• The Korean Journal of Physiology and Pharmacology
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• 제7권3호
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• pp.119-124
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• 2003

To elucidate the molecular mechanism of pharmacological action of local anesthetics, we studied membrane actions of tetracaine, bupivacaine, lidocaine, prilocaine and procaine. Fluorescence polarization of n-(9-anthroyloxy)stearic acid (n-AS) was used to examine the effects of these local anesthetics on differential rotational mobility of different positions of the number of synaptosomal plasma membrane vesicle (SPMV) phospholipid carbon atoms. The four membrane components differed with respect to 3, 6, 9 and 16-(9-anthroyloxy)stearic acid (3-AS, 6-AS, 9-AS and 16-AP) probes, indicating that differences in the membrane fluidity might be present. Degrees of the rotational mobility of 3-AS, 6-AS, 9-AS and 16-AP were different depending on depth of hydrocarbon interior. In a dose-dependentmanner, tetracaine, bupivacaine, lidocaine, prilocaine and procaine decreased anisotropy of 3-AS, 6-AS, 9-AS and 16-AP in the hydrocarbon interior of the SPMV. These results indicate that local anesthetics have significant disordering effects on hydrocarbon interior of the SPMV, thus affecting the transport of $Na^+$ and $K^+$ in nerve membranes and leading to anesthetic action.

• Biomolecules & Therapeutics
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• 제25권6호
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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.

• Molecules and Cells
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• 제39권10호
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• pp.728-733
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• 2016

Mesenchymal stem cells (MSCs) effectively reduce airway inflammation and regenerate the alveolus in cigarette- and elastase-induced chronic obstructive pulmonary disease (COPD) animal models. The effects of stem cells are thought to be paracrine and immune-modulatory because very few stem cells remain in the lung one day after their systemic injection, which has been demonstrated previously. In this report, we analyzed the gene expression profiles to compare mouse lungs with chronic exposure to cigarette smoke with non-exposed lungs. Gene expression profiling was also conducted in a mouse lung tissue with chronic exposure to cigarette smoke following the systemic injection of human cord blood-derived mesenchymal stem cells (hCB-MSCs). Globally, 834 genes were differentially expressed after systemic injection of hCB-MSCs. Seven and 21 genes, respectively, were up-and downregulated on days 1, 4, and 14 after HCB-MSC injection. The Hbb and Hba, genes with oxygen transport and antioxidant functions, were increased on days 1 and 14. A serine protease inhibitor was also increased at a similar time point after injection of hCB-MSCs. Gene Ontology analysis indicated that the levels of genes related to immune responses, metabolic processes, and blood vessel development were altered, indicating host responses after hCB-MSC injection. These gene expression changes suggest that MSCs induce a regeneration mechanism against COPD induced by cigarette smoke. These analyses provide basic data for understanding the regeneration mechanisms promoted by hCB-MSCs in cigarette smoke-induced COPD.

• 한국해양학회지
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• 제25권4호
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• pp.182-188
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• 1990

낙동강 하구역에서의 중금속 분포와 퇴적작용에 대한 연구를 1987년 10월부터 1988년 9월에 걸쳐 수행하였다. 연구지역의 퇴적환경은 하구환경이며 입도분석 특성에 따라 모래섬, 수로 및 조간대 지역으로 분류된다. 모래섬의 퇴적물은 뜬짐, 틤짐, 굴 르기 상태로 운반되었으며, 조간대는 주로 뜬점과 틤틔짐으로 이동되었다. 수로의 퇴적 물은 거의 굴르기와 약간의 뜬짐 상태로 운반되었다. 모래섬은 강한 파도의 영향을 받 으며, 그 후방에 놓인 조간대는 약한 조류의 영향을 받는다. 수중에서 Cu, Cd, $Cr^{6+}$, Pb, Zn의 농도는 각각 최고의 27.9, 6.7, 20.4, 16.3, 37.3 ppb를 기록하였으며, 퇴적물에서는 20.0, 1.65, 25.4, 15.4 132.9 ppm을 나타내었다. 이들 중금속의 재첩 (V. Muller)에 의한 총섭취인자는 각각 1600, 310, 310, 490, 7900g이었다.

