Na 섭취제한,K 투여 및 이뇨 기간중 실혈성 Aldosterone 반응의 변동

고주환,유용운,이장규,성호경,박귀원 대한핵의학회 1977 핵의학 분자영상 Vol.11 No.1

고식염 섭취, Na 섭취제한, K 투여 및 이뇨기간중의 혈강 aldosterone 농도에 미치는 실혈의 영향을 정상 혈압을 유지하고 있는 청년 20명에서 관찰하여 아래와 같은 성적을 얻었다. 1) 실혈로 혈중 aldosterone 농도는 증가하였고 식염섭취제한이나 이뇨중의 실혈성 증가반응은 더욱 증대되었으나, K 투여로 aldosterone 농도가 이미 높은 개체에서는 증가반응을 가려낼 수 없었다. 2) 실혈시의 혈중 renin 활성도의 증가는 고식염식때 보다 Na 섭취제한이나 furosemide 이뇨시에 현저히 높았고 K 투여시의 실혈성 PRA 증가반응은 K를 별도로 투여치 않은 실험군과 별 변동이 없었다. 3) 실혈로 혈중 Na 농도에 큰 변동을 보이지 않았지만 모든 실험 조건하에서 감소경향은 나타내고 있었다. 4) 이상의 성적으로 보아 실혈에 의한 혈중 aldosterone 농도의 증가반응은 식염섭취제한이나 이뇨등의 부신 자극 요인이 있는 경우에 renin-aldosterone계의 활동 증가를 통한 aldosterone 분비의 가중현상을 보이나 K 섭취로 aldosterone 분비가 왕성한 기간중에는 실혈에 의한 renin 계의 aldosterone분비자극 첨가는 회의적이었다. Effect of sodium restriction with or without potassium supplement and furosemide diuresis on plasma aldosterone response to mild hemorrhage wese studied in normotensive young volunteers. After an overnight fast, blood were drawn just before and 10, 20, 30, 50, 70, 90, and 120 minutes after the 3H-aldosterone injection. The sum of blood delivered reached over 100ml (during two hours). Plasma aldosterone and renin were measured by means ot radioimmunoassay. The results were as followed; 1) Hemorrhage resulted in a moderate increase in plasma aldosterone level of volunteers with normal diet. 2) The mean figures of plasma aldosterone in subjects with sodium restriction and diuresis were likewise significantly increased by hemorrhage, however, the figure of the subjects with potassium supplement who already shown higher plasma level was without effect on hemorrhage. 3) Hemorrhage produced slight decrease in serum sodium concentration in every experimental conditions, although the changes were not significant. 4) Plasma renin activities after the hemorrhage followed a similar pattern with that of aldos terone, increased during sodium restriction cr diuresis and unaffected during potassium supplement. $quot;

Local Structural Changes Caused in Ni-Mn-Ga Alloy Films by Thermal Effects

이연승,K. K. Yu,Nina Lee,R. J. Kim,Y. J. Yoo,이영백,Y. V. Kudryavtsev 한국물리학회 2006 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.49 No.3

The local structural changes of Ni-Mn-Ga alloy films were investigated, according to the deposition temperature, by using the Ni, the Mn, and the Ga K-edge X-ray absorption fine structure (XAFS) and glancing-angle X-ray diraction. The structural characters of the film deposited at 720 K are similar to those of bulk Ni2MnGa with a cubic L21 phase, and the film deposited onto a cooled substrate (s150 K) is in a disordered structure. After annealing, the structural changes in the films deposited at 150 K are as follows: the films annealed at temperatures below 440 K are in a disordered phase, the structural ordering starts in the films annealed at 520 K, at 600 K, the films become ordered, and at 680 K, the cubic L21 and the tetragonal phases coexist. By XAFS, the Ni, the Mn and the Ga atoms are found to be arranged as an ordered cubic L21 phase in the ordered film and as Ni-Mn-Ga alloy clusters in the disordered film.

