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Before completing his uncharacteristically hopeful filmic vision of an African Oresteia, Pier Paolo Pasolini invented a theatrical continuation of Aeschylus's trilogy. "Pilade" (1966/70) imagines what happens after Orestes, having being absolved by the Aeropagos in Athens, goes back to Argos. With its clear allusions to political developments in the last century - fascism, the Resistance, and Communist revolutions - the play reads as a mythical allegory for the situation of engaged intellectuals in thetwentieth century. As Christoph F. E. Holzhey's contribution '"La vera Diversità": Multistability, Circularity, and Abjection in Pasolini's "Pilade"' shows, Pasolini's imagined continuation of the Oresteia challenges an ideology of rational foundation and progress by moving through a series of aspect changes prompted by sudden events that allow for some integration while also creating new divisions. After all possible alliances among the principal characters - Orestes, Electra, and Pylades - have been played through, Pylades curses reason for its deceptive, consoling, and violent function and embraces his abjected position of true diversity beyond intelligibility. However, Holzhey argues, rather than functioning as the play's telos, this ending is an open one and participates in the paradoxical performance of a self-contradictory subjectivity and a circular temporality without entirely giving up hope for a truly different alternative.
Molecules of the title compound, C20H14O2, show approximate C s symmetry with the approximate mirror plane perpendicular to the central ring. The torsion angles about the acyclic bonds are 30.05 (15) and 30.77 (15)° in one half compared to −36.62 (14) and −18.60 (15)° in the other half of the molecule. The central aromatic ring makes dihedral angles of 47.78 (4) and 51.68 (3)° with the two terminal rings.
We discuss deviations from the exponential decay law which occur when going beyond the BreitWigner distribution for an unstable state. In particular, we concentrate on an oscillating behavior, remisiscent of the Rabi-oscillations, in the short-time region. We propose that these oscillations can explain the socalled GSI anomaly, which measured superimposed oscillations on top of the exponential law for hydrogen-like nuclides decaying via electron-capture. Moreover, we discuss the possibility that the deviations from the Breit-Wigner in the case of the GSI anomaly are (predominantely) caused by the interaction of the unstable state with the measurement apparatus. The consequences of this scenario, such as the non-observation of oscillations in an analogous experiment perfromed at Berkley, are investigated.
Motivated by the U.S. events of the 2000s, we address whether a too low for too long interest rate policy may generate a boom-bust cycle. We simulate anticipated and unanticipated monetary policies in state-of-the-art DSGE models and in a model with bond financing via a shadow banking system, in which the bond spread is calibrated for normal and optimistic times. Our results suggest that the U.S. boom-bust was caused by the combination of (i) too low for too long interest rates, (ii) excessive optimism and (iii) a failure of agents to anticipate the extent of the abnormally favorable conditions.
In the title compound, C27H37N2 +·Br−·2CH2Cl2, both the cation and the anion are located on a crystallographic mirror plane. Both of the dichloromethane solvent molecules show a disorder across a mirror plane over two equally occupied positions. In the crystal, the cations are connnected to the bromide ions via C—H[cdots, three dots, centered]Br hydrogen bonds.
In the title compound, C27H37N2 +·Cl−·2CH2Cl2, the cation and the anion are each located on a crystallographic mirror plane. Both of the dichloromethane solvent molecules show a disorder across a mirror plane over two equally occupied positions. Additionally, one isopropyl group is also disordered. In the crystal, the cations are connected to the chloride ions via C—H[cdots, three dots, centered]Cl hydrogen bonds.
