8 research outputs found
On the Rapid Collapse and Evolution of Molecular Clouds
Stars generally form faster than the ambipolar diffusion time, suggesting
that several processes short circuit the delay and promote a rapid collapse.
These processes are considered here, including turbulence compression in the
outer parts of giant molecular cloud (GMC) cores and GMC envelopes, GMC core
formation in an initially supercritical state, and compression-induced
triggering in dispersing GMC envelopes. The classical issues related to star
formation timescales are addressed: high molecular fractions, low efficiencies,
long consumption times for CO and HCN, rapid GMC core disruption and the lack
of a stable core, long absolute but short relative timescales with accelerated
star formation, and the slow motions of protostars. We consider stimuli to
collapse from changes in the density dependence of the ionization fraction, the
cosmic ray ionization rate, and various dust properties at densities above
~10^5 cm^{-3}. We favor the standard model of subcritical GMC envelops and
suggest they would be long lived if not for disruption by rapid star formation
in GMC cores. The lifecycle of GMCs is illustrated by a spiral arm section in
the Hubble Heritage image of M51, showing GMC formation, star formation, GMC
disruption with lingering triggered star formation, and envelope dispersal.
There is no delay between spiral arm dustlanes and star formation; the
classical notion results from heavy extinction in the dust lane and triggered
star formation during cloud dispersal. Differences in the IMF for the different
modes of star formation are considered.Comment: 46 pages, 5 figures, scheduled for ApJ 668, October 20, 200
The continuum between GH deficiency and GH insensitivity in children
The continuum of growth hormone (GH)-IGF-I axis defects extends from severe to mild GH deficiency, through short stature disorders of undefined aetiology, to GH insensitivity disorders which can also be mild or severe. This group of defects comprises a spectrum of endocrine, biochemical, phenotypic and genetic abnormalities. The extreme cases are generally easily diagnosed because they conform to well-studied phenotypes with recognised biochemical features. The milder cases of both GH deficiency and GH insensitivity are less well defined and also overlap with the group of short stature conditions, labelled as idiopathic short stature (ISS). In this review the continuum model, which plots GH sensitivity against GH secretion, will be discussed. Defects causing GH deficiency and GH insensitivity will be described, together with the use of a diagnostic algorithm, designed to aid investigation and categorisation of these defects. The continuum will also be discussed in the context of growth-promoting endocrine therapy