• Title/Summary/Keyword: myelination

Search Result 50, Processing Time 0.05 seconds

Demyelination of Neuron by Infection of Semliki Forest Virus (Semliki forest virus 감염에 의한 뉴우런의 탈수초)

  • Kim, Hyun Joo;Kim, Ji-Young;Sa, Young-Hee;Hong, Seong-Karp
    • Proceedings of the Korean Institute of Information and Commucation Sciences Conference
    • /
    • 2016.05a
    • /
    • pp.718-721
    • /
    • 2016
  • Schwann cells and neuron cells from dorsal root ganglion (DRG) in embryos of rat were cultured in vitro respectively. The purified neronal cells added with anti-mitotic agents and purified Schwann cells were cocultured and then accomplished myelination processing. Infection of Semliki forest virus into this myelinated co-culture system was performed and then accomplished demyelination. We identified myelination and demyelination processing using antibody of neuropeptide Y meaning presence of myelinated neuron.

  • PDF

Demyelination of Myelinated Neuronal cells by Infection of Herpes Simplex Virus-1 (Herpes Simplex Virus-1감염에 의한 수초화 뉴우런의 탈수초)

  • Kim, Hyun Joo;Kim, Ji-Young;Sa, Young-Hee;Hong, Seong-Karp
    • Proceedings of the Korean Institute of Information and Commucation Sciences Conference
    • /
    • 2016.10a
    • /
    • pp.919-922
    • /
    • 2016
  • Neuronal cells and Schwann cells from dorsal root ganglion (DRG) in embryos of rat were isolated and cultured in vitro respectively. The purified neuronal cells added with anti-mitotic agents and purified Schwann cells were co-cultured and then accomplished myelination processing. This myelinated co-culture system was infected by herpes simplex virus-1 and then accomplished demyelination processing in this myelinated co-culture. We identified myelination and demyelination processing using antibody of neuropeptide Y meaning presence of myelinated neuron.

  • PDF

Induction of Demyelination of Neuronal cells by Sindbis Virus (Sindbis Virus에 의한 뉴런세포의 탈수초의 유도)

  • Sa, Young-Hee;Kim, Hyun Joo;Kweon, Tae Dong;Kim, Ji-Young;Lee, Bae Hwan;Hong, Seong-Karp
    • Proceedings of the Korean Institute of Information and Commucation Sciences Conference
    • /
    • 2018.05a
    • /
    • pp.584-587
    • /
    • 2018
  • Many viruses including mouse hepatitis virus, corona, measles, and sidbis viruses are known as causative virus of inducing demyelination which means destruction of myelination in nervous system of mice. The purpose of this study is to investigate processing of myelination by co-culture of Schwann cells and neuronal cells and demyelination induced by infection of sindbis virusin rat. Schwann cells and neuronal cells from dorsal root ganglion (DRG) in embryos (E16) of rat were cultured in vitro respectively. The purified neuronal cells with anti-mitotic agents and purified Schwann cells were co-cultured. After that, infection of sindbis virus into this myelinated co-culture system was performed. Myelination and demyelination process were observed using antibody of myelin basic protein meaning presence of myelination.We identified myelination and demyelination processing using antibody of peripheral myelin protein 22 (PMP 22) meaning presence of myelinated neuron. This study was supported by the Basic Research Program through the National Research Foundation (NRF) funded by the Ministry of Science, ICT & Future Planning (NRF-2015R1C1A1A01053484 and 2017R1A2B3005753).

  • PDF

Generation of Demyelination through Use of M. leprae-specific phenolic glycolipid-1 (PGL-1)

  • Kim, Ji-Young;Choi, Chang-Shik;Hong, Seong-Karp
    • Rapid Communication in Photoscience
    • /
    • v.4 no.2
    • /
    • pp.48-49
    • /
    • 2015
  • For myelination, Schwann cells and neuron cells from dorsal root ganglion (DRG) of rat embryos (E16) were cultured in vitro system. The purified DRG cells with anti-mitotic agents and purified Schwann cells were cocultured and then accomplished myelination processing. Treatment of M. leprae-specific phenolic glycolipid-1 (PGL-1) into this coculture system was performed and then accomplished demyelination. Therefore, we identified demyelination processing using antibody of myelin basic protein (MBP).

