• 생물정신의학
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• 제7권1호
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• pp.46-54
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• 2000

외상성 뇌손상으로 외상 후 스트레스 장애, 범불안장애, 공황장애, 강박장애, 공포장애 등의 불안장애가 비교적 흔히 발생할 수 있다. 그러나 빈발하는 불안장애인데 비해 의사들로부터 적절하게 관심을 받지도 못했으며 치료받지도 못하였다. 외상성 뇌손상 후 불안장애는 뇌손상 자체에 의해, 뇌손상과 기능상실에 대한 환자 또는 간호인의 반응에 의해 증상이 발생하기도 하고 지속되기도 한다. 의사는 이들 환자들을 진단하고 치료하기 위해서는 우선 뇌손상의 기전과 양상에 대해 지식이 있어야 하며, 불안증상을 호소하는 외상성 뇌손상 환자를 이해하고 수용하고 지지해주는 태도를 취해야 하며, 불안증상이 뇌손상에 의한 것인지 통상적인 불안 증상인지 확인해야 한다. 이들 뇌손상 환자들은 약물의 부작용에 아주 취약하기 때문에 약물치료시에는 약물의 작용기전은 말할 것도 없고 부작용에 대해 잘 알고 있어야 한다.

• 한국초등과학교육학회지:초등과학교육
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• 제26권1호
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• pp.49-62
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• 2007

The higher cognitive functions of the human brain including teaming are hypothesized to be selectively distributed across large-scale neural networks interconnected to the cortical and subcortical areas. Recently, advances in functional imaging have made it possible to visualize the brain areas activated by certain cognitive activities in vivo. Neural substrates for teaming and motivation have also begun to be revealed. Functional magnetic resonance imaging (fMRI) provides a non-invasive indirect mapping of cerebral activity, based on the blood- oxygen level dependent (BOLD) contrast which is based on the localized hemodynamic changes following neural activities in certain areas of the brain. The fMRI method is now becoming an essential tool used to define the neuro-functional mechanisms of higher brain functions such as memory, language, attention, learning, plasticity and emotion. Further research in the field of education will accelerate the verification of the effects on loaming or help in the selection of model teaching strategies. Thus, the purpose of this study was to review brain study methods using fMRI in science education. In conclusion, a number of possible strategies using fMRI for the study of elementary science education were suggested.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.199.1-199.1
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• 2003

Ischemia-induced changes in protein expression may provide important insights into the mechanisms of cellular damage and their potential recovery. In the present study, to investigate protein patterns changed in ischemic condition, the cortical and striatal tissue samples from the permanent and transient ischemic rat brain obtained by middle cerebral occlusion were analysed by proteomic approchese using 20-PAGE and MALOI-MS. (omitted)

• 생물정신의학
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• 제2권2호
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• pp.157-168
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• 1995

The neuropsychiatric sequelae of traumatic brain unjury(TBI) are effects on complex aspect of behavior, cognition and emotional expression. They include psychiatric disorders such as depression, psychosis, personality change, dementia, and postconcussion syndrome. The damage is done not only to the cortex of the brain but also to subcortical and axial structures. The diffuse degeneration of cerebral white mailer is axonal damage that is caused by mechanical forces shearing the neuronal fiber at the moment of impact(diffuse axonal injury, DAI). The DAI and the changed receptor-agonist mechanism ore the most important mechanisms in genesis of neuropsychiatric sequalae by mild TBI. The most important instrument for diagnosis of neuropsychiatric sequalae of TBI is a physician or psychiatrist with experience and knowledge. The most effective therapeutic tool is a professional who understands the nature of the problem.

• 전자통신동향분석
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• 제36권3호
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• pp.106-118
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• 2021

The field of brain science (or neuroscience in a broader sense) has inspired researchers in artificial intelligence (AI) for a long time. The outcomes of neuroscience such as Hebb's rule had profound effects on the early AI models, and the models have developed to become the current state-of-the-art artificial neural networks. However, the recent progress in AI led by deep learning architectures is mainly due to elaborate mathematical methods and the rapid growth of computing power rather than neuroscientific inspiration. Meanwhile, major limitations such as opacity, lack of common sense, narrowness, and brittleness have not been thoroughly resolved. To address those problems, many AI researchers turn their attention to neuroscience to get insights and inspirations again. Biologically plausible neural networks, spiking neural networks, and connectome-based networks exemplify such neuroscience-inspired approaches. In addition, the more recent field of brain network analysis is unveiling complex brain mechanisms by handling the brain as dynamic graph models. We argue that the progress toward the human-level AI, which is the goal of AI, can be accelerated by leveraging the novel findings of the human brain network.

• Clinical Nutrition Research
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• 제12권2호
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• pp.154-167
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• 2023

Hepatic encephalopathy (HE) associated with liver failure is accompanied by hyperammonemia, severe inflammation, depression, anxiety, and memory deficits as well as liver injury. Recent studies have focused on the liver-brain-inflammation axis to identify a therapeutic solution for patients with HE. Lipocalin-2 is an inflammation-related glycoprotein that is secreted by various organs and is involved in cellular mechanisms including iron homeostasis, glucose metabolism, cell death, neurite outgrowth, and neurogenesis. In this study, we investigated that the roles of lipocalin-2 both in the brain cortex of mice with HE and in Neuro-2a (N2A) cells. We detected elevated levels of lipocalin-2 both in the plasma and liver in a bile duct ligation mouse model of HE. We confirmed changes in cytokine expression, such as interleukin-1β, cyclooxygenase 2 expression, and iron metabolism related to gene expression through AKT-mediated signaling both in the brain cortex of mice with HE and N2A cells. Our data showed negative effects of hepatic lipocalin-2 on cell survival, iron homeostasis, and neurite outgrowth in N2A cells. Thus, we suggest that regulation of lipocalin-2 in the brain in HE may be a critical therapeutic approach to alleviate neuropathological problems focused on the liver-brain axis.

