• Journal of the Korean Society of Tobacco Science
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• v.31 no.1
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• pp.29-38
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• 2009

Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.

• Genomics & Informatics
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• v.12 no.4
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• pp.181-186
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• 2014

Genome-wide association studies have proven the highly polygenic architecture of complex diseases or traits; therefore, single-locus-based methods are usually unable to detect all involved loci, especially when individual loci exert small effects. Moreover, the majority of associated single-nucleotide polymorphisms resides in non-coding regions, making it difficult to understand their phenotypic contribution. In this work, we studied epistatic interactions associated with three common diseases using Korea Association Resource (KARE) data: type 2 diabetes mellitus (DM), hypertension (HT), and coronary artery disease (CAD). We showed that epistatic single-nucleotide polymorphisms (SNPs) were enriched in enhancers, as well as in DNase I footprints (the Encyclopedia of DNA Elements [ENCODE] Project Consortium 2012), which suggested that the disruption of the regulatory regions where transcription factors bind may be involved in the disease mechanism. Accordingly, to identify the genes affected by the SNPs, we employed whole-genome multiple-cell-type enhancer data which discovered using DNase I profiles and Cap Analysis Gene Expression (CAGE). Assigned genes were significantly enriched in known disease associated gene sets, which were explored based on the literature, suggesting that this approach is useful for detecting relevant affected genes. In our knowledge-based epistatic network, the three diseases share many associated genes and are also closely related with each other through many epistatic interactions. These findings elucidate the genetic basis of the close relationship between DM, HT, and CAD.

• Journal of Korea Multimedia Society
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• v.22 no.9
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• pp.1020-1028
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• 2019

Cerebrovascular disease is a common disease in the elderly population. However, we do not have enough understanding of brain-related diseases. Recent advances in microscopy technology have resulted in the acquisition of vast amounts of image data sets for small organs, and it has become possible to handle vast amounts of image data sets due to improved computer performance and software technology. In this paper, the author proposes introduce a method for classifying and analysing only cerebrovascular information in the mouse brain image, as well as a quantitative measure of the portion of the cerebrovascular in the mouse brain. The study of the cerebrovascular structure is significant, and it can be helpful to improve the understanding of cerebrovasculature. As a result, the author expects that this study will be useful for neuroscientists conducting clinical research.

• BMB Reports
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• v.53 no.11
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• pp.551-564
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• 2020

Proper development of the nervous system is critical for its function, and deficits in neural development have been implicated in many brain disorders. A precise and predictable developmental schedule requires highly coordinated gene expression programs that orchestrate the dynamics of the developing brain. Especially, recent discoveries have been showing that various mRNA chemical modifications can affect RNA metabolism including decay, transport, splicing, and translation in cell type- and tissue-specific manner, leading to the emergence of the field of epitranscriptomics. Moreover, accumulating evidences showed that certain types of RNA modifications are predominantly found in the developing brain and their dysregulation disrupts not only the developmental processes, but also neuronal activities, suggesting that epitranscriptomic mechanisms play critical post-transcriptional regulatory roles in development of the brain and etiology of brain disorders. Here, we review recent advances in our understanding of molecular regulation on transcriptome plasticity by RNA modifications in neurodevelopment and how alterations in these RNA regulatory programs lead to human brain disorders.

• The Korean Journal of Health Service Management
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• v.5 no.1
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• pp.159-170
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• 2011

This study aims at providing basic data on brain death by analyzing factors of influencing toward attitude to brain death subject to citizens of Busan City. The data was collected for 47 days from 14 July to 31 August, 2009. Among a total of 2200 cases of the questionaries, only 2042 cases were used. For data analysis, SPSS 17.0 was used, and for the specific analysis method frequency analysis to understand general characteristics of the participants. In addition, examination on T-test and ANOVA analysis were conducted after analyzing the factors for participants' consciousness on brain death, and logistic regression analysis for understanding of relations between participants' will to brain death and general characteristics. The results of this study are summarized as follows; First, attitudes towards brain death according to general characteristics was high in those with will to donate their organs than those without in the attitude factors, namely, death recognition, acceptive, exclusive and religious attitude factors. Second, Significant variables for effects of attitudes towards brain death were gender, patients or their family's chronic or incurable diseases, religion, occupation and death recognition, acceptive, and exclusive attitude factors.

