28 research outputs found
Are There Age Spreads in Star Forming Regions?
A luminosity spread at a given effective temperature is ubiquitously seen in
the Hertzsprung-Russell (HR) diagrams of young star forming regions and often
interpreted in terms of a prolonged period (>=10 Myr) of star formation. I
review the evidence that the observed luminosity spreads are genuine and not
caused by astrophysical sources of scatter. I then address whether the
luminosity spreads necessarily imply large age spreads, by comparing HR diagram
ages with ages from independent clocks such as stellar rotation rate, the
presence of circumstellar material and lithium depletion. I argue that whilst
there probably is a true luminosity dispersion, there is little evidence to
support age spreads larger than a few Myr. This paradox could be resolved by
brief periods of rapid accretion during the class I pre main-sequence phase.Comment: To appear in the proceedings of JENAM10: Star Clusters in the Era of
Large Surveys, 8 page
The stellar and sub-stellar IMF of simple and composite populations
The current knowledge on the stellar IMF is documented. It appears to become
top-heavy when the star-formation rate density surpasses about 0.1Msun/(yr
pc^3) on a pc scale and it may become increasingly bottom-heavy with increasing
metallicity and in increasingly massive early-type galaxies. It declines quite
steeply below about 0.07Msun with brown dwarfs (BDs) and very low mass stars
having their own IMF. The most massive star of mass mmax formed in an embedded
cluster with stellar mass Mecl correlates strongly with Mecl being a result of
gravitation-driven but resource-limited growth and fragmentation induced
starvation. There is no convincing evidence whatsoever that massive stars do
form in isolation. Various methods of discretising a stellar population are
introduced: optimal sampling leads to a mass distribution that perfectly
represents the exact form of the desired IMF and the mmax-to-Mecl relation,
while random sampling results in statistical variations of the shape of the
IMF. The observed mmax-to-Mecl correlation and the small spread of IMF
power-law indices together suggest that optimally sampling the IMF may be the
more realistic description of star formation than random sampling from a
universal IMF with a constant upper mass limit. Composite populations on galaxy
scales, which are formed from many pc scale star formation events, need to be
described by the integrated galactic IMF. This IGIMF varies systematically from
top-light to top-heavy in dependence of galaxy type and star formation rate,
with dramatic implications for theories of galaxy formation and evolution.Comment: 167 pages, 37 figures, 3 tables, published in Stellar Systems and
Galactic Structure, Vol.5, Springer. This revised version is consistent with
the published version and includes additional references and minor additions
to the text as well as a recomputed Table 1. ISBN 978-90-481-8817-
Multiple populations in globular clusters. Lessons learned from the Milky Way globular clusters
Recent progress in studies of globular clusters has shown that they are not
simple stellar populations, being rather made of multiple generations. Evidence
stems both from photometry and spectroscopy. A new paradigm is then arising for
the formation of massive star clusters, which includes several episodes of star
formation. While this provides an explanation for several features of globular
clusters, including the second parameter problem, it also opens new
perspectives about the relation between globular clusters and the halo of our
Galaxy, and by extension of all populations with a high specific frequency of
globular clusters, such as, e.g., giant elliptical galaxies. We review progress
in this area, focusing on the most recent studies. Several points remain to be
properly understood, in particular those concerning the nature of the polluters
producing the abundance pattern in the clusters and the typical timescale, the
range of cluster masses where this phenomenon is active, and the relation
between globular clusters and other satellites of our Galaxy.Comment: In press (The Astronomy and Astrophysics Review
Differential modulation of diet-induced obesity and adipocyte functionality by human apolipoprotein E3 and E4 in mice
OBJECTIVE: Apolipoprotein E (apoE), a key protein in lipid metabolism, is highly expressed in adipose tissues. Studies have shown that human APOE*4 is associated with a lower body mass index but with a greater risk of coronary heart disease compared with other APOE alleles. To define the isoform-specific role of apoE in regulating the expandability and functionality of adipose tissues, we investigated the effects of diet-induced obesity in mice whose endogenous Apoe gene has been replaced by either the human APOE*3 or APOE*4 allele. RESULTS: After 8 weeks on a Western-type high-fat diet, male APOE4 mice displayed impaired tolerance to glucose and fat overload compared with APOE3 mice. Subcutaneous fat tissues in APOE4 and APOE3 mice after high fat feeding were not different. In contrast, although epididymal fat tissues in APOE4 mice gained 30% less weight during the high fat feeding than in APOE3 mice, they showed impaired insulin-stimulated glucose uptake ex vivo. Epididymal APOE4 adipocytes were larger in size than APOE3 adipocytes, and expressed reduced levels of mRNA for peroxisome proliferator-activated receptor Îł2 and adiponectin, important markers of adipocyte functionality. Adenoviral expression of apoE3 in apoE-null culture adipocytes induced adiponectin mRNA in a dose-dependent manner, but the induction was significantly blunted in cells overexpressing apoE4. However, in contrast to the apoE3-expressing cells, Glut1, but not Glut4, expression levels were positively correlated with increased apoE4 mRNA, suggesting that apoE4 expression in adipocyte interferes in insulin-sensing pathways. CONCLUSION: Dysfunctional epididymal adipose tissues contribute to the accelerated impairment of glucose tolerance in APOE4 mice fed a Western-type diet. Our results underscore the importance of functionality of individual fat depots rather than total fat mass as a determinant for metabolic disturbance during diet-induced obesity