• Childhood Kidney Diseases
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• v.17 no.1
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• pp.13-18
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• 2013

Podocytopathy is glomerular lesions characterized by podocyte injury. It is observed in various glomerular diseases, but minimal change disease and focal segmental glomerulosclerosis (FSGS) are the prototypes. In this review, morphologic features of podocyte injury and subtypes of FSGS will be reviewed briefly. Effacement of podocyte foot processes is the most common feature of podocyte injury. As podocytic injury progresses, intracytoplasmic vacuoles, subpodocytic cyst, detachment of podocytes from the glomerular basement membrane and apoptosis develop. Glomerular capillary loops in epithelium-denuded area undergo capillary collapse. Synechia and hyalinosis may accompany this lesion. To manifest segmental sclerosis, podocyte loss above a threshold level may be required. Injured podocytes can injure neighboring intact podocytes, and thereby spread injury within the same lobule. FSGS can be categorized into five subtypes by morphologic characteristics; not otherwise specified (NOS), perihilar, cellular, tip, and collapsing types. Each subtype has been reported to show different clinical courses and associated conditions, but there are controversies on its significance. With recent progress in the discovery of genetic abnormalities causing FSGS and plasma permeability factors, we expect to unravel pathophysiology of FSGS and to understand histological sequences leading to FSGS in near future.

• Korean Journal of Food Science and Technology
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• v.47 no.1
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• pp.87-94
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• 2015

High voltage pulsed electric fields (PEF) treatment is one of the more promising nonthermal technologies to fully or partially replace thermal processing. The objective of this research was to investigate the microbial inactivation mechanisms of PEF treatment in terms of intra- and extracellular changes in the cells. Saccharomyces cerevisae cells treated with PEF showed cellular membrane damage. This resulted in the leakage of UV-absorbing materials and intracelluar ions, which increased with increasing treatment time and electric fields strength. This indicates that PEF treatment causes cell death via membrane damage and physical rupture of cell walls. We further confirmed this by Phloxine B staining, a dye that accumulates in dead cells. Using scanning and transmission electron microscopy, we observed morphological changes as well as disrupted cytoplasmic membranes in PEF treated S. cerevisae cells. In addition, PEF treatment led to damaged chromosomal DNA in S. cerevisiae.

• Journal of the Korea Convergence Society
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• v.7 no.2
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• pp.61-67
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• 2016

The olfactory system is an important model for the study of neuronal degeneration and regeneration, including neuronal diseases. When the olfactory sensory neurons are damaged by nerve injury or are exposed to environmental factors, they degenerate and are replaced by regenerating neurons. To monitor neuronal degeneration in living animal, we established an olfactory-specific GFP transgenic zebrafish. The effects of Triton X-100 or sodium acetate on the olfactory system were examined. A significant decrease in the number of GFP-positive olfactory sensory neurons was observed after chemical lesion. We found a recovery of GFP-positive neurons by 2 days posttreatment. From these results, we expect that further studies of olfactory degeneration and regeneration using this transgenic zebrafish will provide important advances for the study of neuronal degeneration and regeneration.

• Tuberculosis and Respiratory Diseases
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• v.41 no.4
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• pp.319-327
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• 1994

