Subresultants in multiple roots: an extremal case

We provide explicit formulae for the coefficients of the order-d polynomial subresultant of (x-\alpha)^m and (x-\beta)^n with respect to the set of Bernstein polynomials \{(x-\alpha)^j(x-\beta)^{d-j}, \, 0\le j\le d\}. They are given by hypergeometric expressions arising from determinants of binomial Hankel matrices.Comment: 18 pages, uses elsart. Revised version accepted for publication at Linear Algebra and its Application

Finiteness and orbifold Vertex Operator Algebras

In this paper, I investigate the ascending chain condition of right ideals in the case of vertex operator algebras satisfying a finiteness and/or a simplicity condition. Possible applications to the study of finiteness of orbifold VOAs is discussed.Comment: 12 pages, comments are welcom

Regulation of T cell lymphokine production by killer cell inhibitory receptor recognition of self HLA class I alleles.

The killer cell inhibitory receptors (KIRs) are surface glycoproteins expressed by natural killer (NK) and T cells that specifically recognize defined groups of polymorphic human histocompatibility leukocyte antigen (HLA) class I molecules. Interactions between KIRs on NK or T cells and major histocompatibility complex (MHC) class I molecules on potential target cells inhibit cell-mediated cytotoxicity, presumably by delivering a negative signal preventing lymphocyte activation. In this study we examined whether KIRs also regulate cytokine production induced in response to T cell receptor-dependent T cell activation. CD4+ and CD8+ T cell clones were stimulated by bacterial superantigens in the presence or absence of monoclonal antibodies (mAbs) against the KIR NKB1 or MHC class I molecules, and production of tumor necrosis factor alpha and interferon gamma was evaluated. When bacterial superantigen was presented by an autologous antigen-presenting cell (APC) to a KIR+ T cell clone, cytokine production was always enhanced in the presence of anti-MHC class I mAb. Similarly, anti-KIR mAb also augmented cytokine production, provided that the APC expressed a HLA class I allele recognized by the KIR. These results suggest that recognition of autologous MHC class I molecules by KIR+ T cells provides a regulatory mechanism acting to modulate the potency of their responses to antigenic challenge