• Science of Emotion and Sensibility
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• v.15 no.4
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• pp.585-592
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• 2012

Food is crucial for the nutrition and survival of humans. Taste system is one of the fundamental senses. Taste cells detect and respond to five basic taste modalities (sweet, bitter, salty, sour, and umami). However, the cortical processing of taste sensation is much less understood. Recently, there were many efforts to observe the brain activation in response to taste stimulation using functional magnetic resonance imaging (fMRI), magnetoencephalography (MEG), and optical imaging. These different techniques do not provide directly comparable data each other, but the complementary investigations with those techniques allowed the description and understanding of the sequence of events with the dynamics of the spatiotemporal pattern of activation in the brain in response to taste stimulation. The purpose of this study is the understanding of the brain activities to taste stimuli in sensory and affective aspects and the reviewing of the recent research of the gustotopic map by functional brain mapping.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.6
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• pp.491-497
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• 2015

Traumatic brain injury (TBI) is a major cause of mortality and long-term disability, which can decrease quality of life. In spite of numerous studies suggesting that Epigallocatechin-3- gallate (EGCG) has been used as a therapeutic agent for a broad range of disorders, the effect of EGCG on TBI remains unknown. In this study, a weight drop model was established to evaluate the therapeutic potential of EGCG on TBI. Rats were administered with 100 mg/kg EGCG or PBS intraperitoneally. At different times following trauma, rats were sacrificed for analysis. It was found that EGCG (100 mg/kg, i.p.) treatment significantly reduced brain water content and vascular permeability at 12, 24, 48, 72 hour after TBI. Real-time PCR results revealed that EGCG inhibited TBI-induced IL-$1{\beta}$ and TNF-${\alpha}$ mRNA expression. Importantly, CD68 mRNA expression decreasing in the brain suggested that EGCG inhibited microglia activation. Western blotting and immunohistochemistry results showed that administering of EGCG significantly inhibited the levels of aquaporin-4 (AQP4) and glial fibrillary acidic protein (GFAP) expression. TBI-induced oxidative stress was remarkably impaired by EGCG treatment, which elevated the activities of SOD and GSH-PX. Conversely, EGCG significantly reduced the contents of MDA after TBI. In addition, EGCG decreased TBI-induced NADPH oxidase activation through inhibition of $p47^{phox}$ translocation from cytoplasm to plasma membrane. These data demonstrate that EGCG treatment may be an effective therapeutic strategy for TBI and the underlying mechanism involves inhibition of oxidative stress.

• Journal of Microbiology and Biotechnology
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• v.21 no.9
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• pp.903-913
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• 2011

Vibrio parahaemolyticus, which causes gastroenteritis, wound infection, and septicemia, has two sets of type III secretion systems (TTSS), TTSS1 and TTSS2. A TTSS1-deficient vcrD1 mutant of V. parahaemolyticus showed an attenuated cytotoxicity against HEp-2 cells, and a significant reduction in mouse lethality, which were both restored by complementation with the intact vcrD1 gene. V. parahaemolyticus also triggered phosphorylation of mitogen-activated protein kinases (MAPKs) including p38 and ERK1/2 in HEp-2 cells. The ability to activate p38 and ERK1/2 was significantly affected in a TTSS1-deficient vcrD1 mutant. Experiments using MAPK inhibitors showed that p38 and ERK1/2 MAPKs are involved in V. parahaemolyticus-induced death of HEp-2 cells. In addition, caspase-3 and caspase-9 were processed into active forms in V. parahaemolyticus-exposed HEp-2 cells, but activation of caspases was not essential for V. parahaemolyticus-induced death of HEp-2 cells, as shown by both annexin V staining and lactate dehydrogenase release assays. We conclude that secreted protein(s) of TTSS1 play an important role in activation of p38 and ERK1/2 in HEp-2 cells that eventually leads to cell death via a caspase-independent mechanism.

• Journal of Veterinary Science
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• v.24 no.2
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• pp.26.1-26.11
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• 2023

Background: Angiotensin-converting enzyme inhibitor (ACEi) inhibits the catalysis of angiotensin I to angiotensin II and the degradation of substance P (SP) and bradykinin (BK). While the possible relationship between ACEi and SP in nociceptive mice was recently suggested, the effect of ACEi on signal transduction in astrocytes remains unclear. Objectives: This study examined whether ACE inhibition with captopril or enalapril modulates the levels of SP and BK in primary cultured astrocytes and whether this change modulates PKC isoforms (PKCα, PKCβI, and PKCε) expression in cultured astrocytes. Methods: Immunocytochemistry and Western blot analysis were performed to examine the changes in the levels of SP and BK and the expression of the PKC isoforms in primary cultured astrocytes, respectively. Results: The treatment of captopril or enalapril increased the immunoreactivity of SP and BK significantly in glial fibrillary acidic protein-positive cultured astrocytes. These increases were suppressed by a pretreatment with an angiotensin-converting enzyme. In addition, treatment with captopril increased the expression of the PKCβI isoform in cultured astrocytes, while there were no changes in the expression of the PKCα and PKCε isoforms after the captopril treatment. The captopril-induced increased expression of the PKCβI isoform was inhibited by a pretreatment with the neurokinin-1 receptor antagonist, L-733,060, the BK B1 receptor antagonist, R 715, or the BK B₂ receptor antagonist, HOE 140. Conclusions: These results suggest that ACE inhibition with captopril or enalapril increases the levels of SP and BK in cultured astrocytes and that the activation of SP and BK receptors mediates the captopril-induced increase in the expression of the PKCβI isoform.

