• The Journal of Pediatrics of Korean Medicine
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• v.23 no.3
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• pp.241-262
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• 2009

Objectives This study is designed to investigate the effects of Jujadokseo-hwan on the brain ability and inducing oxidative stresses. Methods We measured the changes of regional cerebral blood flow and mean arterial blood pressure. Then we analyzed histological examination, immunohistochemistric response and anti-oxidant activity of Jujadokseo-hwan. Results 1. Treatment of Jujadokseo-hwan significantly increased regional cerebral blood flow but decreased mean arterial blood pressure. 2. Treatment of Jujadokseo-hwan-induced increase of regional cerebral blood flow was significantly inhibited by pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase. 3. In histological examination through TTC stain, group I was no change, but group II showed that discolored in the most cortical part. Group III showed that decreased discolor in the cortical part. 4. In immunohistochemistric response of BDNF, group II showed that lower response effect. Group III showed that increase response effect. 5. Treatment of Jujadokseo-hwan increased proliferation rates of Glial cell effectively 6. Treatment of Jujadokseo-hwan accelerated proliferation rates of C6 cells in vitro. In addition, protective effects on cell death induced by paraquat, rotenone and hydrogen peroxide. In addition, activity of SOD were increased by treatment with Jujadokseo-hwan. Conclusions In conclusion, Jujadokseo-hwan can improve of the brain ability, learning ability, memory ability and induce ischemic brain injuries.

• Biomolecules & Therapeutics
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• v.18 no.1
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• pp.24-31
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• 2010

Taurine, 2-aminoethanesulfonic acid, is an abundant free amino acid present in brain cells and exerts many important biological functions such as anti-convulsant, modulation of neuronal excitability, regulation of learning and memory, anti-aggressiveness and anti-alcoholic effects. In the present study, we investigated to explore whether taurine has any protective actions against oxidative stress-induced damages in neuronal cells. ERK I/II regulates signaling pathways involved in nitric oxide (NO) and reactive oxygen species (ROS) production and plays a role in the regulation of cell growth, and apoptosis. We have found that taurine significantly inhibited AMPA induced cortical depolarization in the Grease Gap assays using rat cortical slices. Taurine also inhibited AMPA-induced neuronal cell damage in MTT assays in the differentiated SH-SY5Y cells. When the neuronal cells were treated with $H_2O_2$, levels of NO were increased; however, taurine pretreatment decreased the NO production induced by $H_2O_2$ to approximately normal levels. Interestingly, taurine treatment stimulated ERK I/II activity in the presence of AMPA or $H_2O_2$, suggesting the potential role of ERK I/II in the neuroprotection of taurine. Taken together, taurine has significant neuroprotective actions against AMPA or $H_2O_2$ induced damages in neuronal cells, possibly via activation of ERK I/II.

• Molecules and Cells
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• v.38 no.4
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• pp.312-317
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• 2015

Depletion of intracellular zinc by N,N,N,N-tetrakis(2-pyridylmethyl) ethylenediamine (TPEN) induces p53-mediated protein synthesis-dependent apoptosis of mouse cortical neurons. Here, we examined the requirement for poly(ADP-ribose) polymerase (PARP)-1 as an upstream regulator of p53 in zinc depletion-induced neuronal apoptosis. First, we found that chemical inhibition or genetic deletion of PARP-1 markedly attenuated TPEN-induced apoptosis of cultured mouse cortical neurons. Poly(ADP-ribosyl)ation of p53 occurred starting 1 h after TPEN treatment. Suggesting the critical role of PARP-1, the TPEN-induced increase of stability and activity of p53 as well as poly(ADP-ribosyl)ation of p53 was almost completely blocked by PARP inhibition. Consistent with this, the induction of downstream pro-apoptotic proteins PUMA and NOXA was noticeably reduced by chemical inhibitors or genetic deletion of PARP-1. TPEN-induced cytochrome C release into the cytosol and caspase-3 activation were also blocked by inhibition of PARP-1. Taken together, these findings indicate that PARP-1 is essential for TPEN-induced neuronal apoptosis.