In the systemic circulation, 11,12-epoxyeicosatrienoic acid (11,12-EET) elicits nitric oxide (NO)- and prostacyclin-independent vascular relaxation, partially through the activation of large conductance Ca2+-activated potassium (BK) channels. However, in the lung 11,12-EET contributes to hypoxia-induced pulmonary vasoconstriction. Since pulmonary artery smooth muscle cells also express BK channels, we assessed the consequences of BKβ1 subunit deletion on pulmonary responsiveness to 11,12-EET as well as to acute hypoxia. In buffer-perfused mouse lungs, hypoxia increased pulmonary artery pressure and this was significantly enhanced in the presence of NO synthase (NOS) and cyclooxygenase (COX) inhibitors. Under these conditions the elevation of tissue EET levels using an inhibitor of the soluble epoxide hydrolase (sEH-I), further increased the hypoxic contraction. Direct administration of 11,12-EET also increased pulmonary artery pressure, and both the sEH-I and 11,12-EET effects were prevented by iberiotoxin and absent in BKβ1−/− mice. In pulmonary artery smooth muscle cells treated with NOS and COX inhibitors and loaded with the potentiometric dye, di-8-ANEPPS, 11,12-EET induced depolarization while the BK channel opener NS1619 elicited hyperpolarization indicating there was no effect of the EET on classical plasma membrane BK channels. In pulmonary artery smooth muscle cells a subpopulation of BK channels is localized in mitochondria. In these cells, 11,12-EET elicited an iberiotoxin-sensitive loss of mitochondrial membrane potential (JC-1 fluorescence) leading to plasma membrane depolarization, an effect not observed in BKβ1−/− cells. Mechanistically, stimulation with 11,12-EET time-dependently induced the association of the BK α and β1 subunits. Our data indicate that in the absence of NO and prostacyclin 11,12-EET contributes to pulmonary vasoconstriction by stimulating the association of the α and β1 subunits of mitochondrial BK channels. The 11,12-EET-induced activation of BK channels results in loss of the mitochondrial membrane potential and depolarization of the pulmonary artery smooth muscle cells.
This volume contains the proceedings of the 12th International Workshop on Termination (WST 2012), to be held February 19–23, 2012 in Obergurgl, Austria. The goal of the Workshop on Termination is to be a venue for presentation and discussion of all topics in and around termination. In this way, the workshop tries to bridge the gaps between different communities interested and active in research in and around termination. The 12th International Workshop on Termination in Obergurgl continues the successful workshops held in St. Andrews (1993), La Bresse (1995), Ede (1997), Dagstuhl (1999), Utrecht (2001), Valencia (2003), Aachen (2004), Seattle (2006), Paris (2007), Leipzig (2009), and Edinburgh (2010). The 12th International Workshop on Termination did welcome contributions on all aspects of termination and complexity analysis. Contributions from the imperative, constraint, functional, and logic programming communities, and papers investigating applications of complexity or termination (for example in program transformation or theorem proving) were particularly welcome. We did receive 18 submissions which all were accepted. Each paper was assigned two reviewers. In addition to these 18 contributed talks, WST 2012, hosts three invited talks by Alexander Krauss, Martin Hofmann, and Fausto Spoto.
The title co-crystal, C9H9NO2·C6H6O2, is composed of one 2,6-diacetylpyridine molecule and one resorcinol molecule as the asymmetric unit. In the 2,6-diacetylpyridine molecule, the two carbonyl groups are antiperiplanar to the pyridine N atom. In the crystal, the 2,6-diacetylpyridine and resorcinol molecules are connected by two O-H...O hydrogen bonds, forming planar chains of alternating components running along [120].
In the title molecule, C18H17N5O2, the dihedral angle between the benzene plane and the benzimidazole plane is 19.8 (1)° and the angle between the benzene plane and the triazole plane is 16.7 (1)°. In the crystal, molecules are connected by O—H[cdots, three dots, centered]N hydrogen bonds, forming zigzag chains along the c-axis direction. The chains are connected by bifurcated N—H[cdots, three dots, centered](N,N) hydrogen bonds into layers parallel to (100). These layers are connected along the a-axis direction by weak C—H[cdots, three dots, centered]O contacts, forming a three-dimensional network.