• Carbon letters
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• v.10 no.4
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• pp.293-299
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• 2009

Potassium hydroxide activated carbons were prepared from Egyptian petroleum cokes with different KOH/coke ratios and at different activation temperatures and times. The textural properties were determined by adsorption of nitrogen at $-196^{\circ}C$. The adsorption of iodine and methylene blue was also investigated at $30^{\circ}C$. The surface area and the non-micropore volume increased whereas the micropore volume decreased with the increase of the ratio KOH/coke. Also the surface area and porosity increased with the rise of activation temperature from 500 to $800^{\circ}C$. Textural parameter considerably increased with the increase of activation time from 1 to 3 h. Further increasing of activation time from 3 to 4 h was associated with a less pronounced increase in textural parameters. The adsorption of iodine shows the same trend of surface area and porosity change exhibited by nitrogen adsorption, with KOH/coke ratio and temperature of activation. Adsorption of methylene blue follows pseudo-first-order kinetics and its equilibrium adsorption follows Langmuir and D-R models.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.251-260
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• 1998

Cromakalim (BRL 34915), known as an airway smooth muscle relaxant, inhibited the releases of mediators in the antigen-induced mast cell activation. It has been suggested that cromakalim, in part, inhibited mediator releases by inhibiting the initial increase of 1,2-diacylglycerol (DAG) produced by the activation of the other phospholipase system which is different from phosphatidylcholine-phospholipase D pathway. The aim of this study is to further examine the inhibitory mechanism of cromakalim on the mediator release in the mast cell activation. Guinea pig lung mast cells were purified by using enzyme digestion and percoll density gradient. In purified mast cells prelabeled with $[^3H]PIP_2$, phospholipase C (PLC) activity was assessed by the production of $[^3H]$insitol phosphates. Protein kinase C (PKC) activity was assessed by measuring the protein phosphorylated from mast cells prelabeled with $[{\gamma}-32P]ATP$, and Phospholipase $A_2\;(PLA_2)$ activity by measuring the lyso-phosphatidylcholine produced from mast cell prelabeled with 1-palmitoyl-2-arachidonyl $phosphatidyl-[^{14}C]choline$. Histamine was assayed by fluorometric analyzer, and leukotrienes by radioimmunoassay. The PLC activity was increased by activation of the passively sensitized mast cells. This increased PLC activity was decreased by cromakalim pretreatment. The PKC activity increased by the activation of the passively sensitized mast cells was decreased by calphostin C, staurosporine and cromakalim, respectively. The $PLA_2$ activity was increased in the activated mast cells. The pretreatment of cromakalim did not significantly decrease $PLA_2$ activity. These data show that cromakalim inhibits histamine release by continuously inhibiting signal transduction processes which is mediated via PLC pathway during mast cell activation, but that cromakalim does not affect $PLA_2$ activity related to leukotriene release.

• Journal of the Korean Institute of Electrical and Electronic Material Engineers
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• v.16 no.7
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• pp.584-592
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• 2003

6H-SiC MOSFETs and digital ICs have been fabricated and characterized. PMOS devices are fabricated on an n-type epilayer while the NMOS devices are fabricated on implanted p-wells. NMOS and PMOS devices use a thermally grown gate oxide. SiC MOSFETs are fabricated using different impurity activation methods such as high temperature and newly proposed laser annealing methods. Several digital circuits, such as resistive road NMOS inverters, CMOS inverters, resistive road NMOS NANDs and NORs are fabricated and characterized.

• Korean Journal of Food Science and Technology
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• v.16 no.1
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• pp.41-46
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• 1984

The pectic enzymes produced from Aspergillus niger were separated into three fractions (F-A, F-I and F-II) by means of Sephadex and DEAF-Sephadex column chromatography. Each enzyme fraction was characterized by determining viscosity change and reducing surgar of the pectic acid-enzyme mixture and analyzing thin layer chromatogram of the reaction products. F-I rapidly reduced the viscosity of pectic acid solution and released reducing groups in a random manner so that appeared to be an endo-polygalacturonase (endo-PG). The optimum pH of endo-PG for viscosity reducing activity was 4.2 and that for releasing reducing surgar was 4.7. In the thermal inactivation of endo-PG of $30-45^{\circ}C$, the enthalpy of activation was 217.3 kj/mole and z-value was $7.5^{\circ}C$. F-II and F-A were determined as endo-polymethylgalacturonase and exo-polygalacturonase, respectively.

• Biomolecules & Therapeutics
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• v.25 no.6
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• pp.593-598
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• 2017

The $Na^+/H^+$ exchanger-1 (NHE-1) is a ubiquitously expressed pH-regulatory membrane protein that functions in the brain, heart, and other organs. It is increased by intracellular acidosis through the interaction of intracellular $H^+$ with an allosteric modifier site in the transport domain. In the previous study, we reported that glutamate-induced NHE-1 phosphorylation mediated by activation of protein kinase C-${\beta}$ (PKC-${\beta}$) in cultured neuron cells via extracellular signal-regulated kinases (ERK)/p90 ribosomal s6 kinases (p90RSK) pathway results in NHE-1 activation. However, whether glutamate stimulates NHE-1 activity solely by the allosteric mechanism remains elusive. Cultured primary cortical neuronal cells were subjected to intracellular acidosis by exposure to $100{\mu}M$ glutamate or 20 mM $NH_4Cl$. After the desired duration of intracellular acidosis, the phosphorylation and activation of PKC-${\beta}$, ERK1/2 and p90RSK were determined by Western blotting. We investigated whether the duration of intracellular acidosis is controlled by glutamate exposure time. The NHE-1 activation increased while intracellular acidosis sustained for >3 min. To determine if sustained intracellular acidosis induced NHE-1 phosphorylation, we examined phosphorylation of NHE-1 induced by intracellular acidosis by transient exposure to $NH_4Cl$. Sustained intracellular acidosis led to activation and phosphorylation of NHE-1. In addition, sustained intracellular acidosis also activated the PKC-${\beta}$, ERK1/2, and p90RSK in neuronal cells. We conclude that glutamate stimulates NHE-1 activity through sustained intracellular acidosis, which mediates NHE-1 phosphorylation regulated by PKC-${\beta}$/ERK1/2/p90RSK pathway in neuronal cells.

