• Interdisciplinary Bio Central
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• v.4 no.3
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• pp.6.1-6.12
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• 2012

Parkinson's disease (PD) is a complicated neurodegenerative disorder although it is oftentimes defined by clinical motor symptoms originated from age dependent and progressive loss of dopaminergic neurons in the midbrain. The pathogenesis of PD involves dopaminergic and nondopaminergic neurons in many brain regions and the molecular mechanisms underlying the death of different cell types still remain to be elucidated. There are indications that PD causing disease processes occur in a global scale ranging from DNA to RNA, and proteins. Several PD-associated genes have been reported to play diverse roles in controlling cellular functions in different levels, such as chromatin structure, transcription, processing of mRNA, translational modulation, and posttranslational modification of proteins. The advent of quantitative high throughput screening (HTS) tools makes it possible to monitor systemic changes in DNA, RNA and proteins in PD models. Combined with dopamine neuron isolation or derivation of dopamine neurons from PD patient specific induced pluripotent stem cells (PD iPSCs), HTS techonologies will provide opportunities to draw PD causing sequences of molecular events in pathologically relevant PD samples. Here I discuss previous studies that identified molecular functions in which PD genes are involved, especially those signaling pathways that can be efficiently studied using HTS methodologies. Brief descriptions of quantitative and systemic tools looking at DNA, RNA and proteins will be followed. Finally, I will emphasize the use and potential benefits of PD iPSCs-derived dopaminergic neurons to screen signaling pathways that are initiated by PD linked gene mutations and thus causative for dopaminergic neurodegneration in PD.

• The Korea Journal of Herbology
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• v.28 no.5
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• pp.21-28
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• 2013

Objectives : The aim of this study was to investigate the neuroprotective effects and mechanisms of Cyperi Rhizoma extracts (CRE) using in vitro and in vivo models of Parkinson's disease (PD). Methods : We evaluated the neuroprotective effect of CRE against 1-methyl-4-phenylpyridinium (MPP+) toxicity using tyrosine hydroxylase immunohistochemistry (IHC) in primary rat mesencephalic dopaminergic neurons. In addition, the effect of CRE was evaluated in mice PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). For evaluations, C57bl/6 mice were orally treated with CRE 50 mg/kg for 5 days and were injected intraperitoneally with MPTP (20 mg/kg) at 2 h intervals on the last day. To identify the CRE affects on MPTP-induced neuronal loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) and striatum of mice, the behavioral tests and IHC analysis were carried out. Also, we conducted nitric oxide (NO) and tumor necrosis factor-alpha (TNF-${\alpha}$) assay in dopaminergic neurons and IHC using glial markers in SNpc of mice to assess the anti-inflammation effects. Results : In primary mesencephalic culture system, CRE protected dopaminergic cells against $10{\mu}M$ MPP+-induced toxicity at 0.2 and $1.0{\mu}g/mL$. In the behavior tests, CRE treated group showed improved motor deteriorations than those in the MPTP only treated group. CRE significantly protected striatal dopaminergic damage from MPTP-induced neurotoxicity in mice. Moreover, CRE inhibited productions of NO and TNF-${\alpha}$ in dopaminergic culture system and activation of astrocyte and microglia in SNpc of the mice. Conclusion : We concluded that CRE shows anti-parkinsonian effect by protecting dopaminergic neurons against MPP+/MPTP toxicities through anti-inflammatory actions.

• The Transactions of the Korean Institute of Electrical Engineers D
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• v.55 no.4
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• pp.154-157
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• 2006

This paper is proposed hybrid artificial intelligent(HAI) controller for high performance of induction motor drive. The design..of this algorithm based on fuzzy-neural network(FNN) controller that is implemented using fuzzy control and neural network. This controller uses fuzzy rule as training patterns of a neural network. Also, this controller uses the back-propagation method to adjust the weights between the neurons of neural network in order to minimize the error between the command output and actual output. A model reference adaptive scheme is proposed in which the adaptation mechanism is executed by fuzzy logic based on the error and change of error measured between the motor speed and output of a reference model. The control performance of the adaptive FNN controller is evaluated by analysis for various operating conditions. The results of experiment prove that the proposed control system has strong high performance and robustness to parameter variation, and steady-state accuracy and transient response.

• 전자공학회논문지 IE
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• v.47 no.3
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• pp.26-34
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• 2010

In this study, a neuro-fuzzy controller based on the characteristics of fuzzy controlling and structure of artificial neural networks(ANN). This neuro-fuzzy controller has each advantage from fuzzy and ANN, respectively. Plus, it can handle their own shortcomings and parameters in the controller can be tuned by on-line. To verify the proposed controller, it has applied to the AC servo motor which is popular item in robot control field. General PID and fuzzy controller are also applied to the same motor so stability and good characteristic of the proposed controller are compared and proved. Especially, the experiment for variable load is investigated and performance result is proved also.

• PNF and Movement
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• v.7 no.1
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• pp.33-46
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• 2009

Purpose : N.A.P.(Neuromuscular Skeletal Plasticity) an integrative neuro-orthopedic concept to facilitate motor strategies in daily life. The primary thesis is, that treatment of body functions and structural impairments should be integrated within goal-oriented activities. The purpose of this article is to demonstrate that the functional activity itself, determines the structure. Material and Methods : A case report of a dentist with brachial plexus lesion after a motor vehicle accident is presented. The necessity for training body functions within relevant tasks is undermined by references which emphasize the importance of training realistic activities to enhance long-term changes in neural representation. Results : The treatment methods presented in this case show significant effects for the patient's ability to participate in his profession within less than a year's time after his motor vehicle accident. Conclusions : Current evidence supports the treatment methods of this concept. The inability to flex his elbow and supinate his forearm placed a considerable doubt to his ability to ever be able to participate in his profession again. Structural reorganization is possible and depends on functional demands, which need to be trained task-specifically. Single case reports may serve as the basis for further randomized controlled studies to support the efficacy of the treatment methods within the N.A.P. concept.

