• The Korean Journal of Physiology and Pharmacology
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• 제1권5호
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• pp.515-521
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• 1997

Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B ($NF-_{\kappa}B$) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha($TNF{\alpha}$) had protective effect of cell death induced by serum deprivation and this protection was related to $NF-_{\kappa}B$ activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by $NF-_{\kappa}B$. And the role of nitric oxide (NO) generated by iNOS on cell viability is still controversial. To elucidate the mechanism of $TNF{\alpha}$ and $NF-_{\kappa}B$ activation on cell death protection, we investigate the effect of NO on the cell death induced by serum- deprivation in bovine cerebral endothelial cells in this study. Addition of $TNF{\alpha}$, which are inducer of iNOS, prevented serum-deprivation induced cell death. Increased expression of iNOS was confirmed indirectly by nitrite measurement. When selective iNOS inhibitors were treated, the protective effect of $TNF{\alpha}$ on cell death was partially blocked, suggesting that iNOS expression was involved in controlling cell death. Exogenously added NO substrate (L-arginine) and NO donors (sodium nitroprusside and S-nitroso-N-acetylpenicillamine) also inhibited the cell death induced by serum deprivation. These results suggest that NO has protective effect on bovine cerebral endothelial cell death induced by serum-deprivation and that iNOS is one of the possible target molecules by which $NF-_{\kappa}B$ exerts its cytoprotective effect.

• Journal of Radiation Protection and Research
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• 제46권1호
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• pp.1-7
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• 2021

Background: The use of computed tomography (CT) device has increased in the past few decades in Japan. Dose optimization is strongly required in pediatric CT examinations, since there is concern that an unreasonably excessive medical radiation exposure might increase the risk of brain cancer and leukemia. To accelerate the process of dose optimization, continual assessment of the dose levels in actual hospitals and medical facilities is necessary. This study presents organ dose estimation using pediatric cerebral CT scans in the Kyushu region, Japan in 2012 and the web-based calculator, WAZA-ARI (https://waza-ari.nirs.qst.go.jp). Materials and Methods: We collected actual patient information and CT scan parameters from hospitals and medical facilities with more than 200 beds that perform pediatric CT in the Kyushu region, Japan through a questionnaire survey. To estimate the actual organ dose (brain dose, bone marrow dose, thyroid dose, lens dose), we divided the pediatric population into five age groups (0, 1, 5, 10, 15) based on body size, and inputted CT scan parameters into WAZA-ARI. Results and Discussion: Organ doses for each age group were obtained using WAZA-ARI. The brain dose, thyroid dose, and lens dose were the highest in the Age 0 group among the age groups, and the bone marrow and thyroid doses tended to decrease with increasing age groups. All organ doses showed differences among facilities, and this tendency was remarkable in the young group, especially in the Age 0 group. This study confirmed a difference of more than 10-fold in organ doses depending on the facility and CT scan parameters, even when the same CT device was used in the same age group. Conclusion: This study indicated that organ doses varied widely by age group, and also suggested that CT scan parameters are not optimized for children in some hospitals and medical facilities.

• 대한한방내과학회지
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• 제31권4호
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• pp.763-774
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• 2010

Objectives : In condition of brain infarction, irreversible axon damage occurs in central nerve system(CNS), because gliosis becomes physical and mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. The current study is to examine the effect of the Uncariae Ramulus et Uncus on CD81 and GFAP expression in the rat brain following middle cerebral artery occlusion. Methods : In order to study ischemic injuries on brain, infarction was induced by middle cerebral artery occlusion(MCAO) using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Results : The following results were obtained 1. Measuring the size of cerebral infartion induced by MCAO in the rat after injection of Uncariae Ramulus et Uncus showed the size was decreased. 2. Intravenous injection of Uncariae Ramulus et Uncus showed pyramidal cell death protection in the hippocampus in the MCAO rat. 3. Water extract injection of Uncariae Ramulus et Uncus decreased GFAP expression significantly in the MCAO rat. 4. Uncariae Ramulus et Uncus water extract decreased CD81 expression in the MCAO rat. 5. The administration of water extract of Uncariae Ramulus et Uncus induced up-regulation of c-Fos expression significantly compared with MCAO. 6. The admistration of water extract of Uncariae Ramulus et Uncus increased ERK expression significantly compared with MCAO. Conclusion : We observed that Uncariae Ramulus et Uncus could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of the rat with cerebral infaction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the up-regulation of c-Fos and ERK. These results suggest that Uncariae Ramulus et Uncus can be a candidate to regenerate CNS injury.

