Spatial modeling of the 3D morphology of hybrid polymer-ZnO solar cells, based on electron tomography data

A spatial stochastic model is developed which describes the 3D nanomorphology of composite materials, being blends of two different (organic and inorganic) solid phases. Such materials are used, for example, in photoactive layers of hybrid polymer zinc oxide solar cells. The model is based on ideas from stochastic geometry and spatial statistics. Its parameters are fitted to image data gained by electron tomography (ET), where adaptive thresholding and stochastic segmentation have been used to represent morphological features of the considered ET data by unions of overlapping spheres. Their midpoints are modeled by a stack of 2D point processes with a suitably chosen correlation structure, whereas a moving-average procedure is used to add the radii of spheres. The model is validated by comparing physically relevant characteristics of real and simulated data, like the efficiency of exciton quenching, which is important for the generation of charges and their transport toward the electrodes.Comment: Published in at http://dx.doi.org/10.1214/11-AOAS468 the Annals of Applied Statistics (http://www.imstat.org/aoas/) by the Institute of Mathematical Statistics (http://www.imstat.org

Noncompaction of the Ventricular Myocardium Is Associated with a De Novo Mutation in the β-Myosin Heavy Chain Gene

Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin. NVM results presumably from a congenital developmental error and has been traced back to single point mutations in various genes. The objective of this study was to determine the underlying genetic defect in a large German family suffering from NVM. Twenty four family members were clinically assessed using advanced imaging techniques. For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12. Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the α- and β-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7. The mutation affects a highly conserved amino acid in the myosin subfragment-1 (R281T). In silico simulations suggest that the mutation R281T prevents the formation of a salt bridge between residues R281 and D325, thereby destabilizing the myosin head. The mutation was exclusively present in morphologically affected family members. A few members of the family displayed NVM in combination with other heart defects, such as dislocation of the tricuspid valve (Ebstein's anomaly, EA) and atrial septal defect (ASD). A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life. The data presented in this report provide first evidence that a mutation in a sarcomeric protein can cause noncompaction of the ventricular myocardium