• Biomolecules & Therapeutics
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• v.30 no.1
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• pp.98-116
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• 2022

The small GTPase RhoA has been studied extensively for its role in actin dynamics. In this study, multiple bioinformatics tools were applied cooperatively to the microarray dataset GSE64714 to explore previously unidentified functions of RhoA. Comparative gene expression analysis revealed 545 differentially expressed genes in RhoA-null cells versus controls. Gene set enrichment analysis (GSEA) was conducted with three gene set collections: (1) the hallmark, (2) the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and (3) the Gene Ontology Biological Process. GSEA results showed that RhoA is related strongly to diverse pathways: cell cycle/growth, DNA repair, metabolism, keratinization, response to fungus, and vesicular transport. These functions were verified by heatmap analysis, KEGG pathway diagramming, and direct acyclic graphing. The use of multiple gene set collections restricted the leakage of information extracted. However, gene sets from individual collections are heterogenous in gene element composition, number, and the contextual meaning embraced in names. Indeed, there was a limit to deriving functions with high accuracy and reliability simply from gene set names. The comparison of multiple gene set collections showed that although the gene sets had similar names, the gene elements were extremely heterogeneous. Thus, the type of collection chosen and the analytical context influence the interpretation of GSEA results. Nonetheless, the analyses of multiple collections made it possible to derive robust and consistent function identifications. This study confirmed several well-described roles of RhoA and revealed less explored functions, suggesting future research directions.

• Journal of applied mathematics & informatics
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• v.23 no.1_2
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• pp.321-327
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• 2007

We say that a triangle ${\Delta}$ tiles the polygon ${\rho}\;if\;{\rho}$ can be decomposed into finitely many non-overlapping triangles similar to ${\Delta}$. Let ${\rho}$ be a parallelogram with angles ${\delta}\;and\;{\pi}-{\delta}\;(0<{\delta}{\leq}{\pi}/2)$ and let ${\Delta}$ be a triangle with angles ${\alpha};{\beta},\;{\gamma}\;({\alpha}{\leq}{\beta}{\leq}{\gamma})$. We prove that if ${\Delta}$ tiles ${\rho}$ then either ${\delta}{\in}\;({\alpha},\;{\beta},\;{\gamma},\;{\pi}-{\gamma},\;{\pi}-2{\gamma})\;or\;dimL_{\rho}=dimL_{{\Delta}}$. We also prove that for every parallelogram P, and for every integer n $(where\;n{\geq}2,\;n{\neq}3)$ there is a triangle ${\Delta}$ so that n similar copies of ${\Delta}\;tile\;{\rho}$.

• Journal of Mechanical Science and Technology
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• v.20 no.2
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• pp.271-277
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• 2006

A numerical study is made of the spin-up from rest of a three-layer fluid in a closed, vertically-mounted cylinder. The densities in the upper layer $\rho_1$, middle layer $\rho_2$ and lower layer $\rho_3\;are\;\rho_3\;>\;\rho_2\;>\;\rho_1$, and the kinematic viscosities are left arbitrary. The representative system Ekman number is small. Numerical solutions are obtained to the time-dependent axisymmetric Navier-Stokes equations, and the treatment of the interfaces is modeled by use of the Height of Liquid method. Complete three-component velocity fields, together with the evolution of the interface deformations, are depicted. At small times, when the kinematic viscosity in the upper layer is smaller than in the middle layer, the top interface rises (sinks) in the central axis (peripheral) region. When the kinematic viscosity in the lower layer is smaller than in the middle layer, the bottom interface rises (sinks) in the periphery (axis) region. Detailed shapes of interfaces are illustrated for several cases of exemplary viscosity ratios.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.3
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• pp.175-182
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• 2022

Translocation of azurophil granules is pivotal for bactericidal activity of neutrophils, the first-line defense cells against pathogens. Previously, we reported that lysophosphatidylcholine (LPC), an endogenous lipid, enhances bactericidal activity of human neutrophils via increasing translocation of azurophil granules. However, the precise mechanism of LPC-induced azurophil granule translocation was not fully understood. Treatment of neutrophil with LPC significantly increased CD63 (an azurophil granule marker) surface expression. Interestingly, cytochalasin B, an inhibitor of action polymerization, blocked LPC-induced CD63 surface expression. LPC increased F-actin polymerization. LPC-induced CD63 surface expression was inhibited by both a Rho specific inhibitor, Tat-C3 exoenzyme, and a Rho kinase (ROCK) inhibitor, Y27632 which also inhibited LPC-induced F-actin polymerization. LPC induced Rho-GTP activation. NSC23766, a Rac inhibitor, however, did not affect LPC-induced CD63 surface expression. Theses results suggest a novel regulatory mechanism for azurophil granule translocation where LPC induces translocation of azurophil granules via Rho/ROCK/F-actin polymerization pathway.

• The Journal of the Institute of Internet, Broadcasting and Communication
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• v.17 no.6
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• pp.19-25
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• 2017

This paper deals with integer factorization of two prime p,q of SHA-256 secure hash value n for Bit coin mining. This paper proposes an algorithm that greatly reduces the execution time of Pollard's rho integer factorization algorithm. Rho(${\rho}$) algorithm computes $x_i=x^2_{i-1}+1(mod\;n)$ and $y_i=[(y^2_{i-1}+1)^2+1](mod\;n)$ for intial values $(x_0,y_0)=(2,2)$ to find the factor 1 < $gcd({\mid}x_i-y_i{\mid},n)$ < n. It however fails to factorize some particular composite numbers. The algorithm proposed in this paper applies multiple initial values $(x_0,y_0)=(2^k,2^k)$ and ($2^k,2$), $2{\leq}k{\leq}10$ to the existing Pollard's Rho algorithm. As a results, the proposed algorithm achieves both the factorization of all the composite numbers and the reduction of the execution time of Pollard's Rho by 67.94%.