특이적 콜레라균 검출법 개발 및 해양 가검물에의 적용

김기상,이영희,황규잠,이광준,박강수,배송미,이점규,오경수,유정식,신영학 국립보건연구원 2000 국립보건원보 Vol.37 No.-

Novel dentin phosphoprotein frameshift mutations in dentinogenesis imperfecta type II

Lee, K‐,E,Kang, H‐,Y,Lee, S‐,K,Yoo, S‐,H,Lee, J‐,C,Hwang, Y‐,H,Nam, KH,Kim, J‐,S,Park, J‐,C,Kim, J‐,W Blackwell Publishing Ltd 2011 Clinical genetics Vol.79 No.4

<P>Lee K‐E, Kang H‐Y, Lee S‐K, Yoo S‐H, Lee J‐C, Hwang Y‐H, Nam KH, Kim J‐S, Park J‐C, Kim J‐W. Novel dentin phosphoprotein frameshift mutations in dentinogenesis imperfecta type II.</P><P>The dentin sialophosphoprotein (<I>DSPP</I>) gene encodes the most abundant non‐collagenous protein in tooth dentin and DSPP protein is cleaved into several segments including the highly phosphorylated dentin phosphoprotein (DPP). Mutations in the <I>DSPP</I> gene have been solely related to non‐syndromic form of hereditary dentin defects. We recruited three Korean families with dentinogenesis imperfecta (DGI) type II and sequenced the exons and exon–intron boundaries of the <I>DSPP</I> gene based on the candidate gene approach. Direct sequencing of PCR products and allele‐specific cloning of the highly repetitive exon 5 revealed novel single base pair (bp) deletional mutations (c.2688delT and c.3560delG) introducing hydrophobic amino acids in the hydrophilic repeat domain of the DPP coding region. All affected members of the three families showed exceptionally rapid pulp chambers obliteration, even before tooth eruption. Individuals with the c.3560delG mutation showed only mild, yellowish tooth discoloration, in contrast to the affected individuals from two families with c.2688delT mutation. We believe that these results will help us to understand the molecular pathogenesis of DGI type II as well as the normal process of dentin biomineralization.</P>

Telomere length, TERT and shelterin complex proteins in hepatocellular carcinomas expressing ''stemness''-related markers

Kim, H.,Yoo, J.E.,Cho, J.Y.,Oh, B.K.,Yoon, Y.S.,Han, H.S.,Lee, H.S.,Jang, J.J.,Jeong, S.H.,Kim, J.W.,Park, Y.N. Elsevier Science Publishers 2013 Journal of hepatology Vol.59 No.4

Background & Aims: Hepatocellular carcinomas (HCCs) expressing ''stemness''-related markers have been associated with aggressive biological behavior and poor prognosis. We examined the relationship between ''stemness''-related protein expression and telomere length, hTERT and shelterin complex protein expression and chromosomal instability. Methods: Quantitative fluorescent in situ hybridization for telomere length, immunohistochemistry for K19, EpCAM, CD133, c-kit, HepPar1, hTERT, TRF1, TRF2, POT1, RAP1 and TPP1, and TUNEL assay were performed in 137 HCCs, and array comparative genomic hybridization was performed with 24 HCCs. Results: Telomeres were significantly longer in HCCs expressing ''stemness''-related proteins (K19: p<0.001, EpCAM: p=0.002, CD133: p=0.002). On analyzing different tumor cells within EpCAM-expressing HCCs, EpCAM-positive tumor cells showed longer telomeres (1.329+/-0.246) compared to EpCAM-negative tumor cells (0.996+/-0.381) within the same HCCs (p=0.031). Telomeres were significantly longer in HCCs expressing hTERT (p=0.048) and RAP1 proteins (p=0.031). K19-expressing HCCs expressed hTERT (p=0.002), TRF2 (p=0.001) and TPP1 (p=0.013) more frequently compared to K19-negative HCCs. EpCAM-positivity was associated with more frequent hTERT (p=0.028), TPP1 (p=0.017), TRF2 (p=0.027) and POT1 (p=0.004) expression. Copy number alterations were more frequent in K19 and EpCAM-expressing HCCs compared to HCCs without these markers (K19: p=0.038, EpCAM: p=0.009). HCCs with longer telomeres were associated with a shorter overall (p=0.019) and disease-free survivals (p=0.049), and decreased disease-free survivals were seen in TRF2-positive HCCs (p=0.018). Conclusions: HCCs expressing ''stemness''-related proteins are characterized by increased telomere length, increased expression of hTERT and shelterin complex proteins, and increased chromosomal instability compared to conventional HCCs. Longer telomeres and TRF2 expression in HCCs are associated with poor patient outcomes.

