226 research outputs found
SN 2016coi/ASASSN-16fp: An example of residual helium in a type Ic supernova?
The optical observations of Ic-4 supernova (SN) 2016coi/ASASSN-16fp, from
to days after explosion, are presented along with analysis
of its physical properties. The SN shows the broad lines associated with SNe
Ic-3/4 but with a key difference. The early spectra display a strong absorption
feature at \AA\ which is not seen in other SNe~Ic-3/4 at this
epoch. This feature has been attributed to He I in the literature. Spectral
modelling of the SN in the early photospheric phase suggests the presence of
residual He in a C/O dominated shell. However, the behaviour of the He I lines
are unusual when compared with He-rich SNe, showing relatively low velocities
and weakening rather than strengthening over time. The SN is found to rise to
peak d after core-collapse reaching a bolometric luminosity of Lp
\ergs. Spectral models, including the nebular epoch, show
that the SN ejected \msun\ of material, with \msun\ below
5000 \kms, and with a kinetic energy of erg. The
explosion synthesised \msun\ of 56Ni. There are significant
uncertainties in E(B-V)host and the distance however, which will affect Lp and
MNi. SN 2016coi exploded in a host similar to the Large Magellanic Cloud (LMC)
and away from star-forming regions. The properties of the SN and the
host-galaxy suggest that the progenitor had of \msun\
and was stripped almost entirely down to its C/O core at explosion.Comment: Accepted for publication in MNRAS. Updated to reflect the published
version, minor typographical changes onl
Identifying the Location in the Host Galaxy of the Short GRB 111117A with the Chandra Sub-arcsecond Position
We present our successful Chandra program designed to identify, with
sub-arcsecond accuracy, the X-ray afterglow of the short GRB 111117A, which was
discovered by Swift and Fermi. Thanks to our rapid target of opportunity
request, Chandra clearly detected the X-ray afterglow, though no optical
afterglow was found in deep optical observations. The host galaxy was clearly
detected in the optical and near-infrared band, with the best photometric
redshift of z=1.31_{-0.23}^{+0.46} (90% confidence), making it one of the
highest known short GRB redshifts. Furthermore, we see an offset of 1.0 +- 0.2
arcseconds, which corresponds to 8.4 +- 1.7 kpc, between the host and the
afterglow position. We discuss the importance of using Chandra for obtaining
sub-arcsecond X-ray localizations of short GRB afterglows to study GRB
environments.Comment: 17 pages, 11 figures, accepted for publication in Ap
Measurement of the CKM angle γ from a combination of B±→Dh± analyses
A combination of three LHCb measurements of the CKM angle γ is presented. The decays B±→D K± and
B±→Dπ± are used, where D denotes an admixture of D0 and D0 mesons, decaying into K+K−, π+π−, K±π∓, K±π∓π±π∓, K0Sπ+π−, or K0S K+K− final states. All measurements use a dataset corresponding to 1.0 fb−1 of integrated luminosity. Combining results from B±→D K± decays alone a best-fit value of
γ =72.0◦ is found, and confidence intervals are set
γ ∈ [56.4,86.7]◦ at 68% CL,
γ ∈ [42.6,99.6]◦ at 95% CL.
The best-fit value of γ found from a combination of results from B±→Dπ± decays alone, is γ =18.9◦,
and the confidence intervals
γ ∈ [7.4,99.2]◦ ∪ [167.9,176.4]◦ at 68% CL
are set, without constraint at 95% CL. The combination of results from B± → D K± and B± → Dπ±
decays gives a best-fit value of γ =72.6◦ and the confidence intervals
γ ∈ [55.4,82.3]◦ at 68% CL,
γ ∈ [40.2,92.7]◦ at 95% CL
are set. All values are expressed modulo 180◦, and are obtained taking into account the effect of D0–D0
mixing
The response of a classical Hodgkin–Huxley neuron to an inhibitory input pulse
A population of uncoupled neurons can often be brought close to synchrony by a single strong inhibitory input pulse affecting all neurons equally. This mechanism is thought to underlie some brain rhythms, in particular gamma frequency (30–80 Hz) oscillations in the hippocampus and neocortex. Here we show that synchronization by an inhibitory input pulse often fails for populations of classical Hodgkin–Huxley neurons. Our reasoning suggests that in general, synchronization by inhibitory input pulses can fail when the transition of the target neurons from rest to spiking involves a Hopf bifurcation, especially when inhibition is shunting, not hyperpolarizing. Surprisingly, synchronization is more likely to fail when the inhibitory pulse is stronger or longer-lasting. These findings have potential implications for the question which neurons participate in brain rhythms, in particular in gamma oscillations
SN 2016coi/ASASSN-16fp: an example of residual helium in a type Ic supernova?
