• Progress in Medical Physics
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• v.28 no.2
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• pp.61-66
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• 2017

The aim of this study is to investigate the characteristics of portal dosimetry in comparison with the MapCHECK2 measurments. In this study, a total of 65 treatment plans including both volumetric modulated arc therapy (VMAT) and intensity-modulated radiation therapy (IMRT) were retrospectively selected and analyzed (45 VMAT plans and 20 IMRT plans). A total of 4 types of linac models (VitalBeam, Trilogy, Clinac 21EXS, and Clianc iX) were used for the comparison between portal dosimetry and the MapCHECK2 measurements. The VMAT plans were delivered with two VitalBeam linacs (VitalBeam1 and VitalBeam2) and one Trilogy while the IMRT plans were delivered with one Clinac 21EXS and one Clinacl iX. The global gamma passing rates of portal dosimetry and the MapCHECK2 measurements were analyzed with a gamma criterion of 3%/3 mm for IMRT while those were analyzed with a gamma criterion of 2%/2 mm for VMAT. Spearman's correlation coefficients (r) were calculated between the gamma passing rates of portal dosimetry and those of the MapCHECK2 measurements. For VMAT, the gamma passing rates of portal dosimetry with the VitalBeam1, VitalBeam2, and Trilogy were $97.3%{\pm}3.5%$, $97.1%{\pm}3.4%$, and $97.5%{\pm}1.9%$, respectively. Those of the MapCHECK2 measurements were $96.8%{\pm}2.5%$, $96.3%{\pm}2.7%$, and $97.4%{\pm}1.3%$, respectively. For IMRT, the gamma passing rates of portal dosimetry with Clinac 21EXS and Clinac iX were $99.7%{\pm}0.3%$ and $99.8%{\pm}0.2%$, respectively. Those of the MapCHECK2 measurements were $96.5%{\pm}3.3%$ and $97.7%{\pm}3.2%$, respectively. Except for the result with the Trilogy, no correlations were observed between the gamma passing rates of portal dosimetry and those of the MapCHECK2 measurements. Therefore, both the MapCHECK2 measurements and portal dosimetry can be used as an alternative to each other for patient-specific QA for both IMRT and VMAT.

• Journal of applied mathematics & informatics
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• v.13 no.1_2
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• pp.201-215
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• 2003

A map is a connected topological graph $\Gamma$ cellularly embedded in a surface. For any connected graph $\Gamma$, by introducing the concertion of semi-arc automorphism group Aut$\_$$\frac{1}{2}$/$\Gamma$ and classifying all embedding of $\Gamma$ undo. the action of this group, the numbers r$\^$O/ ($\Gamma$) and r$\^$N/($\Gamma$) of rooted maps on orientable and non-orientable surfaces with underlying graph $\Gamma$ are found. Many closed formulas without sum ∑ for the number of rooted maps on surfaces (orientable or non-orientable) with given underlying graphs, such as, complete graph K$\_$n/, complete bipartite graph K$\_$m, n/ bouquets B$\_$n/, dipole Dp$\_$n/ and generalized dipole (equation omitted) are refound in this paper.

• Journal of Korea Multimedia Society
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• v.19 no.5
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• pp.837-847
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• 2016

Tone mapping for High Dynamic Range(HDR) image provides matching human visual perception between real world scene and displayable devices. Recently, a tone mapping algorithm based on localized gamma correction is proposed. This algorithm is using human visual properties of contrast and colorfulness with background intensity, generating a weight map for gamma correction. However, this method have limitations of controlling enhancement region as well as generating halo artifacts caused by the weight map construction. To overcome aforementioned limitations, proposed algorithm in this paper modifies previous weight map, considering base layer intensity of input luminance channel. By determining enhancement region locally and globally based on base layer intensity, gamma values are corrected accordingly. Therefore, proposed algorithm selectively enhances local brightness and controls strength of edges. Subjective evaluation using z-score shows that our proposed algorithm outperforms the conventional methods.

