• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.11a
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• pp.80-88
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• 2002

Recent studies demonstrate that collagen IV selectively pro-motes the repair of physiological processes in sublethally injured renal proximal tubular ceils (RPTC). We sought to further define the mechanisms of cell repair by measuring the effects of toxicant injury and stimulation of repair by L-ascorbic acid-2-phosphate (AscP), exogenous collagen IV, or function-stimulating integrin antibodies on the expression and subcellular localization of collagen-binding integrins (CBI) in RPTC. Expression of CBI subunits ${\alpha}_1$, ${\alpha}_2$, and ${\beta}_1$ in RPTC was not altered on day 1 after sublethal injury by S-(1,2-dichlorovinyl)-L-cysteine (DCVC). On day 6, expression of ${\alpha}_1$ and ${\beta}_1$ subunits remained unchanged, whereas a 2.2-fold increase in ${\alpha}_2$ expression was evident in injured RPTC. CBI localization in control RPTC was limited exclusively to the basal membrane. On day 1 after injury, RPTC exhibited a marked inhibition of active $Na^+$ transport and a loss of cell polarity characterized by a decrease in basal CBI localization and the appearance of CBI on the apical membrane. On day 6 after injury, RPTC still exhibited marked inhibition of active $Na^+$ transport and localization of CBI to the apical membrane. However, DCVC-injured RPTC cultured in pharmacological concentrations of AscP (500 ${\mu}$M)or exogenous collagen IV (50 ${\mu}$g/ml) exhibited an increase inactive $Na^+$ transport, relocalization of CBI to the basal membrane, and the disappearance of CBI from the apical membrane on day 6. Function-stimulating antibodies to CBI ${\beta}_1$ did not promote basal relocalization of CBI despite stimulating the repair of $Na^+$/$K^+$-ATPase activity on day 6 after injury. These data demonstrate that DCVC disrupts integrin localization and that physiological repair stimulated by AscP or collagen IV is associated with the basal relocalization of CBI in DCVC-injured RPTC. These data also suggest that CBI-mediated repair of physiological functions may occur independently of integrin relocalization.

• Archives of Craniofacial Surgery
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• v.14 no.1
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• pp.46-49
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• 2013

Facial deformity after nerve injury changes ones' social life. We experienced a few patients with healthy early recovery of muscle contraction after the operation with soft tissue wraparound splint. Under general anesthesia, exploration to find as many injured nerve stumps with ${\times}2.5$ loopes was undertaken at first. Interfascicular repair was done with minimal tension by 10-0 nylon under a microscope, and the suture site was sealed by approximating the surrounding fat flaps. This conjoined adipose tissue flap was a splint as a wraparound environment to reduce the tension in the coaptation site, and to increase the relative concentration of releasing neurotrophic factors by surrounding it. A 45-year-old man fell down in a drunken state and had deep laceration by broken flowerpot fragments with facial muscle weakness on the right cheek. His injured mandibular branches of the facial nerve were found. A 31-year-old female suffered from motionlessnesss of frontalis muscle after a traffic accident. She had four frontal branches injured. The man had his cheek with motion after seven days, and the woman two months after the operation. The nerve conduction test of the woman showed normalized values. Facial nerve repair surrounded by adipose tissue wraparound splint can make the recovery time relatively short.

• Journal of Korean Medicine Rehabilitation
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• v.18 no.3
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• pp.19-39
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• 2008

Objectives : It has been reported that CG was effective in decreasing injury to neural tissues. To investigate neural responses in the injured spinal cord, an extract of CG was examined to determine its effect on neural responses in the injured spinal cords of rats. Methods : After CG treatment was applied to the spinal cord of rats given a contusion injury, the re-growth responses of injured neural tissues and corticospinal tract axons was observed by measuring the number of GAP-43, Cdc2, and phospho-Erk1/2 proteins, CST axons, GFAP-stained astrocytes, and Glial scarring in the injured spinal cord. Results : Levels of GAP-43, Cdc2, and phospho-Erk1/2 proteins were found to have increased in the injured spinal cord region. The number of GFAP-stained astrocytes also increased within and around the injury cavity. Glial scarring, which was identified by CSPG immunofluorescence staining, was reduced by CG treatment. Anterograde tracing by Dil dye showed that the elongation of the CST axons in the dorso-medial white matter area was almost completely prevented at the injury site. Collateral sprouting was observed in the spinal cord rostrally close to the injury site, and CG treatment further increased axonal arborization in the corresponding region. In vivo migration of CST axons and astrocytes using an implanted polymer tube system showed more of an increase in enhanced migration of axons and astrocytes in CG-treated group compared to the injury control group. Conclusions : These results suggest that CG activated neural responses - including astrocyte migration - and promotes axonal regenerative activity in the injured spinal cord area.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.6
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• pp.1666-1672
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• 2005

