• Corrosion Science and Technology
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• v.8 no.3
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• pp.110-115
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• 2009

At the onset of corrosion of steel in concrete, hydrogen ions usually evolve in the process of electrochemical reaction, thereby decreasing the pH of the pore solution, which can be buffered by cement hydration products, as being representatively illustrated by calcium hydroxide. Hence, a fall in the pH is dependent on properties of cement hydration (i.e. hydration products and degree of hydration). The present study tested acid neutralization capacity (ANC) of cementitious binders of OPC(Ordinary Portland Cement), 30% PFA(Pulverized Fuel Ash), 60% GGBS(Ground Granulated Blast Furnace Slag), 10% SF(Silica Fume) to quantify the resistance of cement matrix to a pH fall. Cement pastes were cast at 0.4 of a free W/C ratio with 1.5% chlorides by weight of binder in cast. Powder samples obtained crushed and ground specimen after 200 days of curing were diluted in still water combined with different levels of 1M nitric acid solution, ranging from 0.5 to 20 mol/kg. Then, the pH of diluted solution was monitored until any further change in the pH did not take place. It was seen that the pH of the diluted solution gradually decreased as the molar amount of nitric acid increased. At some particular values of the pH, however, a decrease in the pH was marginal, which can be expressed in the peak resistances to a pH fall in the ANC curve. The peaks occurred at the variations in the pH, depending on binder type, but commonly at about 12.5 in the pH, indicate a resistance of precipitated calcium hydroxide. The measurement of water soluble chloride at the end of test showed that the amount of free chloride was significantly increased at the pH corresponding to the peaks in the ANC curve, which may reflect the adsorption of hydration products to chlorides.

• Journal of Food Hygiene and Safety
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• v.17 no.3
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• pp.117-123
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• 2002

The five main green tea catechin components such as (+)-catechin, (-)-epicatechin, (-)-epigallocatechin, (-)-epicatechin gallate, and (-)-epigallocatechin gallate were analyzed quantitatively from commercial green tea by HPLC. Amounts of catechins decreased in the following order : (+)-catechin > (-)-epigallocatechin gallate >(-)-epigallocatechin >(-)-epicatechin >(-)-epicatechin gallate. In this study, the stability of the following green tea catechins to pH in the range from 3 to 11 was studied using of ultraviolet spectroscopy : (+)-catechin, (-)-epicatechin, (-)-epicatechin gallate, and (-)-epigallocatechin gallate. This study demonstrated that green tea catechins were not stable at high pH and that the pH-, and time-dependent spectral alternatives were not reversible In conclusion, low pH is important to maintain the efficient utilization of green tea catechins.

• Journal of Soil and Groundwater Environment
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• v.27 no.1
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• pp.25-30
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• 2022

Mackinawite (FeS), as a ubiquitous reduced iron mineral, is known as a key controller of redox reactions in anaerobic subsurface environment. The reaction of FeS with redox-sensitive toxic element such as arsenic is substantially affected by pH conditions of the given environments. In this study, the interaction of As(V) with FeS was studied under strict anaerobic conditions with various pH conditions. The pH-dependent arsenic removal tests were conducted under wide ranges of pH conditions and X-ray absorption spectroscopy (XAS) was applied to investigate the reaction mechanisms under pH 5, 7, and 9. The removal efficiency of FeS for As(V) showed the higher removal of As(V) under low pH conditions and its removal efficiency decreased with increasing pH, and no As(V) reduction was observed in 1 g/L FeS solution. However, XAS analysis indicated the reduction of As(V) to As(III) occurred during reaction between FeS and As(V). The reduced form of As(III) was particularly identified as an arsenic sulfide mineral (As₂S₃) in all pH conditions (pH 5, 7, and 9). As₂S₃ precipitation was more pronounced in pH 5 where the solubility of FeS is higher than in other pH conditions. The linear combination fitting results of XAS demonstrated that As(V) removal mechanism is concerted processes of As₂S₃ precipitation and surface complexation of both arsenic species.

• The korean journal of orthodontics
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• v.21 no.1 s.33
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• pp.97-111
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• 1991

