• 대한약리학회:학술대회논문집
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• 2006.10a
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• pp.122.1-122.1
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• 2006

• Journal of the Ergonomics Society of Korea
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• v.16 no.2
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• pp.15-27
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• 1997

Brain potential is described using the mesocolumnar activity defined by averaged firings of excitatory and inhibitory neuron of neocortex. Lagrangian is constructed based on SMNI(Statistical Mechanics of Neocortical Interaction) and then Euler Lagrange equation is obtained. Excitatory neuron firing is assumed to be amplitude- modulated dominantly by the sum of two modes of frequency .omega. and 2 .omega. . Time series of this neuron firing is calculated numerically by Euler Lagrangian equation. I .omega. L related to low frequency distribution of power spectrum, I .omega. H hight frequency, and Sd(standard deviation) were introduced for the effective extraction of the dynamic property in the simulated brain potential. The relative behavior of I .omega. L, I .omega. H, and Sd was found by parameters .epsilon. and .gamma. related to nonlinearity and harmonics respectively. Experimental I .omega L, I .omega. H, and Sd were obtained from EEG of human in rest state and of canine in deep sleep state and were compared with theoretical ones.

• Biomolecules & Therapeutics
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• v.14 no.2
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• pp.106-109
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• 2006

Neprilysin (Nep) is known to be important to degrade $A{\beta}$ derived from amyloid precursor protein (APP) by cleavage with $\beta-and\;\gamma$-secretases. In order to determine whether a correspondence between $A{\beta}-42/{\gamma}-secretase$ activity and Nep levels exists in postnatal aging of transgenic mice expressing either neuron-specific enolase (NSE)-controlled human mutant presenilin-2 (hPS2m) or APPsw alone, the levels of Nep expression and $A{\beta}-42/{\gamma}-secretase$ activity were examined age of 5, 12, and 20 months, respectively. The levels of Nep expression in both types of transgenic brains were decreased relative to those of control mice in a aging-related manner, while the level of $A{\beta}-42/{\gamma}-secretase$ activity was reversibly increased. Thus, changes in $A{\beta}-42$ may all reflect variation in amounts of Nep enzyme.

• PNF and Movement
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• v.1 no.1
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• pp.19-25
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• 2003

Objectives: The purpose of this article is to summarize the effect of stretch stimulus on muscle contraction facilitation. Methods : Some studies of the stretch reflex. ${\gamma}-motor$ system, and the effect of stretch stimulus on muscle activation were reviewed. Results : To facilitate muscle contraction, before the movement is started, the prime mover is in stretched position. The patient must be instructed to occur voluntary muscle contraction after quick stretching. It elicits the functional stretch reflex to produce a more powerful and functional contraction. The intensity of muscle contraction depends on two ways. One is firing rate of ${\alpha}-motor$ neuron by sensory information from the periphery induced in stretched position and stretch reflex. The other is excitation level of the cortical motor area and the corresponding motor neurons. Conclusions: To activate central nervous system and to increase firing rate of ${\alpha}-motor$ neuron. the therapist should apply quick stretch for the patient with stretched position and the patient should make voluntary muscle contraction.

• Journal of the Institute of Convergence Signal Processing
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• v.9 no.3
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• pp.238-244
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• 2008

Dynamic neural networks have been applied to diverse fields requiring temporal signal processing. This paper presents gamma neural network(GAM) to improve the dynamics of multilayer network. The GAM network uses the gamma memory kernel in the hidden layer of feedforword multilayer network. The GAM network is evaluated in linear and nonlinear system identification, and compared with feedforword(FNN) and recurrent neural networks(RNN) for the relative comparison of its performance. Experimental results show that the GAM network performs better with respect to the convergence and accuracy, indicating that it can be a more effective network than conventional multilayer networks in system identification.

