• IMMUNE NETWORK
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• v.20 no.5
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• pp.40.1-40.15
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• 2020

The protein encoded by the Gene Associated with Retinoid-Interferon-Induced Mortality-19 (GRIM-19) is located in the mitochondrial inner membrane and is homologous to the NADH dehydrogenase 1-alpha subcomplex subunit 13 of the electron transport chain. Multiple sclerosis (MS) is a demyelinating disease that damages the brain and spinal cord. Although both the cause and mechanism of MS progression remain unclear, it is accepted that an immune disorder is involved. We explored whether GRIM-19 ameliorated MS by increasing the levels of inflammatory cytokines and immune cells; we used a mouse model of experimental autoimmune encephalomyelitis (EAE) to this end. Six-to-eight-week-old male C57BL/6, IFNγ-knockout (KO), and GRIM-19 transgenic mice were used; EAE was induced in all strains. A GRIM-19 overexpression vector (GRIM19 OVN) was electrophoretically injected intravenously. The levels of Th1 and Th17 cells were measured via flow cytometry, immunofluorescence, and immunohistochemical analysis. IL-17A and IFNγ expression levels were assessed via ELISA and quantitative PCR. IL-17A expression decreased and IFNγ expression increased in EAE mice that received injections of the GRIM-19 OVN. GRIM19 transgenic mice expressed more IFNγ than did wild-type mice; this inhibited EAE development. However, the effect of GRIM-19 overexpression on the EAE of IFNγ-KO mice did not differ from that of the empty vector. GRIM-19 expression was therapeutic for EAE mice, elevating the IFNγ level. GRIM-19 regulated the Th17/Treg cell balance.

• Korean Journal of Biological Psychiatry
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• v.24 no.1
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• pp.1-9
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• 2017

The proton magnetic resonance spectroscopy ($^1H-MRS$) is a tool used to detect concentrations of brain metabolites such as N-acetyl aspartate, choline, creatine, glutamate, and gamma-amino butyric acid (GABA). It has been widely used because it does not require additional devices other than the conventional magnetic resonance scanner and coils. Demyelination, or the neuronal damage due to loss of myelin sheath, is one of the common pathologic processes in many diseases including multiple sclerosis, leukodystrophy, encephalomyelitis, and other forms of autoimmune diseases. Rodent models mimicking human demyelinating diseases have been induced by using virus (e.g., Theiler's murine encephalomyelitis virus) or toxins (e.g., cuprizon or lysophosphatidyl choline). This review is an overview of the MRS findings on brain metabolites in demyelination with a specific focus on rodent models.

• Korean Journal of Veterinary Research
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• v.31 no.2
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• pp.155-161
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• 1991

The mechanisms of demyelination in Theiler's murine encephalomyelitis virus (TMEV)-induced chronic central nervous system(CNS) disease are still unclear and are probably multifactoral. This study was intended to culture spinal cord cells isolated from TMEV-induced demyelinating mice. By Percoll density centrifugation of enzymatically dissociated tissue, the cells were collected and then cultured on poly-L-lysine-coated plastic coverslips for 2 weeks. Oligodendrocytes, astrocytes and macrophages were identified using cell-type specific markers. Viral antigens were not present in oligodendrocytes and in astrocytes by double immunofluorescence. Affected mouse oligodendrocytes had less capacities of sheet formation and galactocerebroside immunoreactivity than those of control cell 3. These findings support the hypothesis that immune mediated mechanisms play an important role in the process of demyelination in this animal model.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.194-194
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• 1996

Pathogenesis of experimental allergic encephalomyelitis was involved with infection, inflammatory reaction, immune reaction etc. We studied on relation of blood vessel system and EAE. So, we measured blood pressure, heart rate and relaxation of isolated blood vessel in control and EAE-induced lewis rats. Blood pressure was decreased before EAE clinical sign (0-20day), but was increased from 23day. In isolated blood vessel, acetylcholine-treated relaxation was different on control, maximum EAE stage, recovery stage. Acetylcholine-treated relaxation was reduced 30% in recovery stage. but, sodium nitroprusside had similar relaxation reaction.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.193-193
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• 1996

Endothelin-1, which is a peptide originally isolated from cultured porcine aortic cell, has been found to play a crucial role in potentiating the vasoconstriction mitogenesis, and chemotaxis. In the present study, we examined the level of endothelin-1 in the brain, spinal cord and blood from rat with experimental allergic encephalomyelitis(EAE). At the peak stage of EAE(grade 3), endothelin-1 level in the spinal cord of rat with EAE increased two folds as compared with that of sham-treated rats, and subsequently decreased to the level of control at the recovery stage. In the endothelin-1 immunocytochemistry, endothelin-1 immunopositive cells and ED-1, macrophage marker immunopositive cells observed in the spinal cord of peak stage(grade 3). These Findings suggest that endothelin-1 play the important role in progression of EAE.

