• The Journal of Korean Physical Therapy
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• v.15 no.3
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• pp.295-345
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• 2003

This study investigated activation of cerebral cortex in patients with hemiplegia that was caused by neural damage. Key-point control movement therapy of Bobath was performed for 9 weeks in 3 subjects with hemiplegia and fMRI was used to compare and analyze activated degree of cerebral cortex in these subjects. fMRI was conducted using the blood oxygen level-dependent(BOLD) technique at 3.0T MR scanner with a standard head coil. The motor activation task consisted of finger flexion-extension exercise in six cycles(one half-cycles = 8 scans = $3\;sec{\times}\;8\;=\;24\;sec$). Subjects performed this task according to visual stimulus that sign of right hand or left hand twinkled(500ms on, 500ms off). After mapping activation of cerebral motor cortex on hand motor function, below results were obtained. 1. Activation decreased in primary motor area, whereas it increased in supplementary motor area and visual association area(p<.001). 2. Activation was observed in bilateral medial frontal gyrus, middle frontal gyrus of left cerebrum, inferior frontal gyrus, inter-hemispheric, fusiform gyrus of right cerebrum, superior parietal lobule of parietal lobe and precuneus in subjedt 1, parahippocampal gyrus of limbic lobe and cingulate gyrus in subject 2, and inferior frontal gyrus of right frontal lobe, middle frontal gyrus, and inferior parietal lobule of left cerebrum in subject 3 (p<.001). 3. Activation cluster extended in declive of right cellebellum posterior lobe in subject 1, culmen of anterior lobe and declive of posterior lobe in subject 2, and dentate gyrus of anterior lobe, culmen and tuber of posterior lobe in subject 3 (p<.001). In conclusion, these data showed that Key-point control movement therapy of Bobath after stroke affect cerebral cortex activation by increasing efficiency of cortical networks. Therefore mapping of brain neural network activation is useful for plasticity and reorganization of cerebral cortex and cortico-spinal tract of motor recovery mechanisms after stroke.

• Journal of Veterinary Clinics
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• v.16 no.2
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• pp.265-271
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• 1999

These experiments were performed to investigate the effect of saline, monosodium L-glutamate(MSG), MSG-phenylalanine, and/or phenylalanine on TH-immunoreactivity in arcuate nucleus of hypothalamus and hind limb area of cerebral cortex in rats using the immunohistochemical methods. The result were as follows: 1. TH-immunoreactive neurons in hind limb area of cerebral cortex and arcuate nucleus of hypothalamus were decreased in MSG treated group compared to the saline treated group and also lesions in arcuate nucleus and median eminence of hypothalamus were increased with MSG treatment 2. TH-immunoreactive neurons in median eminence and arcuate nucleus were increased in phenylalanine treated group compared to the saline treated group and also neurons were more increased in lamina V of hind limb area of cerebral cortex with phenylalanine treatment. 3. TH-immunoreactive neurons in median eminence and arcuate nucleus were decreased in MSG-phenylalanine treated group compared to the phenylalanine treated group and increased compared to the MSG treated group. In lamina V of hind limb area of cerebral cortex, TH-immunoreactive neurons were more decreased in MSG-phenylalanine treated group than that of the phenylalanine treated group, and more increased than that of MSG treated group. These experiments indicated that TH-immunoreactive neurons in hypothalamus and cerebral cortex were increased due to the activation of phenylalanine and decreased by suppressing activation of phenylalanine through MSG treatment.

• Biomolecules & Therapeutics
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• v.13 no.2
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• pp.95-100
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• 2005

This study was performed to investigate the mechanism of cerebral blood flow of adenosine $A_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by nitric oxide (NO) and guanylate cyclase. In pentobarbital-anesthetized, pancuronium-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood flow from cerebral cortex was measured using laser-doppler flowmetry. Topical application of an adenosine $A_{2B}$ receptor agonist, 5'-N-ethylcar-boxamidoadenosine (NECA; $4{\mu}mol/l$) increased cerebral blood flow. This effect of NECA ($4{\mu}mol/l$) was blocked by pretreatment with NO synthase inhibitor, $N^G$-nitro-L-argine methvlester (L-NAME; $40{\mu}mol/l$) and guanylate cyclase inhibitor, LY-83,583 ($10{\mu}mol/l$). These results suggest that adenosine $A_{2B}$ receptor increases cerebral blood flow. It seems that this action of adenosine $A_{2B}$ receptor is mediated via the NO and the activation of guanylate cyclase in the cerebral cortex of the rats.