• Journal of Yeungnam Medical Science
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• v.39 no.3
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• pp.181-189
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• 2022

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative condition characterized by loss of motor neurons, resulting in motor weakness of the limbs and/or bulbar muscles. Pain is a prevalent but neglected symptom of ALS, and it has a significant negative impact on the quality of life of patients and their caregivers. This review outlines the epidemiology, clinical characteristics, underlying mechanisms, and management strategies of pain in ALS to improve clinical practice and patient outcomes related to pain. Pain is a prevalent symptom among patients with ALS, with a variable reported prevalence. It may occur at any stage of the disease and can involve any part of the body without a specific pattern. Primary pain includes neuropathic pain and pain from spasticity or cramps, while secondary pain is mainly nociceptive, occurring with the progression of muscle weakness and atrophy, prolonged immobility causing degenerative changes in joints and connective tissue, and long-term home mechanical ventilation. Prior to treatment, the exact patterns and causes of pain must first be identified, and the treatment should be tailored to each patient. Treatment options can be classified into pharmacological treatments, including nonsteroidal anti-inflammatory drugs, antiepileptic drugs, drugs for cramps or spasticity, and opioid; and nonpharmacological treatments, including positioning, splints, joint injections, and physical therapy. The development of standardized and specific assessment tools for pain-specific to ALS is required, as are further studies on treatments to reduce pain, diminish suffering, and improve the quality of life of patients with ALS.

• Molecules and Cells
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• v.43 no.3
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• pp.228-235
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• 2020

The Drosophila transmembrane semaphorin Sema-1a mediates forward and reverse signaling that plays an essential role in motor and central nervous system (CNS) axon pathfinding during embryonic neural development. Previous immunohistochemical analysis revealed that Sema-1a is expressed on most commissural and longitudinal axons in the CNS and five motor nerve branches in the peripheral nervous system (PNS). However, Sema-1a-mediated axon guidance function contributes significantly to both intersegmental nerve b (ISNb) and segmental nerve a (SNa), and slightly to ISNd and SNc, but not to ISN motor axon pathfinding. Here, we uncover three cis-regulatory elements (CREs), R34A03, R32H10, and R33F06, that robustly drove reporter expression in a large subset of neurons in the CNS. In the transgenic lines R34A03 and R32H10 reporter expression was consistently observed on both ISNb and SNa nerve branches, whereas in the line R33F06 reporter expression was irregularly detected on ISNb or SNa nerve branches in small subsets of abdominal hemisegments. Through complementation test with a Sema-1a loss-of-function allele, we found that neuronal expression of Sema-1a driven by each of R34A03 and R32H10 restores robustly the CNS and PNS motor axon guidance defects observed in Sema-1a homozygous mutants. However, when wild-type Sema-1a is expressed by R33F06 in Sema-1a mutants, the Sema-1a PNS axon guidance phenotypes are partially rescued while the Sema-1a CNS axon guidance defects are completely rescued. These results suggest that in a redundant manner, the CREs, R34A03, R32H10, and R33F06 govern the Sema-1a expression required for the axon guidance function of Sema-1a during embryonic neural development.

• Proceedings of the KIEE Conference
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• 2004.11c
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• pp.450-452
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• 2004

Every movement, perception and thought we perform is associated with distinct neural activation patterns. Neurons in the brain communicate with each other by sending electrical impulses that produce currents. These currents give rise to electrical fields that can be measured outside the head. It shows some variation on the electroencephalographic signals. In recent devices, the EEG signals measured from head surface are a sum of all the momentary brain activation. With these EEG signals, it is difficult to distinguish the patterns correlated with a certain event from the signals. However, the system must discriminate some patterns with some events especially for any kind of device as a brain control interface system. In this experiment, the sensory-motor cortex of humans has been extensively studied. Activation related to several movements on both sides of the sensory-motor cortices in imaginary. The activation patterns during imagination of several movements resemble the activation patterns during preparation of movements. The result represents the system based on the optimal filters discriminated at least 60% of mental imageries.

• Annals of Clinical Neurophysiology
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• v.6 no.1
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• pp.1-13
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• 2004

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that primarily affects motor neurons. The characteristic features of this devastating disorder are the simultaneous presence of upper and lower motor neuron (LMN) signs with progression from one region of the neuraxis to the next and eventual death, typically from respiratory compromise. Electrophysiological studies are an indispensible part of the ALS evaluation, especially serving as an extension of the clinical examination, and most useful in identifying LMN dysfunction. Not only may electrodiagnostic studies reveal characteristic changes in those regions clinically manifesting signs, but it also serves to disclose asymptomatic areas of involvement.

• BMB Reports
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• v.29 no.2
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• pp.151-155
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• 1996

To swimming motor neurons (SMNs) of Polyorchis penicillatus, a hydrozoan medusae, dopamine (DA) acts as an inhibitory neurotransmitter by hyperpolarizing its membrane potential and decreasing its firing rate as well. Such an inhibitory action of DA is caused by an increased permeability to potassium (K) ions. To investigate whether voltage-gated K channels are directly responsible for the membrane hyperpolarization induced by DA, we employed whole-cell voltage clamp configuration. One ${\mu}M$ DA applied to SMNs increased the peak and rear values of voltage-gated K currents by 37 and 54%, respectively, in a reversible manner. Combined with subtraction analysis, this result suggests that the outflux of K ions by DA in SMNs occurs mainly through rectifier-like K channels.