• Journal of Biomedical Engineering Research
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• v.27 no.2
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• pp.64-72
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• 2006

The present study introduces a new cortical patch-based source model for EEG/MEG cortical source imaging to consider anatomical constraints more precisely. Conventional source models for EEG/MEG cortical source imaging have used coarse cortical surface mesh or sampled small number of vertices from fine surface mesh, and thus they failed to utilize full anatomical information which nowadays we can get with sub-millimeter modeling accuracy. Conventional ones placed a single dipolar source on each cortical patch and estimated its intensity by means of various inverse algorithms; whereas the suggested cortical patch-based model integrates whole cortical area to construct lead field matrix and estimates current density that is assumed to be constant in each cortical patch. We applied the proposed and conventional models to realistic EEG data and compared the results quantitatively. The quantitative comparisons showed that the proposed model can provide more precise spatial descriptions of neuronal source distribution.

• Journal of applied mathematics & informatics
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• v.29 no.1_2
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• pp.427-442
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• 2011

Calcium is a vital second messenger for signal transduction in neurons. Calcium plays an important role in almost every part of the human body but in neuronal cytosol, it is of utmost importance. In order to understand the calcium signaling mechanism in a better way a finite element model has been developed to study the flow of calcium in two dimensions with time. This model assumes EBA (Excess Buffering Approximation), incorporating all the important parameters like time, association rate, influx, buffer concentration, diffusion constant etc. Finite element method is used to obtain calcium concentration in two dimensions and numerical integration is used to compute effect of time over 2-D Calcium profile. Comparative study of calcium signaling in two dimensions with time is done with other important physiological parameters. A MATLAB program has been developed for the entire problem and simulated on an x64 machine to compute the numerical results.

• Honam Mathematical Journal
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• v.44 no.3
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• pp.402-418
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• 2022

Noise is a fundamental factor to increased validity and regularity of spike propagation and neuronal firing in the nervous system. In this paper, we examine the stochastic version of the Izhikevich-FitzHugh neuron dynamical model. This approach is based on techniques presented by Luo and Guo, which provide a general framework for the bifurcation and stability analysis of two dimensional stochastic dynamical system as an Itô averaging diffusion system. By using largest lyapunov exponent, local and global stability of the stochastic system at the equilibrium point are investigated. We focus on the two kinds of stochastic bifurcations: the P-bifurcation and the D-bifurcations. By use of polar coordinate, Taylor expansion and stochastic averaging method, it is shown that there exists choices of diffusion and drift parameters such that these bifurcations occurs. Finally, numerical simulations in various viewpoints, including phase portrait, evolution in time and probability density, are presented to show the effects of the diffusion and drift coefficients that illustrate our theoretical results.

• International Journal of Computer Science & Network Security
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• v.23 no.7
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• pp.71-78
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• 2023

Employee turnover is one of the most important challenges facing modern organizations. It causes job experiences and skills such as distinguished faculty members in universities, rare-specialized doctors, innovative engineers, and senior administrators. HR analytics has enhanced the area of data analytics to an extent that institutions can figure out their employees' characteristics; where inaccuracy leads to incorrect decision making. This paper aims to develop a novel model that can help decision-makers to classify the problem of Employee Turnover. By using feature selection methods: Information Gain and Chi-Square, the most important four features have been extracted from the dataset. These features are over time, job level, salary, and years in the organization. As one of the important results of this research, these features should be planned carefully to keep organizations their employees as valuable assets. The proposed model based on machine learning algorithms. Classification algorithms were used to implement the model such as Decision Tree, SVM, Random Frost, Neuronal Network, and Naive Bayes. The model was trained and tested by using a dataset that consists of 1470 records and 25 features. To develop the research model, many experiments had been conducted to find the best one. Based on implementation results, the Neural Network algorithm is selected as the best one with an Accuracy of 84 percents and AUC (ROC) 74 percents. By validation mechanism, the model is acceptable and reliable to help origination decision-makers to manage their employees in a good manner.

