• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.34 no.5
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• pp.578-581
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• 2008

Schwannoma named neurinoma, peripheral glioma, perineural fibriblastoma and Neurilemmoma is a ectodermal benign neoplasm which originates from schwann cell or neuro axons. It usually develops in peripheral systems of sensory nerves of gastrointestinal tract, oral cavity, and bone. It occurs more frequently in soft tissue than hard tissue, and is extremely rare in intraoral area. We report a case of Schwannoma that showed large mass on buccal cheek with Rt. midfacial swelling, pain, tenderness to palpation and involvement with maxillary branch of trigeminal nerve. We present this case and review the literature.

• Proceedings of the KSMRM Conference
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• 2001.11a
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• pp.155-161
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• 2001

Anisotropic DWI - Mapping of the Proton Diffusion "tensor". In neural ordered tissue, it is thought that water diffusion is mainly influenced by the presence of myelin sheaths and intracellular structures. Perpendicular to the fiber tracts, the cholesterol-laden myelin lipid bilayers might restrict or hinder the spins from diffusing through the normally highly permeable cytomembrane. Diffusion along the fiber is more or less determined by subcellular structures, such as the endoplasmatic reticulum, mitochondria, neuro-filaments and macromolecules. In addition to that, the entire complex of axons and stabilizing tissue (i.e., glia cells, astrocytes) is also assumed to influence diffusion due to the tortuosity of proton translation, but the uniform distribution of such cells throughout the brain might render this notion less important as initially anticipated.

• Korean Journal of Biological Psychiatry
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• v.17 no.3
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• pp.119-126
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• 2010

Synaptic adhesion molecules mediate synapse formation, maturation and maintenance. These proteins are localized at synaptic sites in neuronal axons and dendrites. These proteins function as a bridge of synaptic cleft via interaction with another synaptic adhesion molecules in the opposite side. They can interact with scaffold proteins via intracellular domain and recruit many synaptic proteins, signaling proteins and synaptic vesicles. Scaffold proteins function as a platform in dendritic spines or axonal terminals. Recently, many genetic studies have revealed that synaptic adhesion molecules and scaffold proteins are important in neurodevelopmental disorders, psychotic disorders, mood disorders and anxiety disorders. In this review, fundamental mechanisms of synapse formation and maturation related with synaptic adhesion molecules and scaffold proteins are introduced and their psychiatric implications addressed.

• Animal cells and systems
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• v.4 no.3
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• pp.215-221
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• 2000

Our anatomical and behavioral studies of embryonic rats that developed in microgravity suggest that the vestibular sensory system, like the visual system, has genetically mediated precesses of development that establish crude connections between the periphery and the brain. Environmental stimuli also regulate connection formation including terminal branch formation and fine-tuning of synaptic contacts. Axons of vestibular sensory neurons from grabistatic as well as linear acceleration receptors reach their targets in both microgravity and norm81 gravity, suggesting that this is a genetically regulated component of development. However, microgravity exposure delays the development of terminal branches and synapses in gravistatic but not linear acceleration-sensitive neurons and also produces behavioral changes. These latter changes reflect environmentally controlled processes of development.

• Molecules and Cells
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• v.40 no.1
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• pp.10-16
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• 2017

When peripheral axons are damaged, neuronal injury signaling pathways induce transcriptional changes that support axon regeneration and consequent functional recovery. The recent development of bioinformatics techniques has allowed for the identification of many of the regeneration-associated genes that are regulated by neural injury, yet it remains unclear how global changes in transcriptome are coordinated. In this article, we review recent studies on the epigenetic mechanisms orchestrating changes in gene expression in response to nerve injury. We highlight the importance of epigenetic mechanisms in discriminating efficient axon regeneration in the peripheral nervous system and very limited axon regrowth in the central nervous system and discuss the therapeutic potential of targeting epigenetic regulators to improve neural recovery.

• Annals of Clinical Neurophysiology
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• v.2 no.1
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• pp.1-7
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• 2000

From among the group of patients diagnosed clinically to have Guillain-Barre syndrome(GBS), subgroups with pure motor involvement have been identified. Some of such patients appear to have an axonal neuropathy by eletrophysiology. Such cases have been termed acute motor axonal neuropathy(AMAN). Many of these patients are found clinically to have normal sensation and to have electrodiagnostic patterns consistent with selective degeneration of motor axons. A serological survey showed some of individuals with AMAN had evidence of antecedent Campylobacter jejuni(CJ) infection. And AMAN has an association with the presence of anti-ganglioside antibodies. This article reviewed briefly the AMAN and their relationship to CJ infection and anti-ganglioside antibodies.

• International Journal of Industrial Entomology and Biomaterials
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• v.29 no.1
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• pp.120-127
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• 2014

The cerebral neurosecretory cells (NSC) constitute four paired groups, medial (MNC), lateral (LNC-I, LNC-II) and posterior (PNC) in the brain of larvae of tasar silkworm Antheraea mylitta (D) Eco-race Bhandara. The MNC is the largest groups of peptidergic neurosecretory cells and are located in the pars intercerebralis region. The transmission electron microscopic (TEM), ultrastructure of the NSC confirmed the presence of mitochondria, endoplasmic reticulum, Golgi bodies, lysosomes and neurosecretory granules. The median neurosecretory cells shows secretory activity and release of secretory products, the neurosecretory granules (NSG) in the axons of NSC as well as the blood sinus.