• Biomolecules & Therapeutics
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• v.30 no.1
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• pp.55-63
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• 2022

Oleanolic acid (OA), a natural pentacyclic triterpenoid, has been reported to exert protective effects against several neurological diseases through its anti-oxidative and anti-inflammatory activities. The goal of the present study was to evaluate the therapeutic potential of OA against acute and chronic brain injuries after ischemic stroke using a mouse model of transient middle cerebral artery occlusion (tMCAO, MCAO/reperfusion). OA administration immediately after reperfusion significantly attenuated acute brain injuries including brain infarction, functional neurological deficits, and neuronal apoptosis. Moreover, delayed administration of OA (at 3 h after reperfusion) attenuated brain infarction and improved functional neurological deficits during the acute phase. Such neuroprotective effects were associated with attenuation of microglial activation and lipid peroxidation in the injured brain after the tMCAO challenge. OA also attenuated NLRP3 inflammasome activation in activated microglia during the acute phase. In addition, daily administration of OA for 7 days starting from either immediately after reperfusion or 1 day after reperfusion significantly improved functional neurological deficits and attenuated brain tissue loss up to 21 days after the tMCAO challenge; these findings supported therapeutic effects of OA against ischemic stroke-induced chronic brain injury. Together, these findings showed that OA exerted neuroprotective effects against both acute and chronic brain injuries after tMCAO challenge, suggesting that OA is a potential therapeutic agent to treat ischemic stroke.

• Investigative Magnetic Resonance Imaging
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• v.2 no.1
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• pp.104-112
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• 1998

Purpose : To evaluate the clinical utility of diffusion-weighted imaging by analyzing the signal intersity of lesions in patients with various intracranial diseases. Materials and Methods : difusion-weighted MR imaging was prospectively perormed in randomly selected 70 patients with various intracranial idseases. They consisted of 20 patients with acute infarct, 21 patients with chronic infarct of small vessel disease, 14 patients with primary intracranial tumor, three patients with brain metastasis, five patient with brain abscess, five patients with brain abscess, five patients with cerebral hemorrhage, one patient with neurocysticercosis, and one patient with epidermoid cyst. the diffusion-weighted images were obtained immediately after routine T2-weighted imaging on a 1.5T MR unit using single shot spin echo EPI technique with 6500 ms TR, 107ms TE, $128{\times}128$ matrix, 1 number of excitation, $24{\times}24$ field of view, 5-7 mm slice thickness, 2-3 mm inter-slice gap. The diffusion-gradients (b value of ($1000s{\;}/{\;}textrm{mm}^2$)) were applied along three directions(x, y, z). On visual inspection of diffusion-weighted images, the signal intersity of lesions was arbitrarily graded as one of 5 grades. In quantitative assessment, we measured the signal intensity of all the lesions and the contralateral corresponding normal area using round region of interest(ROI), and then calculated the signal intensity ratio of the lesion to the normal brain parenchyma. Results : On visual inspection, markedly hyperintense signals were seen in all cases of acute infarct, brain abscess, epidermoid cyst, and neurocysticercosis in degenerating stage. In all cases of cerebral hematoma, the very high signal internsity was intermingled with low signal intensity. focal very high signal intersity was also seen in a solid portion of the tumor in a patient. the mean signal intensity ratios of all those lesions to the normal brain parenchyma were above 2.5. Gliosis, solid component of brain tumor, brain metastasis, and vasogenic dedma appeared isointense to the normal brain parenchyma in 71%, 64%, 100%, and 67%, respectively ; the mean signal intensity ratios of those lesions to the normal brain parenchyma ranged 1.15 to 1.28 and there was no significant difference among these(p>0.1). Cystic cerebromalacia and necrotic or cystic portions in tumor were markedly or slightly hypointense, and the mean signal intensity ratios were 0.45 and 0.42, respectively. Conclusion : Very high signal intensity of acute infarct, brain abscess, epidermoid cyst, and cystic neurocysticercosis in degenerating stage on diffusion-weighted images may be helpful in differentiating from other diseases that are hypointense or isointense to the normal brain parenchyma. It may be especially useful differentiation of brain abscess from brain tumor with necrotic or cystic portion.

