• The Transactions of the Korean Institute of Electrical Engineers D
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• v.51 no.1
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• pp.8-17
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• 2002

This paper suggests that the immune algorithm can effectively be used in tuning of a PID controller. The artificial immune network always has a new parallel decentralized processing mechanism for various situations, since antibodies communicate to each other among different species of antibodies/B-cells through the stimulation and suppression chains among antibodies that form a large-scaled network. In addition to that, the structure of the network is not fixed, but varies continuously. That is, the artificial immune network flexibly self-organizes according to dynamic changes of external environment (meta-dynamics function). However, up to the present time, models based on the conventional crisp approach have been used to describe dynamic model relationship between antibody and antigen. Therefore, there are some problems with a less flexible result to the external behavior. On the other hand, a number of tuning technologies have been considered for the tuning of a PID controller. As a less common method, the fuzzy and neural network or its combined techniques are applied. However, in the case of the latter, yet, it is not applied in the practical field, in the former, a higher experience and technology is required during tuning procedure. In addition to that, tuning performance cannot be guaranteed with regards to a plant with non-linear characteristics or many kinds of disturbances. Along with these, this paper used immune algorithm in order that a PID controller can be more adaptable controlled against the external condition, including moise or disturbance of plant. Parameters P, I, D encoded in antibody randomly are allocated during selection processes to obtain an optimal gain required for plant. The result of study shows the artificial immune can effectively be used to tune, since it can more fit modes or parameters of the PID controller than that of the conventional tuning methods.

• Sleep Medicine and Psychophysiology
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• v.6 no.1
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• pp.19-25
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• 1999

Sleep alters both breathing pattern and the ventilatory responses to external stimuli. These changes during sleep permit the development or aggravation of sleep-related hypoxemia in patients with respiratory disease and contribute to the pathogenesis of apneas in patients with the sleep apnea syndrome. Fundamental effects of sleep on the ventilatory control system are 1) removal of wakefulness input to the upper airway leading to the increase in upper airway resistance, 2) loss of wakefulness drive to the respiratory pump, 3) compromise of protective respiratory reflexes, and 4) additional sleep-induced compromise of ventilatory control initiated by reduced functional residual capacity on supine position assumed in sleep, decreased $CO_2$ production during sleep, and increased cerebral blood flow in especially rapid eye movement(REM) sleep. These effects resulted in periodic breathing during unsteady non-rapid eye movement(NREM) sleep even in normal subjects, regular but low ventilation during steady NREM sleep, and irregular breathing during REM sleep. Sleep-induced breathing instabilities are divided due primarily to transient increase in upper airway resistance and those that involve overshoots and undershoots in neural feedback mechanisms regulating the timing and/or amplitude of respiratory output. Following ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include 1) hypocapnia, 2) inhibitory effect from lung stretch, 3) baroreceptor stimulation, 4) upper airway mechanoreceptor reflexes, 5) central depression by hypoxia, and 6) central system inertia. While the respiratory control system functions well during wakefulness, the control of breathing is commonly disrupted during sleep. These changes in respiratory control resulting in breathing instability during sleep are related with the pathophysiologic mechanisms of obstructive and/or central apnea, and have the therapeutic implications for nocturnal hypoventilation in patients with chronic obstructive pulmonary disease or alveolar hypoventilation syndrome.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.6
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• pp.603-611
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• 2021

