Seismic structure of the volcanic apron north of Gran Canaria

High-resolution reflection seismic profiles through the volcanic apron north of Gran Canaria collected during Meteor Cruise 24 were interpreted in the light of results from Leg 157 (Sites 953 and 954). The shape of the submarine island flanks of Gran Canaria and the two adjacent islands of Fuerteventura to the east and Tenerife to the west were reconstructed by interpretating seismic profiles that penetrated the sediments covering the deeper portions of the volcanic pedestals. The ~4750-m-deep flank of Fuerteventura is the oldest submarine island flank, influencing the subsequent shield-building of Gran Canaria to the east, whose 16- to 15-Ma shield is ponded against Fuerteventura, forming a topographic barrier between the islands. The associated reduction of the current cross section has caused strong bottom currents, indicated by erosional features and contourites. To the north, the flank of Gran Canaria extends 60 km seaward to a depth of ~4500 m. The shield of the Anaga massif on northeast Tenerife onlaps the flank of Gran Canaria to the east. Seismic correlation of the feathered edge of the Anaga shield (~50 km off Tenerife at a depth of 4000 m) to the bio- and magnetostratigraphy at Site 953 results in an age of ~6 Ma. The surrounding sedimentary basin is characterized by chaotic and discontinuous reflection patterns of the slope facies, turning into well-stratified basin facies ~30–40 km off the coast. The westward decrease of reflectivity in the northern apron is interpreted to be caused by the submarine ridge off Galdar at the western limit of the north coast of Gran Canaria, through which mass flows from Gran Canaria entering the sea in the north were diverted to the northeastern part of the apron. The volcanic activity correlates with the sedimentation rates in the apron. The lowest rate corresponds to the volcanic hiatus on Gran Canaria (9–5 Ma) with 3–4 cm/k.y., and the highest rate (up to 12 cm/k.y.) was found during the voluminous Miocene volcanism on the island. A number of large mass-wasting events could be identified, interbedded with the pelagic background sedimentation. The basaltic breccia drilled at Site 954 (lithologic Unit IV) is interpreted to represent the deposits associated with a slope failure at the northern flank of Gran Canaria at 12 Ma. The seismic mapping reveals >60 km3 of debris advanced at least 70 km into the apron. The volume fits well with the dimensions of an amphitheater at the northern flank of Gran Canaria. The Quaternary volcanism on La Isleta at northeast Gran Canaria extends further seaward, where the seismic data show young lava flows. Other submarine volcanism occurred in the channel between Gran Canaria and Fuerteventura

Comparison of seismic reflection data to a synthetic seismogram in a volcanic apron at Site 953

The volcanic apron of Gran Canaria at Site 953 is characterized by numerous, closely spaced reflectors, allowing a highresolution stratigraphic correlation. The calibration of the presite survey seismic data (during the Meteor Cruise 24) with regard to the lithology and stratigraphy found at the drill site was achieved by computing a synthetic seismogram serving as the link between seismic and borehole data. Because logging data were available for only 53% of the hole, velocity and density measurements taken from the recovered cores were used in the missing intervals to obtain a complete synthetic seismogram. Most reflectors in the upper ~900 m of the sequence (lithologic Units I–V) turned out to be thin volcaniclastic layers intercalated to the nonvolcanic background sediments. Their thicknesses are generally <2 m, and the reflections from their tops and bases overlap, forming a single reflection. The limit of the seismic detection of such interbeds is on the order of several decimeters and thus requires special care for the processing of the velocity and density data to avoid destruction of the signal from these thin layers

Numerical simulation of the thermal fragmentation process in fullerene C60

The processes of defect formation and annealing in fullerene C60 at T=(4000-6000)K are studied by the molecular dynamics technique with a tight-binding potential. The cluster lifetime until fragmentation due to the loss of a C2 dimer has been calculated as a function of temperature. The activation energy and the frequency factor in the Arrhenius equation for the fragmentation rate have been found to be Ea = (9.2 +- 0.4) eV and A = (8 +- 1)10^{19} 1/s. It is shown that fragmentation can occur after the C60 cluster loses its spherical shape. This fact must be taken into account in theoretical calculations of Ea.Comment: 12 pages, 3 figure

