Kwak, Dong Hoon;Kim, Sung Min;Lee, Dea Hoon;Kim, Ji Su;Kim, Sun Mi;Lee, Seo Ul;Jung, Kyu Yong;Seo, Byoung Boo;Choo, Young Kug
Molecules and Cells
/
v.20
no.3
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pp.354-360
/
2005
Neuronal damage subsequent to transient cerebral ischemia is a multifactorial process involving several overlapping mechanisms. Gangliosides, sialic acid-conjugated glycosphingolipids, reduce the severity of acute brain damage in vitro. However their in vivo effects on the cerebral cortex damaged by ischemic infarct are unknown. To assess the possible protective role of gangliosides we examined their expression in the cerebral cortex damaged by ischemic infarct in the rat. Ischemia was induced by middle cerebral artery (MCA) occlusion, and the resulting damage was observed by staining with 2, 3, 5-triphenylterazolium chloride (TTC). High-performance thin-layer chromatography (HPTLC) showed that gangliosides GM3 and GM1 increased in the damaged cerebral cortex, and immunofluorescence microscopy also revealed a significant change in expression of GM1. In addition, in situ hybridization demonstrated an increase in the mRNA for ganglioside GM3 synthase. These results suggest that gangliosides GM1 and GM3 may be synthesized in vivo to protect the cerebral cortex from ischemic damage.
Suh, Sang Heon;Lee, Ko Eun;Park, Jeong Woo;Kim, In Jin;Kim, Ok;Kim, Chang Seong;Choi, Joon Seok;Bae, Eun Hui;Ma, Seong Kwon;Lee, Jong Un;Kim, Soo Wan
The Korean Journal of Physiology and Pharmacology
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v.17
no.5
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pp.435-440
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2013
While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 ${\mu}g/kg/day$) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynucleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.
Journal of Physiology & Pathology in Korean Medicine
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v.17
no.2
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pp.553-559
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2003
In order to make the efficient prescription and cope with various senile dementia, learning and memory functions of Sprague-Dawley model rats were tested with Morris water maze at first. And to evaluate the effects of the sample drug(GM) on choline acetyltranferase and acetylcholine esterase, immunoreactive measurement and enzymatic activity measuring were carried out. Rats were injected with ibotenic acid through hippocampus CA1 and CA3 area. The results are as following. GM improves the learning ability in tile acquisition test and memory function in the retention test significantly. And GM increases the level of ChAT which is synthesizing acetylcholine in CA3 area, and at the same time it increases the level of AChE which is resolving acetylcholine. These results show that GM improve the cholinergic catabolism and anabolism, and the increment of metabolic activity of cholinergic system contributes to the recovery of damaged learning and memory function by ibotenic acid. So it can be concluded that GM will be helpful to cholinergic brain disease induced by primary or senile reduction of acetylcholine secretive activity.
The subsurface damaged layer in ultraprecisison machined single crystal Ge was examined by ion channeling. Single crystal Ge surfaces were prepared by chemo-mechanical polishing, mechanical polishing with 1/4 gm diamond abrasive, single point diamond turning and ultraprecision orthogonal flycutting. The extent of subsurface lattice disorder was compared to the crystal's orginal surface quality. Ion channeling is seen to be useful for quantitative measure of lattice disorder in finely finished surfaces.
Hydraulic concrete buildings in the northwest of China are often subject to the combined effects of low-temperature frost damage, during drying and wetting cycles, and salt erosion, so the study of concrete deterioration prediction is of major importance. The prediction model of the relative dynamic elastic modulus (RDEM) of four different kinds of modified concrete under the special environment in the northwest of China was established using Grey residual Markov theory. Based on the available test data, modified values of the dynamic elastic modulus were obtained based on the Grey GM(1,1) model and the residual GM(1,1) model, combined with the Markov sign correction, and the dynamic elastic modulus of concrete was predicted. The computational analysis showed that the maximum relative error of the corrected dynamic elastic modulus was significantly reduced, from 1.599% to 0.270% for the BS2 group. The analysis error showed that the model was more adjusted to the concrete mixed with fly ash and mineral powder, and its calculation error was significantly lower than that of the rest of the groups. The analysis of the data for each group proved that the model could predict the loss of dynamic elastic modulus of the deterioration of the concrete effectively, as well as the number of cycles when the concrete reached the damaged state.
