• Asian Journal of Turfgrass Science
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• v.11 no.3
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• pp.205-210
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• 1997

The metal spikes evaluated in this study significantly affected more negative on the turf wear and ball speed of putting green than alternative plastic spikes. 1.The metal spikes caused the most amount of wear compared with plastic spikes, athletic shoes and mountain-climbing shoes. On the other hand, athletic shoes caused the least amount of wear. Plastic spikes caused wear more than athletic shoes, hut apparently wear less than metal spikes. The wear from metal spike repaired later than any other tread types. 2.The wear from all kinds of shoe treads in wetcondition green were higher than in dry-condition green and the wear from metal spikes was more severe compared with plastic spikes in both green condition. 3. Ball speed of heavy compaction area by metal spike was reduced about 9% compared with that of light compaction area, hecause metal spikes made many holes in the putting green surface. On the other hand, plastic spikes did not affect hall speed of heavy and light compaction area in the putting green. Key words: Metal spike, Plastic spike, Wear, Ball speed.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.40 no.2
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• pp.245-249
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• 1995

The number of immature spikes of barley (Hordeum vulgare L.) and wheat (Triticum aestivum L) were studied to determine if there could be existed the significant difference among 5 varieties of barley and wheat each. Heritability of 6 characters including the number of immature spikes have also calculated. Correlation between the immature spikes and 5 other characters were also investigated. There were significant difference among 5 varieties of barley and wheat in the number of immature spikes. Heritability estimated were very high in case of number of immature spikes of barley and that of wheat was high. There were highly significant correlation between the number of immature spikes of barley and number of internode and significant correlation between the number of immature spikes and flag leaf. However, in wheat no correlations were found among the 5 characters in wheat and between the number of immature spikes and number of internode were negative.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.6
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• pp.531-540
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• 2022

Group 1 metabotropic glutamate receptors (mGluRs) can positively affect postsynaptic neuronal excitability and epileptogenesis. The objective of the present study was to determine whether group 1 mGluRs might be involved in synaptically-induced intracellular free Ca²⁺ concentration ([Ca²⁺]_i) spikes and neuronal cell death induced by 0.1 mM Mg²⁺ and 10 µM glycine in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using imaging methods for Ca²⁺ and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays for cell survival. Reduction of extracellular Mg²⁺ concentration ([Mg²⁺]_o) to 0.1 mM induced repetitive [Ca²⁺]_i spikes within 30 sec at day 11.5. The mGluR5 antagonist 6-Methyl2-(phenylethynyl) pyridine (MPEP) almost completely inhibited the [Ca²⁺]_i spikes, but the mGluR1 antagonist LY367385 did not. The group 1 mGluRs agonist, 3,5-dihydroxyphenylglycine (DHPG), significantly increased the [Ca²⁺]_i spikes. The phospholipase C inhibitor U73122 significantly inhibited the [Ca²⁺]_i spikes in the absence or presence of DHPG. The IP₃ receptor antagonist 2-aminoethoxydiphenyl borate or the ryanodine receptor antagonist 8-(diethylamino)octyl 3,4,5-trimethoxybenzoate also significantly inhibited the [Ca²⁺]_i spikes in the absence or presence of DHPG. The TRPC channel inhibitors SKF96365 and flufenamic acid significantly inhibited the [Ca²⁺]_i spikes in the absence or presence of DHPG. The mGluR5 antagonist MPEP significantly increased the neuronal cell survival, but mGluR1 antagonist LY367385 did not. These results suggest a possibility that mGluR5 is involved in synaptically-induced [Ca²⁺]_i spikes and neuronal cell death in cultured rat hippocampal neurons by releasing Ca²⁺ from IP₃ and ryanodine-sensitive intracellular stores and activating TRPC channels.

