THE P3-DOMINATION IN GRAPHS

ANWAR ALWARDI,N. D. Soner 장전수학회 2013 Advanced Studies in Contemporary Mathematics Vol.23 No.1

Let G be a graph and u,v be any vertices of G. Then u and v are said to be P3-adjacent vertices of G if there is a subgraph of G, isomorphic to P3, Containing u and v. A P3-dominating set of G is a set D of vertices such that every vertex of G belongs to D or is P3-adjacent to a vertex of D. The P3-domination number of G denoted by P3 (G) is the minimum cardinality among the P3-dominating sets of vertices of G. In this paper we introduce and study the P3-domination of a graph G and analogous to this concept we define the P3-independence number P3 (G), P3-neighbourhood number P3 (G) and P3-domatic number dP3 (G). Some bounds and interesting results are obtained. Also the P3-adjacency motivated us to define new graphs in particular P3-neighbourhood graph, P3-complete graph, P3-regular graph, P3-complement graph and P3-complementary graph, some basic properties of these graphs are introduce and new method to construct any r-regular graph is established. finally we generalize the domination of graphs.

JNK and p38 mitogen-activated protein kinase pathways contribute to porcine epidemic diarrhea virus infection

Lee, Changhee,Kim, Youngnam,Jeon, Ji Hyun Elsevier 2016 VIRUS RESEARCH Vol.222 No.-

<P><B>Abstract</B></P> <P>The mitogen-activated protein kinase (MAPK) pathways, which are central building blocks in the intracellular signaling network, are often manipulated by viruses of diverse families to favor their replication. Among the MAPK family, the extracellular signal-regulated kinase (ERK) pathway is known to be modulated during the infection with porcine epidemic diarrhea virus (PEDV); however, involvement of stress-activated protein kinases (SAPKs) comprising p38 MAPK and c-Jun NH<SUB>2</SUB>-terminal kinase (JNK) remains to be determined. Therefore, in the present study, we investigated whether activation of p38 MAPK and JNK cascades is required for PEDV replication. Our results showed that PEDV activates p38 MAPK and JNK1/2 up to 24h post-infection, whereas, thereafter their phosphorylation levels recede to baseline levels or even fall below them. Notably, UV-irradiated inactivated PEDV, which can enter cells but cannot replicate inside them, failed to induce phosphorylation of p38 MAPK and JNK1/2 suggesting that viral biosynthesis is essential for activation of these kinases. Treatment of cells with selective p38 or JNK inhibitors markedly impaired PEDV replication in a dose-dependent manner and these antiviral effects were found to be maximal during the early times of the infection. Furthermore, direct pharmacological inhibition of p38 MAPK or JNK1/2 activation resulted in a significant reduction of viral RNA synthesis, viral protein expression, and progeny release. However, independent treatments with either SAPK inhibitor did not inhibit PEDV-induced apoptotic cell death mediated by activation of mitochondrial apoptosis-inducing factor (AIF) suggesting that SAPKs are irrelevant to the apoptosis pathway during PEDV infection. In summary, our data demonstrated critical roles of the p38 and JNK1/2 signaling pathways in facilitating successful viral infection during the post-entry steps of the PEDV life cycle.</P> <P><B>Highlights</B></P> <P> <UL> <LI> PEDV infection activated p38 MAPK and JNK1/2 <I>in vitro</I>. </LI> <LI> UV-inactivated virus failed to induce p38 MAPK and JNK1/2 activation. </LI> <LI> Pharmacological inhibition of p38 MAPK or JNK activation impaired PEDV replication. </LI> <LI> SAPK cascades do not affect the apoptosis pathway during PEDV infection. </LI> <LI> PEDV exploits the p38 MAPK and JNK signaling pathways for optimal replication. </LI> </UL> </P>

Insight into phosphate doped BiVO₄ heterostructure for multifunctional photocatalytic performances: A combined experimental and DFT study

Regmi, Chhabilal,Kshetri, Yuwaraj K.,Dhakal, Dipesh,Sohng, Jae Kyung,Rosei, Federico,Lee, Soo Wohn Elsevier 2019 APPLIED SURFACE SCIENCE - Vol.466 No.-