Taste-responsive neurons in the nucleus of the solitary tract (NST), the first gustatory nucleus, often respond to thermal or mechanical stimulation. Alcohol, not a typical taste modality, is a rewarding stimulus. In this study, we aimed to investigate the effects of ethanol (EtOH) and/or temperature as stimuli to the tongue on the activity of taste-responsive neurons in hamster NST. In the first set of experiments, we recorded the activity of 113 gustatory NST neurons in urethane-anesthetized hamsters and evaluated responses to four basic taste stimuli, 25% EtOH, and 40℃ and 4℃ distilled water (dH₂O). Sixty cells responded to 25% EtOH, with most of them also being sucrose sensitive. The response to 25% EtOH was significantly correlated with the sucrose-evoked response. A significant correlation was also observed between sucrose- and 40℃ dH₂O- and between 25% EtOH- and 40℃ dH₂O-evoked firings. In a subset of the cells, we evaluated neuronal activities in response to a series of EtOH concentrations, alone and in combination with 32 mM sucrose (EtOH/Suc) at room temperature (RT, 22℃-23℃), 40℃, and 4℃. Neuronal responses to EtOH at RT and 40℃ increased as the concentrations increased. The firing rates to EtOH/Suc were greater than those to EtOH or sucrose alone. The responses were enhanced when solutions were applied at 40℃ but diminished at 4℃. In summary, EtOH activates most sucrose-responsive NST gustatory cells, and the concomitant presence of sucrose or warm temperatures enhance this response. Our findings may contribute to elucidate the neural mechanisms underlying appetitive alcohol consumption.

• Journal of Audiology & Otology
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• v.23 no.3
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• pp.145-152
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• 2019

Background and Objectives: The present study aims to investigate whether the cochlear implant electrode array design affects the electrophysiological and psychophysical measures. Subjects and Methods: Eighty five ears were used as data in this retrospective study. They were divided into two groups by the electrode array design: lateral wall type (LW) and perimodiolar type (PM). The electrode site was divided into three regions (basal, medial, apical). The evoked compound action potential (ECAP) threshold, T level, C level, dynamic range (DR), and aided air conduction threshold were measured. Results: The ECAP threshold was lower for the PM than for the LW, and decreased as the electrode site was closer to the apical region. The T level was lower for the PM than for the LW, and was lower on the apical region than on the other regions. The C level on the basal region was lower for the PM than for the LW whereas the C level was lower on the apical region than on the other regions. The DRs on the apical region was greater for the PM than for the LW whereas the DR was narrower on the apical region than on the other regions. The aided air conduction threshold was not different for the electrode design and frequency. Conclusions: The current study would support the advantages of the PM over the LW in that the PM had the lower current level and greater DR, which could result in more localized neural stimulation and reduced power consumption.

• Korean Journal of Audiology
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• v.23 no.3
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• pp.145-152
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• 2019

Background and Objectives: The present study aims to investigate whether the cochlear implant electrode array design affects the electrophysiological and psychophysical measures. Subjects and Methods: Eighty five ears were used as data in this retrospective study. They were divided into two groups by the electrode array design: lateral wall type (LW) and perimodiolar type (PM). The electrode site was divided into three regions (basal, medial, apical). The evoked compound action potential (ECAP) threshold, T level, C level, dynamic range (DR), and aided air conduction threshold were measured. Results: The ECAP threshold was lower for the PM than for the LW, and decreased as the electrode site was closer to the apical region. The T level was lower for the PM than for the LW, and was lower on the apical region than on the other regions. The C level on the basal region was lower for the PM than for the LW whereas the C level was lower on the apical region than on the other regions. The DRs on the apical region was greater for the PM than for the LW whereas the DR was narrower on the apical region than on the other regions. The aided air conduction threshold was not different for the electrode design and frequency. Conclusions: The current study would support the advantages of the PM over the LW in that the PM had the lower current level and greater DR, which could result in more localized neural stimulation and reduced power consumption.

