• Journal of Animal Science and Technology
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• v.44 no.5
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• pp.549-560
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• 2002

This study, including two in vitro experiments and an in vivo experiment were conducted to evaluate effects of Passtein$^{(R)}$ on crude protein degradability, ruminal fermentation characteristics and nutrient digestibility. In in vitro experiment protein degradability was examined using borate-phosphate buffer and neutral detergent, and using protease from Stroptomyces griseus at 39$^{\circ}C$ for 0, 2, 4, 8, 12, and 48 h. In addition, an in vivo experiment was conducted in a switch back design and ruminal fermentation and nutrient digestibility were determined. Four ruminal-fistulated Holstein cows weighing 300kg in mean body weight randomly allotted to 2 treatments (control and Passtein$^{(R)}$ supplementation). Although there was no significant difference on protein fraction between treatments, it appears that Passtein$^{(R)}$ supplementation decreased buffer soluble protein fraction compared to control. Protein degradability was not affected by Passtein$^{(R)}$ from 0 h to 4 h, but decreased at 12 h and 48 h compared to control. Degradation of immediately degradable fraction was higher in Passtein$^{(R)}$ treatment, but degradation of fermentable fraction was lower in Passtein$^{(R)}$ treatment compared to control. The pH and $NH_3$-N concentration tended to increase in Passtein$^{(R)}$ treatment, but VFA production, microbial counts and enzyme activity tended to decrease in Passtein$^{(R)}$ treatment compared to control. In addition, nutrient digestibility in the total tract tended to increase in Passtein$^{(R)}$ treatment compared to control.

• Journal of Nuclear Fuel Cycle and Waste Technology(JNFCWT)
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• v.3 no.1
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• pp.49-56
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• 2005

Many different kinds of radwastes are discharged from the nuclear power plants, and $^{129}$I is included in these radwastes. Recovery test of $^{129}$I was evaluated for different radwastes(dry active waste, sludge, spent resin and simulated evaporator bottom). Recovery of $^{129}$I for dry active waste by acid leaching with $1.8\%$ NaClO was $74.3\%$$(RSD,\;2.2\%)$ and l291 for spent rein by alkali fusion method with KOH as a flux agent was $87.7\%$$(RSD,\;0.9\%$), respectively. iodide in simulated evaporator bottom containing a high concentration of borate was adsorbed with anion exchange resin at pH 7 phosphate buffer solution. Recovery of $^{129}$I for anion exchange resin was $92.5\%$ and not affected up to 1,200 $\mu$g/mL $H_3BO)3$(as a Boron). Recovery of $^{129}$I for the spent resin from nuclear power plant was $87.2\%$ $(RSD,\;1.2\%)$.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.3
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• pp.309-316
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• 2017

Transient receptor potential vanilloid 3 (TRPV3) is a non-selective cation channel with modest permeability to calcium ions. It is involved in intracellular calcium signaling and is therefore important in processes such as thermal sensation, skin barrier formation, and wound healing. TRPV3 was initially proposed as a warm temperature sensor. It is activated by synthetic small-molecule chemicals and plant-derived natural compounds such as camphor and eugenol. Schisandra chinensis (Turcz.) Baill (SC) has diverse pharmacological properties including antiallergic, anti-inflammatory, and wound healing activities. It is extensively used as an oriental herbal medicine for the treatment of various diseases. In this study, we investigated whether SC fruit extracts and seed oil, as well as four compounds isolated from the fruit can activate the TRPV3 channel. By performing whole-cell patch clamp recording in HEK293T cells overexpressing TRPV3, we found that the methanolic extract of SC fruit has an agonistic effect on the TRPV3 channel. Furthermore, electrophysiological analysis revealed that ${\gamma}$-schisandrin, one of the isolated compounds, activated TRPV3 at a concentration of $30{\mu}M$. In addition, ${\gamma}$-schisandrin (${\sim}100{\mu}M$) increased cytoplasmic $Ca^{2+}$ concentrations by approximately 20% in response to TRPV3 activation. This is the first report to indicate that SC extract and ${\gamma}$-schisandrin can modulate the TRPV3 channel. This report also suggests a mechanism by which ${\gamma}$-schisandrin acts as a therapeutic agent against TRPV3-related diseases.

• International Journal of Oral Biology
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• v.30 no.1
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• pp.9-15
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• 2005