Oriental medicinal drugs have a broad spectrum of clinical use for the cure of nervous system diseases including brain ischemic damages or neuropathies. Yet, specific drugs or drug components used in the oriental medicine in relation to none fiber regeneration are not known. In the present study, possible growth promoting effects of oriental medicinal drugs were investigated in the injured sciatic nerve system in the rat. By immunofluorescence staining, we found that Jahageo (JHG, Hominis placenta) increased Induction levels of axonal growth associated protein GAP-43 in the rat sciatic none. Small growth promoting activity was found in Golsebo (GSB, Drynariae rhizoma) and Baikhasuo (BHSO, Polygoni multiflori radix) drugs. JHG also increased cell cycle protein Cdc2 levels in the injured area of the sciatic nerves. Immunofluorescence staining indicated that induced Cdc2 protein was mostly localized in the Schwann cells in the injury area, implying that JHG activity might be related to increased Schwann cell proliferation during axonal regeneration. Moreover, levels of phospho-extracellular signal-regulated (ERK) pathway in the injured neNes were elevated by JHG treatment while levels of total ERK were unaltered. In vivo measurement of axonal regeneration using retrograde tracer showed that JHG, GSB and BHSO significantly enhanced Dil-labeled regenerating motor neurons compared with saline control. The present data suggest that oriental medicinal drugs such as JHG, GSB, and BHSO may be a useful target for developing specific drugs of axonal regeneration.

• The Journal of Internal Korean Medicine
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• v.30 no.1
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• pp.24-35
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• 2009

Object : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis makes physical and mechanical barriers. If gliosis formation could be suppressed, irreversible axon damage would be reduced. This could mean that an injured CNS could be regenerated. CD81 and GFAP have close relationships to gliosis. The increase in glial cells at CNS injury gives rise to the expression of CD81 and GFAP. CD81 was postulated to play a central role in the process of CNS scar formation. Method : In this study, the author investigated the effect of the water extract of the Moutan Radicis Cortex on regulation of CD81 and GFAP expression in injured CNS cells. MTT assay was used to examine cell viability, while RT-PCR and ELISA methods were carried out to measure the expression of CD81 and GFAP in the astrocyte. Results : We observed that water extract of the Moutan Radicis Cortex increased cell viability under hypoxia induced by $CoCl_2$ and suppressed the expression of CD81 and GFAP up-regulated by hypoxia. Conclusion : These results suggest that the Moutan Redicis Cortex could promote neural regeneration as a consequence of protecting CNS cells from hypoxia and suppressing the reactive gliosis following CNS injury.

• Journal of Korean Ophthalmic Optics Society
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• v.21 no.1
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• pp.69-76
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• 2016

