Imazethapyr 유도체의 제초활성에 미치는 3-(N-methyl-N-(X)-치환-phenylaminooxoacetyl) group의 영향

성낙도,김현재,장해성,김대황 충남대학교 생물공학연구소 1993 생물공학연구지 Vol.3 No.-

새로운 25종의 Imazethapyr 유도체, (2-(4-isopropyl-4-methyl-5-oxo-2-imidazolin-2-yl)-3-(N-methyl-N-(X)치환 -phenylaminooxoacetyl)-5-methylpyridine)들을 합성하여 치환기(X) 변화에 따른 발아 전 후, 피(Echinochla crus-galli.)의 제초활성에 미치는 3-(N-methyl-N-(X)치환 -phenylaminoozoacetyl) group의 영향을 검토한 바, 발아 전보다 발아 후의 제초활성에 더 큰 영향을 미침을 알 수 있었다. 발아 후의 제초활성은 X-치환기의 전자밀게 효과와 입체상수(E_s)에 의존적이었으며 가장 큰 제초활성을 나타내는 화합물로는 bulky(E_s<O)하고 전자밀게 (б<O)가 치환된 화합물, 15(4-t-butyl group)와 20(3,5-dimethyl group)이었다. 그리고 높은 제초활성을 나타낼 것으로 예상되는 화합물의 조건들이 검토되었다. (1993년 9월 18일 접수, 1993년 9월 22일 수리). New twenty five Imazethapyr derivatives, [2-(4-isopropyl-4-methyl-5-oxo-2-imidazolin-2-yl)-3-(N-methyl-N-X(sub.)-phenylaminooxoacetyl)-5-methylpyridine] were synthesized. and The quantitative structure activity relationships (QSARs) between their post-emergence herbicidal activity(pI_50) values in vivo against Barnyard grass (Echinochloa crus-galli) and physicochemical parameters of substituents(X) of 3-(N-methyl-N-X(sub.)-phenylaminoo-xoacetyl) group have been studied. From the basis on the findings, in case of post-emergence, the activities were dependent on the steric constant(E_s<θ)and electron donating (o<O) effect by subsitituents(X) of 3-(N-methyl-N-X(sub.)phenylaminooxacetyl) group. Therefore, The most effective compound, 15 (4-t-butyl group) and 20 (3,5-dimethyl group) were examined in this study. And the conditions on the compounds predicted to show higher herbicidal activity were also discussed.

An upgrade of the magnetic diagnostic system of the DIII-D tokamak for non-axisymmetric measurements.

King, J D,Strait, E J,Boivin, R L,Taussig, D,Watkins, M G,Hanson, J M,Logan, N C,Paz-Soldan, C,Pace, D C,Shiraki, D,Lanctot, M J,La Haye, R J,Lao, L L,Battaglia, D J,Sontag, A C,Haskey, S R,Bak, J G American Institute of Physics 2014 Review of scientific instruments Vol.85 No.8

<P>The DIII-D tokamak magnetic diagnostic system [E. J. Strait, Rev. Sci. Instrum. 77, 023502 (2006)] has been upgraded to significantly expand the measurement of the plasma response to intrinsic and applied non-axisymmetric '3D' fields. The placement and design of 101 additional sensors allow resolution of toroidal mode numbers 1 n 3, and poloidal wavelengths smaller than MARS-F, IPEC, and VMEC magnetohydrodynamic model predictions. Small 3D perturbations, relative to the equilibrium field (10(-5) < δB/B0 < 10(-4)), require sub-millimeter fabrication and installation tolerances. This high precision is achieved using electrical discharge machined components, and alignment techniques employing rotary laser levels and a coordinate measurement machine. A 16-bit data acquisition system is used in conjunction with analog signal-processing to recover non-axisymmetric perturbations. Co-located radial and poloidal field measurements allow up to 14.2 cm spatial resolution of poloidal structures (plasma poloidal circumference is ~500 cm). The function of the new system is verified by comparing the rotating tearing mode structure, measured by 14 BP fluctuation sensors, with that measured by the upgraded B(R) saddle loop sensors after the mode locks to the vessel wall. The result is a nearly identical 2/1 helical eigenstructure in both cases.</P>

