• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.467-475
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• 1997

Although one of the major physiological functions of taurine(2-aminoethanesulfonic acid) is the inhibitory action on the central nervous system(CNS), the mechanism of taurine in controlling the neuronal excitation in the CNS has been in controversy. Electrically evoked pEPSP and spontaneous activity induced by the perfusion of low $Mg^{++}-ACSF$ were recorded in the CA1 pyramidal cell layer of the hippocampal slice. To test the inhibitory effect of taurine on spontaneous responses, taurine was treated for 2 min at various concentrations(1 mM-10 mM). Taurine reduced the spontaneous activity by 22.2% at 1 mM, and 100% at 2 mM in low $Mg^{++}-ACSF$. Evoked response was induced by electrical stimulation of Schaffer collateral-commissural fibers. Taurine reduced the evoked response by 11.68% at 3 mM, and 24.25% at 5 mM. Even 20 mM of taurine reduced the evoked response only by 24 % after 5 min treatment. That is, the inhibitory efficacy was much higher in spontaneous activity than in evoked response. The $GABA_A$ receptor antagonist, 100 uM bicuculline, blocked the inhibitory action of taurine, while $GABA_B$ receptor antagonist, 700 uM phaclofen, did not. Taurine blocked the spontaneous activity in the presence of CNQX, and did not block the electrically evoked responce in the presence of APV. The results suggest that taurine causes hyperpolarization in the cell by binding to $GABA_A$ receptor and preferentially attenuates NMDA receptor-mediated hyperexcitation, leaving synaptic transmission unmodified.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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• pp.87-91
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• 2002

The aim of this study was to investigate the role of $Ca^{2+}-channel$ blockers in norepinephrine (NE) release from rat hippocampus. Slices and synaptosomes were incubated with $[^3H]-NE$ and the releases of the labelled products were evoked by 25 mM KCl stimulation. Nifedipine, diltiazem, nicardipine, flunarizine and pimozide did not affect the evoked and basal release of NE in the slice. But, diltiazem, nicardipine and flunarizine decreased the evoked NE release with a dose-related manner without any change of the basal release from synaptosomes. Also, a large dose of pimozide produced modest decrement of NE release. ${\omega}-conotoxin$ (CTx) GVIA decreased the evoked NE release in a dose-dependent manner without changing the basal release. And ${\omega}-CTxMVIIC$ decreased the evoked NE release in the synaoptosomes without any effect in the slice, but the effect of decrement was far less than that of ${\omega}-CTxGVIA.$ In interaction experiments with ${\omega}-CTxGVIA,\;{\omega}-CTxMVIIC$ slightly potentiated the effect of ${\omega}-CTxGVIA$ on NE release in the slice and synaptosomal preparations. These results suggest that the NE release in the rat hippocampus is mediated mainly by N-type $Ca^{2+}-channels,$ and that other types such as L-, T- and/or P/Q-type $Ca^{2+}-channels$ could also be participate in this process.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.2
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• pp.59-63
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• 2003

The medial vestibular nucleus (MVN) neurons are controlled by excitatory synaptic transmission from the vestibular afferent and commissural projections, and by inhibitory transmission from interneurons. Spontaneous synaptic currents of MVN neurons were studied using whole cell patch clamp recording in slices prepared from 13- to 17-day-old rats. The spontaneous inhibitory postsynaptic currents (sIPSCs) were significantly reduced by the $GABA_A$ antagonist bicuculline ($20{\mu}M$), but were not affected by the glycine antagonist strychnine ($1{\mu}M$). The frequency, amplitude, and decay time constant of sIPSCs were $4.3{\pm}0.9$ Hz, $18.1{\pm}2.0$ pA, and $8.9{\pm}0.4$ ms, respectively. Spontaneous excitatory postsynaptic currents (sEPSCs) were mediated by non-NMDA and NMDA receptors. The specific AMPA receptor antagonist GYKI-52466 ($50{\mu}M$) completely blocked the non-NMDA mediated sEPSCs, indicating that they are mediated by an AMPA-preferring receptor. The AMPA mediated sEPSCs were characterized by low frequency ($1.5{\pm}0.4$ Hz), small amplitude ($13.9{\pm}1.9$ pA), and rapid decay kinetics ($2.8{\pm}0.2$ ms). The majority (15/21) displayed linear I-V relationships, suggesting the presence of GluR2-containing AMPA receptors. Only 35% of recorded MVN neurons showed NMDA mediated currents, which were characterized by small amplitude and low frequency. These results suggest that the MVN neurons receive excitatory inputs mediated by AMPA, but not kainate, and NMDA receptors, and inhibitory transmission mediated by $GABA_A$ receptors in neonatal rats.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.6
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• pp.295-300
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• 2004

