• 대한핵의학회:학술대회논문집
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• 대한핵의학회 2004년도 추계학술대회 및 총회
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• pp.395.1-395.1
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• 2004

• 대한핵의학회지
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• 제38권5호
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• pp.331-337
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• 2004

Cardiac neurotransmission imaging allows in vivo assessment of presynaptic reuptake, neurotransmitter storage and postsynaptic receptors. Among the various neurotransmitter, I-123 MIBG is most available and relatively well-established. Metaiodobenzylguanidine (MIBG) is an analogue of the false neurotransmitter guanethidine. It is taken up to adrenergic neurons by uptake-1 mechanism as same as norepinephrine. As tagged with I-123, it can be used to image sympathetic function in various organs including heart with planar or SPECT techniques. I-123 MIBG imaging has a unique advantage to evaluate myocardial neuronal activity in which the heart has no significant structural abnormality or even no functional derangement measured with other conventional examination. In patients with cardiomyopathy and heart failure, this imaging has most sensitive technique to predict prognosis and treatment response of betablocker or ACE inhibitor. In diabetic patients, it allow very early detection of autonomic neuropathy. In patients with dangerous arrhythmia such as ventricular tachycardia or fibrillation, MIBG imaging may be only an abnormal result among various exams. In patients with ischemic heart disease, sympathetic derangement may be used as the method of risk stratification. In heart transplanted patients, sympathetic reinnervation is well evaluated. Adriamycin-induced cardiotoxicity is detected earlier than ventricular dysfunction with sympathetic dysfunction. Neurodegenerative disorder such as Parkinson's disease or dementia with Lewy bodies has also cardiac sympathetic dysfunction. Noninvasive assessment of cardiac sympathetic nerve activity with I-123 MIBG imaging nay be improve understanding of the pathophysiology of cardiac disease and make a contribution to predict survival and therapy efficacy.

• Bulletin of the Korean Chemical Society
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• 제35권2호
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• pp.425-430
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• 2014

Amyloidogenic proteins often exhibit fibrillar polymorphism through alternative assembly processes, which has been considered to have possible pathological implications. Here, firefly luciferase (LUC) is shown to induce amyloid polymorphism of ${\alpha}$-synuclein, the major constituent of Lewy bodies found in Parkinson's disease, by acting as a novel template. The drastically accelerated fibrillation kinetics of ${\alpha}$-synuclein with LUC required the nucleation center produced by the active enzyme of LUC. Fluorescent dye binding, transmission electron microscopy, and Fourier transformed infrared spectroscopy revealed the morphologically distinctive amyloid fibrils of ${\alpha}$-synuclein prepared in the absence or presence of LUC. As the altered morphological characteristics became inherent to the mature fibrils, those properties were inherited to next-generations via nucleation-dependent fibrillation process. The seed control, therefore, would be an effective means to modify amyloid fibrils with different biochemical characteristics. In addition, the LUC-directed amyloid fibrillar polymorphism also suggests that other cellular biomolecules including enzymes in general are able to diversify amyloid fibrils, which could be self-propagated with diversified biological activities, if any, inside cells.

• Annals of Clinical Neurophysiology
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• 제22권2호
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• pp.82-91
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• 2020

Electroencephalography (EEG) produces time-series data of neural oscillations in the brain, and is one of the most commonly used methods for investigating both normal brain functions and brain disorders. Quantitative EEG analysis enables identification of frequencies and brain activity that are activated or impaired. With studies on the structural and functional networks of the brain, the concept of the brain as a complex network has been fundamental to understand normal brain functions and the pathophysiology of various neurological disorders. Functional connectivity is a measure of neural synchrony in the brain network that refers to the statistical interdependency between neural oscillations over time. In this review, we first discuss the basic methods of EEG analysis, including preprocessing, spectral analysis, and functional-connectivity and graph-theory measures. We then review previous EEG studies of brain network characterization in several neurological disorders, including epilepsy, Alzheimer's disease, dementia with Lewy bodies, and idiopathic rapid eye movement sleep behavior disorder. Identifying the EEG-based network characteristics might improve the understanding of disease processes and aid the development of novel therapeutic approaches for various neurological disorders.