• The korean journal of orthodontics
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• v.33 no.3 s.98
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• pp.199-210
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• 2003

Tooth movement is the result of bone metabolism in the periodontium, where various cytokines take important roles. Interleukin-6(II-6) and nitrous oxide (NO) were reported to be secreted from osteoblasts in the process of bone resorption. The mechanism of the process has not been clearly understood, but the activation of mitogen-activated protein kinase (MAPK) was known to be an important process in the release of the inflammatory cytotines in macrophages. In this regard, to prove the role of MAPK in the release of IL-6 and NO in MC3T3E-1 osteoblasts, Northern blot analysis, Western blot analysis and immune complex kinase assay were used. As a result, the treatment of MC3T3E-1 osteoblast cultures with combined $interferon-\gamma(IFN-\gamma)$, lipopolysaccharide (LPS) and tumor necrosis $factor-\alpha(TNF-\alpha)$ induces expressions of inducible nitric oxide synthase (iNOS) and IL-6, resulting in sustained releases of large amounts of NO and IL-6. However, $IFN-\gamma,\;LPS,\;and\;TNF-\alpha$ individually induce a non-detectable or small amount of NO and IL-6 in MC3T3E-1 osteoblasts. The role of MAPK activation in the early intracellular signal transduction involved in iNOS and IL-6 transcription in the combined agents-stimulated osteoblasts has been investigated. The p38 MAPK pathway is specifically involved in the combined agents-induced NO and IL-6 release, since NO and IL-6 release in the presence of a specific inhibitor of p38 MAPK, 4-(4-fluorophenyl)-2-(4-metylsulfinylphenyl)-5-(4-metylsulfinylphenyl)-5-(4-pyridyl)imidazole) (SB203580), were significantly diminished. In contrast, PD98059, a specific inhibitor of MEK1, had no effect on NO and IL-6 release. Northern blot analysis showed that the p3a MAPK pathway controlled the iNOS and IL-6 transcription level. These data suggest that p38 MAPK play an important role in the secretion of NO and IL-6 in $LPS/IFN{\gamma}-or\;TNF-\gamma-treated\;MC3T3E-1$ osteoblasts.

• Molecular & Cellular Toxicology
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• v.1 no.3
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• pp.196-202
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• 2005

Nitric oxide (NO) is a small, diffusible, and highly reactive molecule, which plays dichotomous regulatory roles under physiological and pathological conditions. NO promotes apoptosis in some cells, and inhibits apoptosis in other cells. In the present study, we attempted to characterize the NO signaling pathway and cellular response in PC12 cells treated with cytokines. $IFN{\gamma}\;and\;TNF{\alpha}$ treatment resulted in a synergistic increase of nitrite accumulation, with the induction of inducible nitric oxide synthase (iNOS) in the PC12 cells. Moreover, as nitrite concentration increased, cell viability decreased. In order to explore MAP kinase involvement in nitric oxide production resultant from $IFN{\gamma}\;and\;TNF{\alpha}$ stimulation, we measured the activation of MAP kinase using specific MAP kinase inhibitors. PC12 cells pretreated with SB203580, a p38 MAP kinase-specific inhibitor, resulted in the inhibition of iNOS expression and NO production. However, PD98059, an ERK/MAP kinase-specific inhibitor, was not observed to exert such an effect. In addition, Stat1 activated by $IFN{\gamma}\;and\;TNF{\alpha}$ was interacted with p38 MAPK. These data suggest that p38 MAP kinase mediates cytokine-mediated iNOS expression in the PC12 cells, and Jak/Stat pathway interferes with p38 MAPK signaling pathway.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.11a
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• pp.14-40
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• 2002