Serotonin (5-hydroxytroptamine, 5-HT) has been shown to affect the induction of long-term potentiation (LTP) in the cortex such as the hippocampus, the visual cortex and the prefrontal cortex. Fluoxetine, as a selective serotonin reuptake inhibitor, is used in the management of a wide variety of psychological diseases. To study the effect of fluoxetine on the induction of LTP, we recorded the field potential in layer II/III of the frontal cortex from 3-wk-old. LTP was induced in horizontal input by theta burst stimulation (TBS). TBS with two-folds intensity of the test stimulation induced LTP, which was blocked by application of D-AP5 $(50 {\mu}M)$, an NMDA receptor antagonist. Whereas bath application of 5-HT $(10 {\mu}M)$ inhibited the induction of LTP, treatment with the 5-HT depleting agent, para-chloroamphetamine $(PCA,\;10{\mu}M)$, for 2hr did not affect the induction of LTP. Bath application of fluoxetine (1, 3, and $10 {\mu}M)$ suppressed the induction of LTP in concentration-dependent manner, however, fluoxetine did not inhibit the induction of LTP in 5-HT-depleted slices. These results indicate that fluoxetine may inhibit the induction of LTP by modulating serotonergic mechanism in the rat frontal cortex.

• Proceedings of the KOSOMBE Conference
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• v.1997 no.05
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• pp.123-126
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• 1997

We present a method for the estimation of 3D solid angle assessment of the acetabular coverage of the femoral head in 3D space. At first, femoral head and acetabulum is segmented from the original CT scan images. The slice thickness is 1.5mm and the number of slices is usually 30-40 to cover the entire acetabulum. The superior half of the femoral head is modeled as part of a sphere. Thus, the axial cross sections of the upper half of the femoral head are also modeled as circles. A set of points from each outline image of femoral head is fitted recursively into a circle by minimizing root-mean-square (RMS) error. With these fitted circles, a center point of the femoral head model is evaluated. This is a reference point for calculating the solid angle of the acetabular inner surface. Next, the tangent lines connecting from a set of points of the acetabular edge to the center of the fitted sphere are obtained. The lines pass through the unit sphere whose center is the same as that of the femoral head. With the points on the unit sphere, we calculate area and estimate the solid angle. Based on this solid angle, the deformity of the acetabulum is analyzed. In case of normal subject, the solid angle is about 4.3 (rad) and acetabular coverage is 68%.

• Food Science and Preservation
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• v.17 no.2
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• pp.202-207
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• 2010

The effects of ultrasound treatment, in combination with ascorbic acid, on the quality of fresh-cut 'Jonathan' apples was investigated. Prepared apple slices were ultrasonicated in distilled water (US) or in 1%(w/v) ascorbic acid solution (UA) and the other samples were just dipped in 1%(w/v) ascorbic acid solution (AA). All samples were stored at$10^{\circ}C$ for 12 days. UA-treated samples showed high $L^{*}$ and hue values and low $a^{*}$, $b^{*}$, chroma, and ${\Delta}E$ value. Both control and US-treated samples showed considerable browning. A significant inhibition of polyphenol oxidase activity was observed after UA treatment. The level of total phenolics in UA-treated samples was higher on the day of treatment compared with other samples. Total soluble solids, pH, titratable acidity, and gas concentrations were similar in all samples. This study demonstrated that the simultaneous treatment of ultrasound and ascorbic acid was effective in preventing enzymatic browning of fresh-cut 'Jonathan' apples and maintaining total phenolics contents.

• Journal of Korean Neurosurgical Society
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• v.49 no.2
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• pp.107-111
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• 2011

Objective : The aim of this study was to evaluate the utility of volume-rendered helical computerized tomography (CT) angiography focusing tracheostomy tube and innominate artery for prevention of tracheoinnominate artery fistula. Methods : The authors retrospectively analyzed 22 patients with tracheostomy who had checked CT angiography. To evaluate the relationship between tracheostomy tube and innominate artery, we divided into three categories. First proximal tube position based on cervical vertebra, named "tracheostomy tube departure level (TTDL)". Second, distal tube position and course of innominate artery, named "tracheostomy tube-innominate artery configuration (TTIC)". Third, the gap between the tube and innominate artery, named "tracheostomy tube to innominate artery gap (TTIG)". The TTDL/TTIC and TTIG are based on 3-dimensional (3D) reconstruction around tracheostomy and enhanced axial slices of upper chest, respectively. Results : First, mean TTDL was $6.8{\pm}0.6$. Five cases (23%) were lower than C7 vertebra. Second, TTIC were remote to innominate artery (2 cases; 9.1 %), matched with it (14 cases; 63.6%) or crossed it (6 cases; 27.3%). Only 9% of cases were definitely free from innominate artery injury. Third, average TTIG was $4.3{\pm}4.6$ mm. Surprisingly, in 6 cases (27.3%), innominate artery, trachea wall and tracheostomy tube were tightly attached all together, thus have much higher probability of erosion. Conclusion : If low TTDL, match or crossing type TTIC with reverse-L shaped innominate artery, small trachea and thin TTIG are accompanied all together, we may seriously consider early plugging and tube removal.