J/ψ Elliptic Flow in Pb-Pb Collisions at sNN=5.02 TeV

Acharya, S.,Adamová,, D.,Adolfsson, J.,Aggarwal, M. M.,Aglieri Rinella, G.,Agnello, M.,Agrawal, N.,Ahammed, Z.,Ahn, S. U.,Aiola, S.,Akindinov, A.,Al-Turany, M.,Alam, S. N.,Albuquerque, D. S. D. American Physical Society 2017 Physical Review Letters Vol.119 No.24

<P>We report a precise measurement of the J/psi elliptic flow in Pb-Pb collisions at root s(NN) = 5.02 TeV with the ALICE detector at the LHC. The J/psi mesons are reconstructed at midrapidity (|y| < 0.9) in the dielectron decay channel and at forward rapidity (2.5 < y < 4.0) in the dimuon channel, both down to zero transverse momentum. At forward rapidity, the elliptic flow v(2) of the J/psi is studied as a function of the transverse momentum and centrality. A positive v(2) is observed in the transverse momentum range 2<p(T)<8GeV/c in the three centrality classes studied and confirms with higher statistics our earlier results at root s(NN) = 2.76 TeV in semicentral collisions. At midrapidity, the J/psi v(2) is investigated as a function of the transverse momentum in semicentral collisions and found to be in agreement with the measurements at forward rapidity. These results are compared to transport model calculations. The comparison supports the idea that at low p(T) the elliptic flow of the J/psi originates from the thermalization of charm quarks in the deconfined medium but suggests that additional mechanisms might be missing in the models.</P>

D -Meson Azimuthal Anisotropy in Midcentral Pb-Pb Collisions at sNN=5.02 TeV

Acharya, S.,Adamová,, D.,Adolfsson, J.,Aggarwal, M. M.,Aglieri Rinella, G.,Agnello, M.,Agrawal, N.,Ahammed, Z.,Ahmad, N.,Ahn, S. U.,Aiola, S.,Akindinov, A.,Alam, S. N.,Alba, J. L. B.,Albuquerque American Physical Society 2018 Physical Review Letters Vol.120 No.10

<P>The azimuthal anisotropy coefficient v(2) of prompt D-0, D+, D*+, and D-s(+) mesons was measured in midcentral (30%-50% centrality class) Pb-Pb collisions at a center-of-mass energy per nucleon pair root s(NN)=5.02 TeV, with the ALICE detector at the LHC. The D mesons were reconstructed via their hadronic decays at midrapidity, |y| < 0.8, in the transverse momentum interval 1 < p(T) < 24 GeV/c. The measured D-meson v(2) has similar values as that of charged pions. The D-s(+) v(2), measured for the first time, is found to be compatible with that of nonstrange D mesons. The measurements are compared with theoretical calculations of charm-quark transport in a hydrodynamically expanding medium and have the potential to constrain medium parameters.</P>

J/ψ production as a function of charged particle multiplicity in pp collisions at s =7 TeV

ALICE Collaboration,Abelev, B.,Adam, J.,Adamova, D.,Adare, A.M.,Aggarwal, M.M.,Aglieri Rinella, G.,Agocs, A.G.,Agostinelli, A.,Aguilar Salazar, S.,Ahammed, Z.,Ahmad Masoodi, A.,Ahmad, N.,Ahn, S.U.,Aki North-Holland Pub. Co 2012 Physics letters: B Vol.712 No.3