Recently, we reported that high extracellular calcium increased receptor activator of nuclear factor-${\kappa}B$ ligand (RANKL) expression via p44/42 mitogen-activated protein kinase (p44/42 MAPK) activation in mouse osteoblasts. However, the mechanism for p44/42 MAPK activation by high extracellular calcium is unclear. In this study, we examined the role of intracellular calcium increase in high extracellular calcium-induced RANKL induction and p44/42 MAPK activation. Primary cultured mouse calvarial osteoblasts were used. RANKL expression was highly induced by 10 mM calcium treatment. Ionomycin, a calcium ionophore, also increased RANKL expression and activated p44/42 MAPK. U0126, an inhibitor of MEK1/2, an upstream activator of p44/42 MAPK, blocked the RANKL induction by both high extracellular calcium and ionomycin. High extracellular calcium increased the phosphorylation of proline-rich tyrosine kinase 2 (Pyk2), one of the known upstream regulators of p44/42 MAPK activation. Bisindolylmaleimide, an inhibitor of protein kinase C, did not block RANKL induction and p44/42 MAPK activation induced by high extracellular calcium. 2-Aminoethoxydiphenyl borate, an inhibitor of inositol 1,4,5-trisphosphate (IP3) receptor, blocked the RANKL induction by high extracellular calcium. It also partially suppressed the activation of Pyk2 and p44/42 MAPK. Cyclosporin A, an inhibitor of calcineurin, also inhibited high calcium-induced RANKL expression in dose dependent manner. However, cyclosporin A did not affect the activation of Pyk2 and p44/42 MAPK by high extracellular calcium treatment. These results suggest that 1) the increase in intracellular calcium via IP3-mediated calcium release is necessary for RANKL induction by high extracellular calcium treatment, 2) Pyk2 activation, but not protein kinase C, following the increase in intracellular calcium might be involved in p44/42 MAPK activation, and 3) calcineurin-NFAT activation by the increase in intracellular calcium is involved in RANKL induction by high extracellular calcium treatment.

• Clinical and Experimental Pediatrics
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• v.45 no.9
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• pp.1083-1089
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• 2002

Purpose : The prevalence of obese children has recently increased. Obesity is known to be associated with complications such as hypertension, fatty liver, hyperlipidemia, and insulin resistance. L-carnitine is an essential cofactor for the transport of long chain fatty acids into mitochondria for ${\beta}$-oxidation. The purpose of this study is to measure serum free fatty acid and carnitine levels, and evaluate the role of L-carnitine as a therapeutic drug in obese children with fatty liver. Methods : Nine obese children, ranging from seven to 18 years of age, and 10 normal children were examined. Serum lipid(total cholesterol, triglyceride, HDL-cholesterol, and LDL-cholesterol) and fatty acid levels were analyzed. Serum total, free, and acyl carnitine levels were performed also by a new enzymatic cycling technique. Results : Long chain fatty acids(myristic acid, palmitoleic acid, palmitic acid, linoleic acid, oleic acid, and stearic acid)were significantly increased in obese children compared to the control group. Total, and acyl carnitine levels were significantly increased in obese children compared to the control group. Conclusion : Serum free fatty acid and carnitine levels were significantly increased in obese children with fatty liver compared to the normal control. This may suggest that L-carnitine can be used as antilipidemic agent to decrease fatty acid and lipid levels for obese children. Prospective studies will investigate serum fatty acid and carnitine levels after treatment of L-carnitine in obese children in the future.

• Journal of the Korean Society of Radiology
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• v.8 no.7
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• pp.455-459
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• 2014

We grew the $Li_6Gd(BO_3)_3:Ce^{3+}$ scintillator and determined the scintillation and thermoluminescence properties for X-rays. The emission spectrum of $Li_6Gd(BO_3)_3:Ce^{3+}$ is located in the range of 370~500 nm, peaking at 423 nm an 455 nm, due to the $4f{\rightarrow}5d$ transition of $Ce^{3+}$ ions. The fluorescence decay time of the crystal is composed three components. The fast component is 60 ns (25%), the intermediate component is 787 ns (29%) and the slow component is $5.9{\mu}s$ (46%) of the crystal. The after-glow is caused by the electron and hole traps in the crystal lattice. We determined physical parameters of the traps in the crystal. The thermoluminescence trap are composed two traps. The determined activation energy (E), kinetic order (m) and frequency factor (s) of the first trap are 0.65 eV, 1.01 and $6.9{\times}10^8s^{-1}$. And, the determined activation energy, kinetic order and frequency factor of the second trap are 0.96 eV, 1.79 and $3.1{\times}10^{12 }s^{-1}$, respectively.

• Journal of the Korean Ceramic Society
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• v.25 no.3
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• pp.251-260
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• 1988

Ion-exchange porous glasses were prepared by heat treatment and subsequently hydro thermalor acid leaching treatment $10Li_2O$.$(90-x)B_2O_3$.$xSiO_2$ base glasses containing various amount of $Al_2O_3$ or $MoO_3$. It was investigated how the phase separation and the cation exchange capacity(CEC) were affected by the addition of $Al_2O_3$ or $MoO_3$. The optimum condition of phase separation in these glasses was about 48$0^{\circ}C$ for 10 hrs. The degree of phase separation was rapidly suppressed by the addition of $Al_2O_3$ up to 10 mol% and thereafter suppression effect was decreased. The maximum value of CEC, about 252meq/100g, was observed with the $1OLi_2O$.$45B_2O_3$.$45SiO_2＋7.5Al_2O_3$ porous glass prepared by hydrothermal treatment and its mean pore radius was about 16.3A. The addition of $MoO_3$ accelerated phase separation and leaching rate. Looking at the remakable increment of pore diameter and pore volume of these porous glasses by the addition of $MoO_3$, the effect of $MoO_3$ may be ascribed to the lowering of silica concentration in the borate phase and to the forming of water-soluble complex with silica during the leaching treatment.