Background: The pathogenetic mechanism of adult respiratory distress syndrome(ARDS) is not clearly defined yet, but it is well known that increased pulmonary capillary permeabilty is characteristic feature of ARDS. The increased alveolar-capillary permeability is usually preceded by damage of pulmonary artery endothelial cells. The released enzymes and oxygen free radicals from the activated neutrophils seem to play a predominant role in endothelial cell cytotoxicity. The activated neutrophils, however, probably are not the sole contributing factor in this type of damage because many cases of ARDS have been reported in severe neutropenia. Bacterial endotoxin perse and/or oxygen free radicals released from endothelial cells are suggested to be possible factors that contribute to the development of ARDS. The purpose of this study is to investigate the direct cytotoxicity of endotoxin and the role of oxygen free radicals released from the endothelial cells in endotoxin-induced endothelial cell cytotoxicity. Methods: First, to investigate whether endotoxin is cytotoxic to HUVE by itself, various doses of endotoxin were added to culture medium and cytotoxicity was measured. Second, to evaluate the possible role of oxygen free radical in endotoxin-induced HUVE cytotoxicity, various antioxidants were added on the endotoxin-induced HUVE cytotoxicity and cytotoxicity was measured. Third, to verify the release of oxygen free radicals from HUVE, the concentrations of hydrogen peroxide in the endotoxin-treated culture supernatant were measured. Finally, to observe the cytotoxic effect of hydrogen peroxide, HUVE cytotoxicity in the presence of various doses of hydrogen peroxide was measured. The fourth generations of subcultured HUVE from primary culture were used. The cell cytotoxicity was quantified by the chromium-51 release assay. Results: 1) Endotoxin alone showed HUVE cytotoxicity in a dose-dependent fashion. 2) Endotoxin-induced HUVE cytotoxicity was significantly attenuated by the pretreatment of catalase and DMTU. 3) Hydrogen peroxide was released from HUVE after endotoxin treatment in a dose-dependent fashion. 4) Exogenous hydrogen peroxide also showed HUVE cytotoxicity in a dose-dependent fashion. Conclusion: These results suggest that endotoxin alone can directly injure HUVE, and, oxygen-free radicals released from HUVE in response to endotoxin may also participate in the endotoxin-induced HUVE cytotoxicity.

• Korean Journal of Food Science and Technology
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• v.47 no.1
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• pp.81-86
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• 2015

Intense pulsed light (IPL), a nonthermal technology, has attracted increasing interest as a food processing technology. However, its efficacy in inactivating microorganisms has not been evaluated thoroughly. In this study, we investigated the influence of IPL treatment on the inactivation of Escherichia coli O157:H7 depending on light intensity, treatment time, and pulse number. Increased light intensity from 500 V to 1,000 V, raised the inactivation rate at room temperature. At 1000 V, the cell numbers were reduced by 7.1 log cycles within 120 s. In addition, increased pulse number or decreased distance between the light source and sample surface also led to an increase in the inactivation rate. IPL exposure caused a significant increase in the absorption at 260 nm of the suspending agent used in our experiments. This indicates that IPL-treated cells were damaged, consequently releasing intracellular materials. The growth of IPL-irradiated cells were delayed by about 5 h. The degree of damage to the cells after IPL treatment was confimed by transmission electron microscopy.

• Clinical and Experimental Pediatrics
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• v.52 no.12
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• pp.1337-1347
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• 2009

Purpose:Taurine (2-aminoethanesulfonic acid) is a simple sulfur-containing amino acid. It is abundantly present in tissues such as brain, retina, heart, and skeletal muscles. Current studies have demonstrated the neuroprotective effects of taurine, but limited data are available for such effects during neonatal period. The aim of this study was to determine whether taurine could reduce hypoxic-ischemic (HI) cerebral injury via anti-apoptosis mechanism. Methods:Embryonic cortical neurons isolated from Sprague-Dawley (SD) rats at 18 days gestation were cultured in vitro. The cells were divided into hypoxia group, taurine-treated group before hypoxic insult, and taurine-treated group after HI insult. In the in vivo model, left carotid artery ligation was performed in 7-day-old SD rat pups. The pups were exposed to hypoxia, administered an injection of 30 mg/kg of taurine, and killed at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hypoxic insult. We compared the expressions of Bcl-2, Bax, and caspase-3 among the 3 groups by using real- time polymerase chain reaction (PCR) and western blotting. Results:The cells in the taurine-treated group before hypoxic insult, although similar in appearance to those in the normoxia group, were lesser in number. In the taurine-treated group, Bcl-2 expression increased, whereas Bax and caspase-3 expressions reduced. Conclusion:Taurine exerts neuroprotective effects onperinatal HI brain injury due to its anti-apoptotic effect. The neuroprotective effect was maximal at 1-2 weeks after the hypoxic injury.