• Journal of Microbiology and Biotechnology
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• 제17권12호
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• pp.2027-2032
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• 2007

[ ${\alpha}$ ]-Synuclein is the major component of Lewy bodies and responsible for the amyloid deposits observed in Parkinson's disease. Ordered filamentous aggregate formation of the natively unfolded ${\alpha}$-synuclein was investigated in vitro with the periodic ultrasonication. The ultrasonication induced the fibrillation of ${\alpha}$-synuclein, as the random structure gradually converted into a ${\beta}$-sheet structure. The resulting fibrils obtained at the stationary phase appeared heterogeneous in their size distribution, with the average length and height of $0.28\;{\mu}m{\pm}0.21\;{\mu}m$ and $5.6\;nm{\pm}1.9\;nm$, respectively. After additional extensive ultrasonication in the absence of monomeric ${\alpha}$-synuclein, the equilibrium between the fibril formation and its breakdown shifted to the disintegration of the preexisting fibrils. The resulting fragments served as nucleation centers for the subsequent seed-dependent accelerated fibrillation under a quiescent incubation condition. This self-seeding amplification process depended on the seed formation and subsequent alterations in their properties by the ultrasonication to a state that accretes the monomeric soluble protein more effectively than their reassociation of the seeds back to the original fibrils. Since many neurodegenerative disorders have been considered to be propagated via the seed-dependent amyloidosis, this study would provide a novel aspect of the significance of the seed structure and its properties leading to the acce]erated amyloid formation.

• Journal of Korean Neurosurgical Society
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• 제65권2호
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• pp.236-244
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• 2022

Objective : To evaluate the interactions among differentially expressed autophagy and mitophagy markers in subarachnoid hemorrhage (SAH) patients with delayed cerebral ischemia (DCI). Methods : The expression data of autophagy and mitophagy-related makers in the cerebrospinal fluid (CSF) cells was analyzed by real-time reverse transcription-polymerase chain reaction and Western blotting. The markers included death-associated protein kinase (DAPK)-1, BCL2 interacting protein 3 like (BNIP3L), Bcl-1 antagonist X, phosphatase and tensin homolog-induced kinase (PINK), Unc-51 like autophagy activating kinase 1, nuclear dot protein 52, and p62. In silico functional analyses including gene ontology enrichment and the protein-protein interaction network were performed. Results : A total of 56 SAH patients were included and 22 (38.6%) of them experienced DCI. The DCI patients had significantly increased mRNA levels of DAPK1, BNIP3L, and PINK1, and increased expression of BECN1 compared to the non-DCI patients. The most enriched biological process was the positive regulation of autophagy, followed by the response to mitochondrial depolarization. The molecular functions ubiquitin-like protein ligase binding and ubiquitin-protein ligase binding were enriched. In the cluster of cellular components, Lewy bodies and the phagophore assembly site were enriched. BECN1 was the most connected gene among the differentially expressed markers related to autophagy and mitophagy in the development of DCI. Conclusion : Our study may provide novel insight into mitochondrial dysfunction in DCI pathogenesis.

• 정신신체의학
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• 제15권2호
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• pp.73-80
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• 2007

지난 여러 해 동안 치매에서 나타나는 안구운동기능부전에 대해 수많은 논문이 발표되었다. 안구운동검사는 뇌의 기능을 평가하는 비침습적인 검사이며, 치매와 연관된 뇌의 이상을 밝혀내는데 유용한 방법이다. 저자는 치매와 연관된 안구운동이상에 대한 지금까지의 여러 연구들을 고찰해 보았다. 알쯔하이머병에서는 신속안구운동의 잠재기가 증가하고 정확도가 감소하며 항신속안구운동의 오류가 증가 한다. 전측두엽 치매 환자에서는 반사성 신속안구운동 억제의 장애와 항신속안구운동 잠재기와 오류 증가 소견이 나타난다. 그리고 헌팅톤병에서는 수의적인 신속안구운동의 시작 지연, 느린 신속안구운동, 항신속안구운동의 오류와 잠재기 증가 소견이 나타난다. 파킨슨병 치매와 루이체 치매 환자에서는 반사성 신속안구운동과 복합성 신속안구운동 실행 장애가 보고되었다. 크로이츠펠트-야콥 병에 관한 연구는 많지 않으며, 안구운동장애는 치매 증상이 명확해진 이후인 질병의 말기에 나타나고, 이차적으로 소뇌와 전정기관을 침범하게 된다고 한다. 진행성 핵상마비에서는 느린 신속안구운동과 측정저하 신속안구운동이 수직방향주시 장애가 오기 이전에 나타나는 경우가 많다. 수의적인 눈꺼풀 운동의 기능부전도 진행성 핵상마비의 특징적인 증상이다. 결론적으로 치매 환자들은 다양한 비정상적인 안구운동장애를 나타내며 이는 피질, 피질하 기능부전과 연관되어 있다. 치매 환자의 안구운동장애에 대한 다음 단계 연구는 치매에서 나타나는 임상적인 증상이 뇌의 어떤 부위 이상 때문에 발생하는지를 좀 더 명확하게 밝히는 것이 될 것이다.