The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
Gregory J. Tsay - One of the best experts on this subject based on the ideXlab platform.
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a paeonol derivative yph Pa3 promotes the differentiation of monocyte macrophage lineage precursor cells into osteoblasts and enhances their autophagy
European Journal of Pharmacology, 2018Co-Authors: Chun-hao Tsai, Ming Hua Hsu, Po Hao Huang, Chin Tung Hsieh, Ying Ming Chiu, Dong Chen Shieh, Yi-ju Lee, Gregory J. TsayAbstract:Previous studies have indicated that paeonol inhibits RANKL-induced osteoclastogenesis by inhibiting the ERK, p38, and NF-κB pathway. We modified paeonol to form a new compound, YPH-Pa3, and found that it promoted osteoclastogenesis rather than inhibited it the way paeonol does. The aim of this study is to investigate the mechanisms involved in YPH-Pa3-promoted osteoclastogenesis. YPH-Pa3-promoted differentiation of RAW264.7 cells (human monocytes) into osteoclasts is activated through ERK/p38/JNK phosphorylation, affecting c-FOS, NF-κB, and NFATc2. Real-time quantitative PCR and western blot revealed an increased expression of autophagy-related markers during YPH-Pa3-induced osteoclastogenesis. We also demonstrated the relationship between p62/LC3 localization and F-actin ring formation by double-labeling immunofluorescence. Knockdown of p62 small-interfering RNA (siRNA) attenuated YPH-Pa3-induced expression of autophagy-related genes. Our study results indicated that p62 may play a role in YPH-Pa3-induced autophagy and osteoclastogenesis, which may help to develop a novel therapeutic strategy against osteoclastogenesis-related diseases.
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A paeonol derivative, YPH-Pa3 promotes the differentiation of monocyte/macrophage lineage precursor cells into osteoblasts and enhances their autophagy.
European journal of pharmacology, 2018Co-Authors: Chun-hao Tsai, Ming Hua Hsu, Po Hao Huang, Chin Tung Hsieh, Ying Ming Chiu, Dong Chen Shieh, Yi-ju Lee, Gregory J. TsayAbstract:Previous studies have indicated that paeonol inhibits RANKL-induced osteoclastogenesis by inhibiting the ERK, p38, and NF-κB pathway. We modified paeonol to form a new compound, YPH-Pa3, and found that it promoted osteoclastogenesis rather than inhibited it the way paeonol does. The aim of this study is to investigate the mechanisms involved in YPH-Pa3-promoted osteoclastogenesis. YPH-Pa3-promoted differentiation of RAW264.7 cells (human monocytes) into osteoclasts is activated through ERK/p38/JNK phosphorylation, affecting c-FOS, NF-κB, and NFATc2. Real-time quantitative PCR and western blot revealed an increased expression of autophagy-related markers during YPH-Pa3-induced osteoclastogenesis. We also demonstrated the relationship between p62/LC3 localization and F-actin ring formation by double-labeling immunofluorescence. Knockdown of p62 small-interfering RNA (siRNA) attenuated YPH-Pa3-induced expression of autophagy-related genes. Our study results indicated that p62 may play a role in YPH-Pa3-induced autophagy and osteoclastogenesis, which may help to develop a novel therapeutic strategy against osteoclastogenesis-related diseases.
Chun-hao Tsai - One of the best experts on this subject based on the ideXlab platform.
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a paeonol derivative yph Pa3 promotes the differentiation of monocyte macrophage lineage precursor cells into osteoblasts and enhances their autophagy
European Journal of Pharmacology, 2018Co-Authors: Chun-hao Tsai, Ming Hua Hsu, Po Hao Huang, Chin Tung Hsieh, Ying Ming Chiu, Dong Chen Shieh, Yi-ju Lee, Gregory J. TsayAbstract:Previous studies have indicated that paeonol inhibits RANKL-induced osteoclastogenesis by inhibiting the ERK, p38, and NF-κB pathway. We modified paeonol to form a new compound, YPH-Pa3, and found that it promoted osteoclastogenesis rather than inhibited it the way paeonol does. The aim of this study is to investigate the mechanisms involved in YPH-Pa3-promoted osteoclastogenesis. YPH-Pa3-promoted differentiation of RAW264.7 cells (human monocytes) into osteoclasts is activated through ERK/p38/JNK phosphorylation, affecting c-FOS, NF-κB, and NFATc2. Real-time quantitative PCR and western blot revealed an increased expression of autophagy-related markers during YPH-Pa3-induced osteoclastogenesis. We also demonstrated the relationship between p62/LC3 localization and F-actin ring formation by double-labeling immunofluorescence. Knockdown of p62 small-interfering RNA (siRNA) attenuated YPH-Pa3-induced expression of autophagy-related genes. Our study results indicated that p62 may play a role in YPH-Pa3-induced autophagy and osteoclastogenesis, which may help to develop a novel therapeutic strategy against osteoclastogenesis-related diseases.