Journal of Korean Academy of Oral and Maxillofacial Radiology
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v.18
no.1
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pp.31-45
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1988
The author studied the histopathologic changes according to a single or a split dose and the time after irradiation on the acinar cells of rat parotid gland. 99 Sprague Dawley rats, weighing about l20gm, were divided into control and 3 experimental groups. In experimental groups, GroupⅠ and Ⅱ were delivered a single dose of l5Gy, 18Gy and Group Ⅲ and Ⅳ were delivered two equal split doses of 9Gy, 10.5Gy for a 4 hours interval, respectively. The experimental groups were delivered by a cobalt-60 teletherapy unit with a dose rate of 222cGy/min, source-skin distance of 50㎝, depth of l㎝ and a field size of l2×5㎝. The animals were sacrificed at 1, 2, 3, 6, 12 hours, 1, 3, 7 days after irradiation and examined by light and electron microscopy. The results were as follows: 1. As the radiation dose increased and the acinar cells delivered a single dose exposure were more damaged, and the change of acinar cells appeared faster than those of a split dose exposure. 2. The histopathologic change of acinar cells appeared at 1 hour after irradiation. The recovery from damaged acinar cells appeared at 1 day after irradiation and there was a tendency that the recovery from damage of a split dose exposure was somewhat later than that of a single dose exposure. 3. Light microscope showed atrophic change of acinar cells and nucleus, degeneration and vesicle formation of cytoplasm, widening of intercellular space and interlobular space. 4. Electron microscope showed loss of nuclear membrane, degeneration of nucleus and nucleoli, clumping of cytoplasm, widening and degeneration of rough endoplasmic reticulum, loss of cristae of mitochondria, lysosome, autophagosome and lipid droplet. 5. Electron microscopically, the change of rough endoplasmic reticulum was the most prominent and this appeared at 1 hour after irradiation as early changes of acinar cells. The nuclear change appeared at 2 hours after irradiation and the loss of cristae of mitochondria was observed at 2 hours after irradiation in all experimental groups.
This study aims to demonstrate the effect of chitosan, one of the natural chelator, on the ultrastructural changes in the mouse liver caused by cadmium. A total of 60 healthy ICR that weighted 30 gm $({\pm}2gm)$ was used for experiment. The experimental group was divided into three groups; group A, B, and C. The group A and B administrated cadmium (4.0 mg/kg) to the intraperitoneal after pretreated with chitosan (0.5% solution) for 30 and 7 days, respectively. Each group was observed at 12, 24, 48, 72 hours and one week after injected cadmium. The results were as follows: 1. Group A The nuclear membrane and the chromatin were normal shapes at overall the time. The inner and outer membranes of the mitochondria damaged a little but almost normal in shapes. And electron-density showed slightly compacted. some enlarged rER (rough endoplasmic reticulum) showed at 12 hours. At 48 hours, typical lamellae of the rER were reformed, and a lot of transvesicles observed around them. To 48 hours, sER (smooth endoplasmic reticulum) was slightly dilated. From 72 hours, sER rehalizated in normal shape. 2. Group B Nuclear membranes were rounded-shape and chromatin showed evenly. To 72 hours, a lot of mitochondria observed around rER and development of cristae showed weakly. But at one week, cristae were clear and electron-density of matrix showed high. At 72 hours lamellae of rER showed some broken, but were reformed at one week. Also at one week, glycogen granules evenly showed over cytoplasm. 3. Group C At 12 hours, Nucleus showed the condensation of nuclear membrane and clear condensation at 24 hours. However, nuclear membrane had a slightly rounded-shape from 72 hours. From 12 hours to the one week, mitochondria showed the dilation of inner cavity and weak development of cristae. Also electron-density of matrix was a little low. Occasionally, destruction of inner and outer membrane observed at one week. The dilation of cisternae and destruction of lamellae of rER showed from 12 to 48 hours. From 72 hours, rER showed slightly dilated only. And lamella observed at one week. In sER, dilation of inner cavity was observed during whole period. These results suggest that chitosan attenuates the toxic effect of the cadmium in the mouse liver.
