284 research outputs found
The LBDS Hercules sample of mJy radio sources at 1.4 GHz - II. Redshift distribution, radio luminosity function, and the high-redshift cut-off
{Abridged} A combination of spectroscopy and broadband photometric redshifts
has been used to find the complete redshift distribution of the Hercules sample
of millijansky radio sources. These data have been used to examine the
evolution of the radio luminosity function (RLF) and its high-redshift cut-off.
New redshifts have been measured for eleven sources, and a further ten upper
limits are given. The total number of sources with known redshifts in the
sample is now 47 (65%). We calculated broadband photometric redshifts for the
remaining one-third of the sample.
For the luminosity range probed by the present study (P_1.4 > 10^24.5
W/Hz/sr), we use the V/V_max test to show conclusively that there is a deficit
of high-redshift (z > 2-2.5) objects. Comparison with the model RLFs of Dunlop
& Peacock (1990) shows that our data can now exclude pure luminosity evolution.
Two of the models of DP90, and the RLF deduced by direct binning of the data,
both favour a luminosity dependence for the high-redshift cut-off, with
lower-luminosity sources (P_1.4 \simeq 10^24 W/Hz/sr) in decline by z \simeq
1-1.5 while higher-luminosity sources (P_1.4 \simeq 10^{25-26} W/Hz/sr) decline
in comoving number density beyond z \simeq 2-2.5.Comment: Revised version submitted to MNRAS. 16 pages, 12 figure
Mechanism for the formation of the high-altitude stagnant cusp: Cluster and SuperDARN observations
On 16 March 2002, Cluster moved from nightside to dayside, across the high-altitude northern cusp during an extended period of relatively steady positive IMF BY and BZ. Combined Cluster and SuperDARN data imply the existence of two reconnection sites: in the high- latitude northern hemisphere dusk and southern hemisphere dawn sectors. Within the cusp, Cluster encounters 3 distinct plasma regions. First, injections of magnetosheath-like plasma associated with dawnward and sunward convection suggest Cluster crosses newly- reconnected field lines related to the dusk reconnection site. Second, Cluster observes a Stagnant Exterior Cusp (SEC), characterized by nearly isotropic and stagnant plasma. Finally, Cluster crosses a region with significant antifield-aligned flows. We suggest the observed SEC may be located on newly re-closed field lines, reconnected first poleward of the northern hemisphere cusp and later reconnected again poleward of the southern hemisphere cusp. We discuss how the Cluster observations correspond to expectations of ’double reconnection’ model
Altered functional brain network connectivity and glutamate system function in transgenic mice expressing truncated Disrupted-in-Schizophrenia 1
Considerable evidence implicates DISC1 as a susceptibility gene for multiple psychiatric diseases. DISC1 has been intensively studied at the molecular, cellular and behavioral level, but its role in regulating brain connectivity and brain network function remains unknown. Here, we utilize a set of complementary approaches to assess the functional brain network abnormalities present in mice expressing a truncated Disc1 gene (Disc1tr Hemi mice). Disc1tr Hemi mice exhibited hypometabolism in the prefrontal cortex (PFC) and reticular thalamus along with a reorganization of functional brain network connectivity that included compromised hippocampal–PFC connectivity. Altered hippocampal–PFC connectivity in Disc1tr Hemi mice was confirmed by electrophysiological analysis, with Disc1tr Hemi mice showing a reduced probability of presynaptic neurotransmitter release in the monosynaptic glutamatergic hippocampal CA1–PFC projection. Glutamate system dysfunction in Disc1tr Hemi mice was further supported by the attenuated cerebral metabolic response to the NMDA receptor (NMDAR) antagonist ketamine and decreased hippocampal expression of NMDAR subunits 2A and 2B in these animals. These data show that the Disc1 truncation in Disc1tr Hemi mice induces a range of translationally relevant endophenotypes underpinned by glutamate system dysfunction and altered brain connectivity
The Ingredients for a Geomorphological Inversion of Landform Evidence to Reconstruct the Behaviour of the Last British-Irish Ice Sheet
The SCUBA Half Degree Extragalactic Survey (SHADES) - III : Identification of radio and mid-infrared counterparts to submillimetre galaxies
Peer reviewe
Disease consequences of higher adiposity uncoupled from its adverse metabolic effects using Mendelian randomisation
Background:Some individuals living with obesity may be relatively metabolically healthy, whilst others suffer from multiple conditions that may be linked to adverse metabolic effects or other factors. The extent to which the adverse metabolic component of obesity contributes to disease compared to the non-metabolic components is often uncertain. We aimed to use Mendelian randomisation (MR) and specific genetic variants to separately test the causal roles of higher adiposity with and without its adverse metabolic effects on diseases.Methods:We selected 37 chronic diseases associated with obesity and genetic variants associated with different aspects of excess weight. These genetic variants included those associated with metabolically ‘favourable adiposity’ (FA) and ‘unfavourable adiposity’ (UFA) that are both associated with higher adiposity but with opposite effects on metabolic risk. We used these variants and two sample MR to test the effects on the chronic diseases.Results:MR identified two sets of diseases. First, 11 conditions where the metabolic effect of higher adiposity is the likely primary cause of the disease. Here, MR with the FA and UFA genetics showed opposing effects on risk of disease: coronary artery disease, peripheral artery disease, hypertension, stroke, type 2 diabetes, polycystic ovary syndrome, heart failure, atrial fibrillation, chronic kidney disease, renal cancer, and gout. Second, 9 conditions where the non-metabolic effects of excess weight (e.g. mechanical effect) are likely a cause. Here, MR with the FA genetics, despite leading to lower metabolic risk, and MR with the UFA genetics, both indicated higher disease risk: osteoarthritis, rheumatoid arthritis, osteoporosis, gastro-oesophageal reflux disease, gallstones, adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism.Conclusions:Our results assist in understanding the consequences of higher adiposity uncoupled from its adverse metabolic effects, including the risks to individuals with high body mass index who may be relatively metabolically healthy.Funding:Diabetes UK, UK Medical Research Council, World Cancer Research Fund, National Cancer Institute
