Analysis of stabilization operators in a Galerkin least-squares finite element discretization of the incompressible Navier-Stokes equations

In this paper the design and analysis of a dimensionally consistent stabilization operator for a time-discontinuous Galerkin least-squares finite element method for unsteady viscous flow problems governed by the incompressible Navier-Stokes equations, is discussed. The analysis results in a class of stabilization operators which satisfy essential conditions for the stability of the numerical discretization

Subtidal water level variation controlled by river flow and tides

Subtidal water level dynamics in the Berau river, East Kalimantan, Indonesia, feature a pronounced fortnightly variation. The daily mean water levels at a station about 60 km from the sea are 0.2–0.6 m higher during spring tide than during neap tide. To explain the underlying mechanisms, a local subtidal momentum balance is set up from field data, using continuous discharge estimates inferred from measurements taken with a horizontal acoustic Doppler current profiler. It is demonstrated that terms accounting for friction and variation in the water surface gradient are dominant in the subtidal momentum balance. To further investigate the sources of subtidal water level variation, a generic method of analysis is proposed to decompose the subtidal friction term into contributions caused by river flow, by interaction between tidal motions and river flow, and by the tidal motions alone. At the station under study, mainly the river-tide interaction term is responsible for generating fortnightly variation of the subtidal water level. The contribution from interaction between diurnal, semidiurnal, and quarterdiurnal tides to subtidal friction is significantly smaller. Provided that the reduction of tidal velocity amplitudes with increasing discharges can be predicted from a regression model, the results presented herein can be used to predict changes in subtidal water levels as a result of increased river discharges

Novel thin film polymer foaming technique for low and ultra low-k dielectrics

The results presented show a novel route for the preparation of thin ultra-low-k polymer films based on commercial and "non-exotic" (non-expensive) polyimide by a foaming technique. Dependent on the glass transition temperature of the polyimide mechanically and thermally stable (> 300 °C) films having porosities of ca. 40 % and k-values below 2.0 are formed. A further reduction into the ultra low k region may be accomplished by tailoring the shape of the pores from spherical into disc-like void

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The persistence of intertidal mussel beds is governed by both biotic and abiotic processes. Many studies have shown that waves and currents are able to erode mussels from an intertidal mussel bed, but here it is demonstrated that in temperate regions ice action can be important as well. These findings result from a 27-month-long monitoring campaign on a mature intertidal mussel bed in the Dutch Wadden Sea. Daily camera observations revealed two periods in which significant erosion occurred. The first event occurred in a period during which the bed was covered by ice. Ice action resulted in an initial decrease of 19% in mussel covered area around the monitoring station. The losses were concentrated in three erosion hotspots of which the largest two were located close to the beds’ edge. Around these hotspots, up to 0.3 m high ridges of piled up mussels had formed, with the highest ridges located westward of these erosion gaps. The observed topographic changes support the view that the mechanism by which the bed was damaged was, at least partly, due to physical disturbance by scouring ice. Recovery of mussel cover was limited in the 19 months following the ice action event. Due to sedimentation and reorganization of the mussels, initial relief inside the mussel bed was reduced again and mussels spread out over a larger area. Height differences between uncovered parts and mussel covered parts increased as a result of sedimentation in mussel covered areas. Wave action during a storm period caused a further reduction in mussel cover. Especially areas that were previously elevated by ice action suffered from large losses. Wave erosion occurred during multiple wind events, causing initially small erosion gaps to expand outward and increase in extent. The results suggest a twofold impact of wave and ice action on mussel bed cover: firstly, by directly eroding mussels from mussel beds; secondly, by indirectly increasing the exposure of mussel beds to wave induced bed shear stresses

The effects of bedform roughness on hydrodynamics and sediment transport in Delft3D

To contribute to solving scientific and practical questions, numerical morphodynamic models like Delft3D are often used to predict the hydrodynamics, sediment transport processes and morphological development of coastal systems. In such models, many of the processes are parameterized based on a variety of assumptions. One of the parameterized variables is the bedform-related hydraulic roughness ks, which is often assumed to be related to the ripple height. This roughness affects the magnitude and vertical structure of the flow and, consequently, the magnitude of the sediment transport. Yet, their sensitivity to ks is not well understood