• The Korean Journal of Applied Statistics
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• v.35 no.1
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• pp.161-175
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• 2022

Oscillatory magnetic fields produced in the brain due to neuronal activity can be measured by the sensor. Magnetoencephalography (MEG) is a non-invasive technique to record such neuronal activity due to excellent temporal and fair amount of spatial resolution, which gives information about the brain's functional activity. Potential utilization of high spatial resolution in MEG is likely to provide information related to in-depth brain functioning and underlying factors responsible for changes in neuronal waves in some diseases under resting state or task state. This review is a comprehensive report to introduce statistical models from MEG data including graphical network modelling. It is also meaningful to note that statisticians should play an important role in the brain science field.

• Molecules and Cells
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• v.45 no.11
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• pp.855-867
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• 2022

For proper function of proteins, their subcellular localization needs to be monitored and regulated in response to the changes in cellular demands. In this regard, dysregulation in the nucleocytoplasmic transport (NCT) of proteins is closely associated with the pathogenesis of various neurodegenerative diseases. However, it remains unclear whether there exists an intrinsic regulatory pathway(s) that controls NCT of proteins either in a commonly shared manner or in a target-selectively different manner. To dissect between these possibilities, in the current study, we investigated the molecular mechanism regulating NCT of truncated ataxin-3 (ATXN3) proteins of which genetic mutation leads to a type of polyglutamine (polyQ) diseases, in comparison with that of TDP-43. In Drosophila dendritic arborization (da) neurons, we observed dynamic changes in the subcellular localization of truncated ATXN3 proteins between the nucleus and the cytosol during development. Moreover, ectopic neuronal toxicity was induced by truncated ATXN3 proteins upon their nuclear accumulation. Consistent with a previous study showing intracellular calcium-dependent NCT of TDP-43, NCT of ATXN3 was also regulated by intracellular calcium level and involves Importin α3 (Imp α3). Interestingly, NCT of ATXN3, but not TDP-43, was primarily mediated by CBP. We further showed that acetyltransferase activity of CBP is important for NCT of ATXN3, which may acetylate Imp α3 to regulate NCT of ATXN3. These findings demonstrate that CBP-dependent acetylation of Imp α3 is crucial for intracellular calcium-dependent NCT of ATXN3 proteins, different from that of TDP-43, in Drosophila neurons.

• Journal of radiological science and technology
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• v.45 no.3
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• pp.225-232
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• 2022

Fine dust threatens human health in various forms, depending on the particle size, such as by causing respiratory, cardiovascular, and brain diseases, after entering the body via the lungs. The aim of this study was to correlate fine dust exposure with changes in brain blood flow in Sprague Dawley rats by using micro-positron emission tomography and elucidate the possibility of developing cerebrovascular diseases caused by fine dust. The subjects were exposured to an average fine dust (particulate matter 2.5) of 206.2 ± 7.74 to ten rats four times a day, twice a day for 90 min. Before the experiment, they were maintained at NPO to the maximize the intake of ¹⁸F-fluorodeoxy glucose(¹⁸F-FDG) and minimize changes in the ¹⁸F-FDG biomass depending on the ambient environment and body temperature of the rats. PET images were acquired in the list mode 40 min after injecting ¹⁸F-FDG 44.4 MBq into the rats tail vein using a micro-PET scanner pre and post exposure to fine dust. We found that the whole brain level of ¹⁸F-FDG standardized uptake value in rats averaged 5.21 ± 0.52 g/mL pre and 4.22 ± 0.48 g/mL post exposure to fine dust, resulting in a statistically significant difference. Fine dust was able to alter brain activity after entering the body via the lungs in various forms depending on the particle size.