• Journal of Life Science
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• v.23 no.9
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• pp.1096-1103
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• 2013

Chronic traumatic encephalopathy (CTE), which is common in athletes, is a progressive neurodegenerative disease and a long-term consequence of repetitive closed head injuries. CTE is regarded as a chronic brain syndrome due to the effects of repetitive traumatic brain injury (TBI). Because neurotrophic factors are neuroprotective in models of brain and spinal cord injuries, we examined the effects of cerebrolysin, a mixture of various neurotrophic factors, on brain pathology in a mouse model of repetitive mild TBI (rmTBI), which is a good model of CTE. Five groups were created and treated as follows: groups 1 and 2: rmTBI for 4 weeks following cerebrolysin injection for 4 weeks; groups 3 and 4: rmTBI for 8 weeks with or without cerebrolysin injection for 4 weeks; group 5: control. We found that p-tau expression was increased in the pyramidal layer of the cortex and hippocampus, particularly the CA3 region, but not in the CA1 region and the dentate gyrus (DG). Intra-tail vein administration of cerebrolysin ($10{\mu}l$ of 1 mg/ml) after/during rmTBI treatment reduced p-tau expression in both the cortex and hippocampus. Histological analysis revealed mild astrocyte activation (increased expression of glial fibrillary acidic protein (GFAP)) but not microglia activation (ionized calcium binding adaptor molecule 1 (iba-1) expression) and peripheral macrophage infiltration (CD45). Additionally, administration of cerebrolysin after rmTBI resulted in reduced astrocyte activation. These observations in rmTBI demonstrated that cerebrolysin treatment reduces phosphorylation of tau and astrocyte activation, attenuates brain pathology, and mitigates function deficits in TBI. Taken together, our observations suggest that cerebrolysin has potential therapeutic value in CTE.

• Sleep Medicine and Psychophysiology
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• v.3 no.2
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• pp.1-17
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• 1996

To demonstrate the clinical usefulness of electroencephalography (EEG) and factors increasing the usefulness of EEG, the authors evaluated each relationship between EEG related factors and clinical variables, and neuroimaging studies (CT and MRI)-related factors, and factors which are related with routine neurological examination for 207 patients who had been evaluated with both of EEG and neuroimaging study(CT or/and MRI). The results were as follows: 1) Abnormality of EEG findings had significant relationships with chief complaints, diagnosis, medication use, seizure attack, pathological reflex, and level of consciousness. However there were no significant correlations between abnormality of EEG findings and neuroimaging studies (CT and MRI)- related factors. 2) Laterality of EEG findings had significant relationships with abnormality, laterality, and focality of CT findings, and also with abnormality of MRI findings. But there were no significant correlations between laterality of EEG findings and clinical variables, and neurological examination-related factors. 3) Anterior-posterior distribution of EEG findings was significantly related with medication use. 4) Focality of EEG findings had significant relationships with sex, sensory dysfunction sign, and cerebellar dysfunction sign. But there were no significant correlations between focality of EEG findings and neuroimaging studies(CT and MRI) related factors. 5) Abnormal EEG pattern had significant correlations with various factors, such as age, chief complaints, duration from onset of symptom to taking MRI, seizure attack, abnormality and nature of lesion in CT findings, cortical atrophy in MRI findings, motor dysfunction sign, sensory dysfunction sign, and pathological reflex. 6) With abnormality on sleep activation, age, age of onset, seizure attack, ventricular enlargement in CT findings, and abnormality of MRI findings were significantly correlated. 7) With abnormality on hyperventilation activation, duration of illness and laterality of MRI findings were significantly correlated. Above results may suggest that abnormality of EEG findings is more closely related with functional change of the brain than structural changes of the brain and laterality of EEG findings is vice versa. And also that medication use has an influence on anterior versus posterior distribution of EEG findings and focality of EEG findings is not related with structural changes of the brain. Activation with sleep may be effective to show age differences and provocation of seizure activity and hyperventilation may be effective to detect the abnormal EEG findings by cerebrovascular insufficiency.

