• Proceedings of the Korean Society of Toxicology Conference
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• 2006.11a
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• pp.55-64
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• 2006

The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.

• Journal of Korean Academy of Nursing
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• v.34 no.7
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• pp.1255-1264
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• 2004

Purpose: The purpose of this study was to determine the effect of a 3-week somatosensory stimulation program on the integrity of the somatosensory pathway of patients with brain damage. Method: The sample consisted of two groups of patients with brain damage matched by Glasgow Coma Scale (GCS) scores and age:8 patients with a mean age of 56.75 years who were treated with somatosensory stimulation, and 8 patients with a mean age of 58.88 years, who were not treated with sensory intervention program. A repeated measures matched-control group design was used to assess functional recovery of the brain. The instrument used in this study was SSEP (somatosensory evoked potentials), a neurophysiological parameter, for the integrity of the somatosensory pathway. Results: The hypothesis that patients with brain damage who were treated with the somatosensory stimulation program will show higher SSEP wave form scores than the non-treatment group was supported (3rd week.: U=13.000, p=.014). Additional repeated measures analysis showed that there were no significant differences in recovery trends between the groups (F=1.945, p=.159). Conclusion: This study demonstrates that a somatosensory stimulation program is effective in promoting recovery of the integrity of the somatosensory pathway of patients with brain damage.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.5
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• pp.423-431
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• 2020

This study aimed to evaluate the effect of curcumin on brain hypoxic-ischemic (HI) damage in neonatal rats and whether the phosphoinositide 3-kinase (PI3K)/Akt/vascular endothelial growth factor (VEGF) signaling pathway is involved. Brain HI damage models were established in neonatal rats, which received the following treatments: curcumin by intraperitoneal injection before injury, insulin-like growth factor 1 (IGF-1) by subcutaneous injection after injury, and VEGF by intracerebroventricular injection after injury. This was followed by neurological evaluation, hemodynamic measurements, histopathological assessment, TUNEL assay, flow cytometry, and western blotting to assess the expression of p-PI3K, PI3K, p-Akt, Akt, and VEGF. Compared with rats that underwent sham operation, rats with brain HI damage showed remarkably increased neurological deficits, reduced right blood flow volume, elevated blood viscosity and haematocrit, and aggravated cell damage and apoptosis; these injuries were significantly improved by curcumin pretreatment. Meanwhile, brain HI damage induced the overexpression of p-PI3K, p-Akt, and VEGF, while curcumin pretreatment inhibited the expression of these proteins. In addition, IGF-1 treatment rescued the curcumin-induced down-regulated expression of p-PI3K, p-Akt, and VEGF, and VEGF overexpression counteracted the inhibitory effect of curcumin on brain HI damage. Overall, pretreatment with curcumin protected against brain HI damage by targeting VEGF via the PI3K/Akt signaling pathway in neonatal rats.

• Physical Therapy Rehabilitation Science
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• v.7 no.3
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• pp.114-118
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• 2018

Objective: The left and right sides of the brain has different roles. This study investigated the differences in cognitive driving ability between stroke survivors with damage to the left brain and right brain. Therefore, the purpose of this study was to compare the driving cognitive ability of left and right hemispheric drivers following stroke. Design: Cross-sectional study. Methods: The Stroke Drivers' Screening Assessment (SDSA) from the UK was translated to the Korean Stroke Drivers' Screening Assessment (K-SDSA) to meet the specific traffic environments of Korea. The SDSA is composed of 4 tasks :1) a dot cancellation task that measures concentration and visuospatial abilities necessary for driving, 2) a directional matrix task to measure spatio-temporal executive function required for driving, 3) a compass matrix task to measure accurate direction determination ability required for driving, and 4) recognition of traffic signs and reasoning ability to understanding traffic situation. The SDSA assessment time is about 30 minutes. The K-SDSA was used to compare the cognitive driving abilities between 15 stroke survivors with left and 15 stroke survivors with right brain damage. Results: There were significant differences between the persons with stroke patients with left brain lesions (right hemiplegia) compared to the persons with stroke with right brain lesions (left hemiplegia) (p<0.05). It was found that the cognitive driving ability of those with right brain damage was lower than that of the group of left brain damage. Conclusions: This research investigated the driving cognitive ability of persons with stroke. The therapists can use this information as basis for the driving test and training purposes. It could also be used as a basis to understanding if the cognitive ability of not only stroke survivors but also those with brain damage is adequate to actually drive.

• Korean Journal of Biological Psychiatry
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• v.3 no.1
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• pp.66-74
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• 1996

