Cigarette smoking alters intestinal barrier function and Peyer's Patch composition

Smokers have a two-fold increased risk to develop Crohn’s disease (CD). However, little is known about the mechanisms through which smoking affects CD pathogenesis. Interestingly, the Peyer’s patches in the terminal ileum are the sites where the first CD lesions develop. To investigate whether smoke exposure causes alterations in Peyer’s patches, we studied C57BL/6 mice after exposure to air or cigarette smoke for 24 weeks. First, barrier function of the follicle-associated epithelium overlying Peyer’s patches was evaluated. We demonstrate that chronic smoke exposure is associated with increased apoptosis in the follicle-associated epithelium. Furthermore, immune cell numbers and differentiation along with chemokine expression were determined in the ileal Peyer’s patches. We observed significant increases in total dendritic cells (DC), CD4+ T-cells (including regulatory T-cells) and CD8+ T-cells after smoke exposure compared with air-exposed animals. The CD11b+ DC subset almost doubled. Interestingly, these changes were accompanied by an up-regulated mRNA expression of the chemokines CCL9 and CCL20, which are known to attract CD11b+ DC towards the subepithelial dome of Peyer’s patches. Our results demonstrate that cigarette smoke exposure induces apoptosis in follicle-associated epithelium and is associated with immune cell accumulation in Peyer’s patches, changes which can predispose to the development of CD

Local filtering operations on two qubits

We consider one single copy of a mixed state of two qubits and investigate how its entanglement changes under local quantum operations and classical communications (LQCC) of the type $\rho'\sim (A\otimes B)\rho(A\otimes B)^{\dagger}$. We consider a real matrix parameterization of the set of density matrices and show that these LQCC operations correspond to left and right multiplication by a Lorentz matrix, followed by normalization. A constructive way of bringing this matrix into a normal form is derived. This allows us to calculate explicitly the optimal local filterin operations for concentrating entanglement. Furthermore we give a complete characterization of the mixed states that can be purified arbitrary close to a Bell state. Finally we obtain a new way of calculating the entanglement of formation.Comment: 4 page

Mixed Integer Programming for Multi-Vehicle Path Planning

This paper presents a new approach to fuel-optimal path planning of multiple vehicles using a combination of linear and integer programming. The basic problem formulation is to have the vehicles move from an initial dynamic state to a final state without colliding with each other, while at the same time avoiding other stationary and moving obstacles. It is shown that this problem can be rewritten as a linear program with mixed integer /linear constraints that account for the collision avoidance. A key benefit of this approach is that the path optimization can be readily solved using the CPLEX optimization software with an AMPL/Matlab interface. An example is worked out to show that the framework of mixed integer/linear programming is well suited for path planning and collision avoidance problems. Implementation issues are also considered. In particular, we compare receding horizon strategies with fixed arrival time approaches

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Smokers have a twofold increased risk to develop Crohn's disease (CD). However, little is known about the mechanisms through which smoking affects CD pathogenesis. Especially Crohn's ileitis is negatively influenced by smoking. Interestingly, the ileum and, more in particular, the Peyer's patches in the terminal ileum are also the sites where the first CD lesions are found. Several chemokines are implicated in the pathogenesis, among which is the CCL20-CCR6 pathway. Here, we studied the gut-associated lymphoid tissue in C57BL/6 wild-type mice and in CCR6-deficient mice after exposure to air or cigarette smoke for 24 weeks. Apoptotic index of the follicle-associated epithelium overlying the Peyer's patches was evaluated. We found that chronic smoke exposure induced apoptosis in the follicle-associated epithelium. Furthermore, immune cell numbers and differentiation along with chemokine expression were determined in Peyer's patches. Important changes in immune cell composition were observed: total dendritic cells, CD4+ T cells (including regulatory T cells) and CD8+ T cells increased significantly after smoke exposure. The CD11b+ dendritic cell subset almost doubled. Interestingly, these changes were accompanied by an upregulated mRNA expression of the chemokines CCL9 and CCL20. However, no differences in the increase of dendritic cells were observed between wild-type and CCR6-deficient mice. Our results show that cigarette smoke exposure increases apoptosis in the follicle-associated epithelium and is associated with immune cell accumulation in Peyer's patches

The role of ChemR23 in the induction and resolution of cigarette smoke-induced inflammation

Chronic obstructive pulmonary disease is mainly triggered by cigarette smoke (CS) and progresses even after smoking cessation. CS induces an exaggerated influx of inflammatory cells to the bronchoalveolar space and lung parenchyma, likely resulting from a complex interplay between chemoattractants and their respective receptors. In a murine CS model of chronic obstructive pulmonary disease, we studied the importance of chemokine-like receptor ChemR23 for the induction and resolution of inflammation in CS-exposed lungs. Subacute and chronic CS exposure increased protein levels of the ChemR23 ligand and chemoattractant, chemerin, in bronchoalveolar lavage (BAL) fluid of wild-type (WT) mice. Moreover, the proinflammatory chemokines CXCL1, CCL2, and CCL20 were increased in the airways of CS-exposed WT mice, accompanied by a massive accumulation of inflammatory neutrophils and monocytes, CD11b hiCD103- and CD11bloCD103+ dendritic cells (DCs), and CD4+ and CD8+ T cells. The lung parenchyma of WT mice was infiltrated with inflammatory neutrophils, CD11b hiCD103- DCs, and activated CD4+ T cells after CS exposure. CS-induced inflammation was severely attenuated in BAL fluid and lungs of ChemR23 knockout mice with regard to the induction of inflammatory chemokines and the recruitment of inflammatory cells. Neutrophils and CD8 + T cells persisted in the airways of WT mice, as did the airway-derived conventional DCs in the mediastinal lymph nodes, for at least 14 d after smoking cessation. In the BAL fluid of CS-exposed ChemR23 knockout mice, there was a remarkable delayed accumulation of T cells 14 d after the final exposure. Our data support a role for ChemR23 in directing innate and adaptive immune cells to CS-exposed lungs. Copyright © 2011 by The American Association of Immunologists, Inc.SCOPUS: ar.jinfo:eu-repo/semantics/publishe