A linear-time algorithm for finding a paired 2-disjoint path cover in the cube of a connected graph

Ihm, I.,Park, J.H. North Holland ; Elsevier Science Ltd 2017 Discrete Applied Mathematics Vol.218 No.-

<P>For a connected graph G = (V (G), E(G)) and two disjoint subsets of V(G)A = (alpha(1), ..., alpha(k)} and B = {beta(1,) ..., beta(k)}, a paired (many-to-many) k-disjoint path cover of G joining A and B is a vertex-disjoint path cover (beta(1), ..., beta(k)} such that P-i is a path from alpha(i) to beta(i) for 1 <= i <= k. In the recent paper, Park and Ihm (2014) presented a necessary and sufficient condition for a paired 2-disjoint path cover joining two vertex sets to exist in the cube of a connected graph. In this paper, we propose an O vertical bar V(G)vertical bar + vertical bar E(G)vertical bar)-time algorithm that actually finds such a paired 2-disjoint path cover. In particular, we show that, in order to build a desired disjoint path cover, it is sufficient to consider only the edges of a carefully selected spanning tree of the graph and at most one additional edge not in the tree, which allows an efficient linear-time algorithm. (C) 2016 Elsevier B.V. All rights reserved.</P>

Inflexin attenuates proinflammatory responses and nuclear factor-@?B activation in LPS-treated microglia

Ko, H.M.,Koppula, S.,Kim, B.W.,Kim, I.S.,Hwang, B.Y.,Suk, K.,Park, E.J.,Choi, D.K. North-Holland ; Elsevier Science Ltd 2010 european journal of pharmacology Vol.633 No.1

Activated microglia participate in neuroinflammation which contribute to neuronal damage. Suppression of microglial activation would have therapeutic benefits, which lead to alleviation of the progression of neurodegeneration. In this study, the inhibitory effects of inflexin, a putative antiinflammatory agent isolated from Isodon excisus (Max.) Kudo (Labiateae), on the production of proinflammatory mediators were investigated in the lipopolysaccharide (LPS)-stimulated microglia. Inflexin significantly inhibited the release of nitric oxide (NO). Consistently, both the mRNA and the protein levels for the inducible NO synthase were decreased by inflexin in a concentration-dependent manner. Inflexin also inhibited the expression of cyclooxygenase (COX)-2, but not the COX-1 and effectively reduced the LPS-induced expression of proinflammatory cytokines in a dose-dependent manner. Furthermore, inflexin inhibited the degradation of IκB-α and the activation of NF-κB, p65 and Akt, while the MAPKs signal pathway was not affected. Our data suggest that inflexin was able to suppress neuroinflammation via inhibition of NF-κB activation and Akt pathway indicating that inflexin may be developed as a potent therapeutic agent in treating neuroinflammatory diseases.

Anticonvulsant effect of wogonin isolated from Scutellaria baicalensis

Park, H.G.,Yoon, S.Y.,Choi, J.Y.,Lee, G.S.,Choi, J.H.,Shin, C.Y.,Son, K.H.,Lee, Y.S.,Kim, W.K.,Ryu, J.H.,Ko, K.H.,Cheong, J.H. North-Holland ; Elsevier Science Ltd 2007 european journal of pharmacology Vol.574 No.2

In previous studies, we identified sedative effects of Scutellaria baicalensis extracts and found that these extracts or their constituents may also have anticonvulsive effects. Wogonin is a natural product isolated from S. baicalensis, which possesses central nervous system effects such as anxiolytic and neuroprotective activities. In this study, we investigated the effects of wogonin on convulsion related behaviors, such as myorelaxation, motor coordination, and anticonvulsant effects of wogonin on chemical induced seizure and electroshock seizure in mice or rats. The effect of wogonin on membrane potential was also observed. Wogonin was intraperitoneally injected into mice or rats 30 min prior to testing. Animals treated with wogonin did not change locomotor activities as well as endurance times on the rota-rod, which indicates that wogonin did not cause a sedative and myorelaxation effect. Wogonin significantly blocked convulsion induced by pentylenetetrazole and electroshock but not convulsion induced by strychnine. Wogonin also significantly reduced the electrogenic response score, but flumazenil treatment reversed this decrease to the level of the control group. The wogonin treatment increased Cl<SUP>-</SUP>influx into the intracellular area as dose increased. Flumazenil and bicuculline treatment, however, inhibited the Cl<SUP>-</SUP> influx induced by wogonin. These results indicate that the anticonvulsive effects produced by wogonin were mediated by the GABAergic neuron.