There has been an increase in head trauma due to rapid industralization and improvement in transportation. This poses difficulties in differentiating between neuropsychiatric disabilities resulting from real organic changes and those arising from compensation issues. It is the purpose of this study to seek out the differences between normal and abnormal finding group in the structural brain imaging studies via the results of the functional brain imaging studies and psychological tests. Out of 132 subjects, 62 comprised normal and 70 the abnormal finding group. EEG and SPECT were chosen for inspection of functional brain imaging. MMPI and K-WAIS were chosen for psychological test. The subjects were further divided into right hemispheric damage, left hemispheric damage, both hemispheric damage, diffuse damage group and negative group in order to find out whether any differences in the psychological lest results could be localized. The results are as follows : 1) The abnormal finding group, the EEG and SPECT were proven to be a good predictor of brain lesion. This implies that even in the functional brain studies, abnormalities are more easily detected if there are visible brain lesions. 2) The FSIQ of the abnormal finding group is lower than that of normal finding group. this difference is mainly due to low V1Q. The left hemispheric damage group lend to shaw low V1Q. This lowered in was the difference between left hemispheric damage group and negative group. Furthermore, there were no group differences in the PIQ. It is concluded that K-WAIS is effective as evaluator of VIQ mainly of those patients with left hemispheric damage and it is ineffective as a evaluator of PIQ. 3) In the MMPI profile, the both groups displayed high neurotic profiles. There was no difference in the psychotic profiles. The scores of the Depression and Hystery were high in abnormal finding group. This can be seen as one of the lypical findings of chronic head trauma patients. 4) The abnormal finding group tend to be diagnosed as organic mental disorder in the psychological tests more frequently.

• The Journal of Korean Physical Therapy
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• v.13 no.2
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• pp.407-420
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• 2001

This article provide information pertaining to recent scientific findings regarding neural and motor control development and the effects of brain damage on that development. Clinical and scientific issues pertaining to perinatal and adult-onset brain damage are discussed. The article is intended to provide the clinician with new information that will assist in patient assessment and the establishment of therapeutic interventions

• Clinical and Experimental Pediatrics
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• v.56 no.7
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• pp.271-274
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• 2013

Brain insults, including neurotrauma, infection, and perinatal injuries such as hypoxic ischemic encephalopathy, generate inflammation in the brain. These inflammatory cascades induce a wide spectrum of cytokines, which can cause neuron degeneration, have neurotoxic effects on brain tissue, and lead to the development of seizures, even if they are subclinical and occur at birth. Cytokines are secreted by the glial cells of the central nervous system and they function as immune system mediators. Cytokines can be proinflammatory or anti-inflammatory. Interleukin (IL)-$1{\beta}$ and IL-8 are proinflammatory cytokines that activate additional cytokine cascades and increase seizure susceptibility and organ damage, whereas IL-1 receptor antagonist and IL-10 act as anti-inflammatory cytokines that have protective and anticonvulsant effects. Therefore, the immune system and its associated inflammatory reactions appear to play an important role in brain damage. Whether cytokine release is relevant for the processes of epileptogenesis and antiepileptogenesis, and whether epileptogenesis could be prevented by immunomodulatory treatment should be addressed in future clinical studies. Furthermore, early detection of brain damage and early intervention are essential for the prevention of disease progression and further neurological complications. Therefore, cytokines might be useful as biomarkers for earlier detection of brain damage in high-risk infants.

• International Journal of Fuzzy Logic and Intelligent Systems
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• v.16 no.1
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• pp.59-63
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• 2016

Secondary damage to the user is a problem in biometrics. A brain-wave has no shape and a malicious user may not cause secondary damage to a user. However, if user sends brain-wave signals to an authentication system using a network, a malicious user could easily capture the brain-wave signals. Then, the malicious user could access the authentication system using the captured brain-wave signals. In addition, the dataset containing the brain-wave signals is large and the transfer time is long. However, user authentication requires a real-time processing, and an encryption scheme on brain-wave signals is necessary. In this paper, we propose an efficient encryption scheme using a chaos map and adaptive junk data on the brain-wave signals for user authentication. As a result, the encrypted brain-wave signals are produced and the processing time for authentication is reasonable in real-time.

• The Journal of Korean Medicine
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• v.21 no.4
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• pp.37-46
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• 2000

Objective : The purpose of this study was to investigate the effects of Angelicae Gigantis Radix on brain damage and the cardiovascular system. Method : By administration Angelicae Gigantis Radix, we compared treated groups with not treated groups, in view of five points as follows $\circled1$ the intervascular eNOS, $\circled2$ the blood pressure of SHR, $\circled3$ the transcription of the Kir6.2, $\circled4$ the survival time of the rats when common carotid artery was ligated, and $\circled5$ antiplatelet aggregation. Result : In this experiment, Angelicae Gigantis Radix treated group showed significant produced in the intervascular eNOS and decreased the blood pressure of SHR, increased the transcription of the Kir6.2 and SUR significantly in all Treated groups, prolonged the survival time of the rats when common carotid artery, showed the effects on antiplatelet aggregation. Conclusion : According to the above results, Angelicae Gigantis Radix can protect the brain damage and have cardiovascular system effect.

• YAKHAK HOEJI
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• v.35 no.6
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• pp.522-529
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• 1991

The purpose of this research is to evaluate effects of chloramphenicol, phenobarbital and progesterone on damage of DNA, RNA and protein which was induced by dimethylnitrosamine. $N,N-Di[^{14}C]$ methyl-nitrosamine (DMN) was used as a damaging agent and levels of DNA, RNA and protein damage in liver, brain and pancreas were compared with a control group. Pretreatment of mice with chloramphenicol increased protein damage in pancreas two times more than the control level. Liver RNA damage was increased up to 5.8 times and brain DNA damage up to 6.95 times by treatment of phenobarbital but brain RNA damage was decreased significantly down to 21% of the control group. The damage of liver RNA was significantly decreased by treatment of progesterone, although liver protein damage, pancreas RNA damage and pancreas protein damage were increased.