The optical observations of Ic-4 supernova (SN) 2016coi/ASASSN-16fp, from ∼2 to ∼450 d after explosion, are presented along with analysis of its physical properties. The SN shows the broad lines associated with SNe Ic-3/4 but with a key difference. The early spectra display a strong absorption feature at ∼5400 Å which is not seen in other SNe Ic-3/4 at this epoch. This feature has been attributed to He I in the literature. Spectral modelling of the SN in the early photospheric phase suggests the presence of residual He in a C/O dominated shell. However, the behaviour of the He I lines is unusual when compared with He-rich SNe, showing relatively low velocities and weakening rather than strengthening over time. The SN is found to rise to peak ∼16 d after core-collapse reaching a bolometric luminosity of Lp∼3 × 1042 erg s−1. Spectral models, including the nebular epoch, show that the SN ejected 2.5–4 M⊙ of material, with ∼1.5 M⊙ below 5000 km s−1, and with a kinetic energy of (4.5–7) × 1051 erg. The explosion synthesized ∼0.14 M⊙ of 56Ni. There are significant uncertainties in E(B − V)host and the distance, however, which will affect Lp and MNi. SN 2016coi exploded in a host similar to the Large Magellanic Cloud (LMC) and away from star-forming regions. The properties of the SN and the host-galaxy suggest that the progenitor had MZAMS of 23–28 M⊙ and was stripped almost entirely down to its C/O core at explosion
Quantitative Epistasis Analysis and Pathway Inference from Genetic Interaction Data
Inferring regulatory and metabolic network models from quantitative genetic interaction data remains a major challenge in systems biology. Here, we present a novel quantitative model for interpreting epistasis within pathways responding to an external signal. The model provides the basis of an experimental method to determine the architecture of such pathways, and establishes a new set of rules to infer the order of genes within them. The method also allows the extraction of quantitative parameters enabling a new level of information to be added to genetic network models. It is applicable to any system where the impact of combinatorial loss-of-function mutations can be quantified with sufficient accuracy. We test the method by conducting a systematic analysis of a thoroughly characterized eukaryotic gene network, the galactose utilization pathway in Saccharomyces cerevisiae. For this purpose, we quantify the effects of single and double gene deletions on two phenotypic traits, fitness and reporter gene expression. We show that applying our method to fitness traits reveals the order of metabolic enzymes and the effects of accumulating metabolic intermediates. Conversely, the analysis of expression traits reveals the order of transcriptional regulatory genes, secondary regulatory signals and their relative strength. Strikingly, when the analyses of the two traits are combined, the method correctly infers ∼80% of the known relationships without any false positives
α-Arrestins Aly1 and Aly2 Regulate Intracellular Trafficking in Response to Nutrient Signaling
Arrestins, known regulators of endocytosis, take on novel functions in nutrient-regulated endosomal recycling. Yeast α-arrestins, Aly1 and Aly2, redistribute the Gap1 permease from endosomes to the cell surface and interact with clathrin/AP-1. Aly2 is regulated by the Npr1 kinase and acts through mechanisms distinct from Aly1
Membrane Properties and the Balance between Excitation and Inhibition Control Gamma-Frequency Oscillations Arising from Feedback Inhibition
Computational studies as well as in vivo and in vitro results have shown that many cortical neurons fire in a highly irregular manner and at low average firing rates. These patterns seem to persist even when highly rhythmic signals are recorded by local field potential electrodes or other methods that quantify the summed behavior of a local population. Models of the 30–80 Hz gamma rhythm in which network oscillations arise through ‘stochastic synchrony’ capture the variability observed in the spike output of single cells while preserving network-level organization. We extend upon these results by constructing model networks constrained by experimental measurements and using them to probe the effect of biophysical parameters on network-level activity. We find in simulations that gamma-frequency oscillations are enabled by a high level of incoherent synaptic conductance input, similar to the barrage of noisy synaptic input that cortical neurons have been shown to receive in vivo. This incoherent synaptic input increases the emergent network frequency by shortening the time scale of the membrane in excitatory neurons and by reducing the temporal separation between excitation and inhibition due to decreased spike latency in inhibitory neurons. These mechanisms are demonstrated in simulations and in vitro current-clamp and dynamic-clamp experiments. Simulation results further indicate that the membrane potential noise amplitude has a large impact on network frequency and that the balance between excitatory and inhibitory currents controls network stability and sensitivity to external inputs
Expression of the Salmonella Spp. Virulence Factor SifA in Yeast Alters Rho1 Activity on Peroxisomes
SifA is a virulence protein required for assembly and tubulation of a modified phagosome that promotes Salmonella replication. We show that SifA expressed in yeast induces membrane invagination during peroxisome proliferation and requires functional Rho1p. This is consistent with SifA ability to interact with RhoA and the fact that it is a GEF structural homologue
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