Conjugations on 6-manifolds with free integral cohomology

In this article, we show the existence of conjugations on many simply-connected spin 6-manifolds with free integral cohomology. In a certain class the only condition on X^6 to admit a conjugation with fixed point set M^3 is the obvious one: the existence of a degree-halving ring isomorphism between the Z_2-cohomologies of X and M.Comment: 23 page

Conjugations on 6-Manifolds

Conjugation spaces are spaces with involution such that the fixed point set of the involution has Z/2-cohomology isomorphic to the Z/2-cohomology of the space itself, with the little difference that all degrees are divided by two (e.g. CP^n with the complex conjugation). One also requires that a certain conjugation equation is fulfilled. I give a new characterization of conjugation spaces and apply it to the following realization question: given M, a closed orientable 3-manifold, is there a 6-manifold X (with certain additional properties) containing M as submanifold such that M is the fixed point set of an orientation reversing involution on X? My main result is that for every such 3-manifold M there exists a simply connected conjugation 6-manifold X with fixed point set M

Involutions on S^6 with 3-dimensional fixed point set

In this article, we classify all involutions on S^6 with 3-dimensional fixed point set. In particular, we discuss the relation between the classification of involutions with fixed point set a knotted 3-sphere and the classification of free involutions on homotopy CP^3's.Comment: 23 page

One-connectivity and finiteness of Hamiltonian S1S^1-manifolds with minimal fixed sets

Let the circle act effectively in a Hamiltonian fashion on a compact symplectic manifold $(M, \omega)$. Assume that the fixed point set $M^{S^1}$ has exactly two components, $X$ and $Y$, and that $\dim(X) + \dim(Y) +2 = \dim(M)$. We first show that $X$, $Y$ and $M$ are simply connected. Then we show that, up to $S^1$-equivariant diffeomorphism, there are finitely many such manifolds in each dimension. Moreover, we show that in low dimensions, the manifold is unique in a certain category. We use techniques from both areas of symplectic geometry and geometric topology

CagY Is an Immune-Sensitive Regulator of the Helicobacter pylori Type IV Secretion System

BACKGROUND & AIMS: Peptic ulcer disease and gastric cancer are most often caused by Helicobacter pylori strains that harbor the cag pathogenicity island (cagPAI), which encodes a type IV secretion system (T4SS) that injects the CagA oncoprotein into host cells. cagY is an essential gene in the T4SS and has an unusual DNA repeat structure that predicts in-frame insertions and deletions. These cagY recombination events typically lead to a reduction in T4SS function in mouse and primate models. We examined the role of the immune response in cagY-dependent modulation of T4SS function. METHODS: H pylori T4SS function was assessed by measuring CagA translocation and the capacity to induce interleukin-8 (IL8) in gastric epithelial cells. cagY recombination was determined by changes in PCR restriction fragment-length polymorphisms. T4SS function and cagY in H pylori from C57BL/6 mice were compared to strains recovered from Rag1−/− mice, T and B cell deficient mice, mice with deletion of IFNGR or IL10, and Rag1−/− mice that received adoptive transfer of control or Ifng−/− CD4+ T cells. To assess relevance to humans, T4SS function and cagY recombination were assessed in strains obtained sequentially from a patient after 7.4 years of infection. RESULTS: H pylori infection of T-cell deficient and Ifngr1−/− mice, and transfer of CD4+ T cells to Rag1−/− mice, demonstrated that cagY-mediated loss of T4SS function requires a T-helper 1-mediated immune response. Loss of T4SS function and cagY recombination were more pronounced in Il10−/− mice, and in control mice infected with H pylori that expressed a more inflammatory form of cagY. Complementation analysis of H pylori strains isolated from a patient over time demonstrated changes in T4SS function that were dependent on recombination in cagY. CONCLUSIONS: Analysis of H pylori strains from mice and from a chronically infected patient showed that CagY functions as an immune-sensitive regulator of T4SS function. We propose that this is a bacterial adaptation to maximize persistent infection and transmission to a new host under conditions of a robust inflammatory response