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Flexible packaging materials consisting of several layers of very dissimilar materials are currently considered for replacement by multilayer polyolefin films as well as functional flexible paper materials to improve recyclability. Such materials however lead to new challenges in processing on existing packaging machinery. This paper focuses on the sealing process of such materials, especially looking at pillow pouches and the challenges occurring at the junction between cross and fin seals where the total thickness jumps from two to four layers. It is shown that the application of conventional machinery and sealing tools does not lead to a gastight seal within the operational sealing window of such materials. The origin of the permanent failure is the lack of material fraction capable to flow as a viscous melt into the gap at the fin seal. The limited compressibility of the nonmelting materials and their bending stiffness tend to increase the gap. In case of paper, a flexible sealing jaw, equipped with an elastic insert, enables a focused application of pressure at the layer jump of a poorly compressible material. This results in clearly improved gas tightness of all selected materials in the range of the used test methods (leak size 10 mm). The leakage rate of papers was reduced from 3-4 mbar·l/s with rigid tools to 1 mbar·l/s with flexible tools. The leakage of 2 mbar·l/s with OPP/CPP material could be prevented and no leaks were detected. With OPP/PE, leak‐proof results were obtain within reduced temperature at 140°, which is near the level of acceptable seal quality with low shrinkage effect.

COVID-19 is characterized by a dysregulated and excessive inflammatory response and, in severe cases, acute respiratory distress syndrome. We have recently demonstrated a previously unknown high-affinity interaction between the SARS-CoV-2 spike (S) protein and bacterial lipopolysaccharide (LPS), leading to the boosting of inflammation. Here we present a mouse inflammation model employing the coadministration of aerosolized S protein together with LPS to the lungs. Using NF-κB-RE-Luc reporter and C57BL/6 mice followed by combinations of bioimaging, cytokine, chemokine, fluorescence-activated cell sorting, and histochemistry analyses, we show that the model yields severe pulmonary inflammation and a cytokine profile similar to that observed in COVID-19. Therefore, the model offers utility for analyses of the pathophysiological features of COVID-19 and the development of new treatments.

In this paper, we extend the results of [8] by proving exponential asymptotic H1-convergence of solutions to a one-dimensional singular heat equation with L2-source term that describe evolution of viscous thin liquid sheets while considered in the Lagrange coordinates. Furthermore, we extend this asymptotic convergence result to the case of a time inhomogeneous source. This study has also independent interest for the porous medium equation theory.

In this study, DAMASK was used to model and elucidate the microstructural deformation behavior of sintered X3CrMnNi16-7-6 TRIP steel. The recently developed TRIP-TWIP material model was used within the DAMASK framework. Material optimization was performed using the least computationally expensive method, which yielded the desired results. The physical parameters of the material model were identified and tuned to fit the experimental observations. This tuned material model was used to run simulations utilizing 2D EBSD data. The local deformation, transformation, and twinning behaviors of the material under quasi-static tensile and compressive loads were analyzed. The results of this are in good agreement with previous experimental observations. The phenomena of dislocation glide, twinning, martensitic transformation, stress evolution, and dislocation pinning in different deformation stages are discussed.

We present a two-species model with applications in tumour modelling. The main novelty is the coupling of both species through the so-called Brinkman law which is typically used in the context of visco-elastic media, where the velocity field is linked to the total population pressure via an elliptic equation. The same model for only one species has been studied by Perthame and Vauchelet in the past. The first part of this paper is dedicated to establishing existence of solutions to the problem, while the second part deals with the incompressible limit as the stiffness of the pressure law tends to infinity. Here we present a novel approach in one spatial dimension that differs from the kinetic reformulation used in the aforementioned study and, instead, relies on uniform BV-estimates.

Thrombin-derived C-terminal peptides (TCPs), including a major 11-kDa fragment (TCP96), are produced through cleavage by human neutrophil elastase and aggregate lipopolysaccharide (LPS) and the Gram-negative bacterium Escherichia coli. However, the physiological roles of TCP96 in controlling bacterial infections and reducing LPS-induced inflammation are unclear. Here, using various biophysical methods, in silico molecular modeling, microbiological and cellular assays, and animal models, we examined the structural features and functional roles of recombinant TCP96 (rTCP96) in the aggregation of multiple bacteria and the Toll-like receptor (TLR) agonists they produce. We found that rTCP96 aggregates both Gram-negative and Gram-positive bacteria, including Staphylococcus aureus and Pseudomonas aeruginosa, and their cell-wall components LPS, lipid A, and lipoteichoic acid (LTA). The Gram-negative bacteria E. coli and P. aeruginosa were particularly sensitive to aggregation-induced bacterial permeabilization and killing. As a proof of concept, we show that rTCP96 reduces LPS-induced NF-κB activation in human monocytes, as well as in mouse models of LPS-induced subcutaneous inflammation. Moreover, in a mouse model of subcutaneous inoculation with P. aeruginosa, rTCP96 reduced bacterial levels. Together, these results link TCP-mediated aggregation of endotoxins and bacteria in vitro to attenuation of inflammation and bacterial levels in vivo.

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