• Biomolecules & Therapeutics
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• v.13 no.4
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• pp.214-219
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• 2005

Chunghyuldan (Qingxuedan in Chinese) (CHD) has been used for patients with atherosclerosis and brain ischemia in Korea. To evaluate antiischemic activity of CHD, its antiinflammatory effect in lipopolysaccharide-induced BV-2 cells was investigated. CHD potently inhibited nitric oxide (NO) production in LPS-induced BV-2 cells with an $IC_{50}$ value of 4.8${\mu}g/ml$. CHD did not only inhibit mRNA and protein expression levels of inducible NO synthase and cyclooxygenase-2 in LPS-induced BV-2 cells, but also repressed mRNA expression levels of proinflammatory cytokines IL-l$\beta$ and TNF-$\alpha$. CHD also downregulated the activation of NF-kB and AP-l transcription factors induced by LPS. These results suggest that CHD may improve inflammatory brain ischemia by the downregulation the activation of NF-kB and AP-l transcription factors.

• BMB Reports
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• v.30 no.5
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• pp.332-336
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• 1997

The stimulatory effects of leucine on the activities of two soluble forms of brain glutamate dehydrogenase isoproteins (GDH I and GDH II) have been studied at various conditions. There were significant differences between GDH I and GDH II in their sensitivities to the action of leucine. When the effects of varied leucine concentrations on GDH activities were studied in the direction of reductive amination of 2-oxoglutarate with NADPH as a coenzyme, a marked activation was observed for both isoproteins at leucine concentrations up to 10 mM, whereas both isoproteins showed activation to a lesser extent with NADH as a coenzyme. The stimulatory effects of leucine on GDH activities in the direction of the oxidative deamination of glutamate were also observed, but to a much lesser extent. Leucine relieved the inhibition of GDH I by GTP and this resulted in an increase in the apparent activation by leucine in the presence of GTP. 2-Oxoglutarate was found to give rise to high substrate inhibition and leucine significantly reduced the substrate inhibition in the presence of $200\;{\mu}M$ NADH. Thus, the effects of leucine might be composed of a direct effect on the enzyme together with a relief of high substrate inhibition.

• Biomedical Science Letters
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• v.18 no.4
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• pp.428-434
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• 2012

Epilepsy is a chronic neurological disease showing a symptom of repeated seizures without any other physical disorders. Among the diagnostic examination for epilepsy, the electroencephalogram (EEG) has been known as an important test. This study aimed to investigate the EEG with photic stimulation in the pediatric epilepsy patients. They underwent digital sleep and waking EEGs or waking EEGs with photic stimulation. Epilepsy type, seizure history, and season of occurring seizure were analyzed. Epilepsy patients showed more response during the period of photic-on and eye close at the frequency of 10~20 Hz during the EEG activation procedure. Photoparoxysmal response (PPR) was shown in 206 patients out of total 1,551 epilepsy patients. PPR was appeared more frequently during summer and winter seasons, and especially in the patients who had a history of seizure. During the PPR, EEG pattern showed spike (77.18%), theta (9.71%), and spike + theta (13.11%). On the other hand, beta and theta waves were not significantly changed by photic stimulation. However, alpha wave was decreased and delta wave was increased by photic stimulation (P<0.05). These changes may be due to temporarily altered electrophysiological function of the epileptic patient's brain by the photic stimulation. There was no difference in the EEG pattern between the left and right side in the brain. In conclusion, condition of photic-on with closed eyes and frequency of 10~20 Hz during the procedure of EEG activation could be appropriate for obtaining a definite photoparoxysmal response in the electroencephalogram of the pediatric epilepsy patients.

• YAKHAK HOEJI
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• v.28 no.6
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• pp.305-311
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• 1984

Relationship between hypertension and monoamine oxidase (MAO) activity in rat brain and the change of this relationship by presynaptic ${\alpha}-receptor$ agonist were studied. Animals were divided into three groups. Group I was composed of normotensive Sprague-Dawley rats (NR), group II of spontaneously hypertensive rats (SHR) and group III of acquired hypertensive rats induced by deoxycorticosterone acetate (DOCA) and NaCl treatment. Clonidine, a presynaptic ${\alpha}-receptor$ agonist, was administered to groups II and III. Blood pressures and MAO activities were measured in each group. MAO activities in the brain of SHR were lower than those of NR. Animals in group II received clonidine which lowered blood pressures but did not change MAO activities in the brain. DOCA and NaCl induced hypertension 21 days after these treatments in group III and did not cause any changes in brain MAO activity. Clonidine lowered blood pressures of group III but did not change MAO activities. The data from the present study suggest that abnormaly low MAO activities in SHR brain may be one of the underlying factors for the susceptibility to hypertension and that the decrease in noradrenergic neuronal activities through presynaptic ${\alpha}-receptor$ activation by clonidine may not be related to the changes of brain MAO activities.