Cauchy-perturbative matching revisited: tests in spherical symmetry

During the last few years progress has been made on several fronts making it possible to revisit Cauchy-perturbative matching (CPM) in numerical relativity in a more robust and accurate way. This paper is the first in a series where we plan to analyze CPM in the light of these new results. Here we start by testing high-order summation-by-parts operators, penalty boundaries and contraint-preserving boundary conditions applied to CPM in a setting that is simple enough to study all the ingredients in great detail: Einstein's equations in spherical symmetry, describing a black hole coupled to a massless scalar field. We show that with the techniques described above, the errors introduced by Cauchy-perturbative matching are very small, and that very long term and accurate CPM evolutions can be achieved. Our tests include the accretion and ring-down phase of a Schwarzschild black hole with CPM, where we find that the discrete evolution introduces, with a low spatial resolution of \Delta r = M/10, an error of 0.3% after an evolution time of 1,000,000 M. For a black hole of solar mass, this corresponds to approximately 5 s, and is therefore at the lower end of timescales discussed e.g. in the collapsar model of gamma-ray burst engines. (abridged)Comment: 14 pages, 20 figure

Ultrasound-Assisted CO2 Flooding to Improve Oil Recovery

The authors would like to gratefully acknowledge and appreciate the School of Engineering, University of Aberdeen, Aberdeen, Scotland, United Kingdom, for the provision of the laboratory facilities necessary for completing this work.Peer reviewedPostprin

Vasodilator-Stimulated Phosphoprotein (VASP)-dependent and -independent pathways regulate thrombin-induced activation of Rap1b in platelets

BACKGROUND: Vasodilator-Stimulated Phosphoprotein (VASP) is involved in the inhibition of agonist-induced platelet aggregation by cyclic nucleotides and the adhesion of platelets to the vascular wall. α(IIb)β(3) is the main integrin responsible for platelet activation and Rap1b plays a key role in integrin signalling. We investigated whether VASP is involved in the regulation of Rap1b in platelets since VASP-null platelets exhibit augmented adhesion to endothelial cells in vivo. METHODS: Washed platelets from wild type and VASP-deficient mice were stimulated with thrombin, the purinergic receptors agonist ADP, or the thromboxane A2 receptor agonist U46619 and Rap1b activation was measured using the GST-RalGDS-RBD binding assay. Interaction of VASP and Crkl was investigated by co-immunoprecipitation, confocal microscopy, and pull-down assays using Crkl domains expressed as GST-fusion proteins. RESULTS: Surprisingly, we found that activation of Rap1b in response to thrombin, ADP, or U46619 was significantly reduced in platelets from VASP-null mice compared to platelets from wild type mice. However, inhibition of thrombin-induced activation of Rap1b by nitric oxide (NO) was similar in platelets from wild type and VASP-null mice indicating that the NO/cGMP/PKG pathway controls inhibition of Rap1b independently from VASP. To understand how VASP regulated Rap1b, we investigated association between VASP and the Crk-like protein (Crkl), an adapter protein which activates the Rap1b guanine nucleotide exchange factor C3G. We demonstrated the formation of a Crkl/VASP complex by showing that: 1) Crkl co-immunoprecipitated VASP from platelet lysates; 2) Crkl and VASP dynamically co-localized at actin-rich protrusions reminiscent of focal adhesions, filopodia, and lamellipodia upon platelet spreading on fibronectin; 3) recombinant VASP bound directly to the N-terminal SH3 domain of Crkl; 4) Protein Kinase A (PKA) -mediated VASP phosphorylation on Ser157 abrogated the binding of Crkl. CONCLUSIONS: We identified Crkl as a novel protein interacting with VASP in platelets. We propose that the C3G/Crkl/VASP complex plays a role in the regulation of Rap1b and this explains, at least in part, the reduced agonist-induced activation of Rap1b in VASP-null platelets. In addition, the fact that PKA-dependent VASP phosphorylation abrogated its interaction with Crkl may provide, at least in part, a rationale for the PKA-dependent inhibition of Rap1b and platelet aggregation

The algebraic theory of tempered representations of p-adic groups I. Parabolic induction and restriction

This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.In this paper we study the category of non-degenerate modules over the Harish-Chandra Schwartz algebra of a p-adic connected reductive group. We construct functors of parabolic induction and restriction and show that they are exact and both ways adjoint to each other.Peer Reviewe

Decreased reelin expression in the left prefrontal cortex (BA9) in chronic schizophrenia patients