• IE interfaces
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• v.23 no.2
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• pp.176-181
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• 2010

Warranty claim data analysis is a useful tool for the manufacturer because it contains many useful informations regarding reliability of the product in the real-world environments. Because of the nature of uncertainty and the incompleteness of data, some bias patterns are observed on warranty claim rate known as 'spikes'. Two types of spikes are considered. One is due to manufacturing-related failures. The other is caused by customer's behavior. This paper proposes a model by considering two types of spikes. Warranty claim data is analyzed with the proposed model. To represent spikes observed on the early warranty period, we classify failures into manufacturing-related failures and usage-related failures. Uniform distribution is assumed for the time delayed to diagnose and report by customers. By reducing maximum value of the delayed time by customers, the proposed model characterizes customer's rush in the vicinity of the warranty expiration limit. Experimental results by using the real warranty claim data show that the proposed model is better than the existing one in respect to MSE(Mean Squared Error). Moreover it is expected to estimate the failure rate more realistically with proposed model because it considers the delayed time to diagnose and report by customers.

• Proceedings of the KOSOMBE Conference
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• v.1996 no.11
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• pp.203-206
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• 1996

During the electromyographic evaluation, the presence and site of lession may be predicted by a detection of denervation potentials such as fibrllation potentials or positive sharp waves in the group of muscles. Currently, clinicians diagnose the neuropathy by detecting fibrillation potentials during EMG tests, and sometimes it is not easy to distinguish between denervation potentials and endplate spikes. The purpose of this study was to find statistically significant parameters for the quantitative distinction between denervation potentials and endplate spikes. Endplate spikes and denervation potentials from the EDB muscle of 10 patients were extracted. Also, EMG signals were classified by experienced clinicians, and were collected using a 12 bit ADC with a sampling rate of 20KHz for the duration of 400msec. In order to find statistically significant parameters, positive and negative peaks were used for analysis. As a results, standard deviation of the endplate spikes and denervation potentials showed more significant difference than others specially for the positive sharp waves. It was concluded that the results of this study could be used to develope an automated system of a EMG analysis.

• Journal of Power Electronics
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• v.19 no.3
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• pp.727-743
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• 2019

This paper presents a pulse-width modulation strategy to eliminate the common mode voltage (CMV) with reduced CMV spikes in multilevel inverters since a high CMV magnitude and its fast variations dv/dt result in bearing failure of motors, overvoltage at motor terminals, and electromagnetic interference (EMI). The proposed method only utilizes the zero CMV states in a space vector diagram and it is implemented by a carrier-based pulse-width modulation (CBPWM) method. This method is generalized for odd number levels of inverters including neutral-point-clamped (NPC) and cascaded H-bridge inverters. Then it is extended to the over-modulation mode. The over-modulation mode is implemented by using the two-limit trajectory principle to maintain linear control and to avoid look-up tables. Even though the CMV is eliminated, CMV spikes that can cause EMI and bearing current problems still exist due to the deadtime effect. As a result, the deadtime effect is analyzed. By taking the deadtime effect into consideration, the proposed method is capable of reducing CMV spikes. Simulation and experimental results verify the effectiveness of the proposed strategy.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.101-109
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• 2016

Reducing $[Mg^{2+}]_o$ to 0.1 mM can evoke repetitive $[Ca^{2+}]_i$ spikes and seizure activity, which induces neuronal cell death in a process called excitotoxicity. We examined the issue of whether cultured rat hippocampal neurons preconditioned by a brief exposure to 0.1 mM $[Mg^{2+}]_o$ are rendered resistant to excitotoxicity induced by a subsequent prolonged exposure and whether $Ca^{2+}$ spikes are involved in this process. Preconditioning by an exposure to 0.1 mM $[Mg^{2+}]_o$ for 5 min inhibited significantly subsequent 24 h exposure-induced cell death 24 h later (tolerance). Such tolerance was prevented by both the NMDA receptor antagonist D-AP5 and the L-type $Ca^{2+}$ channel antagonist nimodipine, which blocked 0.1 mM $[Mg^{2+}]_o$-induced $[Ca^{2+}]_i$ spikes. The AMPA receptor antagonist NBQX significantly inhibited both the tolerance and the $[Ca^{2+}]_i$ spikes. The intracellular $Ca^{2+}$ chelator BAPTA-AM significantly prevented the tolerance. The nonspecific PKC inhibitor staurosporin inhibited the tolerance without affecting the $[Ca^{2+}]_i$ spikes. While $G{\ddot{o}}6976$, a specific inhibitor of $PKC{\alpha}$ had no effect on the tolerance, both the $PKC{\varepsilon}$ translocation inhibitor and the $PKC{\zeta}$ pseudosubstrate inhibitor significantly inhibited the tolerance without affecting the $[Ca^{2+}]_i$ spikes. Furthermore, JAK-2 inhibitor AG490, MAPK kinase inhibitor PD98059, and CaMKII inhibitor KN-62 inhibited the tolerance, but PI-3 kinase inhibitor LY294,002 did not. The protein synthesis inhibitor cycloheximide significantly inhibited the tolerance. Collectively, these results suggest that low $[Mg^{2+}]_o$ preconditioning induced excitotoxic tolerance was directly or indirectly mediated through the $[Ca^{2+}]_i$ spike-induced activation of $PKC{\varepsilon}$ and $PKC{\xi}$, JAK-2, MAPK kinase, CaMKII and the de novo synthesis of proteins.