• Journal of Korean Neurosurgical Society
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• v.62 no.3
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• pp.272-287
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• 2019

The mechanistic target of rapamycin (mTOR) pathway coordinates the metabolic activity of eukaryotic cells through environmental signals, including nutrients, energy, growth factors, and oxygen. In the nervous system, the mTOR pathway regulates fundamental biological processes associated with neural development and neurodegeneration. Intriguingly, genes that constitute the mTOR pathway have been found to be germline and somatic mutation from patients with various epileptic disorders. Hyperactivation of the mTOR pathway due to said mutations has garnered increasing attention as culprits of these conditions : somatic mutations, in particular, in epileptic foci have recently been identified as a major genetic cause of intractable focal epilepsy, such as focal cortical dysplasia. Meanwhile, epilepsy models with aberrant activation of the mTOR pathway have helped elucidate the role of the mTOR pathway in epileptogenesis, and evidence from epilepsy models of human mutations recapitulating the features of epileptic patients has indicated that mTOR inhibitors may be of use in treating epilepsy associated with mutations in mTOR pathway genes. Here, we review recent advances in the molecular and genetic understanding of mTOR signaling in epileptic disorders. In particular, we focus on the development of and limitations to therapies targeting the mTOR pathway to treat epileptic seizures. We also discuss future perspectives on mTOR inhibition therapies and special diagnostic methods for intractable epilepsies caused by brain somatic mutations.

• Journal of Korean Neurosurgical Society
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• v.46 no.1
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• pp.1-4
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• 2009

Objective: To report an unsuspected adaptive plasticity of single upper motor neurons and of primary motor cortex found after microsurgical connection of the spinal cord with peripheral nerve via grafts in paraplegics and focussed discussion of the reviewed literature. Methods: The research aimed at making paraplegics walk again, after 20 years of experimental surgery in animals. Amongst other things, animal experiments demonstrated the alteration of the motor endplates receptors from cholinergic to glutamatergic induced by connection with upper motor neurons. The same paradigm was successfully performed in paraplegic humans. The nerve grafts were put into the ventral-lateral spinal tract randomly, with out possibility of choosing the axons coming from different areas of the motor cortex. Results: The patient became able to selectively activate the re-innervated muscles she wanted without concurrent activities of other muscles connected with the same cortical areas. Conclusion: Authors believe that unlike in nerve or tendon transfers, where the whole cortical area corresponding to the transfer changes its function a phenomenon that we call "brain plasticity by areas". in our paradigm due to the direct connection of upper motor neurons with different peripheral nerves and muscles via nerve grafts motor learning occurs based on adaptive neuronal plasticity so that simultaneous contractions of other muscles are prevented. We propose to call it adaptive functional "plasticity by single neurons". We speculate that this phenomenon is due to the simultaneous activation of neurons spread in different cortical areas for a given specific movement, whilst the other neurons of the same areas connected with peripheral nerves of different muscles are not activated at the same time. Why different neurons of the same area fire at different times according to different voluntary demands remains to be discovered. We are committed to solve this enigma hereafter.

• Anxiety and mood
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• v.3 no.2
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• pp.91-96
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• 2007

Panic disorder is a common psychiatric illness that causes considerable morbidity. However, the biological basis of panic disorder remains unclear. In this report, we present and summarize the current literature on functional neuroimaging studies related to the neurobiology of panic disorder. The findings were summarized and divided into six groups : (1) known brain structures related to anxiety, especially panic disorder ; (2) structural results ; (3) functional imaging studies at rest ; (4) functional imaging studies with challenge testing ; (5) neuroreceptor studies ; and (6) changes in the treatment of panic disorder. Based on the findings of these neuroimaging studies, it seems as though panic disorder involves the hippocampal and parahippocampal areas, including the amygdala, as well as some cortical regions, such as the temporal and prefrontal cortices. Panic disorder is known to be associated with an imbalance between the right and left hemispheres of the brain at rest or during panic attacks. During a panic attack, patients with panic disorder are likely to experience an increase in local activity in the cingulate, insula, midbrain, and so on. On the other hand, a widespread reduction in the cortical areas has also been reported in most provocation studies. Thus, panic disorder may be related to the excess activation of the fear networks in response to subtle environmental cues and insufficient inhibition from higher cortical control areas ; however ; further studies are recommended in order to fully understand the neurobiology of panic disorder.