15-Deoxy-Δ^12,14-prostaglandin J₂ prevents oxidative injury by upregulating the expression of aldose reductase in vascular smooth muscle cells

Kang, E. S.,Hwang, J. S.,Ham, S. A.,Park, M. H.,Kim, G. H.,Paek, K. S.,Yoo, T.,Lee, W. J.,Kang, K. R.,Lee, J. H.,Choi, Y. J.,Seo, H. G. Informa Healthcare 2014 Free radical research Vol.48 No.2

<P>The omega-6 fatty acid derivative 15-Deoxy-Δ<SUP>12,14</SUP>-prostaglandin J<SUB>2</SUB> (15d-PGJ<SUB>2</SUB>) is believed to play a role in cellular protection against oxidative stress in diverse cell systems. However, the cellular mechanisms by which protection is afforded by 15d-PGJ<SUB>2</SUB> are not fully elucidated in vascular smooth muscle cells (VSMCs). In this study, we report the finding that 15d-PGJ<SUB>2</SUB> elicited a time and concentration- dependent increase in aldose reductase (AR) expression. This induction was independent of the activation of peroxisome proliferator- activated receptor γ. Inhibition of phosphatidylinositol 3-kinase (PI3K) significantly suppressed the increase in expression and promoter activity of AR induced by 15d-PGJ<SUB>2</SUB>. Luciferase reporter assays demonstrated that 15d-PGJ<SUB>2</SUB> targets the multiple stress response regions comprising the antioxidant response element in the promoter of the AR gene. 15d-PGJ<SUB>2</SUB>-mediated induction of AR promoter activity was potentiated in the presence of nuclear factor-erythroid 2-related factor 2 (Nrf2), but not in cells expressing dominant negative Nrf2. Cells treated with 15d-PGJ<SUB>2</SUB> were resistant to oxidant-induced apoptotic cell death by inhibiting production of reactive oxygen species. These effects were significantly attenuated in the presence of an AR inhibitor or small interfering RNA against AR, indicating that AR plays a protective role against oxidative injury. Taken together, these findings demonstrate that activation of PI3K by 15d-PGJ<SUB>2</SUB> increases the expression of AR through Nrf2, and increased AR activity may function as an important cellular response against oxidative injury.</P>

Overview of KSTAR research progress and future plans toward ITER and K-DEMO

Park, H.K.,Choi, M.J.,Hong, S.H.,In, Y.,Jeon, Y.M.,Ko, J.S.,Ko, W.H.,Kwak, J.G.,Kwon, J.M.,Lee, J.,Lee, J.H.,Lee, W.,Nam, Y.B.,Oh, Y.K.,Park, B.H.,Park, J.K.,Park, Y.S.,Wang, S.J.,Yoo, M.,Yoon, S.W.,B IOP 2019 Nuclear fusion Vol.59 No.11

<P>A decade-long operation of the Korean Superconducting Tokamak Advanced Research (KSTAR) has contributed significantly to the operation of superconducting tokamak devices and the advancement of tokamak physics which will be beneficial for the ITER and K-DEMO programs. Even with limited heating capability, various conventional as well as new operating regimes have been explored and have achieved improved performance. As examples, a long pulse high-confinement mode operation with and without an edge-localized mode (ELM) crash was well over 70 and 30 s, respectively. The unique capabilities of KSTAR allowed it to improve the capability of controlling harmful instabilities, and they have been instrumental in uncovering much new physics. The highlights are that the L/H transition threshold power is sensitive to the resonant magnetic perturbation (RMP) and insensitive to non-resonant magnetic perturbation. Co-<I>I</I> <SUB>p</SUB> offset rotation dominated by an electron channel predicted by general neoclassical toroidal viscosity theory was confirmed. Improved heat dispersal in a divertor system using three rows of rotating RMP was demonstrated and predictive control of the ELM-crash with <I>a priori</I> modeling was successfully tested. In magnetohydrodynamic physics, validation of the full reconnection model (i.e. <I>q</I> <SUB>0</SUB>  >  1 right after the sawtooth crash) and self-consistent validation of the anisotropic distribution of turbulence amplitude and flow in the presence of the 2/1 island with theoretical models were achieved. The turbulence amplitude induced by RMP was linearly increased with the slow RMP coil current ramp-up time (i.e. the magnetic diffusion time scale). The <I>D</I> <SUB> <I>α</I> </SUB> spikes (i.e. ELM-crash amplitude) was linearly decreased with the turbulence amplitude and not correlated with the perpendicular electron flow. In the turbulence area, a non-diffusive ‘avalanche’ transport event and the role of a quiescent coherent mode in confinement were studied. To accommodate the anticipation of a higher performance of the KSTAR plasmas with the increased heating powers, a new divertor/internal interface with a full active cooling system will be implemented after a full test of the new heating (neutral beam injection II and electron cyclotron heating) and current drive (CD) (Helicon and lower hybrid CD) systems. An upgrade plan for the internal hardware, heating systems and efficient CD system may allow for a long pulse operation of higher performance plasmas at <I>β</I> <SUB>N</SUB>  >  3.0 with <I>f</I> <SUB>bs</SUB> ~ 0.5 and <I>T</I> <SUB>i</SUB>  >  10 keV.</P>

