The maximal C*-algebra of quotients as an operator bimodule

We establish a description of the maximal C*-algebra of quotients of a unital C*-algebra A as a direct limit of spaces of completely bounded bimodule homomorphisms from certain operator submodules of the Haagerup tensor product of A with itself labelled by the essential closed right ideals of A into A. In addition the invariance of the construction of the maximal C*-algebra of quotients under strong Morita equivalence is proved.

On maximal subgroups of the multiplicative group of a division algebra

This note studies the question whether a multiplicative group of a division ring has a maximal subgroup. It is published in J. Algebra. This is a reputable journal in the subject algebra. Most of submitted papers from 5* schools in RAE was in this journal.

When is the second local multiplier algebra of a C*-algebra equal to the first?

We discuss necessary as well as sufficient conditions for the second iterated local multiplier algebra of a separable C*-algebra to agree with the first.

The C*-algebra of ax+b-like groups

We describe the C*-algebras of " ax+b" -like groups in terms of algebras of operator fields defined over their dual spaces.

The solvable Lie group N_{6, 28}: an example of an almost C_0(\mathcal{K})-C*-algebra

Motivated by the description of the C*-algebra of the affine automorphism group N6,28 of the Siegel upper half-plane of degree 2 as an algebra of operator fields defined over the unitary dual View the MathML source of the group, we introduce a family of C*-algebras, which we call almost C0(K), and we show that the C*-algebra of the group N6,28 belongs to this class.

Using Process Algebra to Model Radiation Induced Bystander Effects

Radiation induced bystander effects are secondary effects caused by the production of chemical signals by cells in response to radiation. We present a Bio-PEPA model which builds on previous modelling work in this field to predict: the surviving fraction of cells in response to radiation, the relative proportion of cell death caused by bystander signalling, the risk of non-lethal damage and the probability of observing bystander signalling for a given dose. This work provides the foundation for modelling bystander effects caused by biologically realistic dose distributions, with implications for cancer therapies.