• 한국수자원학회논문집
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• 제46권7호
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• pp.707-717
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• 2013

충적하천에서 발생하는 하천의 침식과 퇴적은 흐름을 통해 발생하는 자연적인 현상이다. 침식 및 퇴적과 관련된 수치모형을 이용한 분석은 하천에 존재하는 보와 같은 수리구조물들의 유사이송을 연구하는데 중요한 요소이다. 본 연구에서는 다기능보들의 효과적인 운영을 위하여 낙동강수계에 위치해 있는 창녕함안보를 대상으로 하상변동을 예측하였다. 2차원 모형은 CCHE2D를 이용하여 유사이송이 지배적으로 발생하는 다기능보 상 하류 구간 12 km를 대상으로 침식과 퇴적에 대한 모의를 수행하였다. 2003년 태풍 "매미"사상을 대상으로 모형을 검 보정 하였으며, 모의결과와 관측값의 비교를 통하여 전체 모의구간에서 신뢰성 있는 결과가 도출되었다. 함안창녕보가 건설된 이후 태풍사상에 의한 하상변동은 상당히 증가하는 것으로 나타났고 하상변동은 유사의 재분배를 야기하였다. 보와 같은 수리구조물들은 하도내 흐름과 유속을 변화시키기 때문에 세굴과 퇴적 문제를 심화시켰다.

• 한국자동차공학회논문집
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• 제17권1호
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• pp.137-145
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• 2009

The steady-state kinetics of the selective catalytic reduction (SCR) of $NO_X$ with $NH_3$ has been investigated over a commercial ${V_2}{O_5}/TiO_2$ catalyst. In order to account for the influence of transport effects the kinetics are coupled with a fully transient two-phase 1D+1D monolith channel model. The Langmuir-Hinshelwood (L-H) mechanism is adopted to describe the steady-state kinetic behavior of the ${V_2}{O_5}/TiO_2$ catalyst. The reaction rate expressions are based on previously reported papers and are modified to fit the experimental data. The steady-state chemical reaction scheme used in the present mathematical model has been validated extensively with experimental data of selective $NO_X$ reduction efficiency for a wide range of inlet conditions such as space velocity, oxygen concentrations, water concentration, and $NO_2/NO$ ratio. The parametric investigations are performed to examine how the $NH_3$ slip from a SCR $DeNO_X$ catalyst and the conversion of $NO_X$ are affected by the reaction temperature, $NH_3/NO_X$ feed ratio, and space velocity for feed gas compositions with $NO_2/NO_X$ ratios of 0 and 0.5.

• 산업경영시스템학회지
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• 제35권3호
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• pp.192-203
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• 2012

As a leading nation of ubiquitous technology, South Korea has been promoting u-City pilot projects throughout the country. According to 'Fundamental Construction Law of u-City,' u-City projects are classified into old-town and new-town types. However, most projects have focused only on the new-town type. Pushing forward large-scale land development projects, Korea Land and Housing Corporation (LH Co.) under Ministry of Land Transport and Maritime Affairs (MLTM) has gained a development profit out of the u-City infrastructure and then donated the infrastructure to a local government without making any plan for operations. In the process of u-City pilot projects, old-towns have been relatively ignored and various of unexpected problems have emerged. Building the u-City of an old-town is not easy due to many constraints such as huge initial investment, long validity and verification procedures, lack of useful services for citizens, lack of professional outsourcing methods for business promotion, high operating costs of the integrated control center, inadequate law related, insufficient institutional requirements and so on. This paper introduces a case study on u-City development for an old-town, Ansan City, as a private investment project. The case will help boost u-City projects for old-towns by solving their problems and providing an effective operational mechanism. As the first BTL (Build-Transfer-Lease) project for constructing u-City, 'Broadband Information Network Development Project' of Ansan City will provide a reference model of expanding u-City projects for other cities.