Novel signaling axis for ROS generation during K-Ras-induced cellular transformation

Park, M-T,Kim, M-J,Suh, Y,Kim, R-K,Kim, H,Lim, E-J,Yoo, K-C,Lee, G-H,Kim, Y-H,Hwang, S-G,Yi, J-M,Lee, S-J Macmillan Publishers Limited 2014 CELL DEATH AND DIFFERENTIATION Vol.21 No.8

Reactive oxygen species (ROS) are well known to be involved in oncogene-mediated cellular transformation. However, the regulatory mechanisms underlying ROS generation in oncogene-transformed cells are unclear. In the present study, we found that oncogenic K-Ras induces ROS generation through activation of NADPH oxidase 1 (NOX1), which is a critical regulator for the K-Ras-induced cellular transformation. NOX1 was activated by K-Ras-dependent translocation of p47<SUP>phox</SUP>, a subunit of NOX1 to plasma membrane. Of note, PKCδ, when it was activated by PDPK1, directly bound to the SH3-N domain of p47<SUP>phox</SUP> and catalyzed the phosphorylation on Ser348 and Ser473 residues of p47<SUP>phox</SUP> C-terminal in a K-Ras-dependent manner, finally leading to its membrane translocation. Notably, oncogenic K-Ras activated all MAPKs (JNK, ERK and p38); however, only p38 was involved in p47<SUP>phox</SUP>-NOX1-dependent ROS generation and consequent transformation. Importantly, K-Ras-induced activation of p38 led to an activation of PDPK1, which then signals through PKCδ, p47<SUP>phox</SUP> and NOX1. In agreement with the mechanism, inhibition of p38, PDPK1, PKCδ, p47<SUP>phox</SUP> or NOX1 effectively blocked K-Ras-induced ROS generation, anchorage-independent colony formation and tumor formation. Taken together, our findings demonstrated that oncogenic K-Ras activates the signaling cascade p38/PDPK1/PKCδ/p47<SUP>phox</SUP>/NOX1 for ROS generation and consequent malignant cellular transformation.

Features and Properties of $YBa_2$$Cu_3$$O_{7-x}$ Films Grown on SrTi$O_3$ by High Frequency PLD

Shi, D.Q.,Ko, R.K.,Song, K.J.,Chung, J.K.,Choi, S.J.,Park, Y.M.,Shin, K.C.,Yoo, S.I.,Park, C. The Korean Superconductivity Society 2003 Progress in superconductivity Vol.5 No.1

YBCO films were deposited with various thicknesses from 100nm to 1.6$\mu\textrm{m}$ on single crystal $SrTiO_3$ substrates by pulsed laser deposition (PLD). The effects of different deposition conditions, especially different deposition rates by means of changing the pulsed laser frequency up to 200Hz, on the J$_{c}$ value were studied. For YBCO film with the thickness of 200nm, the $J_{c}$ value of $2.1MA/\textrm{cm}^2$ has been achieved under the high deposition rate of 3.2nm/s (190nm/min). The $J_{c}$ can be maintained greater than $1M/\textrm{cm}^2$ with the thickness less than 1$\mu\textrm{m}$. The X-ray analysis was used to examine the texture, crystallization and surface quality. The SEM was employed to analyze the surface of YBCO, and it was shown the surface of YBCO film became rougher with increasing the thickness. There were many large singular outgrowths and networks of outgrowths on the surface of YBCO films which lowered the density of thick YBCO film. The outgrowth network was probably the a-axis YBCO corresponding to XRD $\theta$-2$\theta$scan and $\chi$-scan which were used to characterize a-axis orientation of YBCO film. The reason for J$_{c}$ declining with increasing the thickness was studied and discussed.sed.

生體內 藥劑耐性 및 Plasmid 傳達에 關한 硏究

金鎬薰,李明遠,李英姬,金基湘,兪天權,吳明燉,李悌煥,李点揆,琴東吉,鄭泰華,李潤台 국립보건연구원 1989 국립보건원보 Vol.26 No.