• Journal of Ginseng Research
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• 제47권2호
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• pp.199-209
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• 2023

Background: Due to the interrupted blood supply in cerebral ischemic stroke (CIS), ischemic and hypoxia results in neuronal depolarization, insufficient NAD+, excessive levels of ROS, mitochondrial damages, and energy metabolism disorders, which triggers the ischemic cascades. Currently, improvement of mitochondrial functions and energy metabolism is as a vital therapeutic target and clinical strategy. Hence, it is greatly crucial to look for neuroprotective natural agents with mitochondria protection actions and explore the mediated targets for treating CIS. In the previous study, notoginseng leaf triterpenes (PNGL) from Panax notoginseng stems and leaves was demonstrated to have neuroprotective effects against cerebral ischemia/reperfusion injury. However, the potential mechanisms have been not completely elaborate. Methods: The model of middle cerebral artery occlusion and reperfusion (MCAO/R) was adopted to verify the neuroprotective effects and potential pharmacology mechanisms of PNGL in vivo. Antioxidant markers were evaluated by kit detection. Mitochondrial function was evaluated by ATP content measurement, ATPase, NAD and NADH kits. And the transmission electron microscopy (TEM) and pathological staining (H&E and Nissl) were used to detect cerebral morphological changes and mitochondrial structural damages. Western blotting, ELISA and immunofluorescence assay were utilized to explore the mitochondrial protection effects and its related mechanisms in vivo. Results: In vivo, treatment with PNGL markedly reduced excessive oxidative stress, inhibited mitochondrial injury, alleviated energy metabolism dysfunction, decreased neuronal loss and apoptosis, and thus notedly raised neuronal survival under ischemia and hypoxia. Meanwhile, PNGL significantly increased the expression of nicotinamide phosphoribosyltransferase (NAMPT) in the ischemic regions, and regulated its related downstream SIRT1/2/3-MnSOD/PGC-1α pathways. Conclusion: The study finds that the mitochondrial protective effects of PNGL are associated with the NAMPT-SIRT1/2/3-MnSOD/PGC-1α signal pathways. PNGL, as a novel candidate drug, has great application prospects for preventing and treating ischemic stroke.

• Journal of Acupuncture Research
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• 제18권2호
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• pp.150-160
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• 2001

Objectives ; This study was undertaken to determine whether Carthami-Flos aquacapuncture (CFA) exerts protective effect against oxidant-induced inhibition of $Na^+-K^+$-ATPase activity in cerebral synaptosomes. Methods and Results ; The enzyme activity was dependent on incubation time and enzyme protein concentrations. An oxidant t-butylhydroperoxide (tBHP) at 1 mM concentration caused a significant inhibition of $Na^+-K^+$-ATPase activity, which was prevented by addition of 0.01% CFA. tBHP inhibition and CFA protection were independent on incubation time or enzyme protein concentrations. The enzyme activity was increased by ATP in a dose dependent manner. Effects of tBHP and CFA were not affected by ATP cocentrations. tBHP (1 mM) produced a significant increase in lipid peroxidation in cerebral synaptosomes, which was prevented by 0.01% CFA. CFA decreased oxygen free radicals generated induced by the phorbol-ester in a dose-dependent manner in human neutrophil. Conclusions ; These results suggest that CFA exerts protective effect against tBHP-induced inhibition of $Na^+-K^+$-ATPase activity, which is due to by an antioxidant action resulting from a direct scavenging effect of oxygen free radicals in the cerebral synaptosomes.