• Applied Microscopy
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• v.32 no.3
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• pp.275-284
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• 2002

Granular gland regeneration in the toad after dorsal skin wound histologically was examined using scanning and transmission electron microscopy. After cutaneous wounds were induced by excision, animals were maintained in special cages for up to 20 days. In transmission electron microscopy (TEM), newly formed granular gland, though poorly developed, was seen on 4 day after injury. Epithelial cells moved toward apical region of newly formed gland. The cells had smooth surface and were not connected to other cells by desmosomes. Mitochondria rich cell (MRC) possessing long cytoplasmic processes formed a gland cavity and hemidesmosomes were found under the cell processes. Basal cavity of newly formed gland consisted of MRC, pro-granular producing cells (pGPC), and granular producing cell (GPC). Moreover it was observed that xanthophores moved to the base of the epithelial tissue on 10 day after the injury. These cells contained numerous pterinosomes and carotenoid vesicles. Immature pterinosomes were large and carotenoid vesicles were moderately electron dense. On 13 day after the injury, xanthophores contained abundant carotinoid vesicles and lammelated pterinosomes. Iridophores were also observed adjacent the developing xanthophores on 16 day post-injury. These observations indicated that regeneration of granular gland from glandular precursor cells during wound healing and subsequent expansion of the glandular cells might be dependent on maturation and proliferation of these newly formed cells.

• Journal of Sasang Constitutional Medicine
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• v.11 no.2
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• pp.251-266
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• 1999

1. Purpose : The purpose of this study was to determine the effects of Chungsimyeunjatang on the cerebral neurons injured by hydrogen peroxide($H_2O_2$). 2. Methods : I observed cell viability in mouse cerebral neurons exposed to hydrogen peroxide by NR assay and MTT assay and determined lipid peroxidation and amounts of LDH release in mouse cerebral neurons exposed to hydrogen peroxide. After administration of Chungsimyeunjatang water extracts, I observed significant changes of cell viability, lipid peroxidation and amounts of LDH release in mouse cerebral neurons exposed to hydrogen peroxide. 3. Results : Hydrogen peroxide showed neurotoxicity. Cell viability in mouse cerebral neurons exposed to hydrogen peroxide decreased in NR assay and MTT assay. Lipid peroxidation and amounts of LDH release in mouse cerebral neurons exposed to hydrogen peroxide increased. Chungsimyeunjatang was very effective in blocking hydrogen peroxide-induced neurotoxicity.

• Journal of Acupuncture Research
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• v.25 no.2
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• pp.91-103
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• 2008

목적 : 중완과 족삼리 자침이 neonatal-streptozotocin 모델 실험동물에서 혈당과 베타세포 손상에 대한 보호효과를 알아보고자 하였다. 방법 : 비-비만 제2형 당뇨모델인 neonatal STZ 실험동물을 무처치 대조군, 임의혈 대조군, 중완 자침군, 족삼리 자침군으로 나누어 90일 동안 실험하였다. 체중과 혈당을 3일에 한 번씩 측정하였으며, 90일이 경과 후 혈중 인슐린을 측정하고 당부하 검사를 실시한 후 동물을 희생시켜 이자 조직을 적출하고 표본을 제작하였다. 면역세포화학법을 통하여 이자의 베타세포 손상에 대한 세포보호효과를 관찰하였다. 결과 : 중완 자침군과 족삼리 자침군은 대조군에 비해 유의한 혈당 강하 효과가 관찰되었다. 인슐린 농도는 모든 군에서 상승하였으며 당부하 검사에서는 임의혈 자침군과 중완 자침군 및 족삼리 자침군에서 내당능이 있는 것으로 나타났다. 조직 검사에서는 무처치 대조군과 임의혈 대조군에서는 베타세포 손상이 심했으나, 중완 자침군과 족삼리 자침군에서는 베타세포 손상에 대한 세포보호 효과가 현저하게 관찰되었다. 결론 : 중완과 족삼리 자침은 비-비만 제2형 당뇨모델에서 손상된 베타세포를 회복하고 인슐린 분비를 촉진하여 혈당을 강하시키는 효과가 있는 것으로 사료된다.

• Journal of Convergence for Information Technology
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• v.8 no.2
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• pp.61-65
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• 2018

Our experiment studied that grafted stem cells reduced behavioral deficiency in rodent animal models of clip compressive surgery inducing spinal cord infarction. Our research proved the effect of embryonic stem cells to the spinal cord infarction caused by compressing T9-10 with an aneurysm clip, focusing the application of grafted stem cells for reduction of infarction and regeneration of spinal cord nervous injury. Therefore, our research suggests manifest results that implantation of mouse embryonic stem cell could show behavioral improvement after severe spinal cord damage. Therefore, mouse embryonic stem cell (mESC) could be useful application for the method in neurological injury. Conclusively, stem cell implant therapy may enhance the effectiveness of stem cell implant for central nervous system injury.