Unbound Particles in Dark Matter Halos

We investigate unbound dark matter particles in halos by tracing particle trajectories in a simulation run to the far future (a = 100). We find that the traditional sum of kinetic and potential energies is a very poor predictor of which dark matter particles will eventually become unbound from halos. We also study the mass fraction of unbound particles, which increases strongly towards the edges of halos, and decreases significantly at higher redshifts. We discuss implications for dark matter detection experiments, precision calibrations of the halo mass function, the use of baryon fractions to constrain dark energy, and searches for intergalactic supernovae.Comment: Significant improvements following referee suggestion

The theory of stellar winds

We present a brief overview of the theory of stellar winds with a strong emphasis on the radiation-driven outflows from massive stars. The resulting implications for the evolution and fate of massive stars are also discussed. Furthermore, we relate the effects of mass loss to the angular momentum evolution, which is particularly relevant for the production of long and soft gamma-ray bursts. Mass-loss rates are not only a function of the metallicity, but are also found to depend on temperature, particularly in the region of the bi-stability jump at 21 000 Kelvin. We highlight the role of the bi-stability jump for Luminous Blue Variable (LBV) stars, and discuss suggestions that LBVs might be direct progenitors of supernovae. We emphasize that radiation-driven wind studies rely heavily on the input opacity data and linelists, and that these are thus of fundamental importance to both the mass-loss predictions themselves, as well as to our overall understanding of the lives and deaths of massive stars.Comment: 6 pages, invited review Astrophysics and Space Science, Vol 336, Issue 1, pp. 163-167 (special HEDLA 2010 Issue

Association of maternal Vitamin D status with glucose tolerance and caesarean section in a multi-ethnic Asian cohort: the growing up in Singapore towards healthy outcomes study

10.1371/journal.pone.0142239PLoS ONE10111-16GUSTO (Growing up towards Healthy Outcomes

Detection of Leptospira Antibodies in Dogs by Immunofluorescence

No abstract available

Demographic Correlates for Nutrient Supplementation in 800 Dogs in Scotland

No abstract available

Axonal injury caused by focal cerebral ischemia in the rat

The susceptibility of axons to blunt head injury is well established. However, axonal injury following cerebral ischemia has attracted less attention than damage in gray matter. We have employed immunocytochemical methods to assess the vulnerability of axons to cerebral ischemia in vivo. Immunocytochemistry was performed using antibodies to a synaptosomal-associated protein of 25 kDa (SNAP25), which is transported by fast anterograde transport; the 68-kDa neurofilament subunit (NF68kD); and microtubule-associated protein 5 (MAP5) on sections from rats subjected to 30 min and 1, 2, and 4 h of ischemia induced by permanent middle cerebral artery (MCA) occlusion. After 4 h of occlusion, there was increased SNAP25 immunoreactivity, which was bulbous in appearance, reminiscent of the axonal swellings that occur following blunt head injury. Increased SNAP25 immunoreactivity was present in circumscribed zones in the subcortical white matter and in the axonal tracts at the border of infarction, a pattern similar to that previously described for amyloid precursor protein. Although less marked, similar changes in immunoreactivity in axons were evident following 2 h of ischemia. MAP5 and NF68kD had striking changes in immunoreactivity in axonal tracts permeating the caudate nucleus within the MCA territory at 4 h. The appearance was roughened and disorganized compared with the smooth regular staining in axons within the nonischemic areas. Profiles reminiscent of axonal bulbs were evident in MAP5-stained sections. The changes seen withNF68kD and MAP5 were also evident at 2 h but were more subtle at 1 h. There were no changes in axonal immunoreactivity with SNAP25 or NF68kD at 30 min after MCA occlusion. Altered immunoreactivity following ischemia using SNAP25, MAP5, and NF68kD provides further evidence for the progressive breakdown of the axonal cytoskeleton following an ischemic insult. NF68kD and MAP5 appear to be sensitive markers of the structural disruption of the cytoskeleton, which precedes the subsequent accumulation of SNAP25 within the damaged axons. Axonal cytoskeletal breakdown and disruption of fast axonal transport, which are well-recognized features of traumatic brain injury, are also sequalae of an ischemic insult

Canine Obesity: Do Owners See What You See?

No abstract available

Owner Ability to Assess the Body Condition of their Feline Friends

No abstract available

Megaoesophagus secondary to acquired myasthenia gravis

Fifteen dogs with confirmed adult onset idiopathic megaoesophagus, in which no generalised muscle weakness was observed, were tested for the presence of acetylcholine receptor antibodies. Of these, six were found to have values greater than 0–6 nmol/litre, previously determined to be diagnostic of acquired myasthenia gravis. The mean serum titre value for these dogs was 5–59 nmol/litre (range 0–78 to 8–72 nmol/litre). It appears that a significant proportion of dogs presenting with megaoesophagus have myasthenia gravis and, if a prompt diagnosis and appropriate treatment can be instituted, clinical signs may improve