Formation of the ventral furrow in the Drosophila embryo relies on the apical constriction of cells in the ventral region to produce bending forces that drive tissue invagination. In our recent paper we observed that apical constrictions during the initial phase of ventral furrow formation produce elongated patterns of cellular constriction chains prior to invagination and argued that these are indicative of tensile stress feedback. Here, we quantitatively analyze the constriction patterns preceding ventral furrow formation and find that they are consistent with the predictions of our active-granular-fluid model of a monolayer of mechanically coupled stress-sensitive constricting particles. Our model shows that tensile feedback causes constriction chains to develop along underlying precursor tensile stress chains that gradually strengthen with subsequent cellular constrictions. As seen in both our model and available optogenetic experiments, this mechanism allows constriction chains to penetrate or circumvent zones of reduced cell contractility, thus increasing the robustness of ventral furrow formation to spatial variation of cell contractility by rescuing cellular constrictions in the disrupted regions.

Understanding how heat flows across interfaces is vital to energy efficiency and thermal stability of many electrical devices. However, the thermal resistance caused by the interface between two materials, termed Kapitza resistance, remains poorly understood. To that end, several first‐principles molecular dynamic simulations and a detailed analysis of the phonon processes and associated transfer of heat at the interfaces of both c‐Si|a‐SiO2 and c‐Si|c‐Ge are presented. It is found that in both cases the interface properties are very important. In the case of c‐Si|a‐SiO2, it is found that interface modes cause inelastic phonon interactions and play a significant role in the total energy transferred. In the case of c‐Si|a‐SiO2, one is able to quantify this effect and find that there is a small set of interface modes which carry >10% of the heat, and decrease the ultimate thermal boundary resistance by 26.5%.

A reliable and practical renal-lipid quantification and imaging method is needed. Here, the feasibility of an accelerated MRSI method to map renal fat fractions (FF) at 3T and its repeatability were investigated. A 2D density-weighted concentric-ring-trajectory MRSI was used for accelerating the acquisition of 48 × 48 voxels (each of 0.25 mL spatial resolution) without respiratory navigation implementations. The data were collected over 512 complex-FID timepoints with a 1250 Hz spectral bandwidth. The MRSI sequence was designed with a metabolite-cycling technique for lipid–water separation. The in vivo repeatability performance of the sequence was assessed by conducting a test–reposition–retest study within healthy subjects. The coefficient of variation (CV) in the estimated FF from the test–retest measurements showed a high degree of repeatability of MRSI-FF (CV = 4.3 ± 2.5%). Additionally, the matching level of the spectral signature within the same anatomical region was also investigated, and their intrasubject repeatability was also high, with a small standard deviation (8.1 ± 6.4%). The MRSI acquisition duration was ~3 min only. The proposed MRSI technique can be a reliable technique to quantify and map renal metabolites within a clinically acceptable scan time at 3T that supports the future application of this technique for the non-invasive characterization of heterogeneous renal diseases and tumors.

The key process giving rise to ventral furrow formation (VFF) in the Drosophila embryo 14 is apical (outer side) constriction of cells in the ventral region. A combined effect of the cellular 15 constrictions is a negative spontaneous curvature of the cell layer, which buckles inwards. In our 16 recent paper [Gao et al. (2016). J Phys Condens Matter, 28(41), 414021] we showed that the cell 17 constrictions in the initial phase of VFF produce well-defined cellular constriction chain (CCC) 18 patterns, and we argued that CCC formation is a signature of mechanical signaling that coordinates 19 apical constrictions through tensile stress. In the present study, we provide a statistical comparison 20 between our active granular fluid (AGF) model and time lapses of live embryos. We also 21 demonstrate that CCCs can penetrate regions of reduced constriction probability, and we argue 22 that CCC formation increases robustness of VFF to spatial variation of cell contractility. 23 24 128 determine the essential features of the geometry of constriction patterns without considering 129 complexities of temporal aspects of constrictions of individual cells. 130 The AGF model predicts that tensile-stress feedback between constricting cells re-131 sults in formation of CCCs 132 Description of the AGF model 133 6 of 28