• Molecules and Cells
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• v.38 no.9
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• pp.796-805
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• 2015

Gintonin is a novel ginseng-derived lysophosphatidic acid (LPA) receptor ligand. Oral administration of gintonin ameliorates learning and memory dysfunctions in Alzheimer's disease (AD) animal models. The brain cholinergic system plays a key role in cognitive functions. The brains of AD patients show a reduction in acetylcholine concentration caused by cholinergic system impairments. However, little is known about the role of LPA in the cholinergic system. In this study, we used gintonin to investigate the effect of LPA receptor activation on the cholinergic system in vitro and in vivo using wild-type and AD animal models. Gintonin induced $[Ca^{2+}]_i $ transient in cultured mouse hippocampal neural progenitor cells (NPCs). Gintonin-mediated $[Ca^{2+}]_i $ transients were linked to stimulation of acetylcholine release through LPA receptor activation. Oral administration of gintonin-enriched fraction (25, 50, or 100 mg/kg, 3 weeks) significantly attenuated scopolamine-induced memory impairment. Oral administration of gintonin (25 or 50 mg/kg, 1 2 weeks) also significantly attenuated amyloid-${\beta}$ protein ($A{\beta}$)-induced cholinergic dysfunctions, such as decreased acetylcholine concentration, decreased choline acetyltransferase (ChAT) activity and immunoreactivity, and increased acetylcholine esterase (AChE) activity. In a transgenic AD mouse model, long-term oral administration of gintonin (25 or 50 mg/kg, 3 months) also attenuated AD-related cholinergic impairments. In this study, we showed that activation of G protein-coupled LPA receptors by gintonin is coupled to the regulation of cholinergic functions. Furthermore, this study showed that gintonin could be a novel agent for the restoration of cholinergic system damages due to $A{\beta}$ and could be utilized for AD prevention or therapy.

• Journal of Oral Medicine and Pain
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• v.38 no.4
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• pp.333-338
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• 2013

Purpose: A growing number of studies have been providing evidence for neural connections between the auditory and somatosensory systems that might be a critical part of the mechanisms underlying certain forms of tinnitus. The aim of this study was to investigate the effect of temporomandibular joint (TMJ) movements on tinnitus. Methods: One hundred sixty-three tinnitus patients participated in this study. All patients underwent a thorough audiological examination including pure-tone audiometry, tinnitus handicap inventory, and evaluation of tinnitus loudness, frequency and severity on a visual analog scale. Somatic testing consisting of nine forceful jaw muscle contractions was performed to evaluate the effect of TMJ movements on modulation of tinnitus. Results: 66.9% of patients had unilateral tinnitus. Somatic testing modulated tinnitus loudness in 125 ears (57.6 %) of 217 ears tested. An increase in tinnitus loudness was observed more often than a decrease. Loudness was most commonly increased by opening and clenching jaw. Tinnitus could be induced by opening, clenching and deviating jaw to the left. Conclusion: Our study showed evidence that TMJ movements may aggravate and even evoke tinnitus and somatic testing can be used for evaluating if stimulation of the TMJ induces or aggravates tinnitus.

• Clinical and Experimental Pediatrics
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• v.46 no.7
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• pp.695-701
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• 2003

Purpose : It had been suggested that pain arising from deep somatic body regions influences neural activity within periaqueductal gray(PAG) of midbrain via distinct spinal pathways. Aspirin is one of the popular non-steroidal anti-inflammatory drugs used in the management of pain. Fos expression was used as a marker for neuronal activity throughout central neurons following painful peripheral stimulation. This study was prepared to investigate changes of c-Fos immunoreactivity in midbrain by deep pain and effects of aspirin. Methods : Male Sprague-Dawley rats were injected with 0.1 mL of 5% formalin in the plantar muscle of the right hindpaw. For experimental group II, aspirin was injected intravenously before injection of formalin. An aspirin-untreated group was utilized as group I. Rats were sacrificed at 0.5, 1, 2, 6 and 24 hours after formalin injection. Rat's brains were removed and sliced in rat brain matrix. Brain slices were coronally sectioned at interaural 1.00-1.36 mm. Serial sections were immunohistochemically reacted with polyclonal c-Fos antibody. The numbers of c-Fos protein immunoreactive neurons in ventrolateral periaqueductal gray(VLPAG) and dorsomedial periaqueductal gray(DMPAG) were counted and analyzed statistically with Mann-Whitney U tests. Results : Higher numbers of c-Fos protein immunoreactive neurons were found in VLPAG. In both VLPAG and DMPAG of formalin-treated group, the numbers of c-Fos protein immunoreactive neurons were significantly higher at all time points than the formalin-untreated group, which peaked at two hours. The numbers of c-Fos immunoreactive neuron of the aspirin-treated group were less compared to the aspirin-untreated group at each time point. Conclusion : These results provide some basic knowledge in understanding the mechanism of formalin-induced deep somatic pain and the effects of aspirin.

