The quark Dyson-Schwinger equation and meson Bethe-Salpeter equation are studied in a truncation scheme that extends the rainbow-ladder approximation such that, in the chiral limit, the isovector, pseudoscalar meson remains massless. Quarkquark (diquark) correlations, which are bound in rainbow-ladder approximation, are destabilised by repulsive contributions that only appear at higher order in the Bethe-Salpeter kernel. The net effect of higher order terms on the meson boundstate masses is small.
A Ward-Takahashi identity preserving Bethe-Salpeter kernel can always be
calculated explicitly from a dressed-quark-gluon vertex whose diagrammatic
content is enumerable. We illustrate that fact using a vertex obtained via the
complete resummation of dressed-gluon ladders. While this vertex is planar, the
vertex-consistent kernel is nonplanar and that is true for any dressed vertex.
In an exemplifying model the rainbow-ladder truncation of the gap and
Bethe-Salpeter equations yields many results; e.g., pi- and rho-meson masses,
that are changed little by including higher-order corrections. Repulsion
generated by nonplanar diagrams in the vertex-consistent Bethe-Salpeter kernel
for quark-quark scattering is sufficient to guarantee that diquark bound states
do not exist.Comment: 16 pages, 12 figures, REVTEX
Robustness, the insensitivity of some of a biological system's functionalities to a set of distinct conditions, is intimately linked to fitness. Recent studies suggest that it may also play a vital role in enabling the evolution of species. Increasing robustness, so is proposed, can lead to the emergence of evolvability if evolution proceeds over a neutral network that extends far throughout the fitness landscape. Here, we show that the design principles used to achieve robustness dramatically influence whether robustness leads to evolvability. In simulation experiments, we find that purely redundant systems have remarkably low evolvability while degenerate, i.e. partially redundant, systems tend to be orders of magnitude more evolvable. Surprisingly, the magnitude of observed variation in evolvability can neither be explained by differences in the size nor the topology of the neutral networks. This suggests that degeneracy, a ubiquitous characteristic in biological systems, may be an important enabler of natural evolution. More generally, our study provides valuable new clues about the origin of innovations in complex adaptive systems.
Deconfinement and chiral symmetry restoration are explored in a confining, renormalisable, Dyson-Schwinger equation model of two-flavour QCD. An order parameter for deconfinement is introduced and used to establish that, in the chiral limit, deconfinement and chiral symmetry restoration are coincident at T c ≈ 150 MeV. The transitions are second order and each has the same critical exponent: β ≈ 0.3. The deconfinement transition is found to exhibit sensitivity to the current-quark mass. f π and m π change by no more than 10% for T < 0.7 T c , however, as T → T c , thermal fluctuations cause the pion bound state contribution to the four-point quark-antiquark correlation function to disappear.
We report that M. tuberculosis organisms, but neither PHA nor allogeneic stimulator cells, preferentially activate gamma/delta+ cells within E rosette-purified peripheral blood T cells. gamma/delta+ T cells from purified protein derivative (PPD)-nonimmune healthy donors were enriched by depletion of CD4+ and CD8+ cells; double-negative (DN) cells contained 65-92% gamma/delta+ T cells. Limiting dilution (LD) analyses revealed that 1 of 2-19 purified DN cells proliferated in response to mycobacteria, while frequencies of DN cells proliferating in response to a recombinant 65-kD heat shock protein (hsp 65) of M. tuberculosis/M. bovis were 10-20-fold lower. Established clones of mycobacteria-reactive gamma/delta+ T cells specifically recognized mycobacteria, but neither PPD nor hsp 65. Restimulation of these clones required the presence of PBMC feeder cells; EBV-transformed lymphoblastoid cell lines could not substitute for PBMC. Mycobacteria-reactive gamma/delta+ clones proliferated equally well in the presence of autologous or allogeneic (HLA-DR-different) PBMC feeder cells and thus were not MHC class II restricted. Taken together, these results demonstrate that mycobacteria-reactive gamma/delta+ T cells are present in high frequency in the peripheral blood of healthy individuals, and suggest that hsp 65 of mycobacteria is not a major antigen for gamma/delta+ T cells of normal PPD-nonimmune blood donors.
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