Enhanced sensitivity of postsynaptic serotonin-1A receptors in rats and mice with high trait aggression

Individual differences in aggressive behaviour have been linked to variability in central serotonergic activity, both in humans and animals. A previous experiment in mice, selectively bred for high or low levels of aggression, showed an up-regulation of postsynaptic serotonin-1A (5-HT1A) receptors, both in receptor binding and in mRNA levels, in the aggressive line. The aim of this experiment was to study whether similar differences in 5-HT1A receptors exist in individuals from a random-bred rat strain, varying in aggressiveness. In addition, because little is known about the functional consequences of these receptor differences, a response mediated via postsynaptic 5-HT1A receptors (i.e., hypothermia) was studied both in the selection lines of mice and in the randomly bred rats. The difference in receptor binding, as demonstrated in mice previously, could not be shown in rats. However, both in rats and mice, the hypothermic response to the 5-HT1A agonist alnespirone was larger in aggressive individuals. So, in the rat strain as well as in the mouse lines, there is, to a greater or lesser extent, an enhanced sensitivity of postsynaptic 5-HT1A receptors in aggressive individuals. This could be a compensatory up-regulation induced by a lower basal 5-HT neurotransmission, which is in agreement with the serotonin deficiency hypothesis of aggression.

Stability and Asymmetry of Tide-Influenced River Bifurcations

Bifurcations are important geomorphological features in tide-influenced deltas. At bifurcations, river flow and tides distribute sediment over the channel network and determine the morphodynamic evolution of the entire delta. Using a one-dimensional numerical model, we study the effects of tides on the morphological evolution of bifurcations from river-dominated to tide-dominated systems. In accordance with previous studies, bifurcations with small tidal influence, in which the flood flow hardly drives morphological change, have a larger range of Shields stress and width-to-depth ratio conditions for which symmetric bifurcations are stable to depth perturbations, compared to their river-dominated counterparts. We extended the existing studies to tide-dominated conditions. When bifurcations become increasingly tide-dominated, the range of conditions under which balance discharge partition (symmetric morphology) can exist, shrinks. Under these conditions, the bed can also change during the flood phase and growth of the bed asymmetry is larger than the decay during ebb. However, the bed asymmetry in equilibrium becomes less pronounced with increasing tidal dominance. We conclude that tides reduce the tendency of closure and abandonment of one of the downstream channels compared to river-dominated bifurcations, either by inhibiting the instability or by reducing asymmetry

cGAS-STING pathway expression correlates with genomic instability and immune cell infiltration in breast cancer

Genomic instability, as caused by oncogene-induced replication stress, can lead to the activation of inflammatory signaling, involving the cGAS-STING and JAK-STAT pathways. Inflammatory signaling has been associated with pro-tumorigenic features, but also with favorable response to treatment, including to immune checkpoint inhibition. In this study, we aim to explore relations between inflammatory signaling, markers of replication stress, and immune cell infiltration in breast cancer. Expression levels of cGAS-STING signaling components (STING, phospho-TBK1, and phospho-STAT1), replication stress markers (γH2AX and pRPA), replication stress-related proto-oncogenes (Cyclin E1 and c-Myc) and immune cell markers (CD20, CD4, and CD57) are determined immunohistochemically on primary breast cancer samples (n = 380). RNA-sequencing data from TCGA (n = 1082) and METABRIC (n = 1904) are used to calculate cGAS-STING scores. pTBK1, pSTAT1 expression and cGAS-STING pathway scores are all increased in triple-negative breast cancers compared to other subtypes. Expression of γH2AX, pRPA, Cyclin E1, c-Myc, and immune cell infiltration positively correlate with p-STAT1 expression (P &lt; 0.001). Additionally, we observe significant positive associations between expression of pTBK1 and γH2AX, pRPA, c-Myc, and number of CD4+ cells and CD20+ cells. Also, cGAS-STING scores are correlated with genomic instability metrics, such as homologous recombination deficiency (P &lt; 0.001) and tumor mutational burden (P &lt; 0.01). Moreover, data from the I-SPY2 clinical trial (n = 71) confirms that higher cGAS-STING scores are observed in breast cancer patients who responded to immunotherapy combined with chemotherapy. In conclusion, the cGAS-STING pathway is highly expressed in TNBCs and is correlated with genomic instability and immune cell infiltration.</p

cGAS-STING pathway expression correlates with genomic instability and immune cell infiltration in breast cancer

