| 1. |
- Klimkiewicz, A., et al.
(författare)
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Pygmy Dipole Strength in Exotic Nuclei and the Equation of State
- 2009
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Ingår i: AIP Conference Proceedings. - 1551-7616 .- 0094-243X. ; 1165, s. 181-184 461
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Konferensbidrag (refereegranskat)abstract
- A concentration of dipole strength at energies below the giant dipole resonance was observed in neutron-rich nuclei around Sn-132 in an experiment using the FRS-LAND setup. This so-called "pygmy" dipole strength can be related to the parameters of the symmetry energy and to the neutron skin thickness on the grounds of a relativistic quasiparticle random-phase approximation. Using this ansatz and the experimental findings for Sn-130 and 132 Sri, we derive a value of the symmetry energy pressure of (p) over bar (0) = 2.2 +/- 0.5 MeV/fm(3). Neutron skin thicknesses of R-n-R-p = 0.23 +/- 0.03 fm and 0.24 +/- 0.03 fm for Sn-130 and Sn-132, respectively, have been determined. Preliminary results on Ni-68 from a similar experiment using an improved setup indicate an enhanced cross section at low energies, while the results for Ni-58 are in accordance with results from photoabsorption measurements.
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| 2. |
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| 3. |
- Chatterjee, A., et al.
(författare)
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1n and 2n transfer with the borromean nucleus He-6 near the Coulomb barrier
- 2008
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Ingår i: Physical Review Letters. - 0031-9007 .- 1079-7114. ; 101:3, s. 032701-
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Tidskriftsartikel (refereegranskat)abstract
- Angular distributions for In and 2n transfer are reported for the He-6 + Cu-65 system at E-lab = 22.6 MeV. For the first time, triple coincidences between a particles, neutrons, and characteristic gamma rays from the targetlike residues were used to separate the contributions arising from In and 2n transfer. The differential cross sections for these channels, elastic scattering, and fusion were analyzed using a coupled reaction channels approach. The large measured ratio of the 2n-to-1n cross section and the strong influence of 2n transfer on other channels indicate that the dineutron configuration of He-6 plays a dominant role in the reaction mechanism.
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| 4. |
- Mahata, K., et al.
(författare)
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Study of dipole excitations and the single particle structure of neutron rich Ni isotopes
- 2008
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Ingår i: AIP Conference Proceedings. - 1551-7616 .- 0094-243X. ; 1012, s. 389-391 453
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Konferensbidrag (refereegranskat)abstract
- An experiment was performed using the FRS-LAND setup at GSI to study the dipole strength distributions above neutron separation threshold for neutron-rich Ni isotopes. Measurements, using the same experimental setup, were also carried out to extract single particle occupancies via knockout reactions to investigate the structure and magicity of the neutron-rich Ni isotopes. The status of the data analysis and preliminary results are presented.
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| 5. |
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| 6. |
- Orr, A Wayne, et al.
(författare)
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Molecular Mechanisms of Collagen Isotype-Specific Modulation of Smooth Muscle Cell Phenotype.
- 2009
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Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1524-4636. ; Nov 20, s. 225-231
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Smooth muscle cell (SMC) phenotypic modulation, an important component of atherosclerosis progression, is critically regulated by the matrix, with normal components of the healthy SMC matrix limiting modulation and atherosclerosis-associated transitional matrix proteins promoting phenotypic modulation. We sought to determine how collagen IV (which comprises the healthy artery wall) and monomeric collagen I (which comprises atherosclerotic lesions) differentially affect SMC phenotype. METHODS AND RESULTS: Plating SMCs on collagen IV resulted in elevated expression of SMC contractility proteins compared to collagen I. Concurrent with enhanced contractile gene expression, collagen IV stimulates binding of SRF to CArG boxes in the promoters of smooth muscle actin and smooth muscle myosin heavy chain. Coll IV also stimulated the expression of myocardin, a critical SRF coactivator required to drive expression of SMC specific genes. In contrast to collagen IV, collagen I stimulated enhanced expression of the inflammatory protein vascular cell adhesion molecule (VCAM)-1. NF-kappaB and NFAT-binding sites in the VCAM-1 promoter are critical for collagen I-mediated expression of VCAM-1 promoter activity. However, only inhibitors of NFAT, not NF-kappaB, were able to reduce collagen I-associated VCAM expression, and collagen I but not collagen IV stimulated NFAT transcriptional activity. CONCLUSIONS: These results show for the first time that collagen IV and collagen I differentially affect smooth muscle phenotypic modulation through multiple pathways.
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