An exactly mass conserving space-time embedded-hybridized discontinuous Galerkin method for the Navier-Stokes equations on moving domains

This paper presents a space-time embedded-hybridized discontinuous Galerkin (EHDG) method for the Navier--Stokes equations on moving domains. This method uses a different hybridization compared to the space-time hybridized discontinuous Galerkin (HDG) method we presented previously in (Int. J. Numer. Meth. Fluids 89: 519--532, 2019). In the space-time EHDG method the velocity trace unknown is continuous while the pressure trace unknown is discontinuous across facets. In the space-time HDG method, all trace unknowns are discontinuous across facets. Alternatively, we present also a space-time embedded discontinuous Galerkin (EDG) method in which all trace unknowns are continuous across facets. The advantage of continuous trace unknowns is that the formulation has fewer global degrees-of-freedom for a given mesh than when using discontinuous trace unknowns. Nevertheless, the discrete velocity field obtained by the space-time EHDG and EDG methods, like the space-time HDG method, is exactly divergence-free, even on moving domains. However, only the space-time EHDG and HDG methods result in divergence-conforming velocity fields. An immediate consequence of this is that the space-time EHDG and HDG discretizations of the conservative form of the Navier--Stokes equations are energy stable. The space-time EDG method, on the other hand, requires a skew-symmetric formulation of the momentum advection term to be energy-stable. Numerical examples will demonstrate the differences in solution obtained by the space-time EHDG, EDG, and HDG methods

Analysis of a space--time hybridizable discontinuous Galerkin method for the advection--diffusion problem on time-dependent domains

This paper presents the first analysis of a space--time hybridizable discontinuous Galerkin method for the advection--diffusion problem on time-dependent domains. The analysis is based on non-standard local trace and inverse inequalities that are anisotropic in the spatial and time steps. We prove well-posedness of the discrete problem and provide a priori error estimates in a mesh-dependent norm. Convergence theory is validated by a numerical example solving the advection--diffusion problem on a time-dependent domain for approximations of various polynomial degree

A locally conservative and energy-stable finite element for the Navier--Stokes problem on time-dependent domains

We present a finite element method for the incompressible Navier--Stokes problem that is locally conservative, energy-stable and pressure-robust on time-dependent domains. To achieve this, the space--time formulation of the Navier--Stokes problem is considered. The space--time domain is partitioned into space--time slabs which in turn are partitioned into space--time simplices. A combined discontinuous Galerkin method across space--time slabs, and space--time hybridized discontinuous Galerkin method within a space--time slab, results in an approximate velocity field that is $H({\rm div})$-conforming and exactly divergence-free, even on time-dependent domains. Numerical examples demonstrate the convergence properties and performance of the method

Mitochondrial ROS Signaling in Organismal Homeostasis

Generation, transformation, and utilization of organic molecules in support of cellular differentiation, growth, and maintenance are basic tenets that define life. In eukaryotes, mitochondrial oxygen consumption plays a central role in these processes. During the process of oxidative phosphorylation, mitochondria utilize oxygen to generate ATP from organic fuel molecules but in the process also produce reactive oxygen species (ROS). While ROS have long been appreciated for their damage-promoting, detrimental effects, there is now a greater understanding of their roles as signaling molecules. Here, we review mitochondrial ROS-mediated signaling pathways with an emphasis on how they are involved in various basal and adaptive physiological responses that control organismal homeostasis

Early-life experience reduces excitation to stress-responsive hypothalamic neurons and reprograms the expression of corticotropin-releasing hormone.