Genomic instability, as caused by oncogene-induced replication stress, can lead to the activation of inflammatory signaling, involving the cGAS-STING and JAK-STAT pathways. Inflammatory signaling has been associated with pro-tumorigenic features, but also with favorable response to treatment, including to immune checkpoint inhibition. In this study, we aim to explore relations between inflammatory signaling, markers of replication stress, and immune cell infiltration in breast cancer. Expression levels of cGAS-STING signaling components (STING, phospho-TBK1, and phospho-STAT1), replication stress markers (γH2AX and pRPA), replication stress-related proto-oncogenes (Cyclin E1 and c-Myc) and immune cell markers (CD20, CD4, and CD57) are determined immunohistochemically on primary breast cancer samples (n = 380). RNA-sequencing data from TCGA (n = 1082) and METABRIC (n = 1904) are used to calculate cGAS-STING scores. pTBK1, pSTAT1 expression and cGAS-STING pathway scores are all increased in triple-negative breast cancers compared to other subtypes. Expression of γH2AX, pRPA, Cyclin E1, c-Myc, and immune cell infiltration positively correlate with p-STAT1 expression (P &lt; 0.001). Additionally, we observe significant positive associations between expression of pTBK1 and γH2AX, pRPA, c-Myc, and number of CD4+ cells and CD20+ cells. Also, cGAS-STING scores are correlated with genomic instability metrics, such as homologous recombination deficiency (P &lt; 0.001) and tumor mutational burden (P &lt; 0.01). Moreover, data from the I-SPY2 clinical trial (n = 71) confirms that higher cGAS-STING scores are observed in breast cancer patients who responded to immunotherapy combined with chemotherapy. In conclusion, the cGAS-STING pathway is highly expressed in TNBCs and is correlated with genomic instability and immune cell infiltration.</p

cGAS-STING pathway expression correlates with genomic instability and immune cell infiltration in breast cancer

Genomic instability, as caused by oncogene-induced replication stress, can lead to the activation of inflammatory signaling, involving the cGAS-STING and JAK-STAT pathways. Inflammatory signaling has been associated with pro-tumorigenic features, but also with favorable response to treatment, including to immune checkpoint inhibition. In this study, we aim to explore relations between inflammatory signaling, markers of replication stress, and immune cell infiltration in breast cancer. Expression levels of cGAS-STING signaling components (STING, phospho-TBK1, and phospho-STAT1), replication stress markers (γH2AX and pRPA), replication stress-related proto-oncogenes (Cyclin E1 and c-Myc) and immune cell markers (CD20, CD4, and CD57) are determined immunohistochemically on primary breast cancer samples (n = 380). RNA-sequencing data from TCGA (n = 1082) and METABRIC (n = 1904) are used to calculate cGAS-STING scores. pTBK1, pSTAT1 expression and cGAS-STING pathway scores are all increased in triple-negative breast cancers compared to other subtypes. Expression of γH2AX, pRPA, Cyclin E1, c-Myc, and immune cell infiltration positively correlate with p-STAT1 expression (P &lt; 0.001). Additionally, we observe significant positive associations between expression of pTBK1 and γH2AX, pRPA, c-Myc, and number of CD4+ cells and CD20+ cells. Also, cGAS-STING scores are correlated with genomic instability metrics, such as homologous recombination deficiency (P &lt; 0.001) and tumor mutational burden (P &lt; 0.01). Moreover, data from the I-SPY2 clinical trial (n = 71) confirms that higher cGAS-STING scores are observed in breast cancer patients who responded to immunotherapy combined with chemotherapy. In conclusion, the cGAS-STING pathway is highly expressed in TNBCs and is correlated with genomic instability and immune cell infiltration.</p