• Korean Journal of Acupuncture
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• v.29 no.3
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• pp.396-405
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• 2012

Objectives : To confirm whether acupuncture can suppress the degree of seizure and the activation of astrocytes in hippocampi using kainic acid(KA)-induced epilepsy mouse model. Methods : 8 weeks C57BL/6 mice(20~25 g) were given acupuncture once a day at acupoint HT8(Shaofu) bilaterally during 2 days before KA injection. After an intraperitoneal injection of 30 mg/kg KA, acupuncture treatment was subsequently administered once more(total 3 times), and the degree of seizure was observed for 120 min. The neuronal cell death, pERK expression, and astrocyte activation confirmed 1 hour and 24 hours after KA injection. Results : Acupuncture treatment at HT8 suppressed KA-induced epileptic seizure. One hour after KA injection, the pERK expression was increased, which was reduced by the acupuncture treatment. Twenty four hours after injection, the treatment decreased the KA-induced neuronal cell death, the interleukin-$1{\beta}$ expression and the astrocyte activation in the CA3 region of the mouse hippocampus. Conclusions : Acupuncture treatment at HT8 decreases the KA-induced epileptic seizure, the neural cell inflammation and death.

• Journal of Korean Neurosurgical Society
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• v.63 no.2
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• pp.163-170
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• 2020

Objective : Milk fat globule-epidermal growth factor VIII (MFG-E8) may play a key role in inflammatory responses and has the potential to function as a neuroprotective agent for ameliorating brain injury in cerebral infarction. This study aimed to determine the role of MFG-E8 in brain injury in the subacute phase of cerebral ischemia in a rat model. Methods : Focal cerebral ischemia was induced in rats by occluding the middle cerebral artery with the modified intraluminal filament technique. Twenty-four hours after ischemia induction, rats were randomly assigned to two groups and treated with either recombinant human MFG-E8 or saline. Functional outcomes were assessed using the modified Neurological Severity Score (mNSS), and infarct volumes were evaluated using histology. Anti-inflammation, angiogenesis, and neurogenesis were assessed using immunohistochemistry with antibodies against ionized calcium-binding adapter molecule 1 (Iba-1), rat endothelial cell antigen-1 (RECA-1), and bromodeoxyuridine (BrdU)/doublecortin (DCX), respectively. Results : Our results showed that intravenous MFG-E8 treatment did not reduce the infarct volume; however, the mNSS test revealed that neurobehavioral deficits were significantly improved in the MFG-E8-treated group than in the vehicle group. Immunofluorescence staining revealed a significantly lower number of Iba-1-positive cells and higher number of RECA-1 in the periinfarcted brain region, and significantly higher numbers of BrdU- and DCX-positive cells in the subventricular zone in the MFG-E8-treated group than in the vehicle group. Conclusion : Our findings suggest that MFG-E8 improves neurological function by suppressing inflammation and enhancing angiogenesis and neuronal proliferation in the subacute phase of cerebral infarction.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.197-205
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• 2006

Objectives: Anti-oxidants are known to prevent neuronal diseases with pathological and physiological changes such as the brain atrophy and cognitive impairment. This study was designed to investigate the protective effects of Korean ginseng on the oxidative stress induced pathologic changes, and develop new animal model for the brain atrophy. Korean ginseng has anti-oxidant, anti-aging, and protective effects on the brain ischemia. Methods : The intracerebroventricular (ICV) hydrogen peroxide ($H_2O_2$) injection into mice was conducted to generate oxidative stress. Results : The ICV $H_2O_2$ (1 M, $5\;{\mu}l$ injection did not induce either convulsion or death in the acute phase. At the end of second week, cognitive impairment and pathologic change of the brain were observed. The massive brain atrophy was found in the $H_2O_2-injected$ mice, especially in the hippocampus and thalamus. Treatment with Korean ginseng showed a protective effect against the brain atrophy. The $H_2O_2$ injected mice revealed cognitive impairment in the passive avoidance test, and Korean ginseng alleviated cognitive impairment. Conclusion : The results indicate that Korean ginseng has a protective effect on the oxidative stress-induced neuronal damages.

