No abstract

Finite deformation contact of flexible solids embedded in fluid flows occurs in a wide range of engineering scenarios. We propose a novel three-dimensional finite element approach in order to tackle this problem class. The proposed method consists of a dual mortar contact formulation, which is algorithmically integrated into an eXtended finite element method (XFEM) fluid-structure interaction approach. The combined XFEM fluid-structure-contact interaction method (FSCI) allows to compute contact of arbitrarily moving and deforming structures embedded in an arbitrary flow field. In this paper, the fluid is described by instationary incompressible Navier-Stokes equations. An exact fluid-structure interface representation permits to capture flow patterns around contacting structures very accurately as well as to simulate dry contact between structures. No restrictions arise for the structural and the contact formulation. We derive a linearized monolithic system of equations, which contains the fluid formulation, the structural formulation, the contact formulation as well as the coupling conditions at the fluid-structure interface. The linearized system may be solved either by partitioned or by monolithic fluid-structure coupling algorithms. Two numerical examples are presented to illustrate the capability of the proposed fluid-structure-contact interaction approach.Keywords Finite deformation contact · Contact of solids in fluid · EXtended finite element method · Fluid-structure interaction · Dual mortar contact approach · Partitioned and monolithic fluid-structure coupling

Three-dimensional higher-order eXtended finite element method (XFEM)-computations still pose challenging computational geometry problems especially for moving interfaces. This paper provides a method for the localization of a higher-order interface finite element (FE) mesh in an underlying three-dimensional higher-order FE mesh. Additionally, it demonstrates, how a subtetrahedralization of an intersected element can be obtained, which preserves the possibly curved interface and allows therefore exact numerical integration.The proposed interface algorithm collects initially a set of possibly intersecting elements by comparing their 'eXtended axis-aligned bounding boxes'. The intersection method is applied to a highly reduced number of intersection candidates. The resulting linearized interface is used as input for an elementwise constrained Delaunay tetrahedralization, which computes an appropriate subdivision for each intersected element. The curved interface is recovered from the linearized interface in the last step. The output comprises triangular integration cells representing the interface and tetrahedral integration cells for each intersected element.Application of the interface algorithm currently concentrates on fluid-structure interaction problems on low-order and higher-order FE meshes, which may be composed of any arbitrary element types such as hexahedra, tetrahedra, wedges, etc. Nevertheless, other XFEM-problems with explicitly given interfaces or discontinuities may be tackled in addition. Multiple structures and interfaces per intersected element can be handled without any additional difficulties. Several parallelization strategies exist depending on the desired domain decomposition approach. Numerical test cases including various geometrical exceptions demonstrate the accuracy, robustness and efficiency of the interface handling.

A series of 15 patients with Peters' anomaly observed from 1987-1991 and a patient showing Wolf-Hirschhorn syndrome were studied retrospectively. Combined ocular anomalies were: microphthalmos (9x), myopia (4x), aniridia (2x), cataract (2x). Five of the patients had combined general anomalies: mental retardation, deafness, cardiac malformation (ASD II), and luxatio coxae. In two of them chromosomal anomalies were found: 4p minus syndrome, mosaic trisomy 9. After comparison of these data with those known from the literature the author confirms that Peters' anomaly is a morphologic finding rather than a distinct entity. Treatment depends on individual histopathologic findings and on the psychophysical development of the child.

A male infant is reported with congenital dyskeratosis and pancytopenia Zinsser-Engman-Cole. The bone marrow pathology showed similarities to Fanconi anaemia. Ophthalmological complications were vitreous haemorrhage, haemorrhagic cataracta complicata and glaucoma. Spontaneous and diepoxybutane-induced chromosomal fragility was within the range of normal cells but was elevated through induction with 4-nitroquinoline-oxide. These findings are contrasted with those of Fanconi anaemia.

We investigated four cats with similar clinical skin-related signs strongly suggestive of Ehlers-Danlos syndrome (EDS). Cases no. 1 and 4 were unrelated and the remaining two cases, no. 2 and 3, were reportedly siblings. Histopathological changes were characterized by severely altered dermal collagen fibers. Transmission electron microscopy in one case demonstrated abnormalities in the collagen fibril organization and structure. The genomes of the two unrelated affected cats and one of the affected siblings were sequenced and individually compared to 54 feline control genomes. We searched for private protein changing variants in known human EDS candidate genes and identified three independent heterozygous COL5A1 variants. COL5A1 is a well-characterized candidate gene for classical EDS. It encodes the proα1 chain of type V collagen, which is needed for correct collagen fibril formation and the integrity of the skin. The identified variants in COL5A1 are c.112_118+15del or r.spl?, c.3514A>T or p.(Lys1172*), and c.3066del or p.(Gly1023Valfs*50) for cases no. 1, 2&3, and 4, respectively. They presumably all lead to nonsense-mediated mRNA decay, which results in haploinsufficiency of COL5A1 and causes the alterations of the connective tissue. The whole genome sequencing approach used in this study enables a refinement of the diagnosis for the affected cats as classical EDS. It further illustrates the potential of such experiments as a precision medicine approach in animals with inherited diseases.

A multi-scale optical model for organic light-emitting devices containing scattering layers is presented. This model describes the radiation of embedded oscillating dipoles and scattering from spherical particles. After successful model validation with experiments on a top-emitting white OLED, we show how this tool can be used for optimization with specific targets.

Lack of sensitive diagnostic tests impairs the understanding of the epidemiology of histoplasmosis, a disease whose burden is estimated to be largely underrated. Broad-range PCRs have been applied to identify fungal agents from pathology blocks, but sensitivity is variable. In this study, we compared the results of a specific Histoplasma qPCR (H. qPCR) with the results of a broad-range qPCR (28S qPCR) on formalin-fixed, paraffin-embedded (FFPE) tissue specimens from patients with proven fungal infections (n = 67), histologically suggestive of histoplasmosis (n = 36) and other mycoses (n = 31). The clinical sensitivity for histoplasmosis of the H. qPCR and the 28S qPCR was 94% and 48.5%, respectively. Samples suggestive for other fungal infections were negative with the H. qPCR. The 28S qPCR did not amplify DNA of Histoplasma in FFPE in these samples, but could amplify DNA of Emergomyces (n = 1) and Paracoccidioides (n = 2) in three samples suggestive for histoplasmosis but negative in the H. qPCR. In conclusion, amplification of Histoplasma DNA from FFPE samples is more sensitive with the H. qPCR than with the 28S qPCR. However, the 28S qPCR identified DNA of other fungi in H. qPCR-negative samples presenting like histoplasmosis, suggesting that the combination of both assays may improve the diagnosis.