• Transactions of the Korean Society of Automotive Engineers
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• v.7 no.5
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• pp.162-171
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• 1999

The most important part in automated transport systems is steering control for lane keeping Most of systems developed so far have used the visual information for steering control. In this study, the steering control algorithm based on visual servoing has been developed and tested by applying it on Radio Controlled(R/C) model car equipped with one CCD camera. We also demonstrated the feasibility of using it as a pre-test car before the real car experiment in developing automated vehicles. In order to solve the problem of the limited spave and load of a model car, remote-brained approach has been taken. For steering control of a model car, the PD controller which uses the look ahead offset to generate control input has been implemented and the characteristics of the controller has been explained in view of kinematics. Some experimental results have been also illustrated so as to show the control performance and stability.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.1
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• pp.9-17
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• 2001

It has been demonstrated that multipotent neuronal progenitor cells can be isolated from the developing or adult CNS and proliferated in vitro in response to epidermal growth factor. The present study was undertaken to investigate the differentiation of neuronal progenitor cells after transplantation into the neonatal rat forebrain striatum. Primary cultured progenitor cells were labeled with 3,3'-dioctadecycloxacarbonyl- amine perchlorate (DiO). DiO labeled progenitor cells were implanted into neonatal rat striatum. Implanted DiO labeled progenitor cells were differentiated into astrocytes and GABAergic neurons. These results suggest that implanted progenitor cells can be differentiated into neurons in host forebrain striatum. In addition, our data show that DiO labeling is a useful technique for tracing implanted progenitor cells.

• Journal of mucopolysaccharidosis and rare diseases
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• v.4 no.2
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• pp.37-41
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• 2018

Mucopolysaccharidosis III (MPS III, Sanfilippo syndrome) is a rare autosomal recessive disease caused by a deficiency of one of four enzymes involved in the degradation of glycosaminoglycan (GAG). The resultant cellular accumulation of GAG causes various clinical manifestations. MPS III is divided into four subtypes depending on the deficient enzyme. All the subtypes show similar clinical features and are characterized by progressive degeneration of the central nervous system. A number of genetic and biochemical diagnostic methods have been developed. However, there is no effective therapy available for any form of MPS III, with treatment currently limited to clinical management of neurological symptoms. Main purpose of the treatment for MPS III is to prevent neurologic deterioration. Because conventional intravenous enzyme replacement therapy (ERT) has a limitation due to inability to cross the blood-brain barrier, several innovative therapeutic approaches for MPS III are being developed. This review covers the currently developing new therapeutic options for MPS III including high dose ERT, substrate reduction therapy, intrathecal or intraventricular ERT, fusion protein delivery using bioengineering technology, and gene therapy.

• International Journal of Advanced Culture Technology
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• v.9 no.1
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• pp.196-202
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• 2021

Currently, as Korea enters into a fast aging society, the problem of dementia population is increasing. In this paper, we intend to contribute to the improvement of welfare for the elderly by developing virtual reality technology and related interface technology to effectively perform hand movements known as effective methods for preventing and treating dementia. As the content of the research and development of this paper, it is designed to be easy for the elderly to use and stimulate brain function by applying VR technology using sensors, and to activate mental and physical activities for the elderly who are marginalized in terms of cultural welfare. We intend to develop by classifying the types of games and contents that can induce them. As a result of this thesis, we developed contents using virtual reality to improve cognitive abilities for elderly people with poor cognitive ability to activate the brains of users' cognition, memory, and attention to prevent and treat dementia I want to contribute.

• BMB Reports
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• v.57 no.1
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• pp.19-29
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• 2024

Mitochondrial DNA (mtDNA), a multicopy genome found in mitochondria, is crucial for oxidative phosphorylation. Mutations in mtDNA can lead to severe mitochondrial dysfunction in tissues and organs with high energy demand. MtDNA mutations are closely associated with mitochondrial and age-related disease. To better understand the functional role of mtDNA and work toward developing therapeutics, it is essential to advance technology that is capable of manipulating the mitochondrial genome. This review discusses ongoing efforts in mitochondrial genome editing with mtDNA nucleases and base editors, including the tools, delivery strategies, and applications. Future advances in mitochondrial genome editing to address challenges regarding their efficiency and specificity can achieve the promise of therapeutic genome editing.

• Neonatal Medicine
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• v.16 no.2
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• pp.221-233
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• 2009

Purpose: Erythropoietin (EPO) has neuroprotective effects in many animal models of brain injury, including hypoxic-ischemic (HI) encephalopathy, trauma, and excitotoxicity. Current studies have demonstrated the neuroprotective effects of EPO, but limited data are available for the neonatal periods. Here in we investigated whether recombinant human EPO (rHuEPO) can protect the developing rat brain from HI injury via modulation of NMDA receptors. Methods: In an in vitro model, embryonic cortical neuronal cell cultures from Sprague-Dawley (SD) rats at 19-days gestation were established. The cultured cells were divided into five groups: normoxia (N), hypoxia (H), and 1, 10, and 100 IU/mL rHuEPO-treated (H+E1, H+ E10, and H+E100) groups. To estimate cell viability and growth, a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay was done. In an in vivo model, left carotid artery ligation was performed on 7-day-old SD rat pups. The animals were divided into six groups; normoxia control (NC), normoxia Sham-operated (NS), hypoxia-ischemia only (H), hypoxia-ischemia+vehicle (HV), hypoxia-ischemia+rHuEPO before a HI injury (HE-B), and hypoxia-ischemia+rHuEPO after a HI injury (HE-A). The morphologic changes following brain injuries were noted using hematoxylin and eosin (H/E) staining. Real-time PCR using primers of subunits of NMDA receptors (NR1, NR2A, NR2B, NR2C and NR2D) mRNA were performed. Results: Cell viability in the H group was decreased to less than 60% of that in the N group. In the H+E1 and H+E10 groups, cell viability was increased to >80% of the N group, but cell viability in the H+E100 group did not recover. The percentage of the left hemisphere area compared the to the right hemisphere area were 98.9% in the NC group, 99.1% in the NS group, 57.1% in the H group, 57.0% in the HV group, 87.6% in the HE-B group, and 91.6% in the HE-A group. Real-time PCR analysis of the expressions of subunits of NMDA receptors mRNAs in the in vitro and in vivo neonatal HI brain injuries generally revealed that the expression in the H group was decreased compared to the N group and the expressions in the rHuEPO-treated groups was increased compared to the H group. Conclusion: rHuEPO has neuroprotective property in perinatal HI brain injury via modulation of N-methyl-D-aspartate receptors.

