719 research outputs found

    Electronic and optical properties of graphene and other 2D materials

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    The Physics of Protoplanetesimal Dust Agglomerates. III. Compaction in Multiple Collisions

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    To study the evolution of protoplanetary dust aggregates, we performed experiments with up to 2600 collisions between single, highly-porous dust aggregates and a solid plate. The dust aggregates consisted of spherical SiO2_2 grains with 1.5μ\mum diameter and had an initial volume filling factor (the volume fraction of material) of ϕ0=0.15\phi_0=0.15. The aggregates were put onto a vibrating baseplate and, thus, performed multiple collisions with the plate at a mean velocity of 0.2 m s1^{-1}. The dust aggregates were observed by a high-speed camera to measure their size which apparently decreased over time as a measure for their compaction. After 1000 collisions the volume filling factor was increased by a factor of two, while after 2000\sim2000 collisions it converged to an equilibrium of ϕ0.36\phi\approx0.36. In few experiments the aggregate fragmented, although the collision velocity was well below the canonical fragmentation threshold of 1\sim1 m s1^{-1}. The compaction of the aggregate has an influence on the surface-to-mass ratio and thereby the dynamic behavior and relative velocities of dust aggregates in the protoplanetary nebula. Moreover, macroscopic material parameters, namely the tensile strength, shear strength, and compressive strength, are altered by the compaction of the aggregates, which has an influence on their further collisional behavior. The occurrence of fragmentation requires a reassessment of the fragmentation threshold velocity.Comment: accepted by the Astrophysical Journa

    Contact geometry modification of friction-welded semi-finished products to improve the bonding of hybrid components

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    To improve the bond strength of hybrid components when joined by friction welding, specimens with various front end surface geometries were evaluated. Rods made of aluminum AA6082 (AlSi1MgMn/EN AW-6082) and the case-hardening steel 20MnCr5 (AISI 5120) with adapted joining surface geometries were investigated to create both a form-locked and material-bonded joint. Eight different geometries were selected and tested. Subsequently, the joined components were metallographically examined to analyze the bonding and the resulting microstructures. The mechanical properties were tested by means of tensile tests and hardness measurements. Three geometrical variants with different locking types were identified as the most promising for further processing in a forming process chain due to the observed material bond and tensile strengths above 220 MPa. The hardness tests revealed an increase in the steel’s hardness and a softening of the aluminum near the transition area. Apparent intermetallic phases in the joining zone were analyzed by scanning electron microscopy (SEM) and an accumulation of silicon in the joining zone was detected by energy-dispersive X-ray spectroscopy (EDS). © 2021 by the authors. Licensee MDPI, Basel, Switzerland

    The plasticity of human breast carcinoma cells is more than epithelial to mesenchymal conversion

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    The human breast comprises three lineages: the luminal epithelial lineage, the myoepithelial lineage, and the mesenchymal lineage. It has been widely accepted that human breast neoplasia pertains only to the luminal epithelial lineage. In recent years, however, evidence has accumulated that neoplastic breast epithelial cells may be substantially more plastic in their differentiation repertoire than previously anticipated. Thus, along with an increasing availability of markers for the myoepithelial lineage, at least a partial differentiation towards this lineage is being revealed frequently. It has also become clear that conversions towards the mesenchymal lineage actually occur, referred to as epithelial to mesenchymal transitions. Indeed, some of the so-called myofibroblasts surrounding the tumor may have an epithelial origin rather than a mesenchymal origin. Because myoepithelial cells, epithelial to mesenchymal transition-derived cells, genuine stromal cells and myofibroblasts share common markers, we now need to define a more ambitious set of markers to distinguish these cell types in the microenvironment of the tumors. This is necessary because the different microenvironments may confer different clinical outcomes. The aim of this commentary is to describe some of the inherent complexities in defining cellular phenotypes in the microenvironment of breast cancer and to expand wherever possible on the implications for tumor suppression and progression

    Establishment of a normal-derived estrogen receptor-positive cell line comparable to the prevailing human breast cancer subtype

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    Understanding human cancer increasingly relies on insight gained from subtype specific comparisons between malignant and non-malignant cells. The most frequent subtype in breast cancer is the luminal. By far the most frequently used model for luminal breast cancer is the iconic estrogen receptor-positive (ER(pos)) MCF7 cell line. However, luminal specific comparisons have suffered from the lack of a relevant non-malignant counterpart. Our previous work has shown that transforming growth factor-β receptor (TGFβR) inhibition suffices to propagate prospectively isolated ER(pos) human breast luminal cells from reduction mammoplasties (HBEC). Here we demonstrate that transduction of these cells with hTERT/shp16 renders them immortal while remaining true to the luminal lineage including expression of functional ER (iHBEC(ERpos)). Under identical culture conditions a major difference between MCF7 and normal-derived cells is the dependence of the latter on TGFβR inhibition for ER expression. In a breast fibroblast co-culture model we further show that whereas MCF7 proliferate concurrently with ER expression, iHBEC(ERpos) form correctly polarized acini, and segregate into proliferating and ER expressing cells. We propose that iHBEC(ERpos) may serve to shed light on hitherto unappreciated differences in ER regulation and function between normal breast and breast cancer
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