It is the aim of this study to investigate the effects of sodium fluoride and sodium orthovanadate upon the proliferation and activity of the osteoblast (MC3T3-E1 cells). MC3T3-E1 cells were cultured in $\alpha-MEM$ containing $10\%$ FBS and various concentration of sodium fluoride and sodium orthovanadate was appended to serum free media. DNA synthesis was examined through the $[^3H]$ thymidine incorporation into DNA. Collagen synthesis was examined through the $[^3H]$ proline incorporation into collagenase digestible protein and noncollagen protein. The following results were drawn; 1. Sodium fluoride stimulated the DNA synthesis of osteoblast significantly in dose-dependent manner within the concentration from $2{\mu}M$ to $10{\mu}M$ (P < 0.005). 2. Sodium orthovanadate stimulated the DNA synthesis of osteoblast significantly in dose-dependent manner within the concentration from $2{\mu}M\;to\;8{\mu}M$, however showed diminution at $10{\mu}M$ (P < 0.001). 3. Sodium fluoride and sodium orthovanadate stimulated the percent collagen synthesis of osteoblast significantly in dose-dependent manner within the concentration from $5{\mu}M$ to $10{\mu}M$ (P < 0.001). 4. Sodium fluoride and sodium orthovanadate stimulated the noncollagen synthesis of osteoblast significantly in dose-dependent manner within the concentration from $5{\mu}M\;to\;10{\mu}M$ (P < 0.001). In conclusion, sodium fluoride and sodium orthovanadate stimulate the proliferation and activity of osteoblast by stimulation of DNA synthesis and collagen and noncollagen synthesis in osteoblast.

• Biomedical Science Letters
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• v.29 no.4
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• pp.287-295
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• 2023

Amifostine was developed to protect cells, but it is known to induce cytotoxicity and apoptosis, and the exact mechanism is unknown. In this study, we investigated how the DNA mismatch repair (MMR) system interacts with p53 to prevent apoptosis, cell cycle arrest, and cytoprotective effects induced by amifostine. HCT116 colon cancer cells sublines HCT116/p53+,HCT116/p53+, HCT116/p53-, HCT116/E6 and HCT116+ch3/E6 cells were used for evaluation. Amifostine induced G1 arrest and increased toxicity two-fold in p53- cells regardless of MMR expression. Both G1 cell cycle arrest and induction of p53 protein peaked at 24 h after the start of amifostine exposure. Both G1 cell cycle arrest and induction of p53 protein peaked at 24 h after the start of amifostine exposure. Amifostine induced the expression of p21 protein in both p53+ and p53- cells. As for apoptosis, compared to p53- cells, p53+ cells showed 3.5~4.2 times resistance to amifostine-induced apoptosis. HCT116+E6 with both p53 and MMR loss showed maximum apoptosis at 48 h, and HCT116+ch3/E6HCT116+ch3/E6 with p53 loss showed maximum apoptosis at 24 h. As a result, it was confirmed through in vitro experiments that amifostine-induced G1 cell cycle arrest and apoptosis are mediated through a pathway dependent on MMR and p53 protein.

• Journal of the Korean institute of surface engineering
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• v.37 no.6
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• pp.319-325
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• 2004

Fe thin films containing Si particles were prepared on metallic substrates by electrodeposition method in sulfate solutions and the content of codeposited Si particles in the films was investigated as a function of applied current density, the content of Si particels in the solution, solution pH, solution temperature and concentration of $FeSO_4$$7H_2$O in the solution. The amount of Si codeposited in the film was not dependent on the applied current density, solution pH and solution temperature, while it was dependent on the content of Si particles in the solution and the concentration of $FeSO_4$$7H_2$O in the solution. The amount of Si codeposited in the film increased with increasing content of Si particles in the solution but reached a maximum value of about 6 wt% when the content of Si particles in the solution exceeds 100 g/l. On the other hand, the content of Si codeposited in the film increased up to about 17 wt% with decreasing concentration of $FeSO_4$$7H_2$O in the solution. These results would be applied to the fabrication of very thin Fe-6.5 wt% Si sheets for electrical applications.

• Molecules and Cells
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• v.23 no.1
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• pp.11-16
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• 2007

N,N-dimethyl-D-erythro-sphingosine (DMS) is an N-methyl derivative of sphingosine and an inhibitor of protein kinase C (PKC) and sphingosine kinase (SK). In the present study, we examined the effects of DMS on intracellular $Ca^{2+}$ concentration, pH, and glutamate uptake in human 1321N1 astrocytes. DMS increased intracellular $Ca^{2+}$ concentration and cytosolic pH in a concentration-dependent manner. Pretreatment of the cells with the $G_{i/o}$ protein inhibitor PTX and the PLC inhibitor U73122 had no obvious effect. However, removal of extracellular $Ca^{2+}$ with the $Ca^{2+}$ chelator EGTA or depletion of intracellular $Ca^{2+}$ stores with thapsigargin impeded the DMS-induced increase of intracellular $Ca^{2+}$ concentration. Pretreatment of cells with $NH_4Cl$ or monensin reduced the DMS-induced $Ca^{2+}$ increase. However, inhibition of the DMS-induced $Ca^{2+}$ increase with BAPTA did not influence the DMS-induced pH increase. DMS also inhibited glutamate uptake by the 1321N1 astrocytes in a concentration-dependent manner. It also increased intracellular $Ca^{2+}$ and pH in PC12 neuronal cells. Our observations on the effects of DMS on 1321N1 astrocytes and PC12 neuronal cells point to a physiological role of DMS in the brain.

