Structure in the E2 quasicontinuum spectrum of Dy154

The evolution of the quasicontinuum spectrum with neutron number has been investigated in the sequence of isotopes Dy152,154,156. The three nuclei display a pronounced collective E2 component. In Dy154 this component shows a splitting into two distinct parts, signifying a structural change along the cascade above the yrast line. The E2 and statistical components are reproduced in simple -cascade calculations; in Dy152 and Dy156 only rotational bands are included, whereas in Dy154 additional vibration-like transitions are required to reproduce the two E2 peaks

Evolution of nuclear structure with increasing spin and internal excitation energy in 152Dy

The total γ ray spectrum emitted by 152Dy has been measured in two different reactions and decomposed into its constituent parts. From the measured decay times, multiplicities, multipolarities and spectral shapes, the average decay path has been reconstructed. The yrast single-particle structures have been shown to give way to highly collective bands at internal excitations energies > 1.5 MeV. A model, which takes into account the competition between statistical and collective decay at high spin and temperature, has been used to fit all features of the data, yielding Qt=7.0+2.5-1.5 e b for the collective bands

Structural changes along and above the yrast line of Dy154

States in Dy154 have been located up to I=48+ and their lifetimes measured. Marked structural changes occur along the yrast line with a transition from prolate to oblate shape, followed by an unexpected return to moderate collectivity at the highest spins. Structural changes with increasing energy above the yrast line are also observed

Measuring the value of social engagement in adults with and without autism

Differences in social communication are commonly reported in autism spectrum condition (ASC). A recent theory attributes this to a reduced motivation to engage with others, that is, deficits in social motivation. However, there are currently few simple, direct, behavioural ways to test this claim. This study uses a new behavioural measure of social motivation to test if preferences for direct gaze and face stimuli are linked to autistic traits or an ASC diagnosis. Our novel choose-a-movie (CAM) paradigm measures the effort participants invest to see particular stimuli. This aspect of social motivation is also known as social seeking. Methods In experiment 1, 80 typical adults completed the CAM task and a measure of autistic traits. In experiment 2, 30 adults with ASC and 24 age/IQ-matched typical adults completed the CAM paradigm. Results The results from study one showed that typical adults prefer social stimuli over non-social, but this preference is weaker in those with higher levels of autistic traits. In study two, adults with ASC showed a significant reduction in their preference for direct gaze but little difference in their preference for faces without direct gaze. Conclusions These data show that social motivation can be measured in a simple, direct, behavioural paradigm. Furthermore, adults with ASC prefer direct gaze less than typical adults but may not avoid faces without direct gaze. This data advance our understanding of how social motivation may differ between those with and without autism

Level structure of 148Gd up to I=44

The level scheme of 148Gd has been extended to I=44 by use of a Compton-suppressed Ge spectrometer array. Up to I=38 the observed level spectrum consists of spherical and oblate states of aligned-particle type. A change in structure along the yrast line is indicated at higher spins, where fast E2 transitions suggest the onset of collectivity

Evidence for superdeformation in 148Gd

γ-γ transition energy correlation measurements were performed in 148Gd using Compton-suppressed Ge detectors. A broad first ridge was observed for 1.00<Eγ<1.42 MeV. The deduced moment of inertia I(2)=78 h ℏ2MeV- is consistent with superdeformation in 148Gd. The results can be explained by cranked Strutinsky calculations

Attenuated reovirus displays oncolysis with reduced host toxicity

Background: Although the naturally occurring reovirus causes only mild symptoms in humans, it shows considerable potential as an oncolytic agent because of its innate ability to target cancer cells. In immunocompromised hosts, however, wild-type reovirus can target healthy tissues, including heart, liver, pancreas and neural structures. Methods: We characterized an attenuated form of reovirus (AV) derived from a persistently infected cell line through sequence analysis, as well as western blot and in vitro transcription and translation techniques. To examine its pathogenesis and oncolytic potential, AV reovirus was tested on healthy embryonic stem cells, various non-transformed and transformed cell lines, and in severe combined immunodeficiency (SCID) mice with tumour xenografts. Results: Sequence analysis of AV reovirus revealed a premature STOP codon in its sigma 1 attachment protein. Western blot and in vitro translation confirmed the presence of a truncated ?1. In comparison to wild-type reovirus, AV reovirus did not kill healthy stem cells or induce black tail formation in SCID mice. However, it did retain its ability to target cancer cells and reduce tumour size. Conclusion: Despite containing a truncated attachment protein, AV reovirus still preferentially targets cancer cells, and compared with wild-type reovirus it shows reduced toxicity when administered to immunodeficient hosts, suggesting the potential use of AV reovirus in combination cancer therapy

Gap Junctions and Epileptic Seizures – Two Sides of the Same Coin?

Electrical synapses (gap junctions) play a pivotal role in the synchronization of neuronal ensembles which also makes them likely agonists of pathological brain activity. Although large body of experimental data and theoretical considerations indicate that coupling neurons by electrical synapses promotes synchronous activity (and thus is potentially epileptogenic), some recent evidence questions the hypothesis of gap junctions being among purely epileptogenic factors. In particular, an expression of inter-neuronal gap junctions is often found to be higher after the experimentally induced seizures than before. Here we used a computational modeling approach to address the role of neuronal gap junctions in shaping the stability of a network to perturbations that are often associated with the onset of epileptic seizures. We show that under some circumstances, the addition of gap junctions can increase the dynamical stability of a network and thus suppress the collective electrical activity associated with seizures. This implies that the experimentally observed post-seizure additions of gap junctions could serve to prevent further escalations, suggesting furthermore that they are a consequence of an adaptive response of the neuronal network to the pathological activity. However, if the seizures are strong and persistent, our model predicts the existence of a critical tipping point after which additional gap junctions no longer suppress but strongly facilitate the escalation of epileptic seizures. Our results thus reveal a complex role of electrical coupling in relation to epileptiform events. Which dynamic scenario (seizure suppression or seizure escalation) is ultimately adopted by the network depends critically on the strength and duration of seizures, in turn emphasizing the importance of temporal and causal aspects when linking gap junctions with epilepsy