Port-Hamiltonian formulation of shallow water equations with Coriolis force and topography

We look into the problem of approximating the shallow water equations with Coriolis forces and topography. We model the system as an infinite-dimensional port-Hamiltonian system which is represented by a non-constant Stokes-Dirac structure. We here employ the idea of using different finite elements for the approximation of geometric variables (forms) describing a distributed parameter system, to spatially discretize the system and obtain a lumped parameter port-Hamiltonian system. The discretized model then captures the physical laws of its infinite-dimensional couterpart such as conservation of energy. We present some preliminary numerical results to justify our claims

Port-Hamiltonian discretization for open channel flows

A finite-dimensional Port-Hamiltonian formulation for the dynamics of smooth open channel flows is presented. A numerical scheme based on this formulation is developed for both the linear and nonlinear shallow water equations. The scheme is verified against exact solutions and has the advantage of conservation of mass and energy to the discrete level

On the rate of convergence of the Hamiltonian particle-mesh method

The Hamiltonian Particle-Mesh (HPM) method is a particle-in-cell method for compressible fluid flow with Hamiltonian structure. We present a numer- ical short-time study of the rate of convergence of HPM in terms of its three main governing parameters. We find that the rate of convergence is much better than the best available theoretical estimates. Our results indicate that HPM performs best when the number of particles is on the order of the number of grid cells, the HPM global smoothing kernel has fast decay in Fourier space, and the HPM local interpolation kernel is a cubic spline

Exploring the crosstalk between inflammation and epithelial-mesenchymal transition in cancer

Tumor cells undergo invasion and metastasis through epithelial-to-mesenchymal cell transition (EMT) by activation of alterations in extracellular matrix (ECM) protein-encoding genes, enzymes responsible for the breakdown of ECM, and activation of genes that drive the transformation of the epithelial cell to the mesenchymal type. Inflammatory cytokines such as TGFβ, TNFα, IL-1, IL-6, and IL-8 activate transcription factors such as Smads, NF-κB, STAT3, Snail, Twist, and Zeb that drive EMT. EMT drives primary tumors to metastasize in different parts of the body. T and B cells, dendritic cells (DCs), and tumor-associated macrophages (TAMs) which are present in the tumor microenvironment induce EMT. The current review elucidates the interaction between EMT tumor cells and immune cells under the microenvironment. Such complex interactions provide a better understanding of tumor angiogenesis and metastasis and in defining the aggressiveness of the primary tumors. Anti-inflammatory molecules in this context may open new therapeutic options for the better treatment of tumor progression. Targeting EMT and the related mechanisms by utilizing natural compounds may be an important and safe therapeutic alternative in the treatment of tumor growth

Some studies on the deformation of the membrane in an RF MEMS switch

Radio Frequency (RF) switches of Micro Electro Mechanical Systems (MEMS) are appealing to the mobile industry because of their energy efficiency and ability to accommodate more frequency bands. However, the electromechanical coupling of the electrical circuit to the mechanical components in RF MEMS switches is not fully understood. In this paper, we consider the problem of mechanical deformation of electrodes in RF MEMS switch due to the electrostatic forces caused by the difference in voltage between the electrodes. It is known from previous studies of this problem, that the solution exhibits multiple deformation states for a given electrostatic force. Subsequently, the capacity of the switch that depends on the deformation of electrodes displays a hysteresis behaviour against the voltage in the switch. We investigate the present problem along two lines of attack. First, we solve for the deformation states of electrodes using numerical methods such as finite difference and shooting methods. Subsequently, a relationship between capacity and voltage of the RF MEMS switch is constructed. The solutions obtained are exemplified using the continuation and bifurcation package AUTO. Second, we focus on the analytical methods for a simplified version of the problem and on the stability analysis for the solutions of deformation states. The stability analysis shows that there exists a continuous path of equilibrium deformation states between the open and closed state

Identification of putative candidate gene markers for grain zinc content using recombinant inbred lines (RIL) population of IRRI38 X Jeerigesanna

