The Structure of Molecular Clouds: II - Column Density and Mass Distributions

The formation of stars is inextricably linked to the structure of their parental molecular clouds. Here we take a number of nearby giant molecular clouds (GMCs) and analyse their column density and mass distributions. This investigation is based on four new all-sky median colour excess extinction maps determined from 2MASS. The four maps span a range of spatial resolution of a factor of eight. This allows us to determine cloud properties at a common spatial scale of 0.1pc, as well as to study the scale dependence of the cloud properties. We find that the low column density and turbulence dominated part of the clouds can be well fit by a log-normal distribution. However, above a universal extinction threshold of 6.0 \pm 1.5mag A_V there is excess material compared to the log-normal distribution in all investigated clouds. This material represents the part of the cloud that is currently involved in star formation, and thus dominated by gravity. Its contribution to the total mass of the clouds ranges over two orders of magnitude from 0.1 to 10%. This implies that our clouds sample various stages in the evolution of GMCs. Furthermore, we find that the column density and mass distributions are extremely similar between clouds if we analyse only the high extinction material. On the other hand, there are significant differences between the distributions if only the low extinction, turbulence dominated regions are considered. This shows that the turbulent properties differ between clouds depending on their environment. However, no significant influence on the predominant mode of star formation (clustered or isolated) could be found. Furthermore, the fraction of the cloud actively involved in star formation is only governed by gravity, with the column density and mass distributions not significantly altered by local feedback processes.Comment: 31 pages, 4 tables, 99 figures, accepted for publication by MNRAS, a version with higher resolution figures can be found at http://astro.kent.ac.uk/extinction

Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption and glucose-dependent incretin secretion.

To clarify the physiological role of Na(+)-D-glucose cotransporter SGLT1 in small intestine and kidney, Sglt1(-/-) mice were generated and characterized phenotypically. After gavage of d-glucose, small intestinal glucose absorption across the brush-border membrane (BBM) via SGLT1 and GLUT2 were analyzed. Glucose-induced secretion of insulinotropic hormone (GIP) and glucagon-like peptide 1 (GLP-1) in wild-type and Sglt1(-/-) mice were compared. The impact of SGLT1 on renal glucose handling was investigated by micropuncture studies. It was observed that Sglt1(-/-) mice developed a glucose-galactose malabsorption syndrome but thrive normally when fed a glucose-galactose-free diet. In wild-type mice, passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1, independent the glucose load. High glucose concentrations increased the amounts of SGLT1 and GLUT2 in the BBM, and SGLT1 was required for upregulation of GLUT2. SGLT1 was located in luminal membranes of cells immunopositive for GIP and GLP-1, and Sglt1(-/-) mice exhibited reduced glucose-triggered GIP and GLP-1 levels. In the kidney, SGLT1 reabsorbed ∼3% of the filtered glucose under normoglycemic conditions. The data indicate that SGLT1 is 1) pivotal for intestinal mass absorption of d-glucose, 2) triggers the glucose-induced secretion of GIP and GLP-1, and 3) triggers the upregulation of GLUT2

Changing structures in galactic star clusters

We investigate the structures of embedded and open clusters using statistical methods, in particular the combined parameter \Q, which permits to quantify the cluster structure. Star clusters build up from several subclusters evolving from a structured to a more centrally concentrated stage. The evolution is not only a function of time, but also of the mass of the objects. Massive stars are usually centrally concentrated, while lower-mass stars are more widespread, reflecting the effect of mass segregation. Using this method we find that in IC 348 and the Orion Nebula Cluster the spatial distribution of brown dwarfs does not follow the central clustering of stars, giving important clues to their formation mechanism by supporting the ejected embryo scenario

Evolution of Class 0 protostars; model versus observations

The catalogue of class 0 protostars from an earlier paper by Froebrich et al., was used to quantitatively review how well current evolutionary models of protostars match the observational evidence. The first time usage of such a technique allowed us to discover that the environment influences the observational properties of Class 0 protostars. It furthermore allowed us to constrain several previously arbitrary parameters in the evolutionary models (Impact Factor: 5.325

Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption and glucose-dependent incretin secretion.

To clarify the physiological role of Na(+)-D-glucose cotransporter SGLT1 in small intestine and kidney, Sglt1(-/-) mice were generated and characterized phenotypically. After gavage of d-glucose, small intestinal glucose absorption across the brush-border membrane (BBM) via SGLT1 and GLUT2 were analyzed. Glucose-induced secretion of insulinotropic hormone (GIP) and glucagon-like peptide 1 (GLP-1) in wild-type and Sglt1(-/-) mice were compared. The impact of SGLT1 on renal glucose handling was investigated by micropuncture studies. It was observed that Sglt1(-/-) mice developed a glucose-galactose malabsorption syndrome but thrive normally when fed a glucose-galactose-free diet. In wild-type mice, passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1, independent the glucose load. High glucose concentrations increased the amounts of SGLT1 and GLUT2 in the BBM, and SGLT1 was required for upregulation of GLUT2. SGLT1 was located in luminal membranes of cells immunopositive for GIP and GLP-1, and Sglt1(-/-) mice exhibited reduced glucose-triggered GIP and GLP-1 levels. In the kidney, SGLT1 reabsorbed ∼3% of the filtered glucose under normoglycemic conditions. The data indicate that SGLT1 is 1) pivotal for intestinal mass absorption of d-glucose, 2) triggers the glucose-induced secretion of GIP and GLP-1, and 3) triggers the upregulation of GLUT2