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A paeonol derivative, YPH-Pa3 promotes the differentiation of monocyte/macrophage lineage precursor cells into osteoblasts and enhances their autophagy.
European journal of pharmacology, 2018Co-Authors: Chun-hao Tsai, Ming Hua Hsu, Po Hao Huang, Chin Tung Hsieh, Ying Ming Chiu, Dong Chen Shieh, Yi-ju Lee, Gregory J. TsayAbstract:Previous studies have indicated that paeonol inhibits RANKL-induced osteoclastogenesis by inhibiting the ERK, p38, and NF-κB pathway. We modified paeonol to form a new compound, YPH-Pa3, and found that it promoted osteoclastogenesis rather than inhibited it the way paeonol does. The aim of this study is to investigate the mechanisms involved in YPH-Pa3-promoted osteoclastogenesis. YPH-Pa3-promoted differentiation of RAW264.7 cells (human monocytes) into osteoclasts is activated through ERK/p38/JNK phosphorylation, affecting c-FOS, NF-κB, and NFATc2. Real-time quantitative PCR and western blot revealed an increased expression of autophagy-related markers during YPH-Pa3-induced osteoclastogenesis. We also demonstrated the relationship between p62/LC3 localization and F-actin ring formation by double-labeling immunofluorescence. Knockdown of p62 small-interfering RNA (siRNA) attenuated YPH-Pa3-induced expression of autophagy-related genes. Our study results indicated that p62 may play a role in YPH-Pa3-induced autophagy and osteoclastogenesis, which may help to develop a novel therapeutic strategy against osteoclastogenesis-related diseases.
Paul L. A. Popelier - One of the best experts on this subject based on the ideXlab platform.
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Structures of cubic and orthorhombic phases of acetylene by single-crystal neutron diffraction
Acta Crystallographica Section B Structural Science, 1992Co-Authors: R. K. Mcmullan, Å. Kvick, Paul L. A. PopelierAbstract:C 2 H 2 cristallise dans Pa3, Z=4, avec a T=131, 141K, a o =6.0940,6.1050; et affinement jusqu'a R=0.065,0.052. C 2 D 2 cristallise a T=143K dans Pa3 avec Z=4, a o =6.1020A, et a T=15K dans Acam avec Z=4, a=6.198, b=6.023, c=5.578A. Pour ces deux temperatures, l'affinement atteint R=0.068, 0.081
K. H. Michel - One of the best experts on this subject based on the ideXlab platform.
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Theory of elastic anomalies at the gamma--alpha phase transition in solid Ce
arXiv: Materials Science, 2012Co-Authors: K. H. Michel, A. V. NikolaevAbstract:Starting from a model of 4f-electron generated quadrupolar densities on a compressible fcc lattice, the elastic anomalies at the Fm3m -> Pa3 phase transition are studied by means of analytical theory. The model is taken as representative for the gamma-alpha phase transition in Ce. The coupling of the (linear) lattice displacements to the square of the quadrupolar orientational density fluctuations renormalizes the elastic constants. The condensation of the quadrupolar densities into the orientationally ordered Pa3 structure is studied as function of temperature and pressure. Precursor effects of the transition lead to an anomalous softening of the elastic constant c11 while c44 exhibits no such softening. The theoretical results are in excellent qualitative agreement with pressure experiments on the elastic constants (equivalently on sound velocities) at the $gamma-alpha transition in Ce. Lattice dynamical analogies in theory and striking similarities in experimental results with the Fm3m -> Pa3 transition in C60 fullerite are discussed.