Iron Deficiency and Brain Development in Infancy (철분과 영유아기 뇌 발달)

  • Kim, Ae Suk
    • Pediatric Gastroenterology, Hepatology & Nutrition
    • /
    • v.12 no.sup1
    • /
    • pp.46-52
    • /
    • 2009
  • As the most common nutrition deficiency, iron deficiency not only causes anemia but also influences the central nervous system development. Its pathogenesis is supposed to be the alteration of neurometabolism and neurotransmission in major brain structures, and the disruption of myelination. The first two years after birth is a crucial period for cognitive, behavior, and emotional development with fast brain growth. If iron deficiency occurs in this period, cognitive and psychomotor function cannot be restored in spite of adequate iron supplementation. Thus, iron deficiency in infancy should be considered as a serious disease.

Infection of Semliki Forest Virus Induces Demyelination of Neuron (Semliki Forest Virus 감염은 뉴우런의 탈수초를 유발한다)

  • Kim, Hyun Joo;Sa, Young-Hee;Hong, Seong-Karp
    • Journal of the Korea Institute of Information and Communication Engineering
    • /
    • v.21 no.6
    • /
    • pp.1212-1217
    • /
    • 2017
  • We constructed a population of myelinated cells with co-culture of neuronal cells and Schwann cells from DRG. Schwann cells and neuronal cells were isolated from dorsal root ganglion (DRG) in embryos of rat in vitro respectively. The cultured Schwann cells and cultured neuronal cells, respectively were co-cultured in a same plate. This procedure contains following four steps: first step of suspension of the embryonic dorsal root ganglion cells, second step of addition of anti-mitoticcocktail, third step of purification of dorsal root cells, and fourth step of addition of Schwann cells to dorsal root ganglion cells. These cells were performed accomplishment of myelination. This myelinated co-culture system was infected by Semliki forest virus and then induced demyelination processing in this myelinated co-culture. We identified myelination and demyelination processing using antibody of peripheral myelin protein 22 (PMP 22) meaning presence of myelinated neuron.

Rat Peripheral Nerve Regeneration Using Nerve Guidance Channel by Porcine Small Intestinal Submucosa

  • Yi, Jin-Seok;Lee, Hyung-Jin;Lee, Hong-Jae;Lee, Il-Woo;Yang, Ji-Ho
    • Journal of Korean Neurosurgical Society
    • /
    • v.53 no.2
    • /
    • pp.65-71
    • /
    • 2013
  • Objective : In order to develop a novel nerve guidance channel using porcine small intestinal submucosa (SIS) for nerve regeneration, we investigated the possibility of SIS, a tissue consisting of acellular collagen material without cellular immunogenicity, and containing many kinds of growth factors, as a natural material with a new bioactive functionality. Methods : Left sciatic nerves were cut 5 mm in length, in 14 Sprague-Dawley rats. Grafts between the cut nerve ends were performed with a silicone tube (Silicon group, n=7) and rolled porcine SIS (SIS group, n=7). All rats underwent a motor function test and an electromyography (EMG) study on 4 and 10 weeks after grafting. After last EMG studies, the grafts, including proximal and distal nerve segments, were retrieved for histological analysis. Results : Foot ulcers, due to hypesthesia, were fewer in SIS group than in Silicon group. The run time tests for motor function study were 2.67 seconds in Silicon group and 5.92 seconds in SIS group. Rats in SIS group showed a better EMG response for distal motor latency and amplitude than in Silicon group. Histologically, all grafts contained some axons and myelination. However, the number of axons and the degree of myelination were significantly higher in SIS group than Silicon group. Conclusion : These results show that the porcine SIS was an excellent option as a natural biomaterial for peripheral nerve regeneration since this material contains many kinds of nerve growth factors. Furthermore, it could be used as a biocompatible barrier covering neural tissue.