Purpose: The study was conducted to determine that photoreceptors of mouse having pigment in RPE(retinal pigment epithelium) can be damaged by blue-light and apoptosis of specific cells among photoreceptors are induced by blue-light, and to assist the investigation of AMD(Age-related macular degeneration) mechanisms and development of AMD drugs. Methods: C57Black mice were injured by irradiating $2800{\pm}10lux$ of 463 nm LED for 6 hours after 24 hours dark adaptation and eyes were enucleated 1, 3, 7 days. Damage of retina induced by blue-light was determined by western blotting GFAP(Glial fibrillary acidic protein) expression. In the light-injured retina, cell death of photoreceptors was determined by TUNEL(Terminal deoxynucleotidyl transferase dUTP nick end labeling) assay. ERK(Extracellular signal-regulated kinases), JNK, and SRC(sarcoma) expression were assessed by western blotting to determine regulated pathway. Blue light-injured retina were immunostained with antibodies against Opsin and Rhodopsin as markers of photoreceptors to compared the damage cone cells with rod cells. Results: After 1, 3 and 7 days from exposure to blue-light, thickness of retina was more decreased than control, and more decreased at nuclear layer than at outer plexiform layer and GFAP expression was increased day 1 after blue-light injured. While phosphorylated ERK and SRC protein expressions at day 1 were increased after blue-light injured, phosphorylated c-JUN was decreased. Fluorescence intensity analysis showed that markers of cone and rod cells were decreased after blue-light injured and Opsin was more decreased than Rhodopsin. Conclusions: The study suggests possibilities that the blue-light promotes retinal damage and causes apoptotic cell death via ERK and SRC pathway in mouse retina, and blue-light retinal damage is more induced cone cells apoptosis than rod cells directly.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.36 no.3
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• pp.193-197
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• 2003

Psychrotrophic characteristics of Listeria monocytogenes YM-7 showed similar growth at $8^{\circ}C$ as L. monocytogenes ATCC 15313. But it showed different growth pattern at $4^{\circ}C.$ Thus the isolated strain from the Patient can not grow at $4^{\circ}C,$ while L. monocytogenes ATCC 15313 grow slowly. Number of the injured cells of L. monocytogenes YM-7 was higher at $-3^{\circ}C$ than at $-18^{\circ}C$ in phosphate buffer solution. The rate of the injured cell was higher in the TSB (tryptic soy broth) medium than in phosphate buffer solution at $-3^{\circ}C$ and $-18^{\circ}C.$ When L. monocytogenes YM-7 stored at $-18^{\circ}C$ in homogenized fish muscle, the cell numbers decreased by 2-3 log cycles in 12 weeks.

• Journal of the Korean Society of Visualization
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• v.20 no.2
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• pp.70-77
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• 2022

Skeletal muscle tissues feature cellular heterogeneity, including differentiated myofibers, myoblasts, and satellite cells. Thanks to the presence of undifferentiated myoblasts and satellite cells, skeletal muscle tissues can self-regenerate after injury. In skeletal muscle regeneration, the collective motions among these cell types must play a significant role, but little is known about the dynamic collective behavior during the regeneration. In this study, we constructed in vitro platform to visualize the migration behavior of skeletal muscle cells in specific conditions that mimic the biochemical environment of injured skeletal muscles. We then visualized the spatiotemporal distribution of stresses arising from the differential collectiveness in the cellular clusters under different conditions. From these analyses, we identified that the heterogeneous population of muscle cells exhibited distinct collective migration patterns in the injury-mimicking condition, suggesting selective activation of a specific cell type by the biochemical cues from the injured skeletal muscles.

• BMB Reports
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• v.35 no.1
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• pp.94-105
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• 2002

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

• Journal of International Academy of Physical Therapy Research
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• v.1 no.2
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• pp.91-98
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• 2010

This study is intended to examine the motor skill learning and treadmill exercise on motor performance and synaptic plasticity in the cerebellar injured rats by harmaline. Experiment groups were divided into four groups and assigned 15 rats to each group. Group I was a normal control group(induced by saline); Group II was a experimental control group(cerebellar injured by harmaline); Group III was a group of motor skill learning after cerebellar injured by harmaline; Group IV was a group of treadmill exercise after cerebellar injured by harmaline. In motor performance test, the outcome of group II was significantly lower than the group III, IV(especially group III)(p<.001). In histological finding, the experimental groups were destroy of dendrities and nucleus of cerebellar neurons. Group III, IV were decreased in degeneration of cerebellar neurons(especially group III). In immunohistochemistric response of synaptophysin in cerebellar cortex, experimental groups were decreased than group I. Group III's expression of synaptophysin was more increased than group II, IV. In electron microscopy finding, the experimental groups were degenerated of Purkinje cell. These result suggest that improved motor performance by motor skill learning after harmaline induced is associated with dynamically altered expression of synaptophysin in cerebellar cortex and that is related with synaptic plasticity.