• Clinical and Experimental Pediatrics
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• v.53 no.2
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• pp.136-145
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• 2010

Natural killer T (NKT) cell is a special type of T lymphocytes that has both receptor of natural killer (NK) cell (NK1.1, CD161c) and T cell (TCR) and express a conserved or invariant T cell receptor called $V{\alpha}14J{\alpha}18$ in mice or Va24 in humans. Invariant NKT (iNKT) cell recognizes lipid antigen presented by CD1d molecules. Marine-sponge-derived glycolipid, ${\alpha}-galactosylceremide$ (${\alpha}-GalCer$), binds CD1d at the cell surface of antigen-presenting cells and is presented to iNKT cells. Within hours, iNKT cells become activated and start to secrete Interleukin-4 and $interferon-{\gamma}$. NKT cell prevents autoimmune diseases, such as type 1 diabetes, experimental allergic encephalomyelitis, systemic lupus erythematous, inflammatory colitis, and Graves' thyroiditis, by activation with ${\alpha}-GalCer$. In addition, NKT cell is associated with infectious diseases by mycobacteria, leshmania, and virus. Moreover NKT cell is associated with asthma, especially CD4+ iNKT cells. In this review, I will discuss the characteristics of NKT cell and the association with inflammatory diseases, especially asthma.

• Archives of Pharmacal Research
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• v.3 no.1
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• pp.51-55
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• 1980

Thiamine, in the form of its diphosphate (TDP), is well known to act as a coenzyme, and during the early stage in the study of thiamine it had been believed that the symptoms of thiamine-deficiency were resulted secondarily from the disturbance of metabolic processes in which TDP participated as a coenzyme. However, the neurological symptoms in thiamine deficiency are now separated from the metabolic disturbances in thiamine deficiency. On the other hand, the specific involvement of phosphorylated thiamine in nerve conduction has been suggested by von Muralt, but nature of this involvement has not been elucidated at a molecular level. Recently the possible significance of thiamine triphosphate (TTP) in nervous tissue was suggested by the demonstration that TTP is not present in the brain of patients with subacute necrotizing encephalomyelitis, a fatal disease associated with an abnormality in thiamine metabolism. Furthermore, the studies using membrane fragments of rat brain strongly indicated that ion movement across the nerve membrane is associated with dephosphorylation of phosphorylated thiamine.

• Korean Journal of Veterinary Pathology
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• v.2 no.1
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• pp.31-36
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• 1998

The Opuntia ficus-indica extract(OFE) has been claimed to have several therapeutic properties including anti-inflammation and anti-rheumatoid arthritis in oriental medicine but little is known about their effect on macrophages. This study demonstrated that OFE could stimulate TNF-alpha production in cultured macrophages. which is one of important mediators in autoimmune diseases including experimental autoimmune encephalomyelitis(EAE). In vivo study showed that oral administration of OFE exacerbate the onset of clinical paralysis. This finding suggests that OFE stimulates cytokine production and exacerbates autoimmune inflammatory diseases including EAE.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2005.11a
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• pp.66-67
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• 2005

• Annals of Clinical Neurophysiology
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• v.24 no.2
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• pp.101-106
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• 2022

Neurological complications attributed to coronavirus disease-19 (COVID-19) infection have been reported including acute disseminated encephalomyelitis, Guillain-Barré syndrome, and so on. Herein, we report a 49-year-old woman presented with acute encephalopathy and paraplegia simultaneously after COVID-19 infection. Brain magnetic resonance imaging (MRI) showed symmetric hyperintense basal ganglia lesions on T2-weighted imaging. Cerebrospinal fluid pleocytosis, motor axonal neuropathy and enhancement of conus medullaris nerve roots on spine MRI were observed. We treated her with high-dose corticosteroid and intravenous immunoglobulin.