• Nuclear Engineering and Technology
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• v.21 no.2
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• pp.63-72
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• 1989

An analysis for the gamma radiation fields in the research reactor MAPLE-X10 facility has been peformed under the assumption of partial loss of reactor and service pool water to assess the safety from the view point of design. Four photon source terms considered in the analysis were calculated using the ORIGEN-S code. Gamma dose rate calculations over the reactor and service pools during the water-loss accident conditions were performed using QAD-CG code. MCNP code (Monte Carlo Neuron and Photon Transport code), also, was used to assess the scattered radiation fields away from the pools, which is appropriate for calculating the scattered photon dose rates outside of the solid angle subtended by the source and pool walls.

• Proceedings of the ESK Conference
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• 1997.04a
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• pp.165-175
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• 1997

Brain potential is described by using Euler Lagrange equation derived from Lagrangian based on SMNI(Statistical Mechanics of Neocortical Interaction). It is assumed that excitatory neuron firing is amplitude-modulated dominantly by the sum of two modes of frequency ${\omega}and 2 {\omega}$ . Time series of this neuron firing is numerically calculated. $I_{L}$related to low frequency distribution of power spectrum, $I_{H}$high frequency, and S(standard deviation) are introduced for the effective extraction of the dynamic property in this simulated brain potential. $I_{L}$,$I_{H}$, and S are obtained from EEG of 4 persons in rest state and are compared with thoretical results. It is of importance in various fields related to human well-being such as comfort-pursued industrial design, psychology, medicine to characterize human emotional states by EEG analysis. The pleasant and unpleasant sensation among various emotional states would be demonstrated to be determined in terms of ${\epsilon}$ and ${\gamma}$ parameters estimated by the simulated $I_{L}$-$I_{H}$-S relations.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.12 no.2
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• pp.126-132
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• 2001

Background and Objectives : Signal traduction through phospholipase C(PLC) participate in the regulation of cell growth and differentiation. Growth factors bind to their receptors and thereby induce tyrosine phophorylation of the phospholipase C-${\gamma}$1(PLC-${\gamma}$1). PLC-${\gamma}$1 is a substrate for several receptor tyrosine kinases and its catalytic activity is increased by tyrosine phosphorylation. Tyrosine kinase phosphorylation of PLC-${\gamma}$1 stimulates PLC activation and cell proliferation. However the signal transduction pathway and the significance of PLC in injured recurrent laryngeal nerve regeneration is unknown. Therefore after we obtained fuctionally recovered rats using PEMF in this study, we attempt to provide some evidence that PLC plays a role in nerve regeneration itself and regeneration related to PEMF through the analysis of the difference between fucntional recovery group and non-recovery group in the recurrent laryngeal nerve. Materials and Method : Using 32 healthy male Sprague-Dawley rats, transections and primary anastomosis were performed on their left recurrent laryngeal nerves. Rats were then randomly assigned to 2 groups. The experimental group(n=16) received PEMS by placing them in custom cages equipped with Helm-holz coils(3hr/day, 5days/wk, for 12wk). The control group(n=16) were handled the same way as the experimental group, except that they did not receive PEMS. Laryngo-videoendoscopy was performed before and after surgery and followed up weekly. Laryngeal EMG was obtained in both PCA and TA muscles. Immunohistochemisty staining and Western blotting analysis using monoclonal antibody was performed to detect PLC-${\gamma}$1 in recurrent laryngeal nerve and nodose ganglion. Results : 10 rats(71%) in experimental group and 4 rats(38%) in the control group showed recovery of vocal fold motion. Functionally-recoverd rats show PLC-${\gamma}$1 positive cells in neuron and ganglion cells after 12 weeks from nerve injury. Conclusion : This study shows that PLC1-${\gamma}$ involved in singnal trasduction pathway in functinal recovery of injured recurrent laryngeal nerve and PEMF enhance the functional recovery by effect on this molecule.