• Journal of the Korean Chemical Society
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• v.33 no.5
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• pp.484-495
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• 1989

Reactions of $(Et_4N)_2[MoOCl_5]$ with multidentate ligands containing nitrogen or/and oxygen donor atom (EDTA, DTPA, IDA, CyDTA, OX) produce a series of binuclear molybdate (V) complexes. The prepared Mo (V) complexes has been identified by Elemental Analysis, Infrared Spectra, Proton Magnetic Resonance Spectra, and Electronic Spectra. The electrochemical reduction mechanism has been studied by Cyclic voltammetry, Controlled Potential Coulometry, and Spectrophotometry in pH 3.571-10.375 acetate, borate, phosphate/sodium hydroxide, phosphate, ammonium/ammonia buffers. The cyclic voltammogram of the Mo-EDTA, DTPA, IDA, CyDTA complexes at pH < ca. 6.00 have shown two reduction waves. The first reduction wave shows two electron process and the second reduction wave shows two electron process. The cyclic voltammogram of the Mo-EDTA, DTPA, IDA, CyDTA complexes at pH < ca. 8.00 has shown one reduction wave. This reduction wave show four electron process. The cyclic voltammogram of the Mo-OX complex at pH < ca. 7.2 has shown one reduction wave. This reduction wave show four electron process.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.249-255
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• 2015

Wnk kinase maintains cell volume, regulating various transporters such as sodium-chloride cotransporter, potassium-chloride cotransporter, and sodium-potassium-chloride cotransporter 1 (NKCC1) through the phosphorylation of oxidative stress responsive kinase 1 (OSR1) and STE20/SPS1-related proline/alanine-rich kinase (SPAK). However, the activating mechanism of Wnk kinase in specific tissues and specific conditions is broadly unclear. In the present study, we used a human salivary gland (HSG) cell line as a model and showed that $Ca^{2+}$ may have a role in regulating Wnk kinase in the HSG cell line. Through this study, we found that the HSG cell line expressed molecules participating in the WNK-OSR1-NKCC pathway, such as Wnk1, Wnk4, OSR1, SPAK, and NKCC1. The HSG cell line showed an intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) increase in response to hypotonic stimulation, and the response was synchronized with the phosphorylation of OSR1. Interestingly, when we inhibited the hypotonically induced $[Ca^{2+}]_i$ increase with nonspecific $Ca^{2+}$ channel blockers such as 2-aminoethoxydiphenyl borate, gadolinium, and lanthanum, the phosphorylated OSR1 level was also diminished. Moreover, a cyclopiazonic acid-induced passive $[Ca^{2+}]_i$ elevation was evoked by the phosphorylation of OSR1, and the amount of phosphorylated OSR1 decreased when the cells were treated with BAPTA, a $Ca^{2+}$ chelator. Finally, through that process, NKCC1 activity also decreased to maintain the cell volume in the HSG cell line. These results indicate that $Ca^{2+}$ may regulate the WNK-OSR1 pathway and NKCC1 activity in the HSG cell line. This is the first demonstration that indicates upstream $Ca^{2+}$ regulation of the WNK-OSR1 pathway in intact cells.

• Journal of Ginseng Research
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• v.35 no.1
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• pp.92-103
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• 2011

Ginseng has been used as a general tonic agent to invigorate human body. In the present study, we isolated novel glycolipoproteins from ginseng that activate $Ca^{2+}$-activated $Cl^-$ channel (CaCC) in Xenopus oocytes and transiently increase intracellular free $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in mouse Ehrlich ascites tumor cells. We named the active ingredients as gintonin. Gintonin exists in at least six different forms. The native molecular weight of gintonin is about 67 kDa but its apparent molecular weight is about 13 kDa, indicating that gintonin might be a pentamer. Gintonin is rich in hydrophobic amino acids. Its main carbohydrates are glucose and glucosamine. Its lipid components are linoleic, palmitic, oleic, and stearic acids. Gintonin actions were blocked by U73122, a phospholipase C inhibitor, 2-aminoethxydiphenyl borate, an inositol 1,4,5-trisphosphate receptor antagonist, or bis (o-aminophenoxy) ethane-N,N,N0,N0-tetracetic acid acetoxymethyl ester, a membrane permeable $Ca^{2+}$ chelator. In the present study, we for the first time isolated novel gintonin and showed the signaling pathways on gintonin-mediated CaCC activations and transient increase of $[Ca^{2+}]_i$. Since $[Ca^{2+}]_i$ as a second messenger plays a pivotal role in the regulation of diverse $Ca^{2+}$-dependent intracellular signal pathways, gintonin-mediated regulations of $[Ca^{2+}]_i$ might contribute to biological actions of ginseng.