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Träfflista för sökning "WFRF:(Shepherd J) srt2:(2000-2004)"

Sökning: WFRF:(Shepherd J) > (2000-2004)

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  • Pfohl, J., et al. (författare)
  • Highly deformed rotational structures in 136Pm
  • 2000
  • Ingår i: Physical Review C - Nuclear Physics. - 0556-2813. ; 62:3, s. 313041-313045
  • Tidskriftsartikel (refereegranskat)abstract
    • Four highly deformed structures in the odd-odd nucleus 13661Pm75 were observed via the 105Pd(35Cl,2p2n) reaction at 180 and 173 MeV using the GAMMASPHERE γ-ray spectrometer and the Microball charged-particle detector array. Quadrupole moment measurements were performed on all of the bands. In contrast to lighter odd-Ζ Pm and Pr nuclei, bands based on the g9/2[404]9/2 proton orbital were not observed. Instead, the four observed sequences are assigned as a coupling of an i13/2 neutron with the low-Ω h11/2 and mixed d5/2g7/2 orbitals. Comparisons with neighboring highly deformed structures are discussed and cranked Nilsson-Strutinsky calculations for 136Pm are presented.
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  • Simpson, J., et al. (författare)
  • Discrete line γ-ray spectroscopy in the (50-60)ℏ spin domain of 161,162Er
  • 2000
  • Ingår i: Physical Review C - Nuclear Physics. - 0556-2813. ; 62:2, s. 243211-243218
  • Tidskriftsartikel (refereegranskat)abstract
    • Very high spin states (I=50-60ℏ) have been observed in the transitional nuclei 161Er and 162Er using the Euroball γ-ray spectrometer. In 161Er, three bands are observed well above spin 50ℏ. In the positive parity, positive signature (+, + 1/2) band a discontinuity in the regular rotational behavior occurs at 109/2+ and a splitting into two branches occurs at 97/2- in the negative parity, positive signature (-, + 1/2) band. The ( -, - 1/2) band continues in a regular fashion to 115/2-, tentatively (119/2-). In 162Er the positive parity, even spin (+, 0) yrast band is observed to continue smoothly up to 58+ (60+) and the negative parity, even spin (-,0) and odd spin (-,1) bands are extended from 30- to 34- and from 31- to 47- (49-), respectively. The high spin experimental spectra are compared with both a simple model involving the occupation of specific single neutron states in the absence of neutron pair correlations and with more detailed cranked Nilsson-Strutinsky calculations in which both proton and neutron pairing correlations are neglected. The very high spin domain is found to comprise a series of unpaired rotational bands. Unpaired band crossings between bands with different neutron and proton configurations are identified in 161Er. There is no evidence for aligned oblate or terminating states being close to the yrast line in 161,162Er up to spin ≈60ℏ in contrast to the lighter Er isotopes.
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  • Li, Li, et al. (författare)
  • Insulin induces SOCS-6 expression and its binding to the p85 monomer of phosphoinositide 3-kinase, resulting in improvement in glucose metabolism
  • 2004
  • Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 279:33, s. 34107-34114
  • Tidskriftsartikel (refereegranskat)abstract
    • The suppressors of cytokine signaling ( SOCS) family is thought to act largely as a negative regulator of signaling by cytokines and some growth factors. Surprisingly, the SOCS-6 transgenics had no significant defects in the cytokine signaling and hematopoietic system but displayed significant improvements in glucose metabolism. Insulin stimulation of Akt/protein kinase B was also potentiated. Biochemical analysis showed that, after insulin stimulation, SOCS-6 interacted with the monomeric p85 subunit of class-Ia phosphoinositide ( PI) 3-kinase but not with p85/p110 dimers. Furthermore, SOCS-6 expression is transiently increased by serum and insulin in normal fibroblasts. However, both the mRNA and protein of SOCS-6 were rapidly degraded after induction by insulin. The degradation of the SOCS-6 protein was partially inhibited by a proteasome inhibitor, suggesting a proteasome-mediated degradation mechanism. In contrast, SOCS-6- associated p85 was not degraded and could be recruited to the newly synthesized SOCS-6 molecules in the presence of insulin, suggesting that SOCS-6 expression and its interaction with p85, but not the degradation, is regulated by insulin. The phenotype of SOCS-6 transgenic mice bears a striking resemblance to p85 knock-out mouse models in which glucose metabolism stimulated by insulin is significantly improved despite reduced activation of PI 3-kinase. This suggests that monomeric p85 might play a physiologically important role in attenuating signaling through PI 3-kinase-dependent pathways in unstimulated cells. Therefore, our results indicate that SOCS-6 may provide a dynamically regulated mechanism by which insulin can transiently overcome the negative effects that p85 monomers have on signaling via PI 3-kinase-dependent signaling pathways.
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