• Biomolecules & Therapeutics
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• v.12 no.2
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• pp.108-113
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• 2004

This study was performed to investigate the regulatory mechanism of cerebral blood flow of adenosine $A_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by adenylate cyclase and guanylate cyclase. in pentobarbital-anesthetized, pentobrabital-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood How from cerebral cortex was measured using laser-Doppler flowmetry. Topical application of an adenosine $A_{2B}$ receptor agonist, 5'-N-ethylcar-boxamidoadenosine (NECA; 4 umol/l) increased cerebral blood flow. This effect of NECA (4 umol/l) was not blocked by pretreatment with adenylate cyclase inhibitor, MDL-12330 (20 umol/l). But effect of NECA (4 umol/l) was blocked by pretreatment with guanylate cyclase inhibitor, LY-83383 (10 umol/l). These results suggest that adenosine $A_{2B}$ receptor increases cerebral blood flow. It seems that this action of adenosine $A_{2B}$ receptor is mediated via the activation of guanylate cyclase in the cerebral cortex of the rats.

• Biomolecules & Therapeutics
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• v.13 no.1
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• pp.35-40
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• 2005

This study was performed to investigate the regulatory mechanism of cerebral blood flow of adenosine A$_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by adenylate cyclase, guanylate cyclase and potassium channel. In pentobarbital-anesthetized, pancuronium-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood flow from cerebral cortex was measured using laser-Doppler flowmetry. Topical application of an adenosine A$_{2B}$ receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA; 4 umol/I) increased cerebral blood flow. This effect of NECA (4 umol/I) was not blocked by pretreatment with adenylate cyclase inhibitor, MDL-12,330 (20 umol/I). But effect of NECA (4 umol/I) was blocked by pretreatment with guanylate cyclase inhibitor, LY-83,583 (10 umol/I) and pretreatment with ATP-sensitive potassium channel inhibitor, glipizide (5 umol/I). These results suggest that adenosine A$_{2B}$ receptor increases cerebral blood flow. It seems that this action of adenosine A$_{2B}$ receptor is mediated via the activation of guanylate cyclase and ATP-sensitive potassium channel in the cerebral cortex of the rats.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.179-188
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• 2017

With the explosive increase in exposure to radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones, public concerns have grown over the last few decades with regard to the potential effects of EMF exposure on the nervous system in the brain. Many researchers have suggested that RF-EMFs can effect diverse neuronal alterations in the brain, thereby affecting neuronal functions as well as behavior. Previously, we showed that long-term exposure to 835 MHz RF-EMF induces autophagy in the mice brain. In this study, we explore whether shortterm exposure to RF-EMF leads to the autophagy pathway in the cerebral cortex and brainstem at 835 MHz with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Increased levels of autophagy genes and proteins such as LC3B-II and Beclin1 were demonstrated and the accumulation of autophagosomes and autolysosomes was observed in cortical neurons whereas apoptosis pathways were up-regulated in the brainstem but not in the cortex following 4 weeks of RF exposure. Taken together, the present study indicates that monthly exposure to RF-EMF induces autophagy in the cerebral cortex and suggests that autophagic degradation in cortical neurons against a stress of 835 MHz RF during 4 weeks could correspond to adaptation to the RF stress environment. However, activation of apoptosis rather than autophagy in the brainstem is suggesting the differential responses to the RF-EMF stresses in the brain system.

• Biomolecules & Therapeutics
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• v.12 no.2
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• pp.68-73
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• 2004

This study was performed to investigate the regulatory mechanism of cerebral blood How of adenosine $A_2$ receptor agonist in the rats, and to define whether its mechanism is mediated by nitric oxide (NO), adenylate cyclase and guanylate cyclase. In pentobarbital-anesthetized, pancuronium-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood flow from cerebal cortex was measured using laser-Doppler flowmetry. Topical application of an adenosine $A_2$ receptor agonist [5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA; 4 umol/l)] increased cerebral blood flow. This effect of CPCA (4 umol/l) was blocked by pretreatment with NO synthase inhibitor [$N^G$-nitro-L-argine methylester (L-NAME; 140 umol/l)] and adenylate cyclase inhibitor [MDL-12,330 (20 umol/l)]. But the effect of CPCA (4 umol/l) was not blocked by pretreatment with guanylate cyclase inhibitor [LY-83,583 (10 umol/l)]. These results suggest that adenosine $A_2$ receptor increases cerebral blood How. It seems that this action of adenosine $A_2$ receptor is mediated via the NO and the activation of adenylate cyclase in the cerebral cortex of the rats.

