A nonperturbative study of three dimensional quantum electrodynamics with N flavours of fermion

This work is concerned with the breaking of chiral symmetry in gauge theories and the associated generation of a dynamical mass scale. We investigate this phenomenon in the context of a simple model, three dimensional QED, where the complicating factor of infinite renormalisations is absent. This model possesses an intrinsic scale, set by the coupling [e(^2)] = M, and it is the relationship between this and the dynamically generated mass scale that is of interest. The chiral symmetry breaking mechanism is investigated using the Schwinger Dyson equations which are then truncated in a nonperturbative manner using the Ball-Chiu vertex ansatz. The complexity of the resulting coupled fermion-photon system means that the photon is initially replaced by its perturbative form. Numerical investigations of this simplified system then reveal the existence of an exponential relationship, in terms of the dimensionless parameter N, between the intrinsic and dynamical mass scales, m ~ e(^2) exp(-cN). Contrary to the assertions of Appelquist et al the wavefunction renormalisation was found to be nonperturbative and crucial in determining this behaviour. The sensitivity of this mechanism to the nonperturbative behaviour of the photon is investigated. A simple analysis shows it to be far stronger than previously expected. This is confirmed by a numerical analysis of the coupled photon-fermion system which suggest the relationship between the two scales in the theory is of the form m ~ e(^2) exp(-cN(^2)). This model therefore illustrates how a large hierarchy of scales may naturally occur in a gauge theory, for instance N=3 m/a ~ 10(^-5). Finally an investigation of the gauge dependence of this approach is initiated. The softening of the photon in the low momentum region is shown to amplify automatically any inadequacy of the vertex ansatz by factors of O(a/m) in all but the Landau gauge. It is therefore expected that any incomplete vertex form will result in the generation of a "critical gauge", ɛ(_e), below which chiral symmetry breaking solutions will not exist. A path of further investigation is suggested

Alzheimer's disease: synaptic dysfunction and Aβ

Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia. Accordingly, it has been proposed that synapse loss underlies the memory impairment evident in the early phase of AD and that since plasticity is important for neuronal viability, persistent disruption of plasticity may account for the frank cell loss typical of later phases of the disease. Extensive multi-disciplinary research has implicated the amyloid β-protein (Aβ) in the aetiology of AD and here we review the evidence that non-fibrillar soluble forms of Aβ are mediators of synaptic compromise. We also discuss the possible mechanisms of Aβ synaptotoxicity and potential targets for therapeutic intervention

Morphological and architectural control of hydroxyapatite growth

SIGLEAvailable from British Library Document Supply Centre- DSC:DX185465 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Genetic Correction of Dystrophin Deficiency and Skeletal Muscle Remodeling in Adult MDX Mouse via Transplantation of Retroviral Producer Cells

Duchenne muscular dystrophy (DMD) is an X-linked, lethal disease caused by mutations of the dystrophin gene. No effective therapy is available, but dystrophin gene transfer to skeletal muscle has been proposed as a treatment for DMD. We have developed a strategy for efficient in vivo gene transfer of dystrophin cDNA into regenerating skeletal muscle. Retroviral producer cells, which release a vector carrying the therapeutically active dystrophin minigene, were mitotically inactivated and transplanted in adult nude/ mdx mice. Transplantation of 3 3 10 6 producer cells in a single site of the tibialis anterior muscle resulted in the transduction of between 5.5 and 18% total muscle fibers. The same procedure proved also feasible in immunocompetent mdx mice under short-term pharmacological immunosuppression. Minidystrophin expression was stable for up to 6 mo and led to a -sarcoglycan reexpression. Muscle stem cells could be transduced in vivo using this procedure. Transduced dystrophic skeletal muscle showed evidence of active remodeling reminiscent of the genetic normalization process which takes place in female DMD carriers. Overall, these results demonstrate that retroviral-mediated dystrophin gene transfer via transplantation of producer cells is a valid approach towards the long-term goal of gene therapy of DMD. ( J. Clin. Invest. 1997. 100:620–628 .