• YAKHAK HOEJI
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• v.45 no.4
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• pp.413-418
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• 2001

To investigate action of ATP on ischemia-induced brain injury, we measured phospholipase $A_2$activity and nitric oxide (NO) production in C6 cells. ATP alone did not have any influence on phospholipase $A_2$activity but increased NO production. Glutamate (1 mM) significantly increased phospholipase $A_2$activity whereas did not increased NO production. ATP significantly inhibited phospholipase $A_2$activation induced by 0.1 $\mu$M A23187, 1 mM glutamate and 1 mM $H_2O$$_2$, but did not inhibited 1 $\mu$M PMA-induced phospholipase $A_2$activation. From the above results, it is suggested that the action of ATP in C6 cells has dual actions, such as the inhibition of agonist-induced phospholipase $A_2$activation and the increase of NO production.

• Nuclear Engineering and Technology
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• v.50 no.1
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• pp.132-139
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• 2018

Nanocrystalline reduced activation ferritic/martensitic (RAFM) steel samples were prepared using surface mechanical attrition treatment (SMAT). Un-SMATed and SMATed reduced activation ferritic/martensitic samples were irradiated by helium ions at $200^{\circ}C$ and $350^{\circ}C$ with 2 dpa and 8 dpa, respectively, to investigate the effects of grain boundaries (GBs) and temperature on the formation of He bubbles during irradiation. Experimental results show that He bubbles are preferentially trapped at GBs in all the irradiated samples. Bubble denuded zones are clearly observed near the GBs at $350^{\circ}C$, whereas the bubble denuded zones are not obvious in the samples irradiated at $200^{\circ}C$. The average bubble size increases and the bubble density decreases with an increasing irradiation temperature from $200^{\circ}C$ to $350^{\circ}C$. Both the average size and density of the bubbles increase with an increasing irradiation dose from 2 dpa to 8 dpa. Bubbles with smaller size and lower density were observed in the SMATed samples but not in the un-SMATed samples irradiated in the same conditions, which indicate that GBs play an important role during irradiation, and sink strength increases as grain size decreases.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.14 no.2
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• pp.977-982
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• 2013

Cellulose mixed esters (CME), substituted by various fatty acyl chains, are renewable bio-based polyesters. It has lots of potential due to the biodegradable property. In this study, Alpha cellulose was activated for 2h at $40^{\circ}C$ in deionized water prior to synthesis. Homogeneous esterification of CME was accomplished with water-activated alpha cellulose, various saturated fatty acids and acetic anhydride in lithium chloride/N,N-dimethylacetamide (LiCl/DMAc) medium. CME was obtained after 5 hr at $120^{\circ}C$. The filtrated products were characterized using TGA, FT-IR, 1H-NMR and FE-SEM, and the influence of water activation on the total degree of substitution was investigated.

• Bulletin of the Korean Chemical Society
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• v.12 no.3
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• pp.251-253
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• 1991

• The Journal of Korean Medicine
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• v.21 no.4
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• pp.193-203
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• 2000

Objectives : Hindered barrier function of vascular endothelium has been implicated in the initiation and progression of degenerative vascular diseases such as atherosclerosis. In this study, the effect of Sunghyangchungisan(SHCS) as a protectant against oxidant-induced destruction of endothelial barrier function was assessed. Methods : Toward this end, endothelial cells derived from the human umbilical vein were cultured as monolayers on permeable membrane filters. Endothelial permeability was monitored by measuring transendothelial electrical resistance and movement of low density lipoprotein (LDL) across the endothelial monolayer. Results : Along with increased movement of LDL, $H_2O_2$-induced increase in endothelial permeability was paralleled by a decrease in transendotheliaI electrical resistance. The effect of $H_2O_2$ was mimicked by phorbol 12-myristate 13-acetate (PMA), a potent activator of proteinkinase C. Calphostin-C, a protein kinase C inhibitor, effectively blocked the increase in endothelial permeability induced by $H_2O_2$ or PMA, indicating that activation of protein kinase C is associated with the $H_2O_2-induced$ permeability change. SHCS effectively protected the endothelial monolayer against $H_2O_2-induced$ increase in permeability, whereas, it did not affect PMA-induced change. Forskolin, a potent activator of adenylyl cyclase, antagonized $H_2O_2$ to increase endothelial permeability. In addition, in ${H_2O_2}-treated$ cens, intracenular cAMP concentration was significantly decreased, indicating that impaired cAMP production as well as activation of proteinkinase C is a mechanism underlying ${H_2O_2}>-induced$$H_2O_2$ with regard to its effect on intracellular cAMP content. However, SHCS itself did not affect resting cAMP concentration in endothelial cells. Conclusions : These results suggest that SHCS might operate as an effective protectant against oxidant-induced destruction of endothelial barrier function. The mechanism does not appear to involve direct interaction with protein kinase C- or cAMP-associated signaling mechanism.