintain and improve the daily life ability, cognitive function, depression and upper extremity function of the elderly.

• The Journal of Korean Academy of Orthopedic Manual Physical Therapy
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• v.2 no.1
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• pp.9-19
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• 1996

Type I, II, III are regarded as "true" joint receptors, type IV is considered a class of pain receptor. Type I, II and III mechanoreceptors, via static and dynamic input, signal joint position, intraarticular pressure changes, and the direction, amplitude, and velocity of joint movements. Type I mechanoreceptor subserve both static and dynamic physiologic functions. Type I are found primarily in the stratum fibrosum of the joint capsule and ligaments. Type I receptors have a low threshold for activation and are allow to adapt to changes altering their firing frequency. Type II receptors have a low threshold for activation. These dynamic receptors respond to joint movement. Type II receptors are thus termed rapidly adapting. Type II joint receptors are located at the junction of the synovial membrane and fibrosum of the joint capsule and intraarticular and extraarticular fat pads. Type III receptors have been found in collateral ligaments of the joints of the extremities. Morphologically similar to Golgi tendon organ. These dynamic receptors have a high threshold to stimulation and are slowly adating. Type IV receptors possess free nerve ending that have been found in joint capsule and fat pads. They are not normally active, but respond to extreme mechanical deformation of the joint as well as to direct chemical or mechanical irritation. Small amplitude oscillatory and distraction movements(joint mobilization) techniques are used to stimulate the mechanoreceptors that may inhibit the transmission of nociceptors stimuli at the spinal cord or brain stem levels.

• Biomolecules & Therapeutics
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• v.19 no.4
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• pp.431-437
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• 2011

Aberrant activation of microglia has been reported to cause neuronal damages by releasing a variety of pro-inflammatory cytokines. Besides where microglia become active, damages have been also observed in remote places, which is considered due to the migration of activated microglia. Therefore, an agent that could suppress abnormal activation of microglia and their subsequent migration might be valuable in activated microglia-related brain pathologies. The objective of the present study was to evaluate anti-inflammatory effects of betulinic acid on lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Pretreatment of betulinic acid significantly attenuated LPS-induced NO production and protein expression of iNOS. Betulinic acid also significantly suppressed LPS-induced release and expression of cytokines such as TNF-${\alpha}$ and IL-$1{\beta}$. Furthermore, betulinic acid significantly uppressed LPS-induced MMP-9 expression, which has been suggested to play an important role in the migration of activated microglia. In order to understand the possible mechanism by which betulinic acid suppresses LPS-induced cytokine production and migration of microglia, the role of NF-kB, a major pro-inflammatory transcription factor, was examined. Betulinic acid significantly suppressed LPS-induced degradation of IKB, which retains NF-kB in the cytoplasm. Therefore, nuclear translocation of NF-kB upon LPS stimulation was significantly suppressed with betulinic acid. Taken together, the present study for the first time demonstrates that betulinic acid possesses anti-inflammatory activity through the suppression of nuclear translocation of NF-kB in BV2 microglial cells.

• The Journal of Korean Academy of Sensory Integration
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• v.17 no.1
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• pp.30-42
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• 2019

Objective : The purpose of this study is to analyze non-medication interventions for self-injurious behavior of individuals with autism spectrum disorders, using a systematic review, and to provide evidence of appropriate services for individuals with autism spectrum disorders with self-injury behaviors in the clinical practice of occupational therapy. Methods : Using the electronic databases PubMed, Medline (ProQuest), DBpia, RISS, KISS, and NDSL, we searched for articles published in Korean and international journals from December 2004 to November 2018. The main search term were "Autism OR Autism Spectrum Disorder AND Therapy OR Treatment Or Intervention AND Self Injurious Behavior." Qualitative analysis was performed, and the results are presented in the PICO format. Results : A total of 12 articles were selected. The quality of the evidence was highest in level IV and level V. Single studies with an experimental design were the most common. Behavior therapy was the most common type of intervention. The next most common interventions were behavioral therapy, brain stimulation and control, and sensory integration therapy with behavioral therapy. The self-injury behaviors of individuals autism spectrum disorders were decreased, and was statistically significant. Conclusion : This study investigated the use of non-medication interventions for children with autism spectrum disorders who showed self-injury behavior. Future research should use higher-level designs, and investigate differences between various non-medication interventions.

• 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.