The ALICE Collaboration reports the measurement of the relative J/ψ yield as a function of charged particle pseudorapidity density dN<SUB>ch</SUB>/dη in pp collisions at s=7 TeV at the LHC. J/ψ particles are detected for p<SUB>t</SUB>>0, in the rapidity interval |y|<0.9 via decay into e<SUP>+</SUP>e<SUP>-</SUP>, and in the interval 2.5<y<4.0 via decay into μ<SUP>+</SUP>μ<SUP>-</SUP> pairs. An approximately linear increase of the J/ψ yields normalized to their event average (dN<SUB>J/ψ</SUB>/dy)/<dN<SUB>J/ψ</SUB>/dy> with (dN<SUB>ch</SUB>/dη)/<dN<SUB>ch</SUB>/dη> is observed in both rapidity ranges, where dN<SUB>ch</SUB>/dη is measured within |η|<1 and p<SUB>t</SUB>>0. In the highest multiplicity interval with <dN<SUB>ch</SUB>/dη(bin)≥24.1, corresponding to four times the minimum bias multiplicity density, an enhancement relative to the minimum bias J/ψ yield by a factor of about 5 at 2.5<y<4 (8 at |y|<0.9) is observed.

D_s⁺ meson production at central rapidity in proton-proton collisions at s=7 TeV

ALICE Collaboration,Abelev, B.,Adam, J.,Adamova, D.,Adare, A.M.,Aggarwal, M.M.,Aglieri Rinella, G.,Agocs, A.G.,Agostinelli, A.,Aguilar Salazar, S.,Ahammed, Z.,Ahmad, N.,Ahmad Masoodi, A.,Ahn, S.A.,Ahn North-Holland Pub. Co 2012 Physics letters: B Vol.718 No.2

The p<SUB>T</SUB>-differential inclusive production cross section of the prompt charm-strange meson D<SUB>s</SUB><SUP>+</SUP> in the rapidity range |y|<0.5 was measured in proton-proton collisions at s=7 TeV at the LHC using the ALICE detector. The analysis was performed on a data sample of 2.98x10<SUP>8</SUP> events collected with a minimum-bias trigger. The corresponding integrated luminosity is L<SUB>int</SUB>=4.8 nb<SUP>-1</SUP>. Reconstructing the decay D<SUB>s</SUB><SUP>+</SUP>→φπ<SUP>+</SUP>, with φ→K<SUP>-</SUP>K<SUP>+</SUP>, and its charge conjugate, about 480 D<SUB>s</SUB><SUP>+/-</SUP> mesons were counted, after selection cuts, in the transverse momentum range 2<p<SUB>T</SUB><12 GeV/c. The results are compared with predictions from models based on perturbative QCD. The ratios of the cross sections of four D meson species (namely D<SUP>0</SUP>, D<SUP>+</SUP>, D<SUP>@?+</SUP> and D<SUB>s</SUB><SUP>+</SUP>) were determined both as a function of p<SUB>T</SUB> and integrated over p<SUB>T</SUB> after extrapolating to full p<SUB>T</SUB> range, together with the strangeness suppression factor in charm fragmentation. The obtained values are found to be compatible within uncertainties with those measured by other experiments in e<SUP>+</SUP>e<SUP>-</SUP>, ep and pp interactions at various centre-of-mass energies.

15-Deoxy-Δ^12,14-prostaglandin J₂ induces p53 expression through Nrf2-mediated upregulation of heme oxygenase-1 in human breast cancer cells

Kim, D. H.,Song, N. Y.,Kim, E. H.,Na, H. K.,Joe, Y.,Chung, H. T.,Surh, Y. J. Informa Healthcare 2014 Free radical research Vol.48 No.9

