• Title/Summary/Keyword: Hydrogen transport

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Effects of insulin and IGF on growth and functional differentiation in primary cultured rabbit kidney proximal tubule cells - Effects of IGF-I on Na+ uptake - (초대배양된 토끼 신장 근위세뇨관세포의 성장과 기능분화에 대한 insulin과 IGF의 효과 - Na+ uptake에 대한 IGF-I의 효과 -)

  • Han, Ho-jae;Park, Kwon-moo;Lee, Jang-hern;Yang, IL-suk
    • Korean Journal of Veterinary Research
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    • v.36 no.4
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    • pp.783-794
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    • 1996
  • It has been suggested that ion transport systems are intimately involved in mediating the effects of growth regulatory factors on the growth of a number of different types of animal cells in vivo. The functional importance of the apical membrane $Na^+/H^+$ antiporter in the renal proximal tubule is evidenced by estimates that this transporter mediates the reabsorption of approximately one third of the filtered load of sodium and the bulk of the secretion of hydrogen ions. This study was designed to investigate the pathway utilized by IGF-I in regulating sodium transport in primary cultured renal proximal tubule cells. Results were as follows : 1. $Na^+$ was observed to accumulate in the primary cells as a function of time. Raising the concentration of extracellular NaCl induced an decrease in $Na^+$ uptake compared with control cells in a dose dependent manner. The rate of $Na^+$ uptake into the primary cells was about two times higher in the absence of NaCl($40.11{\pm}1.76pmole\;Na^+/mg\;protein/min$) than in the presence of 140mM NaCl($17.82{\pm}0.94pmole\;Na^+/mg\;protein/min$) at the 30 minute uptake. 2. $Na^+$ uptake was inhibited by IAA($1{\times}10^{-4}M$) or valinomycin($5{\times}10^{-6}M$) treatment($50.51{\pm}4.04$ and $57.65{\pm}2.27$ of that of control, respectively). $Na^+$ uptake by the primary proximal tubule cells was significantly increased by ouabain($5{\times}10^{-5}M$) treatment($140.23{\pm}3.37%$ of that of control). When actinomycin D($1{\times}10^{-7}M$) or cycloheximide($4{\times}10^{-5}M$) was applied, $Na^+$ uptake was decreased to $90.21{\pm}2.39%$ or $89.64{\pm}3.69%$ of control in IGF-I($1{\times}10^{-5}M$) treated cells, respectively. 3. Extracellular cAMP decreased $Na^+$ uptake in a dose-dependent manner($10^{-8}-10^{-4}M$). IBMX($5{\times}10^{-5}M$) also inhibited $Na^+$ uptake. Treatment of cells with pertussis toxin(50pg/ml) or cholera toxin($1{\mu}g/ml$) inhibited $Na^+$ uptake. Extracellular PMA decreased $Na^+$ uptake in a dose-dependent manner(1-100ng/ml). 100 ng/ml PMA concentration significantly inhibited $Na^+$ uptake in IGF-I treated cells. However, staurosporine($1{\times}10^{-7}M$) had no effect on $Na^+$ uptake. When PMA and staurosporine were added together, the inhibition of $Na^+$ uptake was not observed. In conclusion, sodium uptake in primary cultured rabbit renal proximal tubule cells was dependent on membrane potentials and intracellular energy levels. IGF-I stimulates sodium uptake through mechanisms that involve some degree of de novo protein and/or RNA synthesis, and cAMP and/or PKC pathway mediating the action mechanisms of IGF-I.

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Effect of Additives on Paper Aging (종이 첨가제가 종이의 노화에 미치는 영향)

  • 윤병호;이명구;최경화
    • Journal of Korea Foresty Energy
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    • v.21 no.2
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    • pp.25-33
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    • 2002
  • One of the critical problems to preserve books and documents in libraries and archives is the deterioration. Some of previous results showed that the major cause of paper deterioration was the acid-catalyzed hydrolysis of the cellulose in paper fibres and aging rate of acidic paper was faster than that of alkaline paper. Therefore, It is necessary to remove the acid in the paper for reducing the rate of paper deterioration. It has been reported to extend the useful life of acidic paper by three to five times. Recently, It has been recognized the need for an effective method of deacidifying large quantities of books and document. However, in the previous many reports little attention was paid to the effect of paper additives. In this paper, We carried out experiment about the effect of additives on paper aging and the effect of deacidification by the gaseous ethanolamines (monoehtanolamine, diethanolamine, triehtanolamine). In result, it was found that the strength of aging was in the order of the alum+rosin>alum >AKD> control and the rate of deacidification was in the order of the monoethanolamine>diethanolamine>triethanolamine. The treatment with the gaseous ethanolamines caused decreasing of brightness and dropping of fold endurances. However, deacidification by combination treatment of the various gaseous ehtnaolamines prevented from decreasing of brightness and dropping of folding endurances.