• Radiation Oncology Journal
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• v.21 no.4
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• pp.315-321
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• 2003

Purpose: This study was peformed to Investigate apoptosis by radiation In the developing fetal rat brain. Materials and Methods: Fetal blains were Irradiated In utero between the 17th and 19th days of fetal life (El7-19) by linear accelerator. A dose of Irradiation ranging from 1 Gy to 4 Gy was used to evaluate dose dependency. To test time dependency the ra)s were Irradiated with 2 Gy and then the fetal brain specimens were removed at variable 41me course; 1, 3, 5, 12 and 24 hours after the onset of irradiation. Immunohistochemlcal staining using in situ 707-mediated dUTP nick end labelling (TUNEL) technlfue was used for apoptotic cells. The cerebral cortex, including three zones on coriicai zone (Cf). Intermediate zone (if), and ventricular zone (VZ), was examined. Results : TUNEL positive cells revealed typical features of apoptotic cells under light microscope In the fetal rat cerebral cortex. Apoptotic cells were not found In the cerebral cortex of non-Irradiated fetal rats, but did appear In the entire cerebral cortex after 1 Gy Irradiation, and were more expensive at the ventricular and Intermediate zones than at the cortical zone. The extent of apoptosis was Increased with Increasing doses of radiation. Apoptosis reached the peak at S hours after the onset of 2 Gy Irradiation and persisted until 24 hours. Conclusion: Typical morphological features of apoplosis by irradiation were observed In the developing fetal rat cerebral cortex. It was more extensive at the ventricular and Intermediate zones than at the cortical zone, which suggested that stem cells or early differentiated cells are more radiosensitive than differentiated cells of the cortical zone.

• IMMUNE NETWORK
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• v.4 no.1
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• pp.60-64
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• 2004

Background: Microglial cells, major immune effector cells in the central nervous system, become activated in neurodegenerative disorders. Activated microglial cells produce proinflammatory mediators such as nitric oxide (NO), tumor necrosis factor-$\alpha$ and interleukin-$1{\beta}$(IL-$1{\beta}$). These proinflammatory mediators have been shown to be significantly increased in the neurodegenerative disorders such as Alzhimer's disease and Pakinson's disease. It was known that one of the neurodegeneration source is stress and it is important to elucidate mechanisms of the stress response for understanding the stress-related disorders and developing improved treatments. Because one of the neuropeptide which plays a main role in regulating the stress response is corticotropin-releasing hormone (CRH), we analyzed the regulation of NO release by CRH in BV2 murine microglial cell as macrophage in the brain. Methods: First, we tested the CRH receptor expression in the mRNA levels by RT-PCR. To test the regulation of NO release by CRH, cells were treated with CRH and then NO release was measured by Griess reagent assay. Results: Our study demonstrated that CRH receptor 1 was expressed in BV2 murine microglial cells and CRH treatment enhanced NO production. Furthermore, additive effects of lipopolysaccaride (LPS) and CRH were confirmed in NO production time dependantly. Conclusion: Taken together, these data indicated that CRH is an important mediator to regulate NO release on microglial cells in the brain during stress.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3979-3985
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• 2013

Background: Although primary malignant CNS tumors are registered in the national cancer registry (NCR) of Iran, there are no available data on the incidence of the primary malignant or benign CNS tumors and their common histopathologies in the country. This study analyzed the 10-year data of the Iranian NCR from March 21, 2000 to March 20, 2010, including a systematic review. Materials and Methods: The international and national scientific databases were searched using the search keywords CNS, tumor, malignancy, brain, spine, neoplasm and Iran. Results: Of the 1,086 primary results, 9 papers were selected and reviewed, along with analysis of 10-year NCR data. The results showed that primary malignant brain tumors have an overall incidence of 2.74 per 100,000 person-years. The analysis of the papers revealed a benign to malignant ratio of 1.07. The most common histopathologies are meningioma, astrocytoma, glioblastoma and ependymoma. These tumors are more common in men (M/F=1.48). Primary malignant spinal cord tumors constitute 7.1% of the primary malignant CNS tumors with incidence of 0.21/100,000. Conclusions: This study shows that CNS tumors in Iran are in compliance with the pattern of CNS tumors in developing countries. The NCR must include benign lesions to understand the definitive epidemiology of primary CNS tumors in Iran.

• Korean Journal of Biological Psychiatry
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• v.6 no.1
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• pp.12-20
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• 1999

In order to understand the pathogenesis and progression of some synaptic loss related neuropsychiatric diseases, We attempted to develop a computer model in this study. We made a simple autoassociative memory network remembering numbers, transformed it into a disease model by pruning synapses, and measured its memory performance as a function of synaptic deletion. Decline in performance was measured as amount of synaptic loss increases and its mode of decline is sudden or gradual according to the mode of synaptic pruning. The developed computer model demonstrated how synaptic loss could cause memory impairment through a series of computer simulations, and suggested a new way of research in neuropsychiatry.