• The Korean Journal of Pharmacology
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• v.29 no.2
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• pp.165-174
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• 1993

$Ca^{2+}$ is an important regulator of neurite elongation and growth cone movements but the mechanism(s) mediating these $Ca^{2+}-dependent$ effects is unclear. Since cytoskeletal proteins are rapidly degraded by $Ca^{2+}-dependent $ proteinases (calpains) in vitro and in vivo, we investigated whether $Ca^{2+}-induced$ pruning or regression of neuronal processes is mediated by calpains. Isolated hippocampal pyramidal-like neurons were cultured and the ability of the membrane-permeable calpain inhibitors EST (etyl (+)-(2S,3S)-3-[(S)-methyl-1-(3-methlbutylcarbamoyl)-butylcarbamoyl]2-oxiranecarboxylate) and MDL28170 (carbobenzoxyl-Val-Phe-H) to block the $Ca^{2+}$ ionophore A23187-induced suppression in neurite outgrowth was investigated. Addition of 100 nM A23187 to the culture medium resulted in a retraction of dendrites without altering axonal elongation. The addition of 300 nM A23187 to the culture medium resulted in a signiciant decrease in the rate of axonal elongation as well as a retraction of dendritic processes. Administration of EST $(5\;or\;20{\mu}M)$ to the culture medium completely blocked the pruning effect of 100 nM A23187 on dendrites and of 300 nM A23187 on axons, while EST alone did not significantly affect neurite outgrowth rate. MDL 28170 $(20\;{\mu}M)$ showed the same effect as EST in preventing ionophore-induced pruning of dendrites and axons at 100 nM and 300 nM concentrations, respectively, of A23187. EST $(20\;{\mu}M)$ did not block the A23187-induced rise of $[Ca^{2+}]_{i}$ as measured with fura-2. These results show that $Ca^{2+}-induced$ pruning of neurites in isolated hippocampal pyramidal neurons is mediated by calpains.

• Archives of Plastic Surgery
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• v.34 no.3
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• pp.279-284
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• 2007

Purpose: The vein graft was considered as a useful conduit for nerve defect. But the problem is that it might be collapsed in long vein graft state. A new experimental model using vein graft filled with hyaluronic acid was considered. Methods: Thirty rats were used for the experimental animal. In group I, one side of the femoral nerve was exposed and a segment was removed about 15mm. The neural gap was connected with nerve graft. In group II, the nerve gap was connected with vein graft only. In group III, the nerve gap was connected with vein graft filled with hyaluronic acid. A walking track analysis was made periodically for 2 months and NCV(nerve conduction velocity) was executed at the end of the experiment. And morphologic studies were also done for all groups Results: In a walking track analysis, the toe-spread was widen and the foot-length was lengthened. The recovery of the toe-spread and foot length was checked 2 weeks interval, periodically for two months. The SFI (sciatic function index) was $-52.5{\pm}8.2$ in group I, $-68.1{\pm}4$ in group II, $-55.3{\pm}7.9$ in group III. In electrophysiological study, NCV(nerve conduction velocity) was $26.71{\pm}3.11m/s$ in group I, $17.94{\pm}4.35m/s$ in group II, $25.69{\pm}2.81m/s$ in group III. The functional recovery in group I and III was superior to that the group II statistically(p < 0.05) Under electromicroscopic study, the number of the myelinated axons were $1419.1{\pm}240$ in group I, $921.7{\pm}176.8$ in group II, $1322.2{\pm}318$ in group III. The number of the myelinated axons were much more in group I and III than group II statistically (p<0.05). Conclusion: This study suggested that the vein graft filled with hyaluronic acid is more effective than vein graft only for the conduit of the nerve gap. It was thought that the technique could be used in clinical cases with nerve defects as an alternative method to classical nerve grafts.

• Journal of Korean Neurosurgical Society
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• v.29 no.4
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• pp.461-470
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• 2000

Objective : Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury(TBI) in both animals and humans. It has long been recognized that mild to moderate hypothermia improves neurologic outcomes as well as reduces histologic and biochemical sequelae after TBI. In this study, two immunohistochemical staining using terminal deoxynucleotidyl-transferase-mediated biotin dUTP nick end labeling(TUNEL), staining of apoptosis, and ${\beta}$-amyloid precursor protein(${\beta}$-APP), a marker of axonal injury, were done and the authors evaluated the protective effects of hypothermia on axonal and neuronal injury after TBI in rats. Material and Method : The animals were prepared for the delivery of impact-acceleration brain injury as described by Marmarou and colleagues. TBI is achieved by allowing of a weight drop of 450gm, 1 m height to fall onto a metallic disc fixed on the intact skull of the rats. Fourty Sprague-Dawley rats weighing 400 to 450g were subjected to experimental TBI induced by an impact-acceleration device. Twenty rats were subjected to hypothermia after injury, with their rectal temperatures maintained at $32^{\circ}C$ for 1 hour. After this 1-hour period of hypothermia, rewarming to normothermic levels was accomplished over 30-minute period. Following 12 hours, 24 hours, 1 week and 2 weeks later the animals were killed and semiserial sagittal sections of the brain were reacted for visualization of the apoptosis and ${\beta}$-APP. Results : The density of ${\beta}$-APP marked damaged axons within the corticospinal tract at the pontomedullary junction and apoptotic cells at the contused cerebral cortex were calculated for each animal. In comparison with the untreated controls, a significant reduction in ${\beta}$-APP marked damaged axonal density and apoptotic cells were found in all hypothermic animals(p<0.05). Conclusion : This study shows that the posttraumatic hypothermia result in substantial protection in TBI, at least in terms of the injured axons and neurons.