• Journal of the Korean earth science society
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• v.30 no.4
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• pp.454-463
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• 2009

In this study, from January 2006 to February 2009, we observed 107 ice spikes formed in a natural state, and analyzed their environment. We developed an experimental device to reproduce ice spikes in laboratory and successfully made 531 ice spikes. We analyzed the process of the formation and the principle of how those ice spikes grow through videotaped data of the formation in the experiment. In the natural world, when the surface of water and the lower part of a vessel begin to freeze, a vent (breathing hole) develops at the surface where an ice is not frozen; this vent serves as the seed of an ice spike. It is assumed that the volume expansion of ice in the vessel which occurs when water freezes makes the supercooled water go upward through the vent and becomes an ice bar called an ice spike. In the laboratory, however, when distilled water is poured into an ice tray cube and kept in the experimental device for about one and a half hours at a temperature of -12- $-13^{\circ}C$, a thin layer of ice then begins to develop on the surface of the water, the vent is formed, and ice spikes form for about 10-30 minutes. These spikes stop growing when the end becomes clogged. Ice spikes can be described as falling into seven categories of shape, with the apex type topping the list followed by the slant type in the natural state and the vertical type predominating in the laboratory.

• Journal of Biomedical Engineering Research
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• v.2 no.2
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• pp.83-88
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• 1981

A method of detecting abnormal spikes occuring in the EEG of subjects suffering from epilepsy is studied. The detection scheme is to take the first derivative of EEG and to determine if it exceed some threshold value. This study is focused on the digital signal processing for detecting abnormal spikes using microcomputer.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.3
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• pp.213-221
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• 2001

The amygdala is known as a site for inducing analgesia, but its action on the trigeminal nucleus has not been known well. Little information is available on the effect of dynorphin on NMDA receptor-mediated electrophysiological events in the trigeminal nucleus. The purpose of this study was to investigate the changes in the single neuron spikes at the trigeminal nucleus caused by the amygdala and the action of dynorphin on the trigeminal nucleus. In the present study, extracellular single unit recordings were made in the dorsal horn of the medulla (trigeminal nucleus caudalis) and the effects of microiontophoretically applied compounds were examined. When [D-Ala2, N-Me-Phe4, Glys5-ol]enkephalin (DAMGO, 10-25 mM), a ${\mu}-opioid$ receptor agonist, was infused into the amygdala, the number of NMDA-evoked spikes at the trigeminal nucleus decreased. However, the application of naloxone into the trigeminal nucleus while DAMGO being infused into the amygdala increased the number of spikes. Low dose (1 mM) of dynorphin in the trigeminal nucleus produced a significant decrease in NMDA-evoked spikes of the trigeminal nucleus but the NMDA-evoked responses were facilitated by a high dose (5 mM) of dynorphin. After the ${\kappa}$ receptors were blocked with naloxone, dynorphin induced hyperalgesia. After the NMDA receptors were blocked with AP5, dynorphin induced analgesia. In conclusion, dynorphin A exerted dose-dependent dual effects (increased & decreased spike activity) on NMDA-evoked spikes in the trigeminal nucleus. The inhibitory effect of the dynorphin at a low concentration was due to the activation of ${\kappa}$ receptors and the excitatory effect at a high concentration was due to activation of NMDA receptors in the trigeminal neurons.