Specific Y14 domains mediate its nucleo-cytoplasmic shuttling and association with spliced mRNA

Pre-mRNA splicing deposits multi-protein complexes, termed exon junction complexes (EJCs), on mRNAs near exon-exon junctions. The core of EJC consists of four proteins, eIF4AIII, MLN51, Y14 and Magoh. Y14 is a nuclear protein that can shuttle between the nucleus and the cytoplasm, and binds specifically to Magoh. Here we delineate a Y14 nuclear localization signal that also confers its nuclear export, which we name YNS. We further identified a 12-amino-acid peptide near Y14's carboxyl terminus that is required for its association with spliced mRNAs, as well as for Magoh binding. Furthermore, the Y14 mutants, which are deficient in binding to Magoh, could still be localized to the nucleus, suggesting the existence of both the nuclear import pathway and function for Y14 unaccompanied by Magoh

Not1 mediates recruitment of the deadenylase Caf1 to mRNAs targeted for degradation by tristetraprolin

The carbon catabolite repressor protein 4 (Ccr4)–Negative on TATA (Not) complex controls gene expression at two levels. In the nucleus, it regulates the basal transcription machinery, nuclear receptor-mediated transcription and histone modifications. In the cytoplasm, the complex is required for messenger RNA (mRNA) turnover through its two associated deadenylases, Ccr4 and Caf1. Not1 is the largest protein of the Ccr4–Not complex and serves as a scaffold for other subunits of the complex. Here, we provide evidence that human Not1 in the cytoplasm associates with the C-terminal domain of tristetraprolin (TTP), an RNA binding protein that mediates rapid degradation of mRNAs containing AU-rich elements (AREs). Not1 shows extensive interaction through its central region with TTP, whereas binding of Caf1 is restricted to a smaller central domain within Not1. Importantly, Not1 is required for the rapid decay of ARE-mRNAs, and TTP can recruit the Caf1 deadenylase only in presence of Not1. Thus, cytoplasmic Not1 provides a platform that allows a specific RNA binding protein to recruit the Caf1 deadenylase and thereby trigger decay of its target mRNAs

Selectivity, efficacy and toxicity studies of UCCB01-144, a dimeric neuroprotective PSD-95 inhibitor

Inhibition of postsynaptic density protein-95 (PSD-95) decouples N-methyl-d-aspartate (NMDA) receptor downstream signaling and results in neuroprotection after focal cerebral ischemia. We have previously developed UCCB01-144, a dimeric PSD-95 inhibitor, which binds PSD-95 with high affinity and is neuroprotective in experimental stroke. Here, we investigate the selectivity, efficacy and toxicity of UCCB01-144 and compare with the monomeric drug candidate Tat-NR2B9c. Fluorescence polarization using purified proteins and pull-downs of mouse brain lysates showed that UCCB01-144 potently binds all four PSD-95-like membrane-associated guanylate kinases (MAGUKs). In addition, UCCB01-144 affected NMDA receptor signaling pathways in ischemic brain tissue. UCCB01-144 reduced infarct size in young and aged male mice at various doses when administered 30 min after permanent middle cerebral artery occlusion, but UCCB01-144 was not effective in young male mice when administered 1 h post-ischemia or in female mice. Furthermore, UCCB01-144 was neuroprotective in a transient stroke model in rats, and in contrast to Tat-NR2B9c, high dose of UCCB01-144 did not lead to significant changes in mean arterial blood pressure or heart rate. Overall, UCCB01-144 is a potent MAGUK inhibitor that reduces neurotoxic PSD-95-mediated signaling and improves neuronal survival following focal brain ischemia in rodents under various conditions and without causing cardiovascular side effects, which encourages further studies towards clinical stroke trials