<P><B>Abstract</B></P> <P>Doping with non-metals like phosphorous has been extensively investigated to extend radiation absorption and improve the photocatalytic efficiency of TiO<SUB>2</SUB>. However, the effect of non-metal doping in BiVO<SUB>4</SUB>, whose smaller bandgap (2.4 eV) allows for efficient visible light absorption, has been scarcely investigated. Visible light accounts for 45% of solar energy (as compared to only 5% of UV light) reaching the Earth’s surface. Due to its high efficiency in absorbing visible radiation, BiVO<SUB>4</SUB> can, therefore, be a promising material to replace TiO<SUB>2</SUB>. Here we demonstrate the synthesis of phosphate doped visible-light-active BiVO<SUB>4</SUB> by a microwave hydrothermal method as a promising alternative to TiO<SUB>2</SUB>. Subsequently, we investigated its photocatalytic activity for the removal of p-amino salicylic acid and ibuprofen, two cases of major pharmaceutical waste, as well as disinfection of multi-drug resistance <I>Staphylococcus aureus</I> bacteria. In addition, the biofilm elimination efficiency of the undoped and phosphate doped BiVO<SUB>4</SUB> was studied by crystal violet staining method. A 70% reduction in the biofilm biomass by phosphate doped BiVO<SUB>4</SUB> was obtained. Also, a 4.1log reduction in the viable cells count was observed within 180 min when <I>Staphylococcus aureus</I> was irradiated with visible light mixed in phosphate doped BiVO<SUB>4</SUB> powder. Under similar irradiation conditions, the degradation efficiency for p-amino salicylic acid and ibuprofen are 81% and 80% respectively, a 40% enhancement as compared to undoped BiVO<SUB>4</SUB>. First principle density functional theory calculations show that charge transfer from P to O in the doping site of the BiVO<SUB>4</SUB> is responsible for the enhanced photocatalytic activity.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Phosphate doped BiVO<SUB>4</SUB> photocatalyst was prepared by a facile microwave-hydrothermal process. </LI> <LI> The catalyst was highly efficient for the degradation of the ibuprofen and p-amino salicylic acid. </LI> <LI> Effective inactivation of <I>S. aureus</I> bacteria under visible light was observed. </LI> <LI> Substantial inhibition of biofilm formation was observed in the presence of the photocatalyst. </LI> <LI> Underlying mechanism has been proposed through the DFT Calculation. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Enhanced Nogo-P3 amplitudes of mothers compared with non-mother women during an emotional Go/Nogo task

Hayashi, Sayuri,Wada, Hiroko,Kim, Sung-Phil,Motomura, Yuki,Higuchi, Shigekazu,Kim, Yeon-Kyu BioMed Central 2018 Journal of Physiological Anthropology Vol.37 No.1

<P><B>Background</B></P><P>It is known that emotion regulatory responses of humans are changed by the experiences they have, but in particular, they are changed by becoming a mother. A recent study has found how a woman’s emotion regulatory response to a child’s crying changes after becoming a mother. However, mothers’ emotion regulatory responses other than those to children and the association between emotion regulatory response and parental stress are still unknown.</P><P><B>Methods</B></P><P>Eighteen healthy Japanese females (nine mothers and nine non-mothers) participated in the experiment. They performed an emotional Go/Nogo task, with facial expressions of others (angry, happy, and neutral faces) used as emotional stimuli. The percentage of correct responses, response time, and event-related potentials (ERPs) during the task was measured.</P><P><B>Results</B></P><P>This comparison revealed that the mother group had a larger P3 (Nogo-P3) amplitude than the non-mother group when Nogo trials were held. This indicates that in mothers, there was greater activation of the behavioral inhibition-related brain areas than in non-mother women when they inhibited inappropriate behavior following recognition of facial expressions of others. In addition, in the mother group, there was a negative correlation between parental stress levels and Nogo-P3 amplitudes evoked by angry faces. This suggests that there is a relation between the level of parental stress of mothers and their emotion regulatory responses to angry faces.</P><P><B>Conclusions</B></P><P>Our results demonstrate that mothers’ emotion regulatory processes may differ from those of non-mothers in response, not only to a child’s crying but also to expressions of emotions by others, and also suggest that the inhibitory recognition activity of mothers can be affected by parental stress.</P>

P1-P2 하이브리드 시스템의 내장형 댐핑 시스템 검증에 대한 연구

신택현(Taek-hyun Shin),박찬석(Chan-seok Park),백성환(Seong-hwan Bark),강효은(Hyo-eun Kang) 한국자동차공학회 2021 한국자동차공학회 부문종합 학술대회 Vol.2021 No.6

P1-P2 TMED system is a hybrid powertrain to improve performance and fuel economy through the application of a P1 motor. Since the overall length is lengthened due to the addition of the P1 motor, we reduced the length of transmission by applying a torsion damper in the inner space between P1 and P2. In this study, the verification method for the torsion damper system applied inside the P1-P2 system was reviewed. Through the analysis of the damper system, verification targets and methods were discussed, and we divided the verification of the torsion damper into the damper only system, the drivetrain of the P1 rotor, and the total verification of the entire powertrain system.