<P>Heme oxygenase-1 (HO-1) is a stress-responsive enzyme that has antioxidant and cytoprotective functions. However, HO-1 has oncogenic functions in cancerous or transformed cells. In the present work, we investigated the effects of HO-1 on the expression of p53 induced by 15-deoxy-Δ<SUP>12,14</SUP>-prostaglandin J<SUB>2</SUB> (15d-PGJ<SUB>2</SUB>) in human breast cancer (MCF-7) cells. Treatment of MCF-7 cells with 15d-PGJ<SUB>2</SUB> led to time-dependent increases in the expression of p53 as well as HO-1. Upregulation of p53 expression by 15d-PGJ<SUB>2</SUB> was abrogated by si-RNA knock-down of HO-1. In MCF-7 cells transfected with HO-1 si-RNA, 15d-PGJ<SUB>2</SUB> failed to induce expression of p53 as well as HO-1. In addition, HO-1 inducers enhanced the p53 expression. We speculated that iron, a by-product of HO-1-catalyzed reactions, could mediate 15d-PGJ<SUB>2</SUB>-induced p53 expression. Upregulation of p53 expression by 15d-PGJ<SUB>2</SUB> was abrogated by the iron chelator desferrioxamine in MCF-7 cells. Iron released from heme by HO-1 activity is mostly in the Fe<SUP>2+</SUP> form. When MCF-7 cells were treated with the Fe<SUP>2+</SUP>-specific chelator phenanthroline, 15d-PGJ<SUB>2</SUB>-induced p53 expression was attenuated. In addition, levels of the Fe-sequestering protein H-ferritin were elevated in 15d-PGJ<SUB>2</SUB>-treated MCF-7 cells. In conclusion, upregulation of p53 and p21 via HO-1 induction and subsequent release of iron with accumulation of H-ferritin may confer resistance to oxidative damage in cancer cells frequently challenged by redox-cycling anticancer drugs.</P>

Effect of contrast-induced nephropathy on cardiac outcomes after use of nonionic isosmolar contrast media during coronary procedure

Cho, J.Y.,Jeong, M.H.,Hwan Park, S.,Kim, I.S.,Park, K.H.,Sim, D.S.,Yoon, N.S.,Yoon, H.J.,Park, H.W.,Hong, Y.J.,Kim, J.H.,Ahn, Y.,Cho, J.G.,Park, J.C.,Kang, J.C. Japanese College of Cardiology 2010 Journal of cardiology Vol.56 No.3

Contrast-induced nephropathy (CIN) has been increasing and seems to be associated with clinical outcomes in ischemic heart disease. This study aimed to assess the incidence, predictors, and cardiac outcomes of CIN when nonionic isosmolar contrast media (iodixanol, Visipaque<SUP>(</SUP>R), GE Healthcare, Cork, Ireland) was used. Between January 2005 and July 2008, 510 patients (69.2+/-9.0 years of age, 384 men) undergoing diagnostic coronary angiography (CAG) or percutaneous coronary intervention (PCI) were divided into two groups according to the development of CIN (CIN group: n=74; non-CIN group: n=436). CIN developed in 74 patients (14.5%). They were more likely to have diabetes (55.4% vs. 42.9%, p=0.045), decreased left ventricular ejection fraction (LVEF) (50.1+/-12.6% vs. 57.7+/-13.9%, p<0.001), and lower baseline hematocrit level (32.4+/-5.3% vs. 36.6+/-5.5%, p<0.001). Multiple logistic regression analysis revealed baseline hematocrit (odds ratio 0.900, 95% confidence interval 0.851-0.952, p<0.001), decreased LVEF (odds ratio 0.967, 95% confidence interval 0.949-0.986, p=0.001), and baseline creatinine level (odds ratio 2.317, 95% confidence interval 1.252-4.286, p=0.007) as independent predictors of CIN. At 1-year follow-up, patients with CIN were found to have more adverse outcomes than without CIN in Cox proportional hazards analysis (hazard ratio 13.068, 95% confidence interval 2.425-70.434, p=0.003). CIN was mostly associated with baseline creatinine level rather than CM amount using nonionic isosmolar CM. We found that patients with CIN had worse event-free survival than patients without CIN after multifactorial adjustment.

Effects of the novel angiotensin II receptor type I antagonist, fimasartan on myocardial ischemia/reperfusion injury

Han, J.,Park, S.J.,Thu, V.T.,Lee, S.R.,Long, L.T.,Kim, H.K.,Kim, N.,Park, S.W.,Jeon, E.S.,Kim, E.J.,Yoon, C.H.,Cho, G.Y.,Choi, D.J. Elsevier/North-Holland Biomedical Press 2013 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.168 No.3

