A posteriori error estimators for nonconforming finite element methods of the linear elasticity problem

AbstractIn this work we derive and analyze a posteriori error estimators for low-order nonconforming finite element methods of the linear elasticity problem on both triangular and quadrilateral meshes, with hanging nodes allowed for local mesh refinement. First, it is shown that equilibrated Neumann data on interelement boundaries are simply given by the local weak residuals of the numerical solution. The first error estimator is then obtained by applying the equilibrated residual method with this set of Neumann data. From this implicit estimator we also derive two explicit error estimators, one of which is similar to the one proposed by Dörfler and Ainsworth (2005) [24] for the Stokes problem. It is established that all these error estimators are reliable and efficient in a robust way with respect to the Lamé constants. The main advantage of our error estimators is that they yield guaranteed, i.e., constant-free upper bounds for the energy-like error (up to higher order terms due to data oscillation) when a good estimate for the inf–sup constant is available, which is confirmed by some numerical results

Multimodality cardiovascular imaging in pulmonary embolism

Acute pulmonary embolism (APE) is one of the leading causes of cardiovascular (CV) morbidity andmortality. To select appropriate therapeutic strategy and/or to minimize the mortality and morbidity,rapid and correct identification of life-threatening APE is very important. Also, right ventricular (RV)failure usually precedes acute hemodynamic compromise or death, and thus the identification of RVfailure is another important step in risk stratification or treatment of APE. With advances in diagnosisand treatment, the prognosis of APE has been dramatically improving in most cases, but inadequatetherapy or recurrent episodes of pulmonary embolism (PE) may result in negative outcomes or, so called,chronic thromboembolic pulmonary hypertension (CTEPH). CTEPH is a condition characterized byremaining chronic thromboembolic material in the pulmonary vasculature and subsequent chronicpulmonary hypertension.Various imaging modalities include chest computed tomography pulmonary angiography (CTPA),echocardiography, magnetic resonance imaging, and nuclear imaging and each are used for the assessmentof varying status of PE. Assessment of thromboembolic burden by chest CTPA is the first step inthe diagnosis of PE. Hemodynamic assessment can be achieved by echocardiography and also by chestCTPA. Nuclear imaging is useful in discriminating CTEPH from APE.Better perspectives on diagnosis, risk stratification and decision making in PE can be provided bycombining multimodality CV imaging. Here, the advantages or pitfalls of each imaging modality indiagnosis, risk stratification, or management of PE will be discussed

Altered expression of norepinephrine transporter and norepinephrine in human placenta cause pre-eclampsia through regulated trophoblast invasion

Objective: We investigated the norepinephrine transporter (NET) expression in normal and pre-eclamptic placentas and analyzed the invasion activity of trophoblastic cells based on norepinephrine (NE)-NET regulation. Methods: NET and NE expression levels were examined by western blot and enzyme-linked immunosorbent assay, respectively. Trophoblast invasion activity, depending on NE-NET regulation, was determined by NET-small interfering RNA (siRNA) and NET transfection into the human extravillous trophoblast cells with or without NE treatment and invasion rates were analyzed by zymography and an invasion assay. Results: NET mRNA was expressed at a low level in pre-eclamptic placentas compared with normal placentas and NE concentration in maternal plasma increased significantly in pre-eclamptic women compared to normal pregnant women (p<0.05). NET gene upregulation and NE treatment stimulated trophoblast cell invasion up to 2.5-fold (p<0.05) by stimulating matrix metalloproteinase-9 activity via the phosphoinositol-3-kinase/AKT signaling pathway, whereas NET-siRNA with NE treatment reduced invasion rates. Conclusion: NET expression is reduced by inadequate regulation of NE levels during placental development. This suggests that a complementary balance between NET and NE regulates trophoblast cell invasion activities during placental development

Nitric oxide induces MUC5AC mucin in respiratory epithelial cells through PKC and ERK dependent pathways

BACKGROUND: Nitric oxide (NO) is generally increased during inflammatory airway diseases. This increased NO stimulates the secretion of mucin from the goblet cell and submucosal glands but the mechanism is still unknown precisely. In this study, we investigated potential signaling pathways involving protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) in the NO-induced MUC5AC mucin gene and protein expression in A549 cells. METHODS: Nitric oxide was donated to the A549 cells by NOR-1. MUC5AC mucin levels were assayed by enzyme-linked immunosorbent assay (ELISA). MUC5AC promoter activity was determined by measuring luciferase activity after the lysing the transfected cells. Activation of PKC isoforms were measured by assessing the distribution of the enzyme between cytosolic and membrane fractions using immunoblotting. Immunoblotting experiments using a monoclonal antibody specific to PKC isoforms were performed in the cytosol and membrane fractions from A549 cells. Western blot analysis for pERK and p38 were performed using the corresponding antibodies from the cell lysates after donating NO to the A549 cells by NOR-1. RESULTS: The transcriptional activity of MUC5AC promoter was maximal at the concentration of 0.1 mM NOR-1 for 1 hour incubation in transfected A549 cells. (±)-(E)-methyl-2-((E)-hydroxyimino)-5-nitro-6-methoxy-3-hexenamide (NOR-1) markedly displaced the protein kinase C (PKC)α and PKCδ from the cytosol to the membrane. Furthermore, the PKC-α,βinhibitors, GÖ6976 (10 nM) and PKCδ inhibitors, rottlerin (4 μM) inhibited the NOR-1 induced migration of PKCα and PKCδ respectively. NOR-1 also markedly increased the MUC5AC promoter activity and mRNA expression, mucin synthesis and ERK1/2 phosphorylation. The PKC inhibitors also inhibited the NOR-1 induced MUC5AC mRNA and MUC5AC protein synthesis by inhibiting the activation of PKCα and PKCδ with ERK1/2 pathways. CONCLUSION: Exogenous NO induced the MUC5AC mucin gene and protein through the PKCα and PKCδ – ERK pathways in A549 cells. Inhibition of PKC attenuated NO-mediated MUC5AC mucin synthesis. In view of this findings, PKC inhibitors might be useful in the treatment of bronchial asthma and chronic bronchitis patients where NO and mucus are increased in the bronchial airways

Electric field control of nonvolatile four-state magnetization at room temperature

We find the realization of large converse magnetoelectric (ME) effects at room temperature in a multiferroic hexaferrite Ba$_{0.52}$Sr$_{2.48}$Co$_{2}$Fe$_{24}$O$_{41}$ single crystal, in which rapid change of electric polarization in low magnetic fields (about 5 mT) is coined to a large ME susceptibility of 3200 ps/m. The modulation of magnetization then reaches up to 0.62 $\mu$$_{B}$/f.u. in an electric field of 1.14 MV/m. We find further that four ME states induced by different ME poling exhibit unique, nonvolatile magnetization versus electric field curves, which can be approximately described by an effective free energy with a distinct set of ME coefficients

Rudder Gap Flow Control for Cavitation Suppression

For the suppression of rudder cavitation, especially within and around the gap between the stationary and movable parts, flow control devices were developed. In the present study, both experimental and computational analyses of the flow control devices were carried out. The new rudder system is equipped with cam devices, which effectively close the gap between the stationary horn/pintle and movable flaps. Model scale experiments of surface pressure measurements, flow field visualization near the gap using PIV, and cavitation behavior observation were conducted in a cavitation tunnel. The experiments were simulated using a computational fluid dynamics tool and the results are compared for validation. It is confirmed that the flow control devices effectively suppresses the rudder gap cavitation and, at the same time, augments lifthttp://deepblue.lib.umich.edu/bitstream/2027.42/84266/1/CAV2009-final70.pd