• 제목/요약/키워드: Gamma-map

검색결과 100건 처리시간 0.031초

Gamma Evaluation with Portal Dosimetry for Volumetric Modulated Arc Therapy and Intensity-Modulated Radiation Therapy

  • Kim, Jung-in;Choi, Chang Heon;Park, So-Yeon;An, HyunJoon;Wu, Hong-Gyun;Park, Jong Min
    • 한국의학물리학회지:의학물리
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    • 제28권2호
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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.

GROUP ACTION FOR ENUMERATING MAPS ON SURFACES

  • Mao, Linfan;Liu, Yanpei
    • Journal of applied mathematics & informatics
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    • 제13권1_2호
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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.

HDR 영상의 지역적 밝기 및 디테일 향상을 위한 감마 보정 기법 (Gamma Correction for Local Brightness and Detail Enhancement of HDR Images)

  • 이승윤;하호건;송근원;하영호
    • 한국멀티미디어학회논문지
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    • 제19권5호
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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.

조골세포에시 p-38 MAP kinase의 nitric oxide 및 interleukin-6 생성조절에 관한 연구 (A study on the regulatory effect of p-38 MAP kinase on nitric oxide and interleukin-6 in osteoblasts)

  • 이경원;이도훈;강경화;김상철
    • 대한치과교정학회지
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    • 제33권3호
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    • pp.199-210
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    • 2003
  • 치아이동 시 발생하는 골흡수에서 이미 여러 cytokine의 중요성이 강조된 바 있으며 이 가운데 interleukin-6는 구강 및 연골조직 등에서 많은 연구의 초점이 되어 왔으나 확실한 기전은 아직까지 정확히 확립되어 있지 못하다 골흡수 시 조골세포에서 유리되는 interleukin-6 (IL-6)와 nitric oxide (NO) 등이 골흡수의 조절자로 최근 대두되고 있으며 Mitogen-activated Protein kinase (MAPK)의 활성화로 인해 염증성 cytokine등이 유리될 수 있음이 최근 macrophage 등에서 증명된 바 있다. 그러므로 치아이동을 비롯한 구강 내 여러 염증의 조건에서 골흡수의 대표인자인 IL-6및 NO유리가 MAPK등의 활성 등을 통해 조절될 수 있는 가능성을 시사하고 있다. 본 연구에서 조골세포 특징을 대부분 가지고 있는 조골세포주 MC3T3El에서 p-38 MAP kinase을 매개로 NO와 IL-6가 유리됨을 확인하고자 하였다. $10\%$ Fetal Bovine Serum이 첨가된 -MEM 배양액으로 배양한 조골세포주인 MC3T3El 세포에 tumor necrosis $factor-\alpha(TNF-\alpha)$, $interferon-\gamma(IFN-\gamma)$ 및 lipopolysacchalide(LPS) 등의 단독처리 시 NO와 IL-6의 증가는 확인되지 않았으나 $TNF-\alpha/IFN-\gamma$ 혹은 $LPS/IFN-\gamma$ 등의 처치시 NO와 IL-6의 유의한 증가를 보였으며, NO발현에 직접 관여하는 inducible nitric oxide synthase (iNOS)와 IL-6 단백질 및 mRNA의 발현을 관찰하였다. 또한 specific p-38 MAP kinase inhibitor인 SB203580의 NO와 IL-6의 생성 억제를 관찰하고 단백질과 mRNA발현억제를 통해서도 확인함으로써 SB203580은 transcription 단계에서 NO와 IL-6의 생성을 조절하고 있음을 시사하여 주고 있다. $TNF-\alpha/IFN-\gamma$ 혹은 $LPS/IFN-\gamma$ 처치 시 p-38 MAP Kinase의 활성을 관찰하였으나 단독 처치 시 역시 P-38 MAP Kinase의 활성을 확인함으로써 NO와 IL-6생성기전에는 p-38 MAP Kinase이외에 다른 인자 역시 관여하고 있음을 보여주고 있다. 본 연구에서는 치아 등의 골조직의 구성 세포인 조골세포에서 NO와 IL-6유리를 확인하였으며, 또한 이들의 생성기전중의 하나로 p-38 MAP Kinase가 transcription 단계에서 관여하고 있음을 확인하였다.

Molecular Mechanism of NO-induced Cell Death of PC12 Cells by $IFN{\gamma}\;and\;TNF{\alpha}$

  • Yi, Seh-Yoon;Han, Seon-Kyu;Lee, Jee-Yeon;Yoo, Young-Sook
    • Molecular & Cellular Toxicology
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    • 제1권3호
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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.

Expression of peroxisome proliferator activated receptor gamma in the neuronal cells and modulation of their differentiation by PPAR gamma agonists

  • Hong, Jin-Tae
    • 한국환경성돌연변이발암원학회:학술대회논문집
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    • 한국환경성돌연변이발암원학회 2002년도 Molecular and Cellular Response to Toxic Substances
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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.

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Wogonin inhibits Cytokine-induced TARC/CCL17 Expression by Suppression of NF-${\kappa}B$ activation via p38 MAP kinase Signalning Pathways in HaCaT Keratinocytes

  • Jang, Seon-Il
    • 동의생리병리학회지
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    • 제21권4호
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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.

Gamma TiAI 합금의 고온 변형거동 - 미세조직의 변화 및 변형기구 (High Temperature Deformation Behavior of Gamma TiAl Alloy - Microstructural Evolution and Mechanisms)

  • 김정한;장영원;이종수
    • 소성∙가공
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    • 제11권6호
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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.

Expression of peroxisome proliferator activated receptor gamma in the neuronal cells and modulation of their differentiation by PPAR gamma agonists

  • Hong, Jin-Tae
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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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.

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DIFFERENTIAL GEOMETRIC PROPERTIES ON THE HEISENBERG GROUP

  • Park, Joon-Sik
    • 대한수학회지
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    • 제53권5호
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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.