A Simple Model for the Absorption of Starlight by Dust in Galaxies

We present a new model to compute the effects of dust on the integrated spectral properties of galaxies, based on an idealized prescription of the main features of the interstellar medium (ISM). The model includes the ionization of HII regions in the interiors of the dense clouds in which stars form and the influence of the finite lifetime of these clouds on the absorption of radiation. We compute the production of emission lines and the absorption of continuum radiation in the HII regions and the subsequent transfer of line and continuum radiation in the surrounding HI regions and the ambient ISM. This enables us to interpret simultaneously all the observations of a homogeneous sample of nearby UV-selected starburst galaxies, including the ratio of far-IR to UV luminosities, the ratio of Halpha to Hbeta luminosities, the Halpha equivalent width, and the UV spectral slope. We show that the finite lifetime of stellar birth clouds is a key ingredient to resolve an apparent discrepancy between the attenuation of line and continuum photons in starburst galaxies. In addition, we find that an effective absorption curve proportional to lambda^-0.7 reproduces the observed relation between the ratio of far-IR to UV luminosities and the UV spectral slope. We interpret this relation most simply as a sequence in the overall dust content of the galaxies. The shallow wavelength dependence of the effective absorption curve is compatible with the steepness of known extinction curves if the dust has a patchy distribution. In particular, we find that a random distribution of discrete clouds with optical depths similar to those in the Milky Way provides a consistent interpretation of all the observations. Our model for absorption can be incorporated easily into any population synthesis model. (abridged)Comment: To appear in the 2000 July 20 issue of the Astrophysical Journal; 19 pages with 13 embedded PS figures (emulateapj5.sty

AS160 Associates with the Na+,K+-ATPase and Mediates the Adenosine Monophosphate-stimulated Protein Kinase-dependent Regulation of Sodium Pump Surface Expression

The sodium pump interacts with AS160, a protein that regulates the trafficking of the GLUT4 glucose transporter. This interaction drives the internalization of the sodium pump from the cell surface, and this process is in turn controlled by the energy-sensing kinase adenosine monophosphate-stimulated protein kinase

Renal Cystic Disease Proteins Play Critical Roles in the Organization of the Olfactory Epithelium

It was reported that some proteins known to cause renal cystic disease (NPHP6; BBS1, and BBS4) also localize to the olfactory epithelium (OE), and that mutations in these proteins can cause anosmia in addition to renal cystic disease. We demonstrate here that a number of other proteins associated with renal cystic diseases – polycystin 1 and 2 (PC1, PC2), and Meckel-Gruber syndrome 1 and 3 (MKS1, MKS3) – localize to the murine OE. PC1, PC2, MKS1 and MKS3 are all detected in the OE by RT-PCR. We find that MKS3 localizes specifically to dendritic knobs of olfactory sensory neurons (OSNs), while PC1 localizes to both dendritic knobs and cilia of mature OSNs. In mice carrying mutations in MKS1, the expression of the olfactory adenylate cyclase (AC3) is substantially reduced. Moreover, in rats with renal cystic disease caused by a mutation in MKS3, the laminar organization of the OE is perturbed and there is a reduced expression of components of the odor transduction cascade (Golf, AC3) and α-acetylated tubulin. Furthermore, we show with electron microscopy that cilia in MKS3 mutant animals do not manifest the proper microtubule architecture. Both MKS1 and MKS3 mutant animals show no obvious alterations in odor receptor expression. These data show that multiple renal cystic proteins localize to the OE, where we speculate that they work together to regulate aspects of the development, maintenance or physiological activities of cilia

Self-interest And Public Interest: The Motivations Of Political Actors

Self-Interest and Public Interest in Western Politics showed that the public, politicians, and bureaucrats are often public spirited. But this does not invalidate public-choice theory. Public-choice theory is an ideal type, not a claim that self-interest explains all political behavior. Instead, public-choice theory is useful in creating rules and institutions that guard against the worst case, which would be universal self-interestedness in politics. In contrast, the public-interest hypothesis is neither a comprehensive explanation of political behavior nor a sound basis for institutional design

Chloride channels regulate differentiation and barrier functions of the mammalian airway.

The conducting airway forms a protective mucosal barrier and is the primary target of airway disorders. The molecular events required for the formation and function of the airway mucosal barrier, as well as the mechanisms by which barrier dysfunction leads to early onset airway diseases, remain unclear. In this study, we systematically characterized the developmental landscape of the mouse airway using single-cell RNA sequencing and identified remarkably conserved cellular programs operating during human fetal development. We demonstrated that in mouse, genetic inactivation of chloride channel Ano1/Tmem16a compromises airway barrier function, results in early signs of inflammation, and alters the airway cellular landscape by depleting epithelial progenitors. Mouse Ano1-/-mutants exhibited mucus obstruction and abnormal mucociliary clearance that resemble the airway defects associated with cystic fibrosis. The data reveal critical and non-redundant roles for Ano1 in organogenesis, and show that chloride channels are essential for mammalian airway formation and function

Farnesylation of YDJ1p is required for function at elevated growth temperatures in Saccharomyces cerevisiae

The Saccharomyces cerevisiae YDJ1 protein (YDJ1p) contains a C-terminal "CaaX box" motif common to proteins that are modified by prenylation. In the present study we show that YDJ1p is a specific substrate for both yeast and mammalian protein farnesyltransferase enzymes in vitro. A mutant form of YDJ1p, in which the conserved cysteine of the CaaX box is mutated to a serine (ydj1-S406p), cannot be farnesylated in vitro. After expression in S. cerevisiae, ydj1-S406p displays a reduced electrophoretic mobility and an increased cytosolic localization in subcellular fractionation experiments when compared to wild type YDJ1p. Expression of ydj1-S406 in cells lacking YDJ1 results in a temperature-sensitive growth phenotype in S. cerevisiae. These data indicate that farnesylation of YDJ1p is required for its function at elevated temperature