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Symmetry lowering at the structural phase transition in NpO2 and UO2
Physical Review B, 2003Co-Authors: A. V. Nikolaev, K. H. MichelAbstract:The structural phase transitions with electric-quadrupole long-range order in NpO 2 (Fm3m→Pn3m) and UO 2 (Fm3m→Pa3) are analyzed from a group theoretical point of view. In both cases, the symmetry lowering involves three quadrupolar components belonging to the irreducible representation T 2 g (Γ 5 ) of O h and condensing in a triple-q structure at the X point of the Brillouin zone. The Pa3 structure is close to Pn3m, but allows for oxygen displacements. The Pa3 ordering leads to an effective electrostatic attraction between electronic quadrupoles while the Pn3m ordering results in a repulsion between them. It is concluded that the Pn3m structure can be stabilized only through some additional process such as strengthening of the chemical bonding between Np and O. We also derive the relevant structure-factor amplitudes for Pn3m and Pa3, and the effect of domains on resonant x-ray scattering experiments.
Dong Chen Shieh - One of the best experts on this subject based on the ideXlab platform.
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a paeonol derivative yph Pa3 promotes the differentiation of monocyte macrophage lineage precursor cells into osteoblasts and enhances their autophagy
European Journal of Pharmacology, 2018Co-Authors: Chun-hao Tsai, Ming Hua Hsu, Po Hao Huang, Chin Tung Hsieh, Ying Ming Chiu, Dong Chen Shieh, Yi-ju Lee, Gregory J. TsayAbstract:Previous studies have indicated that paeonol inhibits RANKL-induced osteoclastogenesis by inhibiting the ERK, p38, and NF-κB pathway. We modified paeonol to form a new compound, YPH-Pa3, and found that it promoted osteoclastogenesis rather than inhibited it the way paeonol does. The aim of this study is to investigate the mechanisms involved in YPH-Pa3-promoted osteoclastogenesis. YPH-Pa3-promoted differentiation of RAW264.7 cells (human monocytes) into osteoclasts is activated through ERK/p38/JNK phosphorylation, affecting c-FOS, NF-κB, and NFATc2. Real-time quantitative PCR and western blot revealed an increased expression of autophagy-related markers during YPH-Pa3-induced osteoclastogenesis. We also demonstrated the relationship between p62/LC3 localization and F-actin ring formation by double-labeling immunofluorescence. Knockdown of p62 small-interfering RNA (siRNA) attenuated YPH-Pa3-induced expression of autophagy-related genes. Our study results indicated that p62 may play a role in YPH-Pa3-induced autophagy and osteoclastogenesis, which may help to develop a novel therapeutic strategy against osteoclastogenesis-related diseases.
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A paeonol derivative, YPH-Pa3 promotes the differentiation of monocyte/macrophage lineage precursor cells into osteoblasts and enhances their autophagy.
European journal of pharmacology, 2018Co-Authors: Chun-hao Tsai, Ming Hua Hsu, Po Hao Huang, Chin Tung Hsieh, Ying Ming Chiu, Dong Chen Shieh, Yi-ju Lee, Gregory J. TsayAbstract:Previous studies have indicated that paeonol inhibits RANKL-induced osteoclastogenesis by inhibiting the ERK, p38, and NF-κB pathway. We modified paeonol to form a new compound, YPH-Pa3, and found that it promoted osteoclastogenesis rather than inhibited it the way paeonol does. The aim of this study is to investigate the mechanisms involved in YPH-Pa3-promoted osteoclastogenesis. YPH-Pa3-promoted differentiation of RAW264.7 cells (human monocytes) into osteoclasts is activated through ERK/p38/JNK phosphorylation, affecting c-FOS, NF-κB, and NFATc2. Real-time quantitative PCR and western blot revealed an increased expression of autophagy-related markers during YPH-Pa3-induced osteoclastogenesis. We also demonstrated the relationship between p62/LC3 localization and F-actin ring formation by double-labeling immunofluorescence. Knockdown of p62 small-interfering RNA (siRNA) attenuated YPH-Pa3-induced expression of autophagy-related genes. Our study results indicated that p62 may play a role in YPH-Pa3-induced autophagy and osteoclastogenesis, which may help to develop a novel therapeutic strategy against osteoclastogenesis-related diseases.