TP2P: 효율적인 자원탐색을 위한 토폴로지 기반의 P2P 시스템

차봉관(Bongkwan Cha),한동윤(Dongyun Han),손영성(Youngsong Son),김경석(Kyongsok Kim) 한국정보과학회 2007 정보과학회논문지 : 정보통신 Vol.34 No.2

P2P 시스템은 시스템에 참여하는 노드들의 자원을 공유하는 분산 시스템으로 여기에 참여하는 노드들은 서버와 클라이언트의 역할을 모두 수행한다. 현재 분산 해쉬 테이블(Distributed Hash Table)을 기반으로 한 체계적이고 구조화된 P2P 시스템들인 CAN, Chord, Pastry, Tapestry 등이 제안되었으나 이 시스템들은 물리적 거리를 고려하지 않아서 안정적인 성능을 보장하기 어렵다는 약점을 가지고 있다. 이 문제를 해결하기 위해서 우리는 TP2P시스템을 제안한다. 이 시스템은 스스로 조직을 관리하는 계층적 오버레이 네트워크 시스템으로 자원 탐색을 위해 Chord의 라우팅 메커니즘을 사용한다. 이 시스템은 물리적인 거리가 매우 가까운 노드들로 구성된 서브넷과 모든 노드들로 구성된 글로벌 네트워크로 이루어진 시스템이다. 각 서브넷에서 한 노드가 어떤 자원을 탐색하면 그 자원을 서브넷 안에 저장하기 때문에 Chord 시스템에 비해 물리적인 지연이 줄어들 가능성이 높다. 또 자원을 탐색할 때 각 노드들이 가지고 있는 Global-nodeID 정보를 이용함으로써 물리적 지연이 줄어드는 것은 물론이고 탐색 홉 수도 25%정도 감소한다. P2P systems are distributed data sharing systems, and each node in them plays the role of client as well as server. There are several studies using Distributed Hash Table, such as Chord, CAN, Tapestry, Pastry, but these systems don’t consider the physical latency, therefore they have a weakness of difficulty to guarantee stable performance. To improve this problem, we present the TP2P system. This system is a self-organizing hierarchical overlay system and it uses Chord routing mechanism for lookup data. This system is organized by several subnets, each subnet is organized by physically close nodes, and global network organized by all nodes. In each subnet, one node finds a data, it saves in a node in the subnet, therefore it has higher probability to reduce physical lookup latency than Chord system. And each node has global information of some nodes in its subnet, and it is used to lookup data, therefore the number of hops decrease about 25% as well as the physical lookup latecy are reduced.

Enhanced sodium-ion storage capability of P2/O3 biphase by Li-ion substitution into P2-type Na_0.5Fe_0.5Mn_0.5O₂ layered cathode

Veerasubramani, Ganesh Kumar,Subramanian, Yuvaraj,Park, Myung-Soo,Senthilkumar, Baskar,Eftekhari, Ali,Kim, Sang Jae,Kim, Dong-Won Elsevier 2019 ELECTROCHIMICA ACTA Vol.296 No.-