15-Deoxy-${\Delta}^{12, 14}$-prostaglandin $J_2$ (15-deoxy-$PGJ_2$), a naturally occurring ligand activates the peroxisome proliferator-activated $receptor-{\gamma}(PPAR-{\gamma}$). Activation of $PPAR-{\gamma}$ has been found to induce cell differentiation such as adipose cell and macrophage. Here it was investigated whether 15-deoxy-$PGJ_2$ has neuronal cell differentiation and possible underlying molecular mechanisms. Dopaminergic differentiating PC 12 cells treated with 15-deoxy-$PGJ_2$ (0.2 to 1.6 ${\mu}M$) alone showed measurable neurite extension and expression of neurofilament, markers of cell differentiation. However much greater extent of neurite extension and expression of neurofilament was observed in the presence of NGF (50 ng/ml). In parallel with its increasing effect on the neurite extension and expression of neurofilament, 15-deoxy-$PGJ_2$ enhanced NGF-induced p38 MAP kinase expression and its phosphorylation in addition to the activation of transcription factor AP-1 in a dose dependent manner. Moreover, pretreatment of SD 203580, a specific inhibitor of p38 MAP kinase inhibited the promoting effect of 15-deoxy-$PGJ_2$(0.8 ${\mu}M$) on NGF-induced neurite extension. This inhibition correlated well with the ability of SB203580 to inhibit the enhancing effect of 15-deoxy-$PGJ_2$ on the expression of p38 MAP kinase and activation of AP-1, The promoting ability of 15-deoxy-$PGJ_2$ did not occur through $PPAR-{\gamma}$, as synthetic PPAR-${\gamma}$ agonist andantagonist did not change the neurite promoting effect of 15-deoxy-PGJ$_2$. In addition, contrast to other cells (embryonic midbrain and SK-N-MC cells), $PPAR-{\gamma}$ was not expressed in PC-12 cells. Other structure related prostaglandins, PGD$_2$ and $PGE_2$ acting via a cell surface G-protein-coupled receptor (GPCR) did not increase basal or NGF-induced neurite extension. Moreover, GPCR (EP and DP receptor) antagonists did not alter the promoting effect of f 5-deoxy-$PGJ_2$ on neurite extension and activation of p38 MAP kinase, suggesting that the promoting effect of 15-deoxy-$PGJ_2$ may not be mediated GPCR. These data demonstrate that activation of p38 MAP kinase in conjunction with AP-1 single pathway may be important in the promoting activity of 15-deoxy-$PGJ_2$ cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.4
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• pp.1017-1024
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• 2007

Thymus and activation-regulated chemokine (TARC/CCL-17), produced by keratinocytes, is a CC chemokine known to selectively Th2 type T cells via $CCR4^+$ and is implicated in the development of atopic dermatitis (AD). TARC/CCL17 expression was induced by cytokines such as tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interferon-${\gamma}$ (IFN-${\gamma}$). We recently found that the wogonin, a flavone isolated from Scutellaria baicalensis, suppressed TARC expression via heme oxygenase 1 (HO1) in human keratinocytes induced with mite antigen. However, little is known about the inhibitory mechanism of wogonin on TARC/CCL-17 expression stimulated with cytokines. To investigate the inhibitory mechanism, I determined the inhibitory effects of wogonin on the activation of nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and $I{\kappa}B{\alpha}$ phosphorylation, and also examined the activation of p38 MAP kainase in HaCaT keratinocytes stimulated with TNF-${\alpha}$ and IFN-${\gamma}$. Wogonin inhibited NF-${\kappa}B$-DNA complex, NF-${\kappa}B$ binding activity, and the phosphorylation of $I{\kappa}B{\alpha}$ in a dose dependent manner. Wogonin also inhibited the translocation of NF-${\kappa}B$ from cytosol to nucleus. Moreover, the phosphorylation of of p38 MAP kinase in the TNF-${\alpha}$ and IFN-${\gamma}$-stimulated HaCaT keratinocytes were suppressed by wogonin in a dose dependent manner. These results suggest that wogonin may inhibit cytokine-induced NF-${\kappa}B$ activation by $I{\kappa}B{\alpha}$ degradation via suppression of p38 MAP kinase signaling pathway in keratinocytes and modulation of wogonin signaling pathway may be beneficial for the treatment of AD.

