Computational techniques in tribology and material science at the atomic level

Computations in tribology and material science at the atomic level present considerable difficulties. Computational techniques ranging from first-principles to semi-empirical and their limitations are discussed. Example calculations of metallic surface energies using semi-empirical techniques are presented. Finally, application of the methods to calculation of adhesion and friction are presented

Role of subclinical gut inflammation in the pathogenesis of spondyloarthritis

Subclinical gut inflammation occurring in patients affected by spondyloarthritis (SpA) is correlated with the severity of spine inflammation. Several evidences indicate that dysbiosis occurs in SpA, and that may modulate intestinal permeability and intestinal immune responses. The presence of intestinal dysbiosis is accompanied in SpA patients with the presence of zonulin-dependent alterations of gut-epithelial and gut-vascular barriers. The leakage of epithelial and endothelial surface layers is followed by the translocation of bacterial products, such as lipopolysaccharide and intestinal fatty acid binding protein, in the systemic circulation. These bacterial products may downregulate the expression of CD14 on circulating monocytes leading to an "anergic" phenotype. In the gut, IL-23 may induce the expansion of innate immune cells such as mucosal-associated invariant T cells, γδ T cells, and innate lymphoid cells of group 3 that through the interaction with MAdCAM1 may recirculate form the gut to the sites of SpA active inflammation. On the basis of these findings, gut inflammation observed in SpA patient seems to be not only an epiphenomenon of the on going systemic inflammatory process but may also represent the base camp in which inflammatory cells are activated and from whom they shuttle

Pathogenesis of polymyalgia rheumatica

Polymyalgia rheumatica (PMR) is a chronic, inflammatory disorder of unknown cause, almost exclusively occurring in people aged over 50 and often associated with giant cell arteritis. The evidence that PMR occurs almost exclusively in individuals aged over 50 may indicate that age-related immune alterations in genetically predisposed subjects contribute to development of the disease. Several infectious agents have been investigated as possible triggers of PMR even though the results are inconclusive. Activation of the innate and adaptive immune systems has been proved in PMR patients as demonstrated by the activation of dendritic cells and monocytes/macrophages and the altered balance between Th17 and Treg cells. Disturbed B cell distribution and function have been also demonstrated in PMR patients suggesting a pathogenesis more complex than previously imagined. In this review we will discuss the recent findings regarding the pathogenesis of PMR

L-2 State Estimation With Guaranteed Convergence Speed in the Presence of Sporadic Measurements

This paper deals with the problem of estimating the state of a nonlinear time-invariant system in the presence of sporadically available measurements and external perturbations. An observer with a continuous intersample injection term is proposed. Such an intersample injection is provided by a linear dynamical system, whose state is reset to the measured output estimation error whenever a new measurement is available. The resulting system is augmented with a timer triggering the arrival of a new measurement and analyzed in a hybrid system framework. The design of the observer is performed to achieve exponential convergence with a given decay rate of the estimation error. Robustness with respect to external perturbations and L2-external stability from plant perturbations to a given performance output are considered. Computationally efficient algorithms based on the solution to linear matrix inequalities are proposed to design the observer. Finally, the effectiveness of the proposed methodology is shown in an example

Histopathology of the gut in rheumatic diseases

The gastrointestinal tract regulates the trafficking of macromolecules between the environment and the host through an epithelial barrier mechanism and is an important part of the immune system controlling the equilibrium between tolerance and immunity to non-self-antigens. Various evidence indicates that intestinal inflammation occurs in patients with rheumatic diseases. In many rheumatic diseases intestinal inflammation appears to be linked to dysbiosis and possibly represents the common denominator in the pathogenesis of different rheumatic diseases. The continuative interaction between dysbiosis and the intestinal immune system may lead to the aberrant activation of immune cells that can re-circulate from the gut to the sites of extraintestinal inflammation as observed in patients with ankylosing spondylitis. The exact contribution of genetic factors in the development of intestinal inflammation in rheumatic diseases needs to be clarified