Alternative Interpretation of Sharply Rising E0 Strengths in Transitional Regions

It is shown that strong 0+2 -> 0+1 E0 transitions provide a clear signature of phase transitional behavior in finite nuclei. Calculations using the IBA show that these transition strengths exhibit a dramatic and robust increase in spherical-deformed shape transition regions, that this rise matches well the existing data, that the predictions of these E0 transitions remain large in deformed nuclei, and that these properties are intrinsic to the way that collectivity and deformation develop through the phase transitional region in the model, arising from the specific d-boson coherence in the wave functions, and that they do not necessarily require the explicit mixing of normal and intruder configurations from different IBA spaces.Comment: 6 pages, 3 figure

Exactly separable version of the Bohr Hamiltonian with the Davidson potential

An exactly separable version of the Bohr Hamiltonian is developed using a potential of the form u(beta)+u(gamma)/beta^2, with the Davidson potential u(beta)= beta^2 + beta_0^4/beta^2 (where beta_0 is the position of the minimum) and a stiff harmonic oscillator for u(gamma) centered at gamma=0. In the resulting solution, called exactly separable Davidson (ES-D), the ground state band, gamma band and 0_2^+ band are all treated on an equal footing. The bandheads, energy spacings within bands, and a number of interband and intraband B(E2) transition rates are well reproduced for almost all well-deformed rare earth and actinide nuclei using two parameters (beta_0, gamma stiffness). Insights regarding the recently found correlation between gamma stiffness and the gamma-bandhead energy, as well as the long standing problem of producing a level scheme with Interacting Boson Approximation SU(3) degeneracies from the Bohr Hamiltonian, are also obtained.Comment: 35 pages, 11 postscript figures, LaTe

CTL epitope distribution patterns in the Gag and Nef proteins of HIV-1 from subtype A infected subjects in Kenya: Use of multiple peptide sets increases the detectable breadth of the CTL response

BACKGROUND: Subtype A is a major strain in the HIV-1 pandemic in eastern Europe, central Asia and in certain regions of east Africa, notably in rural Kenya. While considerable effort has been focused upon mapping and defining immunodominant CTL epitopes in HIV-1 subtype B and subtype C infections, few epitope mapping studies have focused upon subtype A. RESULTS: We have used the IFN-γ ELIspot assay and overlapping peptide pools to show that the pattern of CTL recognition of the Gag and Nef proteins in subtype A infection is similar to that seen in subtypes B and C. The p17 and p24 proteins of Gag and the central conserved region of Nef were targeted by CTL from HIV-1-infected Kenyans. Several epitope/HLA associations commonly seen in subtype B and C infection were also observed in subtype A infections. Notably, an immunodominant HLA-C restricted epitope (Gag 296–304; YL9) was observed, with 8/9 HLA-C(W)0304 subjects responding to this epitope. Screening the cohort with peptide sets representing subtypes A, C and D (the three most prevalent HIV-1 subtypes in east Africa), revealed that peptide sets based upon an homologous subtype (either isolate or consensus) only marginally improved the capacity to detect CTL responses. While the different peptide sets detected a similar number of responses (particularly in the Gag protein), each set was capable of detecting unique responses not identified with the other peptide sets. CONCLUSION: Hence, screening with multiple peptide sets representing different sequences, and by extension different epitope variants, can increase the detectable breadth of the HIV-1-specific CTL response. Interpreting the true extent of cross-reactivity may be hampered by the use of 15-mer peptides at a single concentration and a lack of knowledge of the sequence that primed any given CTL response. Therefore, reagent choice and knowledge of the exact sequences that prime CTL responses will be important factors in experimentally defining cross-reactive CTL responses and their role in HIV-1 disease pathogenesis and validating vaccines aimed at generating broadly cross-reactive CTL responses