A New Color-Magnitude Diagram for Palomar 11

We present new photometry for the Galactic thick disk globular cluster Palomar 11 extending well past the main sequence turn-off in the V and I bands. This photometry shows noticeable red giant and subgiant branches. The difference in magnitude between the red horizontal branch (red clump) and the subgiant branch is used to determine that Palomar 11 has an age of 10.4+/-0.5 Gyr. The red clump is used to derive a distance d_\sun=14.3+/-0.4 kpc, and a mean cluster reddening of E(V-I)=0.40+/-0.03. There is differential reddening across the cluster, of order \delta E(V-I)~0.07. The colour magnitude diagram of Palomar 11 is virtually identically to that of the thick disk globular cluster NGC 5927, implying that these two clusters have a similar age and metallicity. Palomar 11 has a slightly redder red giant branch than 47 Tuc, implying that Palomar 11 is 0.15 dex more metal-rich, or 1 Gyr older than 47 Tuc. Ca II triplet observations (Rutledge et al. 1997) favour the hypothesis that Palomar 11 is the same age as 47 Tuc, but slightly more metal-rich.Comment: to appear in AJ (19 pages, 4 B&W figures, 1 colour figure

Assisting Dislocated Workers: Dimensions, Needs and Tax Policy Options

The involvement of the federal government in retraining of dislocated workers raises the specter of rigidity, bureaucracy, paternalism, and cost. After examining the dimensions of the dislocated worker problem and the need for governmental involvement, this article examines the use of tax policy to enable workers to bridge the gap between old and new jobs and to thrive in an economy in transition. The policy making challenge can be succinctly stated: is it possible to use the federal income tax system to the advantage of society by creating tax incentives for a retraining program based on individual choice and limited government involvement

Array-based carbon black-polymer composite vapor detectors for detection of DNT in environments containing complex analyte mixtures

Thin films of carbon black-organic polymer composites have been deposited across two metallic leads, with sorption of vapors producing swelling-induced resistance changes of the detector films. To identify and classify vapors, arrays of such vapor sensing elements have been constructed in which each element of the array contains a different polymer as the insulating phase and a common conductor, carbon black, as the conducting phase. The differing gas-solid partition coefficients for the various polymers of the detector array produce a pattern of differential resistance changes that is used to classify vapors and vapor mixtures. The performance of this detector array system towards 2,4-dinitrotoluene, the predominant signature in the vapor phase above land mines, in the presence high concentrations of water or of acetone has been evaluated

Vapor Detection, Classification, and Quantification Performance Using Arrays of Conducting Polymer