• Korean Journal of Digital Imaging in Medicine
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• v.9 no.2
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• pp.31-38
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• 2007

To evaluate the accuracy and extent in the localization of cerebral motor coutex activation using a gradient- echo echo planar imaging(GE-EPI) compared to spin-echo echo planar iimaging(SE-EPI) on 3T MR imaging. Functional MR imaging of cerebral motor cortex activation was examined in GE-EPI and SE-EPI in five healthy male volunteers. A right finger movement was accomplished with a paradigm of 6 task and rest, periods and the cross-correlation was used for a statistical mapping algorithm. We evaluated any sorts of differenced of the time seried and the signal intensity changes between the rest and task periods obtained with two technoques. The qualitative analysis was distributed with activation sites of large veins and small veins by using two techniques and was found that both the techniques were clinically uesful for delineating large veins and small veins in fMRL Signal intensity charge of the rest and activation periods provided simmilar activations in both methods(GE-EPI : 0.93$\pm$0.11, SE-EPI : 0.80$\pm$.015) but the signal intensity in GE-EPI(133.95$\pm$15.76) was larger than in SE-EPI(74.5$\pm$18.90). The average SNRs of EPI raw data were higher at SMA in SE-EPI(48.54$\pm$12.37) than GE-EPI(41.4$\pm$12.54) and at M1 in SE-EPI(43.24$\pm$11.77) than GE-EPI(38.27$\pm$6.53). The localization of activation voxels of the GE-EPI showed a larger vein but the SE-EPI generally showed small vein. Then the analysis results of the two techniques were used for a statistacal paired student t-test. SE-EPI was found clinically useful for localizing the cerebral moter cortex cativation on 3.0T, but showed a little different activation patterns comparad to GE-EPI. In conclusion, SE-EPI may be feasible and can detect true cortical activation from capillaries and GE-EPI can obtain the large veins in the motor cortex activation on 3T MR imaging.

• Annals of Clinical Neurophysiology
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• v.7 no.1
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• pp.34-36
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• 2005

Two hemiplegic cerebral palsy patients were studied to investigate the cortical mechanisms underlying preserved somatosensory capacity, using functional MRI(fMRI). Tactile stimulation was performed by brushing of palm, during fMRI study. By the affected hand stimulation, contralateral primary somatosensory cortex was activated in patient 1 and cortical area anterior to the lesion site was activated in patient 2. We suggest that reorganization of the somatosensory cortex after brain injury can be induced by recruitment of undamaged areas adjacent to lesion site.

• Journal of Biomedical Engineering Research
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• v.28 no.1
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• pp.139-147
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• 2007

The aim of this study was to evaluate effects of short-tenn repetitive-bilateral excercise on the activation of motor network using functional magnetic resonance imaging (fMRI). The training program was performed at 1 hr/day, 5 days/week during 6 weeks. Fugl-Meyer Assessments (FMA) were performed every two weeks during the training. We compared cerebral and cerebellar cortical activations in two different tasks before and after the training program: (1) the only unaffected hand movement (Task 1); and (2) passive movements of affected hand by the active movement of unaffected hand (Task 2). fMRI was performed at 3T with wrist flexion-extension movement at 1 Hz during the motor tasks. All patients showed significant improvements of FMA scores in their paretic limbs after training. fMRI studies in Task 1 showed that cortical activations decreased in ipsilateral sensorimotor cortex but increased in contralateral sensorimotor cortex and ipsilateral cerebellum. Task 2 showed cortical reorganizations in bilateral sensorimotor cortex, premotor area, supplemetary motor area and cerebellum. Therefore, this study demonstrated that plastic changes of motor network occurred as a neural basis of the improvement subsequent to repetitive-bilateral excercise using the symmetrical upper-limb ann motion trainer.