• Journal of Yeungnam Medical Science
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• v.6 no.1
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• pp.151-163
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• 1989

Nerve conduction studies help delineate the extent and distribution of the neural lesion. The nerve conduction was studied on upper(median, ulnar and radial nerves) and lower(personal, posterior tibial and sural nerves) extremities in 83 healthy subjects 23 to 66 years of age. and normal values were established(Table 1). The mean motor terminal latency (TL) were : median. 3.6(${\pm}0.6$)milliseconds ; ulnar. 2.9(${\pm}0.5$) milliseconds ; radial nerve. 2.3(${\pm}0.4$) milliseconds. Mean motor nerve conduction velocity(MNCV) along distal and proximal segments: median. 61.2(${\pm}9.1$) (W-E) and 57.8(${\pm}13.2$) (E-Ax) meters per second ; ulnar. 63.7(${\pm}9.1$) (W-E) and 50.(${\pm}10.0$) meters per second. Mean sensory nerve conduction velocity(SNCV) : median. 34.7(${\pm}6.7$) (F-W), 63.7(${\pm}7.1$) (W-E) and 62.8(${\pm}12.3$) (E-Ax)meters per second ; ulnar. 38.0(${\pm}6.7$)(F-W), 63.4(${\pm}7.5$) (W-E) and 57.0(${\pm}10.1$) (E-Ax)meters per second ; radial, 45.3(${\pm}6.8$) (F-W) and 64.2(${\pm}11.0$) (W-E) meters per second ; sural nerve, 43.4(${\pm}6.1$) meters per second. The amplitudes of action potential and H-reflex were also standardized. Mean H latency was 28.4(${\pm}3.2$) milliseconds. And. the fundamental principles, several factors altering the rate of nerve conduction and clinical application of nerve stimulation techniques were reviewed.

• The Korean Journal of Pharmacology
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• v.16 no.1 s.26
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• pp.25-34
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• 1980

The in vitro guinea pig ureter responded to 5 sec trains of electrical stimuli with two contractions; the first an 'on response' (ON) occurred with $0.1{\sim}0.3$ sec after the onset o the stimulus train, the second an 'off response'(OFF) occurred $0.2{\sim}1.0$ sec after the termination of the stimulus train. Relaxation occurred between the two responses during a time when the stimulus was still being delivered. Longer duration and/or higher frequencies of stimuli within the train were required to elicit the OFF than the ON. Decreasing temperature from $37^{\circ}$ to $22^{\circ}$ decreased ON amplitude and increased OFF amplitude. $Ca^{++}$-free solution, 2 mM EDTA, 1 mM $Mn^{++}$ or $1{\mu}M$ verapamil rapidly abolished ON. OFF persisted when ON had disappeared by repeated stimulation at 0.12 train per sec. Conversely, caffeine, $50{\mu}M$ and theophylline, $10{\mu}M$ abolished OFF with only slight reduction of ON, and sodium nitroprusside decreased preferentially ON amplitude rather than OFF. Relaxation between ON and OFF was incomplete in low $Na^+$ solution. ON and OFF were not affected by the neural blockers tetrodotoxin, atropine or phentolamine, also pyrilamine and methysergide, and relaxation between ON and OFF was $Na^+$ dependent. Furthermore, ON depends on free $Ca^{++}$ and OFF is more dependent on bound or stored $Ca^{++}$.