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Unbounded *-representations of tensor product locally convex *-algebras induced by unbounded C*-seminorms

100%

Fragoulopoulou M. , Inoue A.

Studia Mathematica

2007

tom 183

nr 3

259-271

The existence of unbounded *-representations of (locally convex) tensor product *-algebras is investigated, in terms of the existence of unbounded *-representations of the (locally convex) factors of the tensor product and vice versa.

Spectral well-behaved *-representations

80%

Bhatt S. , Fragoulopoulou M. , Inoue A.

Banach Center Publications

2005

tom 67

nr 1

123-131

In this brief account we present the way of obtaining unbounded *-representations in terms of the so-called "unbounded" C*-seminorms. Among such *-representations we pick up a special class with "good behaviour" and characterize them through some properties of the Pták function.

Pathogenic immunity in Theiler?s virus-induced demyelinating disease: a viral model for multiple sclerosis

80%

Kim B. S. , Palma J. P. , Inoue A. , Koh C.-S.

nr 5

373-380

Multiple sclerosis involves inflammatory immune responses in the central nervous system and is considered as an autoimmune disease potentially associated with viral infection. The majority of experimental models rely heavily on the autoimmune components since similar diseases can be induced following immunization with various myelin antigens. A very attractive alternative model is the Theiler?s murine encephalomyelitis virus-induced demyelinating disease. This disease is primarily a CD4+ T cell-mediated, inflammatory demyelinating disease, induced following viral infection. Virus-specific inflammatory Th1 cell responses, rather than cytotoxic T lymphocyte response, play a critical role in the pathogenic immune responses. The major pathogenic epitopes have been identified and these are correlated with a Th1 type response to the epitopes following viral infection. In addition, the initial virus-specific immune response is followed by the autoimmune responses to myelin antigens. Assessment of cytokines produced locally in the CNS during the course of disease suggests involvement of inflammatory cytokines in the disease. Furthermore, the manipulation of inflammatory cytokine levels by administration of either recombinant cytokines or antibodies to the cytokines strongly influences the induction and/or progression of disease, supporting the importance of these inflammatory cytokines in this virus-induced demyelinating disease.