<P><B>Abstract</B></P> <P>Integration of P2 and O3 phases in Na<SUB>0.5</SUB>Fe<SUB>0.5</SUB>Mn<SUB>0.5</SUB>O<SUB>2</SUB> cathode via Li-ion substitution is proposed to enhance its electrochemical performance for sodium-ion battery applications. The formation of P2 and the combination of P2/O3 intergrowth were confirmed by X-ray diffraction refinement, high resolution transmission electron microscopy and X-ray photoelectron microscopy analyses. Various content of lithium was used to find optimum P2+O3 combinations. The optimized Li-ion substituted Na<SUB>0.5</SUB>(Li<SUB>0.10</SUB>Fe<SUB>0.45</SUB>Mn<SUB>0.45</SUB>)O<SUB>2</SUB> showed a high initial discharge capacity of 146.2 mAh g<SUP>−1</SUP> with improved cycling stability, whereas the pristine Na<SUB>0.5</SUB>Fe<SUB>0.5</SUB>Mn<SUB>0.5</SUB>O<SUB>2</SUB> initially delivered a discharge capacity of 127.0 mAh g<SUP>−1</SUP>. In addition, the combination of P2+O3 increased its average voltage, which is important for achieving high energy density sodium-ion batteries. Overall, the prepared Na<SUB>0.5</SUB>(Li<SUB>0.10</SUB>Fe<SUB>0.45</SUB>Mn<SUB>0.45</SUB>)O<SUB>2</SUB> electrode exhibited the improved cycling performance in terms of reversible capacity and rate capability compared to pristine Na<SUB>0.5</SUB>Fe<SUB>0.5</SUB>Mn<SUB>0.5</SUB>O<SUB>2</SUB> electrode material.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Facile sol-gel route is used to synthesis of layered cathode via Li-ion substitution. </LI> <LI> Combination of P2 and O3 phases is confirmed using XRD refinement results. </LI> <LI> P2+O3 Na<SUB>0.5</SUB>[Li<SUB>0.10</SUB>Fe<SUB>0.45</SUB>Mn<SUB>0.45</SUB>]O<SUB>2</SUB> biphasic cathode exhibits good cycling performance. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Oxide formation mechanism and its effect on the microstructure and thermoelectric properties of <i>p-type</i> Bi_0.5Sb_1.5Te₃ alloys

Lwin, May Likha,Dharmaiah, Peyala,Madavali, Babu,Lee, Chul-Hee,Shin, Dong-won,Song, Gian,Lee, Kap-Ho,Hong, Soon-Jik Elsevier 2018 Intermetallics Vol.103 No.-

<P><B>Abstract</B></P> <P>Bismuth antimony telluride based thermoelectric (TE) materials have been intensively developed and synthesized using different mechanisms, for the room temperature TE applications. In particular, bismuth antimony telluride based TE alloys are very sensitive to deviations in their composition, and to contamination during the materials synthesis. Oxygen contamination during Bi-Sb-Te based materials synthesis is one of the critical factors that alters or diminishes thermoelectric-transport properties. Thus, in this study, how the oxide formation mechanism on the powder surface and bulks of p-type Bi<SUB>0.5</SUB>Sb<SUB>1.5</SUB>Te<SUB>3</SUB> alloys affected the microstructural features and thermoelectric properties were elucidated quantitatively. While applying heat treatment (HT) to Bi<SUB>0.5</SUB>Sb<SUB>1.5</SUB>Te<SUB>3</SUB> powder, the constituent elements interacted with the ambient atmosphere and formed a new oxide phase which acted as a barrier to carrier transport. At the initial stage (300 °C) of heat treatment, only the powder surface was oxidized due to the reaction of outer surface atoms with atmospheric air and moisture. While increasing in temperature during HT, this surface oxygen contamination diffused further inside the powder through the grain boundaries. More diffusion and spreading occurred throughout the matrix at 450 °C. The increment of oxygen content from 0.05 to 0.82 wt% drastically decreased the electrical conductivity by 67%, and thermal conductivity by 7% at the heat treatment temperature of 450 °C. This reduction behavior is mainly due to severe scattering of the carriers/phonons at the new formation of oxide (Sb<SUB>2</SUB>O<SUB>3</SUB>) phase near grain boundaries and within the matrix. At a glance, a small increase in the oxygen content wouldn't significantly influence the thermoelectric properties; however, at a certain level of oxide formation (0.82 wt%), severe effects could occur due to the intensified scattering or trapping of carriers by the oxide barrier formation at the grain boundaries.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Determined the oxygen concentration of different heat-treated GA powder and SPS bulks. </LI> <LI> Elucidation the relation between the mechanism of oxide formation and the thermoelectric properties of Bi<SUB>0.5</SUB>Sb<SUB>1.5</SUB>Te<SUB>3</SUB> alloys. </LI> <LI> Identified Sb<SUB>2</SUB>O<SUB>3</SUB> phase at the grain boundary and within the grains. </LI> <LI> Demonstrated the thermoelectric performance in Bi<SUB>0.5</SUB>Sb<SUB>1.5</SUB>Te<SUB>3</SUB> alloys with oxygen content. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

p53-dependent and -independent mechanisms are involved in (<i>E</i>)-1-(2-hydroxyphenyl)-3-(2-methoxynaphthalen-1-yl)prop-2-en-1-one (HMP)-induced apoptosis in HCT116 colon cancer cells

Shin, Soon Young,Ahn, Seunghyun,Koh, Dongsoo,Lim, Yoongho Elsevier 2016 Biochemical and biophysical research communication Vol.479 No.4