• Journal of Biomedical Engineering Research
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• v.39 no.3
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• pp.124-133
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• 2018

We tried to investigate the changes in cortical activities according to emotional valence states during watching video clips. We examined the neural basis of two emotional states (positive and negative) using spectral power analysis and brain functional connectivity analysis of cortical current density time-series reconstructed from high-density electroencephalograms (EEGs). Fifteen healthy participants viewed a series of thirty-two 2 min emotional video clips. Sixty-four channel EEGs were recorded. Distributed cortical sources were reconstructed using weighted minimum norm estimation. The temporal and spatial characteristics of spectral source powers showing significant differences between positive and negative emotion were examined. Also, correlations between gamma-band activities and affective valence ratings were determined. We observed the changes of cortical current density time-series according to emotional states modulated by video clip. Gamma-band activities showed significant difference between emotional states for thirty seconds at the middle and the latter half of the video clip, mainly in prefrontal area. It was also significantly anti-correlated with the self-ratings of emotional valence. In addition, the gamma-band activities in frontal and temporal areas were strongly phase-synchronized, more strongly for negative emotional states. Cortical activities in frontal and temporal areas showed high spectral power and inter-regional phase synchronization in gamma-band during negative emotional states. It is inferred that the higher amygdala activation induced by negative stimuli resulted in strong emotional effects and caused strong local and global synchronization of neural activities in gamma-band in frontal and temporal areas.

• Progress in Medical Physics
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• v.16 no.1
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• pp.1-9
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• 2005

The effect of the developed symmetric upper extremity motion trainer on the cortical activation pattern was investigated in three chronic hemiparetic patients using both fMRI and Fugl-Meyer test. The training program was performed at 1 hr/day, 5 days/week during 6 weeks. Fugl-Meyer tests were performed every two weeks during the training. fMRI was performed at 3T scanner with wrist flexion-extension in two different tasks before and after the training program: the only unaffected hand movement (Task 1) and passive movements of affected hand by the active movement of unaffected hand (Task 2). fMRI studies in Task 1 showed that cortical activations decreased in ipsilateral SMC but increased in contralateral SMC. Task 2 showed cortical reorganizations in bilateral SMC, PMA and SMA. Therefore, it seems that the cortical reorganization in chronic hemiparetic patients can be induced by the training with the developed symmetric upper extremity motion trainer.

• Proceedings of the Korean Society for Emotion and Sensibility Conference
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• 2009.11a
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• pp.183-185
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• 2009

As imaging technology develops, magnetic resonance imaging (MRI) techniques have contributed to the understanding of brain function by providing anatomical structure of the brain and functional imaging related to information processing. Manganese-enhanced MRI (MEMRI) techniques can provide useful information about functions of the nervous system. However, systematic studies regarding information processing of pain have not been conducted. The purpose of this study was to detect brain activation during painful electrical stimulation using MEMRI with high spatial resolution. Male Sprague-Dawley rats (250-300 g) were divided into 3 groups: normal control, sham stimulation, and electric stimulation. Rats were anesthetized with 2.5% isoflurane for surgery. Polyethylene catheter (PE-10) was placed in the external carotid artery to administrate mannitol and MnCl2. The blood brain barrier (BBB) was broken by 20% D-mannitol under anesthesia mixed with urethane and a-chloralose. The hind limb was electrically stimulated with a 2Hz (10V) frequency while MnCl2 was infused. Brain activation induced by electrical stimulation was detected using a 4.7 T MRI. Remarkable signal enhancement was observed in the primary sensory that corresponds to sensory tactile stimulation at the hind limb region. These results suggest that signal enhancement is related to functional activation following electrical stimulation of the peripheral receptive field.

• Journal of Acupuncture Research
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• v.21 no.2
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• pp.57-71
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• 2004

Objective : Physiological evidence regarding acupuncture's effect in human patients is not yet well established, despite considerable evidence for its therapeutic efficacy. Besides target or disease specificity of acupuncture, acupuncture analgesia (AA) appears to be another large subclass that poses many questions, such as whether there is point specificity with respect to which acupoint is most effective for a particular condition. Methods : We observed brain activation with functional magnetic resonance imaging (fMRI) using a set of stimuli that consist of pain, pain following Meridian acupuncture, and pain following Sham acupuncture. Results : Among the new observations, the most interesting fact is that data sets of both Meridian acupuncture and Sham acupuncture show decreased activation of the same brain areas related to the pain processing signals. Present functional MRI study demonstrate two important biological observations that could elucidate AA mechanism in human participants: the effects of acupuncture occur through mediation of the higher brain areas. Sham acupuncture stimulation appears to be almost as effective as traditional Meridian acupoint stimulation, suggesting that acupuncture is not entirely point specific. Decreased activation in the limbic paleo cortical areas appears to be the probable neurological manifestation of AA and strongly implies that acupuncture stimulation inhibits the transmission of ascending pain signals to the higher cortical areas by the previously known descending pain inhibitory circuit. Conclusion : We, therefore, a hypothesized that this pain inhibitory circuit is initiated and mediated via the broad sense Hypothalamus Pituitary Adrenal (BS HPA) axis in conjunction to the "sensory stimulation."