Background: The aim of this study was to investigate the cardioprotective effect of fimasartan, a newly developed angiotensin II receptor type I blocker (ARB), against myocardial ischemia/reperfusion (I/R) injury and to identify the mechanism by which it reduces mitochondrial damage. Methods: Fimasartan was administered intravenously to Sprague-Dawley rats (3mg/kg), cardiomyocytes (50μM), and H9c2 cells (50μM) before ischemia or hypoxia. Myocardial infarction (MI), echocardiograms, DNA fragmentation, terminal deoxynucleotidyl transferase-mediated dUTP in situ nick-end labeling, immunoblotting, oxygen consumption, confocal microscopic appearance, and L-type Ca<SUP>2+</SUP> current (I<SUB>Ca,L</SUB>) were then assessed. Results: Fimasartan pretreatment remarkably reduced the rate of MI and improved cardiac performance well after I/R (n=9/group). Fimasartan also reduced apoptotic cell death both in vivo and in hypoxia/reoxygenation (H/R)-treated H9c2 cells (n=5~8/group). H/R-induced mitochondrial O<SUB>2</SUB><SUP>-</SUP> production and collapse of membrane potential were markedly attenuated in fimasartan-treated cardiomyocytes (n=4~6/group). Additionally, mitochondrial Ca<SUP>2+</SUP> overload during reoxygenation was suppressed by fimasartan (n=4~6/group), and this was found to be possibly related to the inhibition of I<SUB>Ca,L</SUB> and mitochondrial Ca<SUP>2+</SUP> uniporter. Furthermore, fimasartan pretreatment increased phosphorylations of Akt and glycogen synthase kinase-3β (n=5~7/group), decreased pro-apoptotic p53 levels, and increased anti-apoptotic Bcl-2 levels (n=4) during reperfusion. Conclusions: Fimasartan preconditioning has the potential to modulate Bcl-2 and suppress I/R-induced Ca<SUP>2+</SUP> overload by inhibiting I<SUB>Ca,L</SUB> and MCU. These beneficial effects could prevent the mitochondrial dysfunction and apoptosis accompanied by I/R.

Loss of NDRG2 promotes epithelial-mesenchymal transition of gallbladder carcinoma cells through MMP-19-mediated Slug expression

Lee, D.G.,Lee, S.H.,Kim, J.S.,Park, J.,Cho, Y.L.,Kim, K.S.,Jo, D.Y.,Song, I.C.,Kim, N.,Yun, H.J.,Park, Y.J.,Lee, S.J.,Lee, H.G.,Bae, K.H.,Lee, S.C.,Shim, S.,Kim, Y.M.,Kwon, Y.G.,Kim, J.M.,Lee, H.J.,Mi Elsevier Science Publishers 2015 Journal of hepatology Vol.63 No.6

Background & Aims: Gallbladder carcinoma (GBC) is the most common malignancy of the biliary tract and one of the most lethal forms of human cancer. However, there is limited information about the molecular pathogenesis of GBC. Here, we examined the functional role of the tumor suppressor N-myc downstream-regulated gene 2 (NDRG2) and the underlying molecular mechanisms of disease progression in GBC. Methods: Clinical correlations between NDRG2 expression and clinicopathological factors were determined by immunohistochemical analysis of tumor tissues from 86 GBC patients. Biological functions of NDRG2 and NDRG2-mediated signaling pathways were determined in GBC cell lines with NDRG2 knockdown or overexpression. Results: Loss of NDRG2 expression was an independent predictor of decreased survival and was significantly associated with a more advanced T stage, higher cellular grade, and lymphatic invasion in patients with GBC. GBC cells with loss of NDRG2 expression showed significantly enhanced proliferation, migration, and invasiveness in vitro, and tumor growth and metastasis in vivo. Loss of NDRG2 induced the expression of matrix metalloproteinase-19 (MMP-19), which regulated the expression of Slug at the transcriptional level. In addition, MMP-19-induced Slug, increased the expression of a receptor tyrosine kinase, Axl, which maintained Slug expression through a positive feedback loop, and stabilized epithelial-mesenchymal transition of GBC cells. Conclusions: The results of our study help to explain why the loss of NDRG2 expression is closely correlated with malignancy of GBC. These results strongly suggest that NDRG2 could be a favorable prognostic indicator and promising target for therapeutic agents against GBC.