<P><B>Abstract</B></P> <P>(<I>E</I>)-1-(2-hydroxyphenyl)-3-(2-methoxynaphthalen-1-yl)prop-2-en-1-one (HMP) is a novel synthetic naphthal chalcone derivative. The aim of this study was to investigate the mode of action underlying the antitumor activity of HMP. We found that treatment with HMP potently inhibited the clonogenicity and triggered cell death in HCT116 colon cancer cells. Flow cytometry showed that HMP induced an increase in the population of sub-G<SUB>0</SUB>/G<SUB>1</SUB>-phase cells. Annexin V binding assay revealed that HMP triggered apoptotic cell death. Furthermore, HMP stimulated the cleavages of caspase-7 and its substrate poly (ADP-ribose) polymerase (PARP). HMP promoted γ-H2AX formation and the production of reactive oxygen species (ROS), and up-regulated expression of the tumor suppressor p53. Interestingly, HMP-induced caspase-7 processing was not completely abrogated in p53-null (p53<SUP>−/−</SUP>) HCT116 cells, suggesting that p53-dependent and -independent mechanisms are involved in HMP-induced apoptosis. Egr-1, a zinc finger transcription factor, was upregulated by HMP. Silencing of Egr-1 by shRNA significantly reduced HMP-induced caspase-7 and PARP cleavages, regardless of p53 status. These results suggest that HMP triggers caspase-mediated apoptosis through two distinct mechanisms involving p53-dependent and p53-independent, Egr-1-dependent pathways.</P> <P><B>Highlights</B></P> <P> <UL> <LI> HMP is a novel synthetic naphthal chalcone derivative. </LI> <LI> HMP inhibits clonogenicity of HCT116 colon cancer cells. </LI> <LI> HMP induces ROS production and activates the caspase cascade. </LI> <LI> HMP induces apoptosis through both p53-and Egr-1-dependent pathways. </LI> </UL> </P>

DUSP1 induces paclitaxel resistance through the regulation of p-glycoprotein expression in human ovarian cancer cells

Kang, Yu-Seon,Seok, Hyun-Jeong,Jeong, Eun-Jeong,Kim, Yuna,Yun, Seok-Joong,Min, Jeong-Ki,Kim, Sun Jin,Kim, Jang-Seong Elsevier 2016 Biochemical and biophysical research communication Vol.478 No.1

<P><B>Abstract</B></P> <P>The heterogeneity and genetic instability of ovarian cancer cells often lead to the development of drug resistance, closely related with the increased cancer-related mortality. In this study, we investigated the role of dual-specificity phosphatase 1 (DUSP1) in the development of the resistance in human ovarian cancer cells against paclitaxel. Overexpression of DUSP1 in HeyA8 human ovarian cancer cells (HeyA8-DUSP1) up-regulated the expression of the drug efflux pump, p-glycoprotein. Consequently, HeyA8-DUSP1 cells are highly resistant to paclitaxel, with the resistance comparable to that of a multi-drug resistance cell line (HeyA8-MDR). Moreover, over expression of DUSP1 significantly increased the activation of p38 MAPK, leaving the activation of ERK1/2 and JNK1/2 unaffected. Pharmacological suppression of p38 MAPK activity prevents the up-regulation of p-glycoprotein expression and the consequent resistance against paclitaxel in HeyA8-DUSP1 cells. By contrast, HeyA8-MDR cells expressed a significantly higher level of DUSP1, but treatment with small interference RNA against DUSP1 significantly suppressed the expression of p-glycoprotein and the resistance against paclitaxel in HeyA8-MDR cells. Ectopic expression of MKK3, an upstream activator of p38 MAPK, significantly up-regulated the expression of p-glycoprotein and increased the consequent resistance against paclitaxel in HeyA8 cells. Collectively, these data indicated that DUSP1 may induce the resistance against paclitaxel through the p38 MAPK-mediated overexpression of p-glycoprotein in human ovarian cancer cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> DUSP1 induces Pgp expression and paclitaxel resistance in ovarian cancer cells. </LI> <LI> DUSP1 mediates p38 MAPK activation leading to Pgp-mediated paclitaxel resistance. </LI> <LI> Inhibition of DUSP1 or p38 MAPK reverses Pgp-mediated paclitaxel resistance. </LI> <LI> DUSP1-p38 MAPK-Pgp axis is a novel mechanism for paclitaxel resistance. </LI> </UL> </P>