Effect of a Type of Loading on Stresses at a Planar Boundary of a Nanomaterial

Abstract A two-dimensional model of an elastic body at nanoscale is considered as a half-plane under the action of a periodic load at the boundary. An additional surface stress, and constitutive equations of the Gurtin-Murdoch surface linear elasticity are assumed. Using Goursat-Kolosov complex potentials and Muskhelisvili technique, the solution of the boundary value problem in the case of an arbitrary load is reduced to a hypersingular integral equation in an unknown surface stress. For the case of a periodic load, the solution of this equation is found in the form of Fourier series. The influence of the surface stress on the stresses at the boundary of the half-plane under the tangential and normal periodic loading is analyzed. In particular, it is found out the size effect which becomes apparent in the dependence of the stresses on a length of the load period of the order 10 nm. Moreover, the tangential stresses appear under the action of the normal loads

A mitochondrial pathway for biosynthesis of lipid mediators

The central role of mitochondria in metabolic pathways and in cell death mechanisms requires sophisticated signaling systems. Essential in this signaling process is an array of lipid mediators derived from polyunsaturated fatty acids. However, the molecular machinery for the production of oxygenated polyunsaturated fatty acids is localized in the cytosol and their biosynthesis has not been identified in mitochondria. Here we report that a range of diversified polyunsaturated molecular species derived from a mitochondria-specific phospholipid, cardiolipin, are oxidized by the intermembrane space hemoprotein, cytochrome c. We show that an assortment of oxygenated cardiolipin species undergoes phospholipase A2-catalyzed hydrolysis thus generating multiple oxygenated fatty acids, including well known lipid mediators. This represents a new biosynthetic pathway for lipid mediators. We demonstrate that this pathway including oxidation of polyunsaturated cardiolipins and accumulation of their hydrolysis products – oxygenated linoleic, arachidonic acids and monolyso-cardiolipins – is activated in vivo after acute tissue injury