• Molecules and Cells
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• v.42 no.11
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• pp.773-782
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• 2019

Cellular senescence is an irreversible form of cell cycle arrest. Senescent cells have a unique gene expression profile that is frequently accompanied by senescence-associated heterochromatic foci (SAHFs). Protein kinase CK2 (CK2) downregulation can induce trimethylation of histone H3 Lys 9 (H3K9me3) and SAHFs formation by activating SUV39h1. Here, we present evidence that the PI3K-AKT-mTOR-reactive oxygen species-p53 pathway is necessary for CK2 downregulation-mediated H3K9me3 and SAHFs formation. CK2 downregulation promotes SUV39h1 stability by inhibiting its proteasomal degradation in a p53-dependent manner. Moreover, the dephosphorylation status of Ser 392 on p53, a possible CK2 target site, enhances the nuclear import and subsequent stabilization of SUV39h1 by inhibiting the interactions between p53, MDM2, and SUV39h1. Furthermore, $p21^{Cip1/WAF1}$ is required for CK2 downregulation-mediated H3K9me3, and dephosphorylation of Ser 392 on p53 is important for efficient transcription of $p21^{Cip1/WAF}$. Taken together, these results suggest that CK2 downregulation induces dephosphorylation of Ser 392 on p53, which subsequently increases the stability of SUV39h1 and the expression of $p21^{Cip1/WAF1}$, leading to H3K9me3 and SAHFs formation.

• Korean Journal of Microbiology
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• v.30 no.4
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• pp.269-277
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• 1992

Several insertion mutants of Escherichia coli in the ant gene, coding for $Na^{+}$ $H^{+}$ antiport activity, showed littel, if any, reduction in the antiport activity. $Na^{+}$ dependent transport activity also remained at wild type level. These facts led to the idea that E. coli has evolved at least two distinct systems for extrusion of $Na^{+}$ The antiport activities were studied under various conditions to reveal different properties of these systems. For convenience these activities are referred to as major and minor activities. The distinguishing properties of the two systems include : kinetics (Km, Vm) at pH 7.8, competition pattern between $Na^{+}$ and Li$^{+}$ , pH profiles, pattern of the change in kinetic parameters as a function of pH, and sensitivity to protease, chemicals and heat.

• The Korean Journal of Physiology
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• v.21 no.1
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• pp.47-58
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• 1987

It has been reported that the luteal function may be regulated by the intracellular $Ca^{++}$ level which may be adjusted partially by the high affinity $Ca^{++}-ATPase$ in luteal cell membranes. Then, one may expect that luteotropic and/or luteolytic agents, such as gonadotropins, prostaglandin $F_{2{\alpha}}\;(PGF_{2{\alpha}})$ and ouabain, affect the intracellular $Ca^{++}$ level. In this present study, therefore, we examined the effects of luteinizing hormone (LH, or human chorionic gonadotropin, hCG), $PGF_{2{\alpha}}$ and ouabain on the kinetic properties of the high affinity $Ca^{++}-ATPase$ in light membrane, heavy membrane, and microsomal fractions from the highly luteinized ovary. LH (or hCG) increased the affinity and the Vmax for $Ca^{++}$ both in light membrane and heavy membrane. $PGF_{2{\alpha}}$ increased the Vmax in light membrane and decreased the Km in heavy membrane for $Ca^{++}$ at low concentration $(5\;{\mu}g/ml)$. At higher concentration, however, $PGF_{2{\alpha}}$ oppositly affected on kinetic properties, that shown at low concentration. Ouabain, a potent inhibitor of $Na^+-K^+-ATPase$, increased the Km at high concentration $(10^{-4}\;M)$, however, decreased the Vmax for $Ca^{++}$ in light membrane at low concentration $(10^{-6}\;M)$. Also, ouabain increased the Km for $Ca^{++}$ in heavy membrane without changes in the Vmax at both concentrations. It seems that LH and low dose of $PGF_{2{\alpha}}$ increase the intracellular $Ca^{++}$ level and cause in activation of $Ca^{++}-ATPase$, however, higher dose of $PGF_{2{\alpha}}$ and ouabain inhibit directly $Ca^{++}-ATPase$ activity and result in increase in intracellular $Ca^{++}$ level. According to the above results, we suggest that luteotropic and/or luteolytic agents regulate the luteal progesterone $(P_4)$ production through two different pathways; one is cyclic adenosine monophosphate (cAMP)-dependent and another is $Ca^{++}-dependent$. Intracellula. $Ca^{++}$ level regulated by the high affinity $Ca^{++}-ATPase$ may affect both pathways in a time-dependent fashion. LH (or hCG) acts on the luteal $P_4$ production via both pathways. The initial step is $Ca^{++}$ dependent, and the late step is cAMP dependent. $PGF_{2{\alpha}}$ and ouabain increase the intracellular $Ca^{++}$ concentration so that basal luteal $P_4$ production is increased and LH-stimulated $P_4$ production is inhibited by the inhibiting LH-dependent adenylate cyclase activity.