• 대한핵의학회:학술대회논문집
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• 2004.11a
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• pp.395.1-395.1
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• 2004

• The Korean Journal of Nuclear Medicine
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• v.38 no.5
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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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• v.35 no.2
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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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• v.22 no.2
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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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• v.17 no.12
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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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• v.65 no.2
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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.

• Korean Journal of Psychosomatic Medicine
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• v.15 no.2
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• pp.73-80
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• 2007

Anumber of prior studies have reported eye movement dysfunction in patients with dementia. The eye movement test which is non-invasive can evaluate the local brain function quantitatively. Therefore, it can be a useful method for characterizing regional brain abnormalities of patients with dementia. The aim of this paper is to review the literatures on eye movement abnormalities in dementia patients. Saccade system dysfunctions in Alzheimer disease include increased latency, reduced accuracy, and increased antisaccade error rates. Patients with frontotemporal dementia showed impaired reflexive saccade inhibition and increased latency and errors of antisaccade task. And delayed initiation of voluntary saccades, slow saccades, and increased errors and latency on antisaccade task were found in Huntington's disease. Patients with Parkinson’s disease dementia and dementia with Lewy bodies have characteristics of impaired in both reflexive saccade execution and complex saccade performance. However, there were few reports of abnormal eye movements in Creutzfeldt-Jakob disease; they could be found at the later stages after symptoms of dementia came to be evident, and secondary to cerebellar and vestibular involvement. Slowing of saccades and hypometric saccades might precede the supranuclear limitation of vertical gaze in PSP. Dysfunction of voluntary eyelid movements was a characteristic finding of PSP as well. In conclusion, patients with dementia can show various abnormal eye movements and they are related with cortial and subcortical brain dysfunctions. The research on localization of brain relevant to each symptom can promise more clinical implications of eye movement of dementia.