| 1. |
- Xiong, Wei, et al.
(författare)
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Thermodynamic reassessment of the Cu-Mg-Ni system with brief comments on the thermodynamic modeling of the sub-systems
- 2008
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Ingår i: Calphad. - : Elsevier BV. - 0364-5916 .- 1873-2984. ; 32:4, s. 675-685
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Tidskriftsartikel (refereegranskat)abstract
- The Cu-Mg-Ni system was reassessed using the CALPHAD (CALculation of PHAse Diagram) approach, in order to provide a reliable thermodynamic description. A set of self-consistent thermodynamic parameters for the Cu-Mg-Ni system was obtained. The liquidus projection and the reaction scheme were generated by using the present thermodynamic parameters. Significant improvements have been made, compared with the previous assessments. Thermodynamic modeling for the three sub-systems was briefly reviewed. Further work is of interest to refine the thermodynamic description of the binary systems, in order to avoid the appearance of the artificial phase equilibria in liquid above 2500 degrees C.
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| 2. |
- Zhang, Wei-Wei, et al.
(författare)
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Phase equilibria of the Fe-Ni-Si system at 850 degrees C
- 2009
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Ingår i: Journal of Alloys and Compounds. - : Elsevier BV. - 0925-8388 .- 1873-4669. ; 481:1-2, s. 509-514
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Tidskriftsartikel (refereegranskat)abstract
- By means of X-ray diffraction, metallography, scanning electron microscopy with energy dispersive Xray analysis, and electron probe microanalysis, the constitution of the ternary Fe-Ni-Si system at 850 degrees C over the entire composition range was established with 24 alloys. Ten of the three-phase equilibria were well determined at 850 degrees C. The existence of the ternary compound Fe5Ni3Si2 (tau(1)) with a cubic crystal structure at 850 degrees C is confirmed. The homogeneity ranges were measured and the lattice parameters were determined for most observed phases.
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| 3. |
- Zhang, Wei-Wei, et al.
(författare)
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Thermodynamic Assessment of the Cu-B System Supported by Key Experiment and First-Principles Calculations
- 2009
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Ingår i: Journal of Phase Equilibria and Diffusion. - : Springer Science and Business Media LLC. - 1547-7037 .- 1863-7345. ; 30:5, s. 480-486
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Tidskriftsartikel (refereegranskat)abstract
- The Cu-B system was investigated via a hybrid approach of key experiment and thermodynamic modeling. Based on the critically assessed Cu-B phase diagram, seven crucial alloys were selected and prepared by arc melting the pure elements. An inductively coupled plasma-atomic emission spectrometric analysis was conducted to determine the compositions of the prepared alloys. The phase equilibria were determined by using x-ray diffraction, electron probe microanalysis, and differential thermal analysis. The temperature associated with the eutectic reaction, L double left right arrow (B) + (Cu); was measured to be 1028 +/- 2 degrees C. First-principles calculations indicate that the energy of inserting a B atom into the interstitial vacancy (Va) site of the lattice for Cu atoms is marginally lower than that of substituting for a Cu atom with a B atom. Consequently, the sublattice model (Cu)(B, Va) in which B atoms occupy the interstitial sites was employed for the fcc (Cu) phase rather than the model (Cu, B)(Va) in which B atoms substitute for Cu atoms. A thermodynamic modeling of the Cu-B system was then performed by considering the reliable literature data and the present experimental results. A good agreement between modeling and experiment was obtained.
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| 4. |
- Ablikim, M., et al.
(författare)
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Measurements of (XcJ)-> K+K-K+K- decays
- 2006
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Ingår i: Physics Letters B. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 642:3, s. 197-202
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Tidskriftsartikel (refereegranskat)abstract
- Using 14M psi(2S) events taken with the BESII detector, chi(cJ) -> 2(K+K-) decays are studied. For the four-kaon final state, the branching fractions are B(chi(c0,1,2) ->.2(K+K-)) = (3.48 +/- 0.23 +/- 0.47) x 10(-3), (0.70 +/- 0.13 +/- 0.10) x 10(-3), and (2.17 +/- 0.20 +/- 0.31) x 10(-3). For the phi K+K- final state, the branching fractions, which are measured for the first time, are B(chi(c0,1,2) -> phi K+K-) = (1.03 +/- 0.22 +/- 0.15) x 10(-3), (0.46 +/- 0.16 +/- 0.06) x 10(-3), and (1.67 +/- 0.26 +/- 0.24) x 10(-4). For the phi phi final state, B(chi(c0,2) -> phi phi) = (0.94 +/- 0.21 +/- 0.13) x 10(-3) and (1.70 +/- 0.30 +/- 0.25) x 10(-3).
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| 5. |
- Chien, Ming-Hsien, et al.
(författare)
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Vascular endothelial growth factor-C (VEGF-C) promotes angiogenesis by induction of COX-2 in leukemic cells via the VEGF-R3/JNK/AP-1 pathway.