• International Journal of Oral Biology
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• v.33 no.3
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• pp.117-123
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• 2008

Reactive oxygen species (ROS) are toxic agents that may be involved in various neurodegenerative diseases. Recent studies indicate that ROS can act as modulators of neuronal activity, and are critically involved in persistent pain primarily through spinal mechanisms. In the present study, whole cell patch clamp recordings were carried out to investigate the effects of tert-buthyl hydroperoxide (t-BuOOH), an ROS, on neuronal excitability and the mechanisms underlying changes of membrane excitability. In current clamp condition, application of t-BuOOH caused a reversible membrane depolarization and firing activity in substantia gelatinosa (SG) neurons. When slices were pretreated with phenyl-N-tert-buthylnitrone (PBN) and ascorbate, ROS scavengers, t-BuOOH failed to induce membrane depolarization. However, isoascorbate did not prevent t-BuOOH-induced depolarization, suggesting that the site of ROS action is intracellular. The t-BuOOH-induced depolarization was not blocked by pretreatment with dithiothreitol (DTT), a sulfhydryl-reducing agent. The membrane-impermeant thiol oxidant 5,5-dithiobis 2-nitrobenzoic acid (DTNB) failed to induce membrane depolarization, suggesting that the changes of neuronal excitability by t-BuOOH are not caused by the modification of extrathiol group. The t-BuOOH-induced depolarization was suppressed by the phospholipase C (PLC) blocker U-73122 and inositol triphosphate ($IP_3$) receptor antagonist 2-aminoethoxydiphenylbolate (APB), and after depletion of intracellular $Ca^{2+}$ pool by thapsigargin. These data suggest that ROS generated by peripheral nerve injury can induce central sensitization in spinal cord, and t-BuOOH-induced depolarization may be regulated by intracellular $Ca^{2+}$ store mainly via $PLC-IP_3$ pathway.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2679-2683
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• 2015

Background: Phenethyl isothiocyanate (PEITC), the most comprehensively studied aromatic isothiocyanate, has been shown to act as an anti-cancer agent mainly through modulation of biotransformation enzymes responsible for metabolizing carcinogens in the human body. Humans are often exposed to carcinogenic factors, some of which through the diet, such as polycyclic aromatic hydrocarbon benzo[a]pyrene via the consumption of over-cooked meats. Inhibition of the enzymes responsible for the bioactivation of this carcinogen, for example CYP1A1, the major enzyme required for polycyclic aromatic hydrocarbons (PAHs) bioactivation, is recognized as a chemoprevention strategy. Objective: To evaluate the inhibitory effects of PEITC against benzo[a]pyrene-induced rise in rat liver CYP1A1 mRNA and apoprotein levels. Materials and Methods: Precision cut rat liver slices were treated with benzo[a]pyrene at 1 and $5{\mu}M$ in the presence of PEITC ($1-25{\mu}M$) for 24 hours, followed by determination of CYP1A1 mRNA and apoprotein levels using quantitative polymerase chain reaction and immunoblotting. Results: Findings revealed that PEITC inhibited benzo[a]pyrene-induced rise in rat liver CYP1A1 mRNA in a dose-dependent manner as well as the apoprotein levels of CYP1A. Conclusions: It was demonstrated that PEITC can directly inhibit the bioactivation of benzo[a]pyrene, indicating chemopreventive potential.

• Korean Journal of Computational Design and Engineering
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• v.2 no.3
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• pp.195-210
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• 1997

In Rapid Prototyping process, the time required to build multiple prototype parts can be reduced by packing several parts optimally in a work volume. Interactive arrangement of the multiple parts is a tedious process and does not guarantee the optimal placement of all the parts. In this case, packing is a kind of 3-D nesting problem because parts are represented by STL files with 3-D information. 3-D nesting is well known to be a problem requiring an intense computation and an efficient algorithm to solve the problem is still under investigation. This paper proposes that packing 3-D parts can be simplified into a 2-D irregular polygon nesting problem by using the characteristic of rapid prototyping process that the process uses 2-dimensional slicing data of the parts and that slice of the STL parts are composed of polygons. Our algorithm uses no-fit-polygon (NFP) to place each slice without overlapping other slices in the same z-level. The allowable position of one part at a fixed orientation for given parts already packed can be determined by obtaining the union of all NFP's that are obtained from each slice of the part. Genetic algorithm is used to determine the order of parts to be placed and orientations of each part for the optimal packing. Optimal orientation of a part is determined while rotating it about the axis normal to the slice by finite angles and flipping upside down. This algorithm can be applied to any rapid prototyping process that does not need support structures.