An, Byeong Kil;Ha, Young Soo;Hyun, Dong Keun;Park, Chong Oon;Kim, Joon Mee
Journal of Korean Neurosurgical Society
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v.29
no.4
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pp.461-470
/
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.
The Journal of Korean Academy of Sensory Integration
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v.2
no.1
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pp.21-32
/
2004
Objective : Effect of treadmill exercise on hippocampal neural cell proliferation under normal conditions and alcohol intoxication conditions has been recently studied; however, this effect under sensory stimulation application has not clarified yet. In the present study, the effect of compression stimulation application on hippocampal neural cell proliferation in the dentate gyrus in normal and alcohol intoxicated rats was investigated. Methods : Experimental design: comparative investigation on number of 5-Bromo-2'-deoxyuridine(BrdU)B-positive cells in dentate gyrus 5 days after commencement. Setting: animal laboratory. Participants: male Sprague-Dawley rats of 3weeks old in age weighing $80{\pm}10gm$. Intervention: animals were randomly assigned into 4 groups; control-rest group(n=8), control-compression group(n=8), alcohol intoxication-rest group(n=8) and alcohol intoxication-compression group(n=8). Animals of the alcohol intoxicated groups were injected intraperitoneally with alcohol(2g/kg) twice per day for 3 days. All animals were injected BrdU(50mg/kg) intraperitoneally, and rats compression stimulation application groups were compressed using sphygmomanometer cuff times per day, for 5 days following alcohol administration. Measures: mean number of BrdU-positive cells in dentate gyrus was observed via immunohistochemistry. Results : Compression stimulation application significantly increased the number of BrdU-positive cells in the dentate gyrus. Also, treatment with alcohol for 3 days inhibited cell proliferation, and compression stimulation application alleviated alcohol-induced inhibition of new cell formation. Conclusion : These results suggest the possibility that compression stimulation application may help in improvement following alcohol-induced brain damaged.
Kwon, Mi Hye;Yoon, Jee-Hyun;Kim, Eun Hye;Lee, Jee Young;Yoon, Seong Woo
Journal of Korean Traditional Oncology
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v.25
no.1
/
pp.11-24
/
2020
Objective : Radiodermatitis is a common sequelae in 95% of patients receiving radiation therapy, which is important to be well managed as it can affect the patient's quality of life as well as the cancer treatment schedule. The aim of this study is to review and summarize the interventions available for the treatment of acute radiodermatitis, including traditional Korean medicine, and to propose treatment algorithms for clinicians. Methods : To collect studies about managements for radiodermatitis, domestic and foreign database were used such as Korean journal of traditional knowledge portal (KTKP), Korean studies information service system (KISS), national discovery or science leaders (NDSL), and oriental medicine advance searching integrated system (OASIS), Pubmed, Google scholar and Scopus. Results : Thirty-two studies were selected. There were nine studies on usual care and dressing, eleven studies on chemical agents, two studies on biological preparations, and ten studies on herbal medicines. Conclusion : Hygienic options and dressings have proved to be useful in the management of radiodermatitis. Chemical agents such as corticosteroid, statin, and topical antibiotic agent have proved to alleviate symptoms and severity, regenerate damaged skin, and prevent secondary infection. In biological preparations, EGF (epidermal growth factor) and GM-CSF (granulocyte-macrophage colony-stimulating factor) could be used to protect skin and prevent radiodermatitis. For herbal medicines, Calendula, catechin, β-sitosterol, and Jaungo (紫雲膏) may be effective for symptoms including pain, itching, and burning sensation induced by radiation therapy. Because of some research with conflicting results, further studies are needed to propose an algorithm for more optimal treatments.
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