• Biomolecules & Therapeutics
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• v.29 no.1
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• pp.83-89
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• 2021

Multiple system atrophy (MSA) is a neurodegenerative disease characterized by presence of α-synuclein-positive inclusions in the cytoplasm of oligodendrocytes. These glial cytoplasmic inclusions (GCIs) are considered an integral part of the pathogenesis of MSA, leading to demyelination and neuronal demise. What is most puzzling in the research fields of GCIs is the origin of α-synuclein aggregates in GCIs, since adult oligodendrocytes do not express high levels of α-synuclein. The most recent leading hypothesis is that GCIs form via transfer and accumulation of α-synuclein from neurons to oligodendrocytes. However, studies regarding this subject are limited due to the absence of proper human cell models, to demonstrate the entry and accumulation of neuronal α-synuclein in human oligodendrocytes. Here, we generated mature human oligodendrocytes that can take up neuronderived α-synuclein and form GCI-like inclusions. Mature human oligodendrocytes are derived from neural stem cells via "oligosphere" formation and then into oligodendrocytes, treating the cells with the proper differentiation factors at each step. In the final cell preparations, oligodendrocytes consist of the majority population, while some astrocytes and unidentified stem cell-like cells were present as well. When these cells were exposed to α-synuclein proteins secreted from neuron-like human neuroblastoma cells, oligodendrocytes developed perinuclear inclusion bodies with α-synuclein immunoreactivity, resembling GCIs, while the stem cell-like cells showed α-synuclein-positive, scattered puncta in the cytoplasm. In conclusion, we have established a human oligodendrocyte model for the study of GCI formation, and the characterization and use of this model might pave the way for understanding the pathogenesis of MSA.

• Journal of Ginseng Research
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• v.46 no.4
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• pp.572-584
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• 2022

Background: Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion of trinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HD involve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinase ataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM is involved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays a critical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expanded mutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effective component of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HD remains unclear and warrants further investigation. Methods: This study used the R6/2 transgenic mouse model of HD and performed behavioral tests, survival rate, histological analyses, and immunoblot assays. Results: The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK and reduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density and lifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2 protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions: Thus, the oral administration of CK reduced the disease progression and markedly enhanced lifespan in the transgenic mouse model (R6/2) of HD.

• Biomolecules & Therapeutics
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• v.29 no.3
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• pp.295-302
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• 2021

Microglial priming is the process of microglial proliferation and activation in response to neurodegeneration and abnormal protein accumulation. Priming makes microglia susceptible to secondary inflammatory stimuli and causes exaggerated inflammatory responses. In the present study, we established a microglial priming model in mice by administering a single injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg). MPTP induced microglial activation without dopaminergic degeneration; however, subsequent treatment with a sub-toxic dose of lipopolysaccharides (LPS) induced an amplified inflammatory response and caused nigrostriatal dopaminergic degeneration. These pathological and inflammatory changes, including microglial activation and dopaminergic cell loss in the substantia nigra (SN) area were reversed by papaverine (PAP) administration. In addition, MPTP/LPS enhanced interleukin-1β (IL-1β) expression and processing via nod-like receptor protein 3 (NLRP3) inflammasome activation in the SN region of mice. However, PAP treatment suppressed inflammasome activation and subsequent IL-1β maturation. Moreover, PAP inhibited nuclear factor-κB (NF-κB) and enhanced cAMP-response element binding protein (CREB) activity in the SN of MPTP/LPS mice. These results suggest that PAP inhibits the activation of NLRP3 inflammasome by modulating NF-κB and CREB signaling pathways, which results in reduced microglial activation and neuronal cell death. Thus, PAP may be a potential candidate for the treatment of Parkinsons's disease, which is aggravated by systemic inflammation.