We study the Mott transition as a function of interaction strength in the half-filled Hubbard chain with next-nearest-neighbor hopping t' by calculating the response to an external electric field using the density matrix renormalization group. The electric susceptibility chi diverges when approaching the critical point from the insulating side. We show that the correlation length xi characterizing this transition is directly proportional to fluctuations of the polarization and that chi approximately xi2. The critical behavior shows that the transition is infinite order for all t', whether or not a spin gap is present, and that hyperscaling holds.

To investigate a possible role of phospholipase A, (PLA,) in the respiratory burst in bovine eosinophilic and neutrophilic leukocytes dependent on GTP-binding protein (G-protein), we permeabilized these cells with Staphylococcus aureus a-toxin and induced NADPH oxidase activity with the non-hydrolysable GTP analogue GTP [S] or the aluminium tetrafluoro complex AlF,-. Under same experimental conditions, cells responded with different onset times. The onset time for eosinophils was 50-200 s, for neutrophils it was only a few seconds. GTP[S] stimulated in neutrophils only 5 % of the respiratory burst compared to eosinophils, whereas AlF,--induced comparable responses (neutrophils 120% of eosinophils). GDP inhibited these responses with an IC,, value of 2.4 mM. Arachidonic acid showed, with the exception of AIF,-stimulated neutrophils, on both stimuli and cell types an enhancing effect (150%) that reached its maximum at 0.1-1 pM. The PLA, inhibitor 4-bromophenacylbromide reduced the GTP[S]-and AlF,--induced response almost completely (10 pM) and the inhibition was not significantly different for eosinophils and neutrophils (IC50 1 -3 pM). If the respiratory burst was reduced with 4-bromophenacylbromide to 1 -4% of the original value, 10% of the basal NADPH oxidase activity could be restored by addition of only 20-100 nM arachidonic acid. In addition, the PLA, activator adriamycin enhanced the response in a dose-dependent manner and in the same order as arachidonic acid did. The results presented above suggest that the respiratory burst may be regulated by different low-molecular-mass and/or heterotrimeric G-proteins and an active role for arachidonic acid or its metabolites in the activation and the maintenance of the direct G-protein-stimulated respiratory burst in bovine eosinophils and neutrophils.When stimulated by particulate or soluble stimuli like opsonized zymosan, formyl-methionyl-leucyl-phenylalanine, leuktriene B,, platelet-activating factor or the anaphylatoxine C,a, phagocytes of the immune system generate superoxide (O;-) and other reduced oxygen species by using an NADPH oxidase, for reviews, see [l -31. of Fribourg, me du mussCe 5 , CH-1700 Fribourg, Switzerland cytosolic factors p47ph0" and p67ph"", the small G-protein p21r"'1'2 and an associated GDP dissociation inhibitor that have been identified as components of the activating mechanism at least in the cell-free system [4-61.The phosphorylation of several proteins has been reported. The phosphorylation of the p47phoX occurs in normal cells but has been reported to be absent in patients with autosomal recessive chronic granulomatous disease 171. There have been reports suggesting that phospholipase A, (PLA,) is involved in the activation of the respiratory burst oxidase. An increase in PLA, activity and a release of arachidonic acid has been shown to occur following the stimulation of NADPH oxidase by different stimuli in neutrophils as well as in macrophages [8-101. Quinacrine and 4-bromophenacylbromide, inhibitors of PLA,, have previously be...

We discuss the effect of disorder on the coherent propagation of the bound state of two attracting particles. It is shown that a result analogous to the Anderson theorem for dirty superconductors is also valid for the Cooper problem, namely, that the pair wave function is extended beyond the singleparticle localization length if the latter is large. A physical justification is given in terms of the Thouless block-scaling picture of localization. These arguments are supplemented by numerical simulations. With increasing disorder we find a transition from a regime in which the interaction delocalizes the pair to a regime in which the interaction enhances localization.

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