• Transactions of Materials Processing
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• v.11 no.6
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• pp.529-537
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• 2002

A series of load-relaxation tests and tensile tests were conducted to study the high temperature deformation mechanism of fine duplex gamma TiAl alloy at temperatures ranging from 800 to 105$0^{\circ}C$. Results of load relaxation test showed that deformation behavior at a small imposed strain ($\varepsilon$≒0.05) was dominated by dislocation glide and dislocation climb. To investigate the deformation behavior at a large amount of strain, the processing map was constructed using a dynamic materials model. Two domains were characterized in the processing map obtained at a strain level of 0.6. One domain was found at the region of 98$0^{\circ}C$ and $10^{-3}/sec$ with a peak efficiency of 48%, which was identified as a domain of dynamic recrystallization from the microstructural observation. The order was observed at the region of 125$0^{\circ}C$ and $10^{-4}/sec$ with a peak efficiency of 64%. The strain rate sensitivity measured indicates that the material was deformed by the superplasticity in the region.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.14-40
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• 2002

15-Deoxy- Δ$\^$12,14/-prostaglandin J$_2$ (15-deoxy-PGJ$_2$), a naturally occurring ligand activates the peroxisome proliferator-activated receptor-${\gamma}$ (PPAR-${\gamma}$). Activation of PPAR-y has been found to induce cell differentiation such as adipose cell and macrophage. Here it was investigated whether 15-deoxy-PGJ$_2$ has neuronal cell differentiation and possible underlying molecular mechanisms. Dopaminergic differentiating PC 12 cells treated with 15-deoxy-PGJ$_2$ (0.2 to 1.6 ${\mu}$M) alone showed measurable neurite extension and expression of neurofilament, markers of cell differentiation. However much greater extent of neurite extension and expression of neurofilament was observed in the presence of NGF (50 ng/$m\ell$). In parallel with its increasing effect on the neurite extension and expression of neurofilament, 15-deoxy-PGJ$_2$ enhanced NGF-induced p38 MAP kinase expression and its phosphorylation in addition to the activation of transcription factor AP-1 in a dose dependent manner. Moreover, pretreatment of SD 203580, a specific inhibitor of p38 MAP kinase inhibited the promoting effect of 15-deoxy-PGJ$_2$ (0.8 ${\mu}$M) on NGF-induced neurite extension. This inhibition correlated well with the ability of SB203580 to inhibit the enhancing effect of 15-deoxy-PGJ$_2$ on the expression of p38 MAP kinase and activation of AP-1. The promoting ability of 15-deoxy-PGJ$_2$ did not occur through PPAR-${\gamma}$, as synthetic PPAR-${\gamma}$ agonist and antagonist did not change the neurite promoting effect of 15-deoxy-PGJ$_2$. In addition, contrast to other cells (embryonic midbrain and SK-N-MC cells), PPAR-${\gamma}$ was not expressed in PC-12 cells. Other structure related prostaglandins, PGD$_2$ and PGE$_2$ acting via a cell surface G-protein-coupled receptor (GPCR) did not increase basal or NGF-induced neurite extension. Moreover, GPCR (EP and DP receptor) antagonists did not alter the promoting effect of 15-deoxy-PGJ$_2$ on neurite extension and activation of p38 MAP kinase, suggesting that the promoting effect of 15-deoxy-PGJ$_2$ may not be mediated GPCR. These data demonstrate that activation of p38 MAP kinase in conjunction with AP-1 signal pathway may be important in the promoting activity of 15-deoxy-PGJ$_2$ on the differentiation of PC12 cells.

• Journal of the Korean Mathematical Society
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• v.53 no.5
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• pp.1149-1165
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• 2016

In this paper, we show that there exists no left invariant Riemannian metric h on the Heisenberg group H such that (H, h) is a symmetric Riemannian manifold, and there does not exist any H-invariant metric $\bar{h}$ on the Heisenberg manifold $H/{\Gamma}$ such that the Riemannian connection on ($H/{\Gamma},\bar{h}$) is a Yang-Mills connection. Moreover, we get necessary and sufficient conditions for a group homomorphism of (SU(2), g) with an arbitrarily given left invariant metric g into (H, h) with an arbitrarily given left invariant metric h to be a harmonic and an affine map, and get the totality of harmonic maps of (SU(2), g) into H with a left invariant metric, and then show the fact that any affine map of (SU(2), g) into H, equipped with a properly given left invariant metric on H, does not exist.