Nutrients in food crops can be enriched by adopting biofortification. Identifying the target quantitative trait loci (QTL) genes will help achieve biofortification with greater precision and accuracy. The objective of this experiment is to estimate grain zinc content, evaluation of candidate gene markers in recombinant inbred lines (RIL) derived from IRRI38 X Jeerigesanna and validation of putative candidate gene markers with rice accessions. Grain zinc content ranged from 16.1 to 35.5 ppm with an average of 23.7 ppm. Among twenty four candidate gene markers, eight showed polymorphism and out of three simple sequence repeats (SSR) markers, three showed polymorphism. Single marker analysis revealed that four (OsNAC, OsZIP8a, OsZIP8c and OsZIP4b) candidate gene markers showed significant variation among RIL population with a phenotypic variation of 4.5, 19.0, 5.1 and 10.2% respectively. Validation with 96 rice genotypes showed three markers (OsZIP8a, OsNAC and OsZIP4b) with phenotypic variation of 11.0, 5.8 and 4.8%, respectively.Keywords: Zinc, biofortification, single-marker analysis (SMS) and marker assisted selection (MAS)African Journal of Biotechnology, Vol. 13(5), pp. 657-663, 29 January, 201

Variational water-wave model with accurate dispersion and vertical vorticity

A new water-wave model has been derived which is based on variational techniques and combines a depth-averaged vertical (component of) vorticity with depth-dependent potential flow. The model facilitates the further restriction of the vertical profile of the velocity potential to n-th order polynomials or a finite-element profile with a small number of elements (say), leading to a framework for efficient modeling of the interaction of steepening and breaking waves near the shore with a large-scale horizontal flow. The equations are derived from a constrained variational formulation which leads to conservation laws for energy, mass, momentum and vertical vorticity. It is shown that the potential-flow water-wave equations and the shallow-water equations are recovered in the relevant limits. Approximate shock relations are provided, which can be used in numerical schemes to model breaking waves

cGAS Drives Noncanonical-Inflammasome Activation in Age-Related Macular Degeneration

Geographic atrophy is a blinding form of age-related macular degeneration characterized by retinal pigmented epithelium (RPE) death; the RPE also exhibits DICER1 deficiency, resultant accumulation of endogenous Alu-retroelement RNA, and NLRP3-inflammasome activation. How the inflammasome is activated in this untreatable disease is largely unknown. Here we demonstrate that RPE degeneration in human-cell-culture and mouse models is driven by a noncanonical-inflammasome pathway that activates caspase-4 (caspase-11 in mice) and caspase-1, and requires cyclic GMP-AMP synthase (cGAS)-dependent interferon-β production and gasdermin D-dependent interleukin-18 secretion. Decreased DICER1 levels or Alu-RNA accumulation triggers cytosolic escape of mitochondrial DNA, which engages cGAS. Moreover, caspase-4, gasdermin D, interferon-β, and cGAS levels were elevated in the RPE in human eyes with geographic atrophy. Collectively, these data highlight an unexpected role of cGAS in responding to mobile-element transcripts, reveal cGAS-driven interferon signaling as a conduit for mitochondrial-damage-induced inflammasome activation, expand the immune-sensing repertoire of cGAS and caspase-4 to noninfectious human disease, and identify new potential targets for treatment of a major cause of blindness

Gut microbiota and microbiota-derived metabolites promotes endometriosis

Endometriosis is a pathological condition of the female reproductive tract characterized by the existence of endometrium-like tissue at ectopic sites, affecting 10% of women between the age 15 and 49 in the USA. However, currently there is no reliable non-invasive method to detect the presence of endometriosis without surgery and many women find hormonal therapy and surgery as ineffective in avoiding the recurrences. There is a lack of knowledge on the etiology and the factors that contribute to the development of endometriosis. A growing body of recent evidence suggests an association between gut microbiota and endometriosis pathophysiology. However, the direct impact of microbiota and microbiota-derived metabolites on the endometriosis disease progression is largely unknown. To understand the causal role of gut microbiota and endometriosis, we have implemented a novel model using antibiotic-induced microbiota-depleted (MD) mice to investigate the endometriosis disease progression. Interestingly, we found that MD mice showed reduced endometriotic lesion growth and, the transplantation of gut microbiota by oral gavage of feces from mice with endometriosis rescued the endometriotic lesion growth. Additionally, using germ-free donor mice, we indicated that the uterine microbiota is dispensable for endometriotic lesion growth in mice. Furthermore, we showed that gut microbiota modulates immune cell populations in the peritoneum of lesions-bearing mice. Finally, we found a novel signature of microbiota-derived metabolites that were significantly altered in feces of mice with endometriosis. Finally, we found one the altered metabolite, quinic acid promoted the survival of endometriotic epithelial cells in vitro and lesion growth in vivo, suggesting the disease-promoting potential of microbiota-derived metabolites. In summary, these data suggest that gut microbiota and microbiota-derived metabolome contribute to lesion growth in mice, possibly through immune cell adaptations. Of translational significance, these findings will aid in designing non-invasive diagnostics using stool metabolites for endometriosis