• The Korean Journal of Pain
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• 제21권2호
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• pp.119-125
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• 2008

Background: Cerebral blood vessels are innervated by sympathetic nerves from the superior cervical ganglia (SCG), and these nerves may influence the cerebral blood flow. The purpose of the present study was to evaluate the neuroprotective effect of superior cervical sympathetic ganglion block in rats that were subjected to focal cerebral ischemia/reperfusion injury. Methods: Eighty male Sprague-Dawley rats (270-320 g) were randomly assigned to one of two groups (the ropivacaine group and a control group). In all the animals, brain injury was induced by middle cerebral artery (MCA) reperfusion that followed MCA occlusion for 2 hours. The animals of the ropivacaine group received $30{\mu}l$ of 0.75% ropivacaine, and their SCG. Neurologic score was assessed at 1, 3, 7 and 14 days after brain injury. Brain tissue samples were then collected. The infarct ratio was measured by 2.3.5-triphenyltetrazolium chloride staining. The terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeled (TUNEL) reactive cells and the cells showing caspase-3 activity were counted as markers of apoptosis at the caudoputamen and frontoparietal cortex. Results: The death rate, the neurologic score and the infarction ratio were significantly less in the ropivacaine group 24 hr after ischemia/reperfusion injury. The number of TUNEL positive cells in the ropivacaine group was significantly lower than those values of the control group in the frontoparietal cortex at 3 days after injury, but the caspase-3 activity was higher in the ropivacaine group than that in the control group at 1 day after injury. Conclusions: The study data indicated that a superior cervical sympathetic ganglion block may reduce the neuronal injury caused by focal cerebral ischemia/reperfusion, but it may not prevent the delayed damage.

• Journal of Chest Surgery
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• 제54권6호
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• pp.513-516
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• 2021

An 87-year-old man presented with a saccular aneurysm at the proximal descending thoracic aorta. As computed tomography revealed a shaggy aorta, we planned hybrid thoracic endovascular aortic repair (TEVAR) with embolic protection devices (EPDs) in both internal carotid arteries to prevent a cerebrovascular accident. We inserted an Emboshield NAV⁶ Embolic Protection System (Abbott Vascular, Abbott Park, IL, USA) into both internal carotid arteries before performing the TEVAR procedure. The patient was discharged from the hospital on postoperative day 4 without any neurological complications.

• Journal of Chest Surgery
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• 제33권6호
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• pp.445-468
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• 2000

Background: Retrograde cerebral perfusion(RCP) is currently used for brain protection during aorta surgery, however, for the safety of it, various data published so far are insufficient. We performed RCP using pig and investiaged various parameters of cerebral metabolism and brain injury after RCP under deep hypothermia. Material and Method: We used two experimental groups: in group I(7 pigs, 20 kg), we performed RCP for 120 minutes and in group II (5 pigs, 20 kg), we did it for 90 minutes. Nasopharyngeal temperature, jugular venous oxygen saturation, electroencephalogram were continuously monitored, and we checked the parameters of cerebral metabolism, histological changes and serum levels of neuron-specific enolose(NSE) and lactic dehydrogenase(LDH). Central venous pressure during RCP was mainained in the range of 25 to 30 mmHg. Result: Perfusion flow rates(ml/min) during RCP were 130$\pm$57.7(30 minutes), 108.6$\pm$55.2(60 minutes), 107.1$\pm$58.8(90 minutes), 98.6$\pm$58.7(120 minutes) in group I and 72$\pm$11.0(30 minutes), 72$\pm$11.0(60 minutes), 74$\pm$11.4(90 minutes) in group II. The ratios of drain flow to perfusion flow were 0.18(30 minutes), 0.19(60 minutes), 0.17(90 minutes), 0.16(120 minutes) in group I and 0.21, 0.20, 0.17 in group II. Oxygen consumptions(ml/min) during RCP were 1.80$\pm$1.37(30 minutes), 1.72$\pm$1.23(60 minutes), 1.38$\pm$0.82(90 minutes), 1.18$\pm$0.67(120 minutes) in group I and 1.56$\pm$0.28(30 minutes), 1.25$\pm$0.28(60 minutes), 1.13$\pm$0.26(90 minutes). We could observe an decreasing tendency of oxygen consumption after 90 minutes of RCP in group I. Cerebrovascular resistance(dynes.sec.cm-5) during RCP in group I incrased from 71370.9$\pm$369145.5 to 83920.9$\pm$49949.0 after the time frame of 90 minutes(p<0.05). Lactate(mg/min) appeared after 30 minutes of RCP and the levels were 0.15$\pm$0.07(30 minutes), 0.18$\pm$0.10(60 minutes), 0.19$\pm$0.19(90 minutes), 0.18$\pm$0.10(120 minutes) in group I and 0.13$\pm$0.09(30 minutes), 0.19$\pm$0.03(60 minutes), 0.29$\pm$0.11(90 minutes) in group II. Glucose utilization, exudation of carbon dioxide, differences of cerebral tissue acidosis between perfusion blood and drain blood were maintained constantly during RCP. Oxygen saturation levels(%) in drain blood during RCP were 22.9$\pm$4.4(30 minutes), 19.2$\pm$4.5(60 minutes), 17.7$\pm$2.8(90 minutes), 14.9$\pm$2.8(120 minutes) in group I and 21.3$\pm$8.6(30 minutes), 20.8$\pm$17.6(60 minutes), 21.1$\pm$12.1(90 minutes) in group II. There were no significant changes in cerebral metabolic parameters between two groups. Differences in serum levels of NSE and LDH between perfusion blood and drain blood during RCP showed no statistical significance. Serum levels of NSE and LDH after resuming of cardipulmonary bypass decreased to the level before RCP. Brain water contents were 0.73$\pm$0.03 in group I and 0.69$\pm$0.06 in group II and were higher than those of the controls(p<0.05). The light microscopic findings of cerebral neocortex, basal ganglia, hippocampus(CA1 region) and cerebellum showed no evidence of cerebral injury in two groups and there were no different electron microscopy in both groups(neocortex, basal ganglia and hippocampus), but they were thought to be reversible findings. Conclusion: Although we did not proceed this study after survival of pigs, we could perform the RCP successfully for 120 minutes with minimal cerebral metabolism and no evidence of irreversible brain damage. The results of NSE and LDH during and after RCP should be reevaluated with survival data.