Background: Reelin is under epigenetic control and has been reported to be decreased in cortical regions in schizophrenia. Methods: To establish if expression of reelin is altered in specific cortical, hippocampal or thalamic regions of schizophrenia patients, we measured gene expression of reelin in a postmortem study of elderly patients with schizophrenia and non-affected controls in both hemispheres differentiating between gray and white matter. We compared cerebral postmortem samples (dorsolateral prefrontal cortex BA9 and BA46, superior temporal cortex BA22, entorhinal cortex BA28, sensoric cortex BA1-3, hippocampus, CA4, mediodorsal nucleus of the thalamus) from 12 schizophrenia patients with 13 normal subjects investigating gene expression of reelin in the gray and white matter of both hemispheres by in situ-hybridization. Results: The left prefrontal area (BA9) of schizophrenia patients revealed a decreased expression of reelin-mRNA of 29.1% in the white (p = 0.022) and 13.6% in the gray matter (p = 0.007) compared to the control group. None of the other regions examined showed any statistically significant differences. Conclusion: Since reelin is responsible for migration and synapse formation, the decreased gene expression of reelin in the left prefrontal area of schizophrenia patients points to neurodevelopmental deficits in neuronal migration and synaptic plasticity. However, our study group was small, and results should be verified using larger samples. Copyright © 2012 S. Karger AG, Base

The Second Transmembrane Domain of P2X7 Contributes to Dilated Pore Formation

Activation of the purinergic receptor P2X7 leads to the cellular permeability of low molecular weight cations. To determine which domains of P2X7 are necessary for this permeability, we exchanged either the C-terminus or portions of the second transmembrane domain (TM2) with those in P2X1 or P2X4. Replacement of the C-terminus of P2X7 with either P2X1 or P2X4 prevented surface expression of the chimeric receptor. Similarly, chimeric P2X7 containing TM2 from P2X1 or P2X4 had reduced surface expression and no permeability to cationic dyes. Exchanging the N-terminal 10 residues or C-terminal 14 residues of the P2X7 TM2 with the corresponding region of P2X1 TM2 partially restored surface expression and limited pore permeability. To further probe TM2 structure, we replaced single residues in P2X7 TM2 with those in P2X1 or P2X4. We identified multiple substitutions that drastically changed pore permeability without altering surface expression. Three substitutions (Q332P, Y336T, and Y343L) individually reduced pore formation as indicated by decreased dye uptake and also reduced membrane blebbing in response to ATP exposure. Three others substitutions, V335T, S342G, and S342A each enhanced dye uptake, membrane blebbing and cell death. Our results demonstrate a critical role for the TM2 domain of P2X7 in receptor function, and provide a structural basis for differences between purinergic receptors. © 2013 Sun et al

Zusammensetzung polarer stratosphärischer Wolkenteilchen simuliert in einer Aerosolkammer

In einer Aerosolkammer können Teilchenänderungen unter kontrollierten Bedingungen untersucht werden. Dies ermöglicht ein besseres Verständnis für den Bildungsprozeß polarer stratosphärischer Wolkenteilchen, die für den Ozonabbau wichtig sind. Hierfür wurde ein Aerosolstrahl-Massenspektrometer entwickelt, um die Zusammensetzung der Wolkenteilchen in der Kammer zu messen. Die Teilchen werden von der Umgebungsluft durch eine aerodynamische Linse und ein differentiell gepumptes Vakuumsystem getrennt. Nach anschließendem Verdampfen wird das entstehende Gas massenspektrometrisch untersucht. Das Instrument besitzt eine hohe Empfindlichkeit. Dies ist nötig, um trotz abnehmender Aerosolmenge in der Kammer lange Beobachtungszeiten zu gewährleisten. Die Zusammensetzung der Teilchen wurde für flüssige binäre H2SO4/H2O- und ternäre HNO3/H2SO4/H2O-Teilchen über Tage hinweg gemessen. Währenddessen wurden die Konzentrationen in der Gasphase und die Temperaturen im Bereich von 185 bis 230 K variiert. Durch diese Experimente konnte die Gültigkeit von Modellrechnungen für niedrigere Temperaturen bestätigt werden, als bisher untersucht wurden. Trotz langer Beobachtungszeiten bei Übersättigungen gegenüber festen Hydraten blieben die Teilchen flüssig. Auch bei Eisübersättigungen größer als 1,4 kam es nicht zu Phasenübergängen. Die Bildung fester Teilchen war nur durch die schnelle Zugabe von HNO3- und H2O-Gas möglich. In diesem Experiment wurde die Koexistenz von Eis und Salpetersäuretrihydrat unter Bedingungen der polaren Stratosphäre beobachtet

Replication factory activation can be decoupled from the replication timing program by modulating Cdk levels

In the metazoan replication timing program, clusters of replication origins located in different subchromosomal domains fire at different times during S phase. We have used Xenopus laevis egg extracts to drive an accelerated replication timing program in mammalian nuclei. Although replicative stress caused checkpoint-induced slowing of the timing program, inhibition of checkpoint kinases in an unperturbed S phase did not accelerate it. Lowering cyclin-dependent kinase (Cdk) activity slowed both replication rate and progression through the timing program, whereas raising Cdk activity increased them. Surprisingly, modest alteration of Cdk activity changed the amount of DNA synthesized during different stages of the timing program. This was associated with a change in the number of active replication factories, whereas the distribution of origins within active factories remained relatively normal. The ability of Cdks to differentially effect replication initiation, factory activation, and progression through the timing program provides new insights into the way that chromosomal DNA replication is organized during S phase