• International Journal of Oral Biology
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• v.31 no.4
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• pp.113-118
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• 2006

In the primary sensory neuron of the mesencephalic trigeminal nucleus (MTN), the peripheral axon supplies a large number of annulospiral endings surrounding intrafusal fibers encapsulated in single muscle spindles while the central axon sends only a few number of synapses onto single ${\alpha}-motoneurons({\alpha}-MNs)$. Therefore, the ${\alpha}-{\gamma}$ linkage is thought to be very crucial in the jaw-closing movement. Spike activity in a ${\gamma}-motoneuron\;({\gamma}-MN)$ would induce a large number of impulses in single peripheral axons by activating many intrafusal fibers simultaneously, subsequently causing an activation of ${\alpha}-MNs$ in spite of the small number of synapses. Thus, the activity of ${\gamma}-MNs$ may be vital for modulation of jaw-closing movements. Independently of such a spindle activity modulated by ${\gamma}-MNs$, somatic depolarization in MTN neurons is known to trigger the oscillatory spike activity. Nevertheless, the trafficking of these spikes arising from the two distinct sources of MTN neurons is not well understood. In this short review, switching among multiple functional modes of MTN neurons is discussed. Subsequently, it will be discussed which mode can support the ${\alpha}-{\gamma}$ linkage. In our most recent study, simultaneous patch-clamp recordings from the soma and axon hillock revealed a spike-back-propagation from the spike-initiation site in the stem axon to the soma in response to a somatic current pulse. The persistent $Na^+$ current was found to be responsible for the spike-initiation in the stem axon, the activation threshold of which was lower than those of soma spikes. Somatic inputs or impulses arising from the sensory ending, whichever trigger spikes in the stem axon first, would be forwarded through the central axon to the target synapse. We also demonstrated that at hyperpolarized membrane potentials, 4-AP-sensitive $K^+$ current ($IK_{4-AP}$) exerts two opposing effects on spikes depending on their origins; the suppression of spike initiation by increasing the apparent electrotonic distance between the soma and the spike-initiation site, and the facilitation of axonal spike invasion at higher frequencies by decreasing the spike duration and the refractory period. Through this mechanism, the spindle activity caused by ${\gamma}-MNs$ would be safely forwarded to ${\alpha}-MNs$. Thus, soma spikes shaped differentially by this $IK_{4-AP}$ depending on their origins would reflect which one of the two inputs was forwarded to the target synapses.

• Journal of Life Science
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• v.21 no.5
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• pp.647-655
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• 2011

The neurotoxicity of aggregated amyloid ${\beta}$ ($A{\beta}$) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease (AD). It can cause neurotoxicity in AD by evoking a cascade of apoptosis to neuron. Here, we investigated the neuroprotective effects of cilostazol, which acts as a phosphodiesterase III inhibitor, on $A{\beta}_{25-35}$-induced cytotoxicity in mouse neuronal cells and cognitive decline in the C57BL/6J AD mouse model via peroxisome proliferator-activated receptor (PPAR)-${\gamma}$ activation. $A{\beta}_{25-35}$ significantly reduced cell viability and increased the number of apoptotic-like cells. Cilostazol treatment recovered cells from $A{\beta}$-induced cell death as well as rosiglitazone, a PPAR-${\gamma}$ activator. These effects were suppressed by GW9662, an antagonist of PPAR-${\gamma}$ activity, indicative of a PPAR-${\gamma}$-mediated signaling. In addition, cilostazol and rosiglitazone also restored PPAR-${\gamma}$ activity levels that had been altered as a result of $A{\beta}_{25-35}$ treatment, which were antagonized by GW9662. Furthermore, cilostazol also markedly decreased the number of apoptotic-like cells and decreased the Bax/Bcl-2 ratio. Intracerebroventricular injection of $A{\beta}_{25-35}$ in C57BL/6J mice resulted in impaired cognitive function. Oral administration of cilostazol (20 mg/kg) for 2 weeks before $A{\beta}_{25-35}$ injection and once a day for 4 weeks post-surgery almost completely prevented the $A{\beta}_{25-35}$-induced cognitive deficits, as did rosiglitazone. Taken together, our findings suggest that cilostazol could attenuate $A{\beta}_{25-35}$-induced neuronal cell injury and apoptosis as well as promote the survival of neuronal cells, subsequently improving cognitive decline in AD, partly because of PPAR-${\gamma}$ activation. The phosphodiesterase III inhibitor cilostazol may be the basis of a novel strategy for the therapy of AD.