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Low temperature plasma deposition of microcrystalline silicon thin films for active matrix displays: opportunities and challenges

  • Cabarrocas, Pere Roca I;Abramov, Alexey;Pham, Nans;Djeridane, Yassine;Moustapha, Oumkelthoum;Bonnassieux, Yvan;Girotra, Kunal;Chen, Hong;Park, Seung-Kyu;Park, Kyong-Tae;Huh, Jong-Moo;Choi, Joon-Hoo;Kim, Chi-Woo;Lee, Jin-Seok;Souk, Jun-H.
    • 한국정보디스플레이학회:학술대회논문집
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    • 2008.10a
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    • pp.107-108
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    • 2008
  • The spectacular development of AMLCDs, been made possible by a-Si:H technology, still faces two major drawbacks due to the intrinsic structure of a-Si:H, namely a low mobility and most important a shift of the transfer characteristics of the TFTs when submitted to bias stress. This has lead to strong research in the crystallization of a-Si:H films by laser and furnace annealing to produce polycrystalline silicon TFTs. While these devices show improved mobility and stability, they suffer from uniformity over large areas and increased cost. In the last decade we have focused on microcrystalline silicon (${\mu}c$-Si:H) for bottom gate TFTs, which can hopefully meet all the requirements for mass production of large area AMOLED displays [1,2]. In this presentation we will focus on the transfer of a deposition process based on the use of $SiF_4$-Ar-$H_2$ mixtures from a small area research laboratory reactor into an industrial gen 1 AKT reactor. We will first discuss on the optimization of the process conditions leading to fully crystallized films without any amorphous incubation layer, suitable for bottom gate TFTS, as well as on the use of plasma diagnostics to increase the deposition rate up to 0.5 nm/s [3]. The use of silicon nanocrystals appears as an elegant way to circumvent the opposite requirements of a high deposition rate and a fully crystallized interface [4]. The optimized process conditions are transferred to large area substrates in an industrial environment, on which some process adjustment was required to reproduce the material properties achieved in the laboratory scale reactor. For optimized process conditions, the homogeneity of the optical and electronic properties of the ${\mu}c$-Si:H films deposited on $300{\times}400\;mm$ substrates was checked by a set of complementary techniques. Spectroscopic ellipsometry, Raman spectroscopy, dark conductivity, time resolved microwave conductivity and hydrogen evolution measurements allowed demonstrating an excellent homogeneity in the structure and transport properties of the films. On the basis of these results, optimized process conditions were applied to TFTs, for which both bottom gate and top gate structures were studied aiming to achieve characteristics suitable for driving AMOLED displays. Results on the homogeneity of the TFT characteristics over the large area substrates and stability will be presented, as well as their application as a backplane for an AMOLED display.

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Effect of $H_2O_2$ on Alveolar Epithelial Barrier Properties (폐상피세포 장벽에 대한 $H_2O_2$의 영향)

  • Suh, Duk-Joon;Cho, Se-Heon;Kang, Chang-Woon
    • Tuberculosis and Respiratory Diseases
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    • v.40 no.3
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    • pp.236-249
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    • 1993
  • Background: Among the injurious agents to which the lung airspaces are constantly exposed are reactive species of oxygen. It has been widely believed that reactive oxygen species may be implicated in the etiology of lung injuries. In order to elucidated how this oxidant causes lung cell injury, we investigated the effects of exogenous $H_2O_2$ on alveolar epithelial barrier characteristics. Methods: Rat type II alveolar epithelial cells were plated onto tissue culture-treated polycarbonate membrane filters. The resulting confluent monolayers on days 3 and 4 were mounted in a modified Ussing chamber and bathed on both sides with HEPES-buffered Ringer solution. The changes in short-circuit current (Isc) and monolayer resistance (R) in response to the exogenous hydroperoxide were measured. To determine the degree of cellular catalase participation in protection against $H_2O_2$ injury to the barrier, experiments were repeated in the presence of 20 mM aminotriazole (ATAZ, an inhibitor of catalase) in the same bathing fluid as the hydroperoxide. Results: These monolayers have a high transepithelial resistance (>2000 ohm-$cm^2$) and actively transport $Na^+$ from apical fluid. $H_2O_2$(0-100 mM) was then delivered to either apical or basolateral fluid. Resulting indicated that $H_2O_2$ decreased Isc and R gradually in dose-dependent manner. The effective concentration of apical $H_2O_2$ at which Isc (or R) was decreased by 50% at one hour ($ED_{50}$) was about 4 mM. However, basolateral $H_2O_2$ exposure led to $ED_{50}$ for Isc (and R) of about 0.04 mM. Inhibition of cellular catalase yielded $ED_{50}$ for Isc (and R) of about 0.4 mM when $H_2O_2$ was given apically, while $ED_{50}$ for basolateral exposure to $H_2O_2$ did not change in the presence of ATAZ. The rate of $H_2O_2$ consumption in apical and basolateral bathing fluids was the same, while cellualr catalase activity rose gradually with time in culture. Conclusion: Our data suggest that basolateral $H_2O_2$ may affect directly membrane component (e.g., $Na^+,\;K^+$-ATPase) located on the basolateral cell surface. Apical $H_2O_2$, on the other hand, may be largely degraded by catalase as it passes through the cells before reaching these membrane components. We conclude that alveolar epithelial barrier integrity as measured by Isc and R are compromised by $H_2O_2$ being relatively sensitive to basolateral (and insensitive to apical) $H_2O_2$.

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