| 1. |
- Fynbo, H. O. U., et al.
(author)
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News on C-12 from beta-decay studies
- 2004
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In: Nuclear Physics A. - : Elsevier BV. - 0375-9474. ; 738, s. 59-65
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Conference paper (peer-reviewed)abstract
- We discuss the importance of the spectroscopic properties of the resonances of C-12 just above the 3alpha-threshold, and review the existing experimental information of this region with emphasis on 0(+) and 2(+) states. A new experimental approach for studying the beta-decays of B-12 and N-12 is presented based on techniques developed in the context of Radioactive beam (rare isotope) physics. Finally preliminary results from an ongoing analysis of two recent experiments are given.
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| 2. |
- Zhang, Shi-Li, et al.
(author)
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Abnormal anti-Stokes Raman scattering of carbon nanotubes
- 2002
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In: Physical Review B. Condensed Matter and Materials Physics. - 1098-0121 .- 1550-235X. ; 66:3
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Journal article (peer-reviewed)abstract
- Abnormal anti-Stokes Raman scattering (AASR) was unambiguously observed in carbon nanotubes (CNT's). In contrast to traditional Raman scattering theory, the absolute value of the Raman frequency of the anti-Stokes peak is not the same as that of the corresponding Stokes peak. It was demonstrated that AASR scattering originates from the unique nanoscale cylindrical structure of CNT's that can be considered naturally as a graphite structure with an intrinsic defect from its rolling. The double-resonance Raman scattering theory was applied to interpret the scattering mechanism of the AASR phenomenon successfully and quantitatively.
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| 3. |
- Beyer, K., et al.
(author)
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Association and linkage of atopic dermatitis with chromosome 13q12-14 and 5q31-33 markers
- 2000
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In: Journal of Investigative Dermatology. - : Elsevier BV. - 0022-202X .- 1523-1747. ; 115:5, s. 906-908
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Journal article (peer-reviewed)abstract
- Atopic dermatitis is a chronic inflammatory skin disease that affects 10-20% of the population. Linkage of atopy, asthma, allergic rhinitis, and total serum IgE levels to several different chromosomal regions have been described extensively, but little is known about the genetic control of atopic dermatitis. We tested for the association and linkage between atopic dermatitis and five chromosomal regions: 5q31-33, 6p21.3, 12q15-24.1, 13q12-31, and 14q11.2/14q32.1-32.3. Marker analysis was performed in two Caucasian populations: (i) 192 unrelated German children with atopic dermatitis and 59 non-atopic children from a German birth cohort study (MAS '90), parental DNA was tested in 77 of 192 children with atopic dermatitis, (ii) 40 Swedish families with at least one family member with atopic dermatitis selected from the International Study of Asthma and Allergy in Children. Evidence for linkage and allelic association for atopic dermatitis was observed for markers on chromosome 13q12-14 and 5q31-33.
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| 4. |
- Grundberg, E, et al.
(author)
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A deletion polymorphism in the RIZ gene, a female sex steroid hormone receptor coactivator, exhibits decreased response to estrogen in vitro and associates with low bone mineral density in young Swedish women
- 2004
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In: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 89:12, s. 6173-6178
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Journal article (peer-reviewed)abstract
- Low bone mineral density (BMD) is a major risk factor for osteoporotic fracture, and the trait is under genetic control by a large number of genes. It is recognized that estrogen plays an important role in the maintenance of bone mass by binding to estrogen receptor a (ERa). RIZ1 has previously been shown to be a specific ERa coactivator and strongly enhances its function both in vivo and in vitro. We performed in vitro studies comparing the abilities of RIZ1 P704 polymorphic variants (homozygous presence, P704+; absence, P704-; heterozygosity P704+/- of a proline at position 704) to coactivate the ERa and also examined the polymorphism associated to BMD of 343 Swedish women, aged 20-39 yr. The expression vector containing P704- RIZ1 showed an impaired response in coactivating ERa in a ligand- and dose-dependent manner compared with P704+ RIZ (P < 0.0001). The genotype frequencies were 19% (P704+), 32% (P704-), and 49% (P704+/-) and were in Hardy-Weinberg equilibrium. BMD at the heel was higher in the P704+ genotype group than in the P704+/- group (P = 0.02), which was evident also after corrections for fat and lean mass (P = 0.03). We conclude that RIZ1 may be a new candidate gene for involvement in the variation seen in BMD.