Magnetic resonance imaging and spectroscopic analysis in 5 cases of Pelizaeus-Merzbacher disease: metabolic abnormalities as diagnostic tools

  • Lee, Eun;Yum, Mi-Sun;Choi, Hae-Won;Yoo, Han-Wook;You, Su Jeong;Lee, Eun-Hye;Ko, Tae-Sung
    • Clinical and Experimental Pediatrics
    • /
    • v.55 no.10
    • /
    • pp.397-402
    • /
    • 2012
  • Pelizaeus-Merzbacher disease (PMD) is a rare, X-linked recessive disorder characterized by dysmyelination in the central nervous system. PMD results from deletion, mutation, or duplication of the proteolipid protein gene (PLP1) located at Xq22, leading to the failure of axon myelination by oligodendrocytes in the central nervous system. PMD may be suspected when there are clinical manifestations such as nystagmus, developmental delays, and spasticity, and genetic analysis can confirm the diagnosis. Further diagnostic manifestations of the disease include a lack of myelination on brain magnetic resonance (MR) imaging and aberrant N-acetyl aspartate (NAA) and choline concentrations that reflect axonal and myelination abnormalities on phroton MR spectroscopy. We report 5 cases of PMD (in 1 girl and 4 boys). PLP1 duplication was detected in 2 patients. Brain MR analyses and MR spectroscopy were performed for all the patients. The brain MR images showed white matter abnormalities typical of PMD, and the MR spectroscopic images showed diverse patterns of NAA, creatinine, and choline concentrations. We propose that MR spectroscopic analysis of metabolic alterations can aid the PMD diagnosis and can contribute to a better understanding of the pathogenesis of the disease.

Myelination by co-culture of neurons and schwann cells and demyelination by virus infection (뉴런세포와 슈반세포의 공동배양에 의한 수초화와 바이러스 감염에 의한 탈수초화)

  • Sa, Young-Hee;Kweon, Tae Dong;Kim, Ji-Young;Kim, Hyun Joo;Lee, Bae Hwan;Hong, Seong-Karp
    • Proceedings of the Korean Institute of Information and Commucation Sciences Conference
    • /
    • 2018.10a
    • /
    • pp.448-451
    • /
    • 2018
  • The purpose of this study was to investigate the developmental process of myelination by neuron and Schwann cell cultures and the development of demyelination by herpes simplex virus-1 infection by electron microscopy and molecular biological analysis. The dorsal root ganglion (DRG) was isolated from the mouse embryo and Schwann cells and neuronal cells were cultured in vitro. Neuronal cells treated with mitotic inhibitors and purified Schwann cells were co-cultured together to induce myelination. The herpes simplex virus-1 was infected with the co-cultured cells, and the demyelination was induced. The myelin protein zero (MPZ) antibody, which means the presence of myelin formation, was used and electron microscopy was used to observe the development of myelin and dehydration.

  • PDF

Generation of myelination with neural cell cultures in rats and suppression of myelination by infection of sindbis virus (쥐의 신경세포 배양에 의한 수초 발생과 sindbis 바이러스 감염에 의한 수초 억제)

  • Sa, Young-Hee;Kim, Hyun Joo;Lee, Bae Hwan;Hong, Seong-Karp
    • Proceedings of the Korean Institute of Information and Commucation Sciences Conference
    • /
    • 2019.05a
    • /
    • pp.528-532
    • /
    • 2019
  • The dorsal root ganglion (DRG) was isolated from mouse embryos and Schwann cells and neuronal cells were cultured in vitro. The neurons and Schwann cells were cultured separately and the two kinds of cells were cultured together for three weeks. Generation of myelination was confirmed by transmission electron microscope and confocal microscope using a myelinaion protein, myelin protein zero (MPZ) antibody. The sindbis virus was infected for three days in the myelinated culture cells and then demyelination was carried out. The process of demyelination was also confirmed by transmission electron microscopy and confocal microscopy using myelin protein zero (MPZ) antibody. The study was supported by a Basic Research Program through the National Research Foundation (NRF) funded by the Ministry of Science and Technology, ICT and Future Plans (NRF-2016R1A2B4016552 and 2017R1A2B3005753).

  • PDF