• BMB Reports
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• 제57권4호
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• pp.200-205
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• 2024

We conducted a comprehensive series of molecular biological studies aimed at unraveling the intricate mechanisms underlying the anti-fibrotic effects of triamcinolone acetonide (TA) when used in conjunction with fully covered self-expandable metal stents (FCSEMS) for the management of benign biliary strictures (BBS). To decipher the molecular mechanisms responsible for the anti-fibrotic effects of corticosteroids on gallbladder mucosa, we conducted a comprehensive analysis. This analysis included various methodologies such as immunohisto-chemistry, ELISA, real-time PCR, and transcriptome analysis, enabling us to examine alterations in factors related to fibrosis and inflammation at both the protein and RNA levels. Overall, our findings revealed a dose-dependent decrease in fibrosis-related signaling with higher TA concentrations. The 15 mg of steroid treatment (1X) exhibited anti-fibrosis and anti-inflammatory effects after 4 weeks, whereas the 30 mg of steroid treatment (2X) rapidly reduced fibrosis and inflammation within 2 weeks in BBS. Transcriptomic analysis results consistently demonstrated significant downregulation of fibrosis- and inflammation-related pathways and genes in steroid-treated fibroblasts. Use of corticosteroids, specifically TA, together with FCSEMS was effective for the treatment of BBS, ameliorating fibrosis and inflammation. Our molecular biological analysis supports the potential development of steroid-eluted FCSEMS as a therapeutic option for BBS in humans resulting from various surgical procedures.

• International Journal of Oral Biology
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• 제32권2호
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• pp.51-57
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• 2007

Cyclosporin A (CsA) plays an important role in clinical medicine and basic biology as an immunosuppressant and a mitochondrial permeability blocker, respectively. It was reported that CsA has a protective role by preventing apoptosis and promoting the proliferation in severed neurons. However, the molecular mechanisms for CsA-induced neuronal cell proliferation are unclear. In this study, we examined the mechanisms underlying the CsA-induced proliferation of PC12 cells. CsA increased the viability of PC12 cells in a dose(over $0.1{\sim}10\;{\mu}M$)-and time-dependent manner. The level of ROS generation was decreased in the CsA-treated PC12 cells. Expression of Bcl-2, an antiapoptotic molecule that inhibits the release of cytochrome c from the mitochondria into the cytosol, was upregulated, whereas Bax, a proapototic molecule, was not changed in the CsA-treated PC12 cells. CsA downregulated the mRNA expression of VDAC 1 and VDAC 3, but VDAC 2 was not changed in the CsA-treated PC12 cells. The level of cytosolic cytochrome c released from the mitochondria and the caspase-3 activity were attenuated in the CsA-treated PC12 cells. These results suggest that the mitochondria-mediated apoptotic signal and Bcl-2 family may play an important role in CsA-induced proliferation in PC12 cells.

• Clinical Psychopharmacology and Neuroscience
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• 제16권4호
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• pp.422-433
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• 2018

Objective: Neuropsychiatric manifestations like depression and cognitive dysfunction commonly occur in inflammatory bowel disease (IBD). In the context of the brain-gut axis model, colitis can lead to alteration of brain function in a bottom-up manner. Here, the changes in the response of the hypothalamic-pituitary-adrenal axis and inflammation-related markers in the brain in colitis were studied. Methods: Dextran sodium sulfate (DSS) was used to generate a mouse model of colitis. Mice were treated with DSS for 3 or 7 days and sacrificed. We analyzed the gene expression of brain-derived neurotrophic factor (BDNF), cyclooxygenase 2 (COX-2), and glial fibrillary acidic protein (GFAP), and the expression of GFAP, in the hippocampus, hypothalamus, and amygdala. Additionally, the levels of C-reactive protein (CRP) and serum cortisol/corticosterone were measured. Results: Alteration of inflammatory-related markers varied depending on the brain region and exposure time. In the hippocampus, COX-2 mRNA, GFAP mRNA, and GFAP expression were upregulated during exposure to DSS. However, in the hypothalamus, COX-2 mRNA was upregulated only 3 days after treatment. In the amygdala, BDNF and COX-2 mRNAs were downregulated. CRP and corticosterone expression increased with DSS treatment at day 7. Conclusion: IBD could lead to neuroinflammation in a bottom-up manner, and this effect varied according to brain region. Stress-related hormones and serum inflammatory markers, such as CRP, were upregulated from the third day of DSS treatment. Therefore, early and active intervention is required to prevent psychological and behavioral changes caused by IBD, and region-specific studies can help understand the precise mechanisms by which IBD affects the brain.

• Toxicological Research
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• 제17권
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• pp.71-77
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• 2001

The brain of the aged dog possesses senile plaques and amyloid angiopathy, which characterize Alzheimer's disease brains. We have defined the dementia condition of aged dogs and examined which mechanism(s) is responsible for the condition. A series of studies revealed that the dementia condition in aged dogs is significantly related to the number of apoptotic brain cells including both neurons and glial cells, but not to the number of senile plaques. On the other hand, 5-azacytidine (5AzC) is a cytidine analogue, and is thought to induce kinds of cell differentiation possibly through hypomethylation of genomic DNA. We have revealed neuronal apoptosis induced in 5AzC-treated fetal mice and PC12 cells. The ribosomal protein L4 (rpL4) gene is expressed prior to the apoptosis in the PC12 cell system. Therefore, the involvement of the rpL4 gene expression in age-related brain cell apoptosis in dogs may contribute to the investigation of Alzheimer's dementia.