- 2009
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Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 30:12, s. 2005-13
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Tidskriftsartikel (refereegranskat)abstract
- Vascular endothelial growth factor (VEGF)-C is recognized as a tumor lymphangiogenic factor based on the effects of activated VEGF-R3 on lymphatic endothelial cells. Many tumor cells express VEGF-R3 but the function of this receptor in tumor cells is largely unknown. It has been reported that the VEGF-C/VEGF-R3 axis is activated in subsets of leukemia patients. Herein, we have shown that VEGF-C induces angiogenic activity in the tube formation assay invitro and Matrigel plug assay in vivo by upregulating an angiogenic factor, cyclooxygenase-2 (COX-2), through VEGF-R3 in the human acute myeloid leukemia (AML) cell line, THP-1. COX-2 induction by VEGF-C was also observed in other VEGF-R3(+) human AML cell lines (U937 and HL60). Moreover, immunohistochemical analysis of bone marrow specimens of 37 patients diagnosed with AML revealed that VEGF-C expression in specimens was associated with the expression of COX-2 (P < 0.001). The manner by which signaling pathways transduced by VEGF-C is responsible for COX-2 upregulation was further investigated. Blocking the p42/44 mitogen-activated protein kinase (MAPK) pathway with the MAPK kinase inhibitor, PD 98059, failed to inhibit VEGF-C-mediated COX-2 expression. However, VEGF-C-induced COX-2 upregulation was effectively abolished by overexpression of dominant-negative c-Jun N-terminal kinase (JNK) or treatment with the JNK inhibitor, SP 600125. VEGF-C induced JNK-dependent nuclear translocation of c-Jun. Furthermore, chromatin immunoprecipitation and reporter assays revealed that VEGF-C enhanced c-Jun binding to the cyclic adenosine 3',5'-monophosphate-response element of the COX-2 promoter and induced COX-2 expression. In sum, the data herein highlight the pathogenic role of VEGF-C in leukemia via regulation of angiogenesis through upregulation of COX-2.
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| 6. |
- Liao, Zhong-Wei, et al.
(författare)
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Robust Low Voltage Program-Erasable Cobalt-Nanocrystal Memory Capacitors with Multistacked Al2O3/HfO2/Al2O3 Tunnel Barrier
- 2009
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Ingår i: Chinese Physics Letters. - 0256-307X .- 1741-3540. ; 26:8, s. 087303-
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Tidskriftsartikel (refereegranskat)abstract
- An atomic-layer-deposited Al2O3/HfO2/Al2O3 (A/H/A) tunnel barrier is investigated for Co nanocrystal memory capacitors. Compared to a single Al2O3 tunnel barrier, the A/H/A barrier can significantly increase the hysteresis window, i. e., an increase by 9V for +/- 12V sweep range. This is attributed to a marked decrease in the energy barriers of charge injections for the A/H/A tunnel barrier. Further, the Co-nanocrystal memory capacitor with the A/H/A tunnel barrier exhibits a memory window as large as 4.1V for 100 mu s program/erase at a low voltage of +/- 7V, which is due to fast charge injection rates, i. e., about 2.4 x 10(16) cm(-2) s(-1) for electrons and 1.9 x 10(16) cm(-2) s(-1) for holes.
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| 7. |
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| 8. |
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| 9. |
- Wang, Wei-Zhou, et al.
(författare)
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Comparative analysis of gene expression profiles between the normal human cartilage and the one with endemic osteoarthritis.
- 2009
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Ingår i: Osteoarthritis and Cartilage. - : Saunders Elsevier. - 1063-4584 .- 1522-9653. ; 17:1, s. 83-90
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate the differences in gene expression profiles of adult articular cartilage with endemic osteoarthritis (OA), Kashin-Beck disease (KBD), and the same regions in the normal joint.METHODS: The messenger RNA expression profiles of articular cartilage with KBD diagnosed according to "Diagnosing Criteria of Kashin-Beck Disease in China" were compared with the normal cartilage. Total RNA isolated separately from four pairs of the KBD and normal cartilage samples were evaluated by oligonucleotide microarray analysis. The microarray data were confirmed by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) amplification and were compared with previously published experiments.RESULTS: About 4100 transcripts, which corresponded to 35% of the expressed transcripts, showed >or=twofold differences in expression between the cartilage tissues in pairs. Approximately 2% of the expressed genes (79, 55 genes expressed in KBD>normal; 24 genes expressed in KBDCONCLUSION: Differences between KBD cartilage and the normal exhibited a similar pattern among the four pairs examined, indicating the presence of common mechanisms mainly including chondrocyte metabolism and apoptosis that contribute to cartilage destruction in KBD.
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| 10. |
- Wei, Jian-Feng, et al.
(författare)
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Formation of Kv2.1-FAK complex as a mechanism of FAK activation, cell polarization and enhanced motility
- 2008
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Ingår i: Journal of Cellular Physiology. - : Wiley. - 0021-9541 .- 1097-4652. ; 217:2, s. 544-557
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Tidskriftsartikel (refereegranskat)abstract
- Focal adhesion kinase (FAK) plays key roles in cell adhesion and migration. We now report that the delayed rectifier Kv2.1 potassium channel, through its LD-like motif in N-terminus, may interact with FAK and enhance phosphorylation of FAK(397) and FAK(576/577) Overlapping distribution of Kv2.1 and FAK was observed on soma and proximal dendrites of cortical neurons. FAK expression promotes a polarized membrane distribution of the Kv2.1 channel. In Kv2.1-transfected CHO cells, formation of the Kv2.1-FAK complex was stimulated by fibronectin/integrin and inhibited by the K channel blocker tetraethylammonium (TEA). FAK phosphorylation was minimized by shRNA knockdown of the Kv2.1 channel, point mutations of the N-terminus, and TEA, respectively. Cell migration morphology was altered by Kv2.1 knockdown or TEA, hindering cell migration activity. In wound healing tests in vitro and a traumatic injury animal model, Kv2.1 expression and co-localization of Kv2.1 and FAK significantly enhanced directional cell migration and wound closure. It is suggested that the Kv2.1 channel may function as a promoting signal for FAK activation and cell motility.
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