• 대한소아치과학회지
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• 제35권2호
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• pp.351-356
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• 2008

뇌성마비(cerebral palsy)는 비진행성의 정신, 운동 장애를 총칭하는 용어로, 소아 장애의 흔한 원인이 된다. 자해 행위란(self-injurious behavior) 자살 의도없이 자신의 신체 일부를 고의적으로 손상시키는 것으로, 종종 반복적인 행동으로 나타난다. 소아에서의 이러한 자해 습관은 정상적인 어린이에서는 드물며, 증후군, 유전질환, 정신지체 어린이 등에서 그 발생률이 높게 보고된다. 구강 내 자해 행위의 가장 흔한 유형은 혀나 입술 혹은 구강 점막을 물어뜯는 것이다. 이러한 자해 행위를 조절하기 위하여 행동 수정법, 약물 치료, 신체 속박술, 치과적 장치의 적용, 외과적 수술 또는 치아 발치술 등의 다양한 방법들이 제시되었다. 이 중 마우스가드 등의 치과적 장치를 이용한 방법은 구강 내 자해 행위의 감소와 조직의 보호를 위해 가장 보존적이며 적합한 방법이라고 사료된다. 본 증례에서는 자해 습관에 의해 하순과 협점막에 궤양성 병소를 가진 뇌성마비 환아에 있어서, 변형된 마우스가드를 이용하여 자해에 의한 손상을 방지하고 만족할 만한 치유 양상을 보였기에 이를 보고하는 바이다.

• 한국해양생명과학회지
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• 제5권2호
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• pp.92-98
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• 2020

Heat shock proteins (HSPs) are highly conserved cellular proteins that contribute to adaptive responses of organisms to a variety of stressors. In response to stressors, cellular levels of HSPs are increased and play critical roles in protein stability, folding and molecular trafficking. The mRNA expression pattern of two well-known heat shock protein transcripts, HSP70 and HSP90 were studied in two tissues of nerve ganglia, cerebral ganglion and pleuropedal ganglion of Pacific abalone (Haliotis discus hannai). It was observed that both HSP70 and HSP90 transcripts were upregulated under heat stress in both ganglion tissues. Expression level of HSP70 was found higher than HSP90 in both ganglia whereas cerebral ganglion showed higher expression than pleuropedal ganglion. The HSP70 and HSP90 showed higher expression at Day-1 after exposed to heat stress, later decreased at Day-3 and Day-7 onwards. The present result suggested that HSP70 and HSP90 synthesize in nerve ganglion tissues and may provide efficient protection from stress.