Increased sensory input from maternal care attenuates neuroendocrine and behavioral responses to stress long term and results in a lifelong phenotype of resilience to depression and improved cognitive function. Whereas the mechanisms of this clinically important effect remain unclear, the early, persistent suppression of the expression of the stress neurohormone corticotropin-releasing hormone (CRH) in hypothalamic neurons has been implicated as a key aspect of this experience-induced neuroplasticity. Here, we tested whether the innervation of hypothalamic CRH neurons of rat pups that received augmented maternal care was altered in a manner that might promote the suppression of CRH expression and studied the cellular mechanisms underlying this suppression. We found that the number of excitatory synapses and the frequency of miniature excitatory synaptic currents onto CRH neurons were reduced in "care-augmented" rats compared with controls, as were the levels of the glutamate vesicular transporter vGlut2. In contrast, analogous parameters of inhibitory synapses were unchanged. Levels of the transcriptional repressor neuron-restrictive silencer factor (NRSF), which negatively regulates Crh gene transcription, were markedly elevated in care-augmented rats, and chromatin immunoprecipitation demonstrated that this repressor was bound to a cognate element (neuron-restrictive silencing element) on the Crh gene. Whereas the reduced excitatory innervation of CRH-expressing neurons dissipated by adulthood, increased NRSF levels and repression of CRH expression persisted, suggesting that augmented early-life experience reprograms Crh gene expression via mechanisms involving transcriptional repression by NRSF

Investigation of the Possible Functions of PACAP in Human Trophoblast Cells

Pituitary adenylate cyclase activating polypeptide (PACAP) is an endogenous neuropeptide having a widespread distribution both in the nervous system and peripheral organs including the female reproductive system. Both the peptide and its receptors have been shown in the placenta but its role in placental growth, especially its human aspects, remains unknown. The aim of the present study was to investigate the effects of PACAP on invasion, proliferation, cell survival, and angiogenesis of trophoblast cells. Furthermore, cytokine production was investigated in human decidual and peripheral blood mononuclear cells. For in vitro studies, human invasive proliferative extravillous cytotrophoblast (HIPEC) cells and HTR-8/SVneo human trophoblast cells were used. Both cell types were used for testing the effects of PACAP on invasion and cell survival in order to investigate whether the effects of PACAP in trophoblasts depend on the examined cell type. Invasion was studied by standardized invasion assay. PACAP increased proliferation in HIPEC cells, but not in HTR-8 cells. Cell viability was examined using MTT test, WST-1 assay, and annexin V/propidium iodide flow cytometry assay. Survival of HTR-8/SVneo cells was studied under oxidative stress conditions induced by hydrogen peroxide. PACAP as pretreatment, but not as co-treatment, significantly increased the number of surviving HTR-8 cells. Viability of HIPEC cells was investigated using methotrexate (MTX) toxicity, but PACAP1-38 could not counteract its toxic effect. Angiogenic molecules were determined both in the supernatant and the cell lysate by angiogenesis array. In the supernatant, we found that PACAP decreased the secretion of various angiogenic markers, such as angiopoietin, angiogenin, activin, endoglin, ADAMTS-1, and VEGF. For the cytokine assay, human decidual and peripheral blood lymphocytes were separated and treated with PACAP1-38. Th1 and Th2 cytokines were analyzed with CBA assay and the results showed that there were no significant differences in control and PACAP-treated cells. In summary, PACAP seems to play various roles in human trophoblast cells, depending on the cell type and microenvironmental influences

Laterality of deep white matter hyperintensities correlates with basilar artery bending and vertebral artery dominance

Aim To investigate whether vertebrobasilar geometry contributes to the presence, severity, and laterality of white matter hyperintensities (WMH). Methods We retrospectively reviewed 290 cerebral scans of patients who underwent time-of-flight and fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) between 2017 and 2018. WMH were counted, localized, and grouped according to laterality on the FLAIR sequence. A 3D mesh of the posterior circulation was reconstructed (with ITK SNAP software) and the morphology of the vertebrobasilar system analyzed with an in-house software written in Python. Results Patients were assigned into a group with WMH (n=204) and a group without WMH (n=86). The severity of WMH burden was mainly affected by age and hypertension, while the localization of the WMH (or laterality) was mainly affected by the vertebrobasilar system morphology. Basilar artery morphology only affected the parietooccipital region significantly if both posterior communicating arteries were hypoplastic or absent. The dominant vertebral artery and basilar artery curve had an opposite directional relationship. Conclusions An unequal vertebral artery flow is an important hemodynamic contributor to basilar bending. Increased basilar artery curvature and increased infratentorial WMH burden may signal inadequate blood flow and predict cerebrovascular events