• 약학회지
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• 제40권1호
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• pp.102-111
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• 1996

LB10522 is a new parenteral broad spectrum cephalosporin with a catechol moiety at C-7 position of beta-lactam ring. This compound can utilize tonB-dependent iron transp ort system in addition to porin proteins to enter bacterial periplasmic space and access to penicillin-binding proteins (PBPs) which are the lethal targets of ${\beta}$-lactam antibiotics. The chelating activity of LB10522 to metal iron was measured by spectrophotometrically scanning the absorbance from 200 to 900nm. When $FeCl_3$ was added, optical density was increased between 450 and 800nm. LB10522 was more active against gram-negative strains in iron-depleted media than in iron-replete media. This is due to the increased expression of iron transport channels in iron-depleted condition. LB10522 showed a similar activity against E. coli DC2 (permeability mutant) and E. coli DCO (wild type strain) in both iron-depleted and iron-replete media, indicating a minimal permeaility barrier for LB10522 uptake. LB10522 had high affinities to PBP 3 and PBP 1A, 1B of E. coli. By blocking these proteins, LB10522 caused inhibition of cell division and the eventual death of cells. This result was correlated well with the morphological changes in E. coli exposed to LB10522. Although the in vitro MIC of LB10522 against P. aeruginosa 1912E mutant (tonB) was 8-times higher than that of the P. aeruginosa 1912E parent strain, LB10522 showed a similar in vivo protection efficacy against both strains in the mouse systemic infection model. This result suggested that tonB mutant, which requires a high level of iron for normal growth, might have a difficulty in surviving in their host with an iron-limited environment.

• 대한화학회지
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• 제60권3호
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• pp.169-176
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• 2016

Borate 완충용액에서 Al의 부식과 부동화에 관하여 변전위법, 대 시간 전류법 그리고 다중 주파수 전기화학적 임피던스 측정법으로 조사하였다. 공기 또는 산소의 영향은 환원과정에 영향을 주었지만 산화반응에는 영향을 미치지 못 하는 것으로 보인다. 부동화 영역에서 생성되는 피막의 전기적 성질은 Mott-Schottky 식이 적용되는 n-type 반도체 성질을 보였다. 낮은 전극전위에서 생성되는 Al의 산화피막은 Al(OH)₃로 충분한 부동화 효과를 보이지 못하나, 전극전위가 증가하면서 Al₂O₃로 변하였다. Al₂O₃ 피막은 “전기장에 의한-이온의 이동” 과정에 의하여 성장하는 것으로 보인다.

• Molecules and Cells
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• 제39권3호
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• pp.266-279
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• 2016

The mechanism by which 12-O-tetradecanoylphorbol-13-acetate (TPA) bypasses cellular senescence was investigated using human diploid fibroblast (HDF) cell replicative senescence as a model. Upon TPA treatment, protein kinase C (PKC) ${\alpha}$ and $PKC{\beta}1$ exerted differential effects on the nuclear translocation of cytoplasmic pErk1/2, a protein which maintains senescence. $PKC{\alpha}$ accompanied pErk1/2 to the nucleus after freeing it from $PEA-15pS^{104}$ via $PKC{\beta}1$ and then was rapidly ubiquitinated and degraded within the nucleus. Mitogen-activated protein kinase docking motif and kinase activity of $PKC{\alpha}$ were both required for pErk1/2 transport to the nucleus. Repetitive exposure of mouse skin to TPA downregulated $PKC{\alpha}$ expression and increased epidermal and hair follicle cell proliferation. Thus, $PKC{\alpha}$ downregulation is accompanied by in vivo cell proliferation, as evidenced in 7, 12-dimethylbenz(a)anthracene (DMBA)-TPA-mediated carcinogenesis. The ability of TPA to reverse senescence was further demonstrated in old HDF cells using RNA-sequencing analyses in which TPA-induced nuclear $PKC{\alpha}$ degradation freed nuclear pErk1/2 to induce cell proliferation and facilitated the recovery of mitochondrial energy metabolism. Our data indicate that TPA-induced senescence reversal and carcinogenesis promotion share the same molecular pathway. Loss of $PKC{\alpha}$ expression following TPA treatment reduces pErk1/2-activated SP1 biding to the $p21^{WAF1}$ gene promoter, thus preventing senescence onset and overcoming G1/S cell cycle arrest in senescent cells.