Rosuvastatin inhibits norepinephrine-induced cardiac hypertrophy via suppression of G_h

Choi, E.Y.,Chang, W.,Lim, S.,Song, B.W.,Cha, M.J.,Kim, H.J.,Choi, E.,Jang, Y.,Chung, N.,Hwang, K.C. North-Holland ; Elsevier Science Ltd 2010 european journal of pharmacology Vol.627 No.1

Statins have recently been shown to produce anti-cardiac hypertrophic effects via the regulation of small GTPases. However, the effects of statins on G protein-mediated cardiac hypertrophy, which is the main pathway of cardiac hypertrophy, have not yet been studied. We sought to evaluate whether statin treatment directly suppresses cardiac hypertrophy through a large G protein-coupled pathway regardless of the regulation of small GTPases. Using neonatal rat cardiomyocytes, we evaluated norepinephrine-induced cardiac hypertrophy for suppressibility of rosuvastatin and the pathways involved by analyzing total protein/DNA content, cell surface area, immunoblotting and RT-PCR for the signal transduction molecule. In a concentration-dependent manner, rosuvastatin inhibited total protein synthesis and downregulated basal and norepinephrine-induced expressions of myosin light chain2 and the c-fos proto-oncogene in cardiomyocytes. Treatment with norepinephrine induced cardiac hypertrophy accompanied by G<SUB>h</SUB> expression and membrane translocation. Rosuvastatin inhibited G<SUB>h</SUB> protein activity in cardiomyocytes by inhibiting basal and norepinephrine-stimulated mRNA transcription, protein expression and membrane translocation; however, norepinephrine-stimulated G<SUB>q</SUB> protein expression was not inhibited. In addition, the norepinephrine-stimulated protein kinase C (PKC)-mitogen-activated protein kinase (MEK 1,2)-extracellular signal-regulated kinases (ERKs) signaling cascade was inhibited by pretreatment with rosuvastatin. Rosuvastatin treatment also helped maintain expression levels of SERCA2a and intracellular calcium concentration. G<SUB>h</SUB> protein is a novel target of statins in myocardial hypertrophy, and statin treatment may directly suppress cardiac hypertrophy through a large G<SUB>h</SUB> protein-coupled pathway regardless of the regulation of small GTPases.

Dimerization of HCN in the gas phase: A theoretical mechanistic study

Yim, M.K.,Choe, J.C. North Holland ; Elsevier Science Ltd 2012 Chemical physics letters Vol.538 No.-

Potential energy surfaces for the formation of covalently bound HCN dimers from two molecules of HCN or HNC were determined from CBS-QB3/APNO calculations. Several novel pathways, with and without the aid of protons, were found for the formation of iminoacetonitrile (HN?CHCN), an intermediate in adenine synthesis from HCN by oligomerization. Covalent C-C or C-N bonds between the two monomers were formed after rearrangement of bimolecular complex intermediates. Energetic and kinetic analyses suggest that the proton-catalyzed dimerizations substantially lower reaction barriers but cannot occur efficiently under interstellar conditions.

An unconditionally stable hybrid method for image segmentation

Li, Y.,Kim, J. North-Holland ; Elsevier Science Ltd 2014 Applied numerical mathematics Vol.82 No.-

In this paper, we propose a new unconditionally stable hybrid numerical method for minimizing the piecewise constant Mumford-Shah functional of image segmentation. The model is based on the Allen-Cahn equation and an operator splitting technique is used to solve the model numerically. We split the governing equation into two linear equations and one nonlinear equation. One of the linear equations and the nonlinear equation are solved analytically due to the availability of closed-form solutions. The other linear equation is discretized using an implicit scheme and the resulting discrete system of equations is solved by a fast numerical algorithm such as a multigrid method. We prove the unconditional stability of the proposed scheme. Since we incorporate closed-form solutions and an unconditionally stable scheme in the solution algorithm, our proposed scheme is accurate and robust. Various numerical results on real and synthetic images with noises are presented to demonstrate the efficiency, robustness, and accuracy of the proposed method.

