The microscopic nature of localization in the quantum Hall effect

The quantum Hall effect arises from the interplay between localized and extended states that form when electrons, confined to two dimensions, are subject to a perpendicular magnetic field. The effect involves exact quantization of all the electronic transport properties owing to particle localization. In the conventional theory of the quantum Hall effect, strong-field localization is associated with a single-particle drift motion of electrons along contours of constant disorder potential. Transport experiments that probe the extended states in the transition regions between quantum Hall phases have been used to test both the theory and its implications for quantum Hall phase transitions. Although several experiments on highly disordered samples have affirmed the validity of the single-particle picture, other experiments and some recent theories have found deviations from the predicted universal behaviour. Here we use a scanning single-electron transistor to probe the individual localized states, which we find to be strikingly different from the predictions of single-particle theory. The states are mainly determined by Coulomb interactions, and appear only when quantization of kinetic energy limits the screening ability of electrons. We conclude that the quantum Hall effect has a greater diversity of regimes and phase transitions than predicted by the single-particle framework. Our experiments suggest a unified picture of localization in which the single-particle model is valid only in the limit of strong disorder.     

Immunomodulation of experimental allergic encephalomyelitis by antibodies to the antigen-Ia complex.

Autoimmune diseases occur when T lymphocytes become activated on recognizing self antigen linked to the autologous class II molecule of the major histocompatibility complex (MHC). The resulting complex of antigen MHC T-cell receptor could be a target for treatment of autoimmune diseases. Studies in which each component is blocked separately might be limited by interference in non-relevant immune responses that either use the same set of T-cell-receptor V gene segments or are linked to the same MHC. We report here an attack by a specific antibody on the unique antigenic site formed by the binding of two components of the trimolecular complex, the autoantigen bound to the self MHC. We tested its effect in experimental allergic encephalomyelitis, an acute neurological autoimmune disease which is widely regarded as a model for autoimmune disorders and which is mediated by CD4+ T cells recognizing myelin basic protein (BP), or its peptides, in association with self Ia. We made monoclonal antibodies which bound only the complex of BP and I-As. These antibodies blocked the proliferative response in vitro to the encephalitogenic determinant of BP and reduced the response to intact BP, without affecting the response to a nonrelevant antigen-purified protein derivative of tuberculin presented on syngeneic macrophages. They also inhibited experimental allergic encephalomyelitis in H-2s mice. Hence, antibodies directed specifically to the autoantigen-Ia complex, may offer a highly selective and effective treatment in autoimmune diseases.     

Mice deficient in Abl are osteoporotic and have defects in osteoblast maturation

The c-Abl protein is a non-receptor tyrosine kinase involved in many aspects of mammalian development. c-Abl kinase is widely expressed, but high levels are found in hyaline cartilage in the adult, bone tissue in newborn mice, and osteoblasts and associated neovasculature at sites of endochondrial ossification in the fetus. Mice homozygous for mutations in the gene encoding c-Abl (AIM) display increased perinatal mortality, reduced fertility, foreshortened crania and defects in the maturation of B cells in bone marrow. Here we demonstrate that Abl-/- mice are also osteoporotic. The long bones of mutant mice contain thinner cortical bone and reduced trabecular bone volume. The osteoporotic phenotype is not due to accelerated bone turnover--both the number and activity of osteoclasts are similar to those of control littermates--but rather to dysfunctional osteoblasts. In addition, the rate of mineral apposition in the mutant animals is reduced. Osteoblasts from both stromal and calvarial explants showed delayed maturation in vitro as measured by expression of alkaline phosphatase (ALP), induction of mRNA encoding osteocalcin and mineral deposition.