• Polymer(Korea)
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• v.36 no.3
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• pp.281-286
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• 2012

Experimental study was performed regarding the effects of disc-like filler orientation and contents on the coefficient of thermal expansion (CTE) of polypropylene composites using the three dimensional ellipsoids ($a_1$ > $a_2$ > $a_3$) analyzed by two aspect ratios(${\rho}_{\alpha}=a_1/a_3$and ${\rho}_{\beta}=a_1/a_2$). Measured data were compared with the theoretical approaches proposed by Lee et al. Mica and talc were useed as disk-like fillers in the composites. As experimental results, ${\alpha}_{11}/{\alpha}_m$ decreased down to ca. 0.56 with mica content of 20 wt% and the aspect ratios, ${\rho}_{\alpha}=13.5$, ${\rho}_{\beta}=1.8$. However, ${\alpha}_{33}/{\alpha}_m$ increased to more than 1. In the case of talc, ${\alpha}_{11}/{\alpha}_m$ decreased to ca. 0.63 with 20 wt% and ${\rho}_{\alpha}=3.7$, ${\rho}_{\beta}=1.4$. Finally, the longitudinal CTEs (${\alpha}_{11}$) of polypropylene composites decreased as filler contents increased, but normal CTE (${\alpha}_{33}$) increased in the low filler contents like the theory.

• Molecules and Cells
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• v.26 no.4
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• pp.396-403
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• 2008

The first ORF of the ARV S1133 S1 segment encodes the nonstructural protein p10, which is responsible for the induction of cell syncytium formation. However, p10-dependent signaling during syncytium formation is fully unknown. Here, we show that dominant negative RhoA, Rho inhibitor C3 exoenzyme, ROCK/Rho-kinase inhibitor Y-27632 and Rac1 inhibitor NSC23766 inhibit p10-mediated cell fusion. p10 over-expression is concomitant with activation and membrane translocation of RhoA and Rac1, but not cdc42. RhoA and Rac1 downstream events, including JNK phosphorylation and transcription factor AP-1 and $NF-{\kappa}B$ activation, as well as MLC expression and phosphorylation are simultaneously activated by p10. p10 point mutant T13M possessed 20% fusion-inducing ability and four p10 fusion-deficient mutants V15M, V19M, C21S and L32A reduced or lost their ability to activate RhoA and Rac1 signaling. We conclude that p10-mediated syncytium formation proceeds by utilizing RhoA and Rac1-dependent signaling.

• Communications of the Korean Mathematical Society
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• v.10 no.4
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• pp.789-795
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• 1995

For nonintegrable weight $-\rho$, some weight multiplicities of the irreducible module $L(-\rho)$ over $A^{(1)}_{(1)}$ affine Lie algebras are expressed in terms of the colored partition functions. Also we find the multiplicity of $L(-\rho)$ in ther Verma module $M(-\rho)$ for any affine Lie algebras.

• Bulletin of the Korean Mathematical Society
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• v.32 no.1
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• pp.25-34
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• 1995

S. Tachibana [10] has defined a confornal Killing tensor in a n-dimensional Riemannian manifold M by a skew symmetric tensor $u_[ji}$ satisfying the equation $$ \nabla_k u_{ji} + \nabla_j u_{ki} = 2\rho_i g_{kj} - \rho_j g_{ki} - \rho_k g_{ji}, $$ where $g_{ji}$ is the metric tensor of M, $\nabla$ denotes the covariant derivative with respect to $g_{ji}$ and $\rho_i$ is a associated covector field of $u_{ji}$. In here, a covector field means a 1-form.

• YAKHAK HOEJI
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• v.50 no.4
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• pp.293-299
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• 2006

The aim of present study was to investigate the possible influence of Rho-kinase inhibition on the plant-derived estrogen-like compounds-induced arterial relaxation. Agonist- or depolarization-induced vascular smooth muscle contractions involve the activation of Rho-kinase pathway. However there are no reports addressing the question whether this pathway is involved in genistein-or daidzein-induced vascular relaxation in rat aortae precontracted with phenylephrine or thromboxane $A_2$ mimetic U-46619. We hypothesized that Rho-kinase inhibition plays a role in vascular relaxation evoked by genistein or daidzein in rat aortae. Endothelium-intact and denuded arterial rings from male Sprague-Dawley rats were used and isometric contractions were recorded using a computerized data acquisition system. Genistein concentration-dependently inhibited phenylephrine or thromboxane $A_2-induced$ contraction regardless of endothelial function. Surprisingly, in the agonists-induced contraction, similar results were also observed in aortae treated with daidzein, the inactive congener for protein tyrosine kinase inhibition, suggesting that Rho-kinase might act upstream of tyrosine kinases in phenylephrine-induced contraction. In conclusion, in the agonists-precontracted rat aortae, genistein and daidzein showed similar relaxant response regardless of tyrosine kinase inhibition or endothelial function.