Inhibition of recombinant Ca_v3.1 (@?_1G) T-type calcium channels by the antipsychotic drug clozapine

Choi, K.H.,Rhim, H. North-Holland ; Elsevier Science Ltd 2010 european journal of pharmacology Vol.626 No.2

Low voltage-activated T-type calcium channels are involved in the regulation of the neuronal excitability, and could be subject to many antipsychotic drugs. The effects of clozapine, an atypical antipsychotic drug, on recombinant Ca<SUB>v</SUB>3.1 T-type calcium channels heterologously expressed in human embryonic kidney 293 cells were examined using whole-cell patch-clamp recordings. At a standard holding potential of -100mV, clozapine inhibited Ca<SUB>v</SUB>3.1 currents with an IC<SUB>50</SUB> value of 23.7+/-1.3μM in a use-dependent manner. However, 10μM clozapine inhibited more than 50% of the Ca<SUB>v</SUB>3.1 currents in recordings at a more physiologically relevant holding potential of -75mV. Clozapine caused a significant hyperpolarizing shift in the steady-state inactivation curve of the Ca<SUB>v</SUB>3.1 channels, which is presumably the main mechanism accounting for the inhibition of the Ca<SUB>v</SUB>3.1 currents. In addition, clozapine slowed Ca<SUB>v</SUB>3.1 deactivation and inactivation kinetics but not activation kinetics. Clozapine-induced changes in deactivation and inactivation rates of the Ca<SUB>v</SUB>3.1 channel gating would likely facilitate calcium influx via Ca<SUB>v</SUB>3.1 T-type calcium channels. Thus, clozapine may exert its therapeutic and/or side effects by altering cell's excitability and firing properties through actions on T-type calcium channels.

Sulforaphane inhibition of TPA-mediated PDCD4 downregulation contributes to suppression of c-Jun and induction of p21-dependent Nrf2 expression

Cho, J.H.,Kim, Y.W.,Choi, B.Y.,Keum, Y.S. North-Holland ; Elsevier Science Ltd 2014 european journal of pharmacology Vol.741 No.-

Programmed cell death 4 (PDCD4) is a bona fide tumor suppressor protein and plays a critical role in controlling the rate of protein synthesis. Here, we show that TPA selectively activated the S6K1 and ERK½ kinases, contributing to PDCD4 proteolysis and Pdcd4 mRNA degradation in HepG2 cells, respectively. In addition, we observed that sulforaphane suppression of TPA-induced S6K1 and ERK½ activation played a critical role in attenuating PDCD4 poly-ubiquitination and Pdcd4 mRNA downregulation. Moreover, we observed that silencing Pdcd4 led to not only an increased expression of c-Jun, but also a decreased expression of p21, the latter of which contributed to suppression of Keap1-dependent Nrf2 poly-ubiquitination. Finally, we demonstrate that the expression of PDCD4, p21 and Nrf2 is higher, but that of c-Jun is lower in normal human liver tissues, compared with hepatoma tissues. Collectively, our study illustrates that attenuating the rate of PDCD4 proteolysis and Pdcd4 mRNA degradation serves as a novel anti-inflammatory and cytoprotective mechanism of sulforaphane.

Diketopyrrolopyrrole-based narrow band gap donors for efficient solution-processed organic solar cells

Bagde, S.S.,Park, H.,Yang, S.n.,Jin, S.H.,Lee, S.H. North Holland ; Elsevier Science Ltd 2015 Chemical physics letters Vol.630 No.-

<P>This study involves the development of two new small molecules comprising a diketopyrrolopyrrole (DPP) core flanked with donor units of triphenylamine (TPA-DPP-TPA) and fluorine (FL-DPP-FL) for application in bulk heterojunction (BHJ) organic solar cells (OSCs). The OSCs based on FL-DPP-FL and PC71 BM exhibited a PCE of 1.73%, compared to 1.45% for that obtained from devices of TPA-DPP-TPA. The morphological studies reveal that the enhancement in OSCs of FL-DPP-FL is mainly attributed to the improved nanoscale film morphology of the FL-DPP-FL:PC71 BM blend, which promoted the formation of smaller domains and greater donor-acceptor interpenetrated networks within the active layer. (C) 2015 Elsevier B.V. All rights reserved.</P>

Effect of amino acid immobilization on the impedance of graphene oxide

Tran, M.H.,Han, J.,Min, B.J.,Lee, C.,Jang, S.H.,Jeong, H.K. North Holland ; Elsevier Science Ltd 2015 Chemical physics letters Vol.627 No.-

A single residue, dipeptide, or tripeptide of alanine or histidine is covalently attached to graphene oxide (GO), and the effect of the amino acid immobilization on the impedance of GO is investigated using the impedance spectroscopy. The histidine of a tripeptide exhibits the lowest resistance compared to the single or dipeptide histidine in the KCl electrolyte, and the single alanine residue shows the lowest resistance in an acidic electrolyte compared to the dipeptide or tripeptide alanine. The peculiar behavior of the impedance could be explained by different net charges of the amino acids, chain length, and π-π stacking interaction.