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| 5. |
- Huang, X., et al.
(author)
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Full dimensional quantum calculations of vibrational energies of H5O2
- 2003
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In: Journal of Physical Chemistry A. - : American Chemical Society (ACS). - 1089-5639 .- 1520-5215. ; 107:37, s. 7142-7151
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Journal article (peer-reviewed)abstract
- The full dimensional (15 degrees-of-freedom) quantum calculations of vibrational energies of H5O2+ are reported using the global potential energy surface (OSS) of Ojamäe et al. (J. Chem. Phys. 1998, 109, 5547). One set of calculations uses the diffusion Monte Carlo (DMC) method with a highly flexible initial trial wave function. This method is limited to the ground vibrational state, but produces what we believe is a highly accurate, benchmark energy and wave function for that state. The DMC wave function is analyzed to identify coordinates that are strongly correlated in zero-point fluctuations. A simple harmonic model is developed to elucidate the energetic consequences of these correlations. The other set of calculations is based on the code MULTIMODE, which does configuration interaction (CI) calculations using a basis determined from a vibrational self-consistent field (VSCF) Hamiltonian, but which uses a representation of the potential with mode coupling limited to a maximum of four modes. Good agreement is obtained between the DMC and the CI MULTIMODE energies for the ground vibrational state. When less sophisticated theoretical treatments are applied, either variational Monte Carlo or vibrational self-consistent field, fairly large errors are found. Vibrationally excited-state energies obtained with MULTIMODE are also reported.
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| 6. |
- Lumpkin, A. H., et al.
(author)
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Evidence for microbunching "sidebands" in a saturated free-electron laser using coherent optical transition radiation
- 2002
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In: Physical Review Letters. - 1079-7114. ; 88:23, s. 4-4
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Journal article (peer-reviewed)abstract
- We report the first measurements of z -dependent coherent optical transition radiation (COTR) due to electron-beam microbunching at high gains (>10(4) ) including saturation of a self-amplified spontaneous emission free-electron laser (FEL). In these experiments the fundamental wavelength was near 530 nm, and the COTR spectra exhibit the transition from simple spectra to complex spectra (5% spectral width) after saturation. The COTR intensity growth and angular distribution data are reported as well as the evidence for transverse spectral dependencies and an "effective" core of the beam being involved in microbunching.
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| 7. |
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| 8. |
- Wang, X., et al.
(author)
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Involvement of the MKK6-p38? cascade in ?-radiation-induced cell cycle arrest
- 2000
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In: Molecular and Cellular Biology. - 0270-7306 .- 1098-5549. ; 20:13, s. 4543-4552
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Journal article (peer-reviewed)abstract
- The p38 group of kinases belongs to the mitogen-activated protein (MAP) kinase superfamily with structural and functional characteristics distinguishable from those of the ERK, JNK (SAPK), and BMK (ERK5) kinases. Although there is a high degree of similarity among members of the p38 group in terms of structure and activation, each member appears to have a unique function. Here we show that activation of p38-? (also known as ERK6 or SAPK3), but not the other p38 isoforms, is required for ?-irradiation- induced G2 arrest. Activation of the MKK6-p38? cascade is sufficient to induce G2 arrest in cells, and expression of dominant negative alleles of MKK6 or p38? allows cells to escape the DNA damage-induce G2 delay. Activation of p38? is dependent on ATM and leads to activation of Cds1 (also known as Chk2). These data suggest a model in which activation of ATM by ? irradiation leads to the activation of MKK6, p38?, and Cds1 and that activation of both MKK6 and p38? is essential for the proper regulation of the G2 checkpoint in mammalian cells.
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| 10. |
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