Disease consequences of higher adiposity uncoupled from its adverse metabolic effects using Mendelian randomisation
Background:Some individuals living with obesity may be relatively metabolically healthy, whilst others suffer from multiple conditions that may be linked to adverse metabolic effects or other factors. The extent to which the adverse metabolic component of obesity contributes to disease compared to the non-metabolic components is often uncertain. We aimed to use Mendelian randomisation (MR) and specific genetic variants to separately test the causal roles of higher adiposity with and without its adverse metabolic effects on diseases.Methods:We selected 37 chronic diseases associated with obesity and genetic variants associated with different aspects of excess weight. These genetic variants included those associated with metabolically ‘favourable adiposity’ (FA) and ‘unfavourable adiposity’ (UFA) that are both associated with higher adiposity but with opposite effects on metabolic risk. We used these variants and two sample MR to test the effects on the chronic diseases.Results:MR identified two sets of diseases. First, 11 conditions where the metabolic effect of higher adiposity is the likely primary cause of the disease. Here, MR with the FA and UFA genetics showed opposing effects on risk of disease: coronary artery disease, peripheral artery disease, hypertension, stroke, type 2 diabetes, polycystic ovary syndrome, heart failure, atrial fibrillation, chronic kidney disease, renal cancer, and gout. Second, 9 conditions where the non-metabolic effects of excess weight (e.g. mechanical effect) are likely a cause. Here, MR with the FA genetics, despite leading to lower metabolic risk, and MR with the UFA genetics, both indicated higher disease risk: osteoarthritis, rheumatoid arthritis, osteoporosis, gastro-oesophageal reflux disease, gallstones, adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism.Conclusions:Our results assist in understanding the consequences of higher adiposity uncoupled from its adverse metabolic effects, including the risks to individuals with high body mass index who may be relatively metabolically healthy.Funding:Diabetes UK, UK Medical Research Council, World Cancer Research Fund, National Cancer Institute
Single Spin Asymmetry in Polarized Proton-Proton Elastic Scattering at GeV
We report a high precision measurement of the transverse single spin
asymmetry at the center of mass energy GeV in elastic
proton-proton scattering by the STAR experiment at RHIC. The was measured
in the four-momentum transfer squared range \GeVcSq, the region of a significant interference between the
electromagnetic and hadronic scattering amplitudes. The measured values of
and its -dependence are consistent with a vanishing hadronic spin-flip
amplitude, thus providing strong constraints on the ratio of the single
spin-flip to the non-flip amplitudes. Since the hadronic amplitude is dominated
by the Pomeron amplitude at this , we conclude that this measurement
addresses the question about the presence of a hadronic spin flip due to the
Pomeron exchange in polarized proton-proton elastic scattering.Comment: 12 pages, 6 figure
Longitudinal double-spin asymmetry and cross section for inclusive neutral pion production at midrapidity in polarized proton collisions at sqrt(s) = 200 GeV
We report a measurement of the longitudinal double-spin asymmetry A_LL and
the differential cross section for inclusive Pi0 production at midrapidity in
polarized proton collisions at sqrt(s) = 200 GeV. The cross section was
measured over a transverse momentum range of 1 < p_T < 17 GeV/c and found to be
in good agreement with a next-to-leading order perturbative QCD calculation.
The longitudinal double-spin asymmetry was measured in the range of 3.7 < p_T <
11 GeV/c and excludes a maximal positive gluon polarization in the proton. The
mean transverse momentum fraction of Pi0's in their parent jets was found to be
around 0.7 for electromagnetically triggered events.Comment: 6 pages, 3 figures, submitted to Phys. Rev. D (RC
High non-photonic electron production in + collisions at = 200 GeV
We present the measurement of non-photonic electron production at high
transverse momentum ( 2.5 GeV/) in + collisions at
= 200 GeV using data recorded during 2005 and 2008 by the STAR
experiment at the Relativistic Heavy Ion Collider (RHIC). The measured
cross-sections from the two runs are consistent with each other despite a large
difference in photonic background levels due to different detector
configurations. We compare the measured non-photonic electron cross-sections
with previously published RHIC data and pQCD calculations. Using the relative
contributions of B and D mesons to non-photonic electrons, we determine the
integrated cross sections of electrons () at 3 GeV/10 GeV/ from bottom and charm meson decays to be = 4.0({\rm
stat.})({\rm syst.}) nb and =
6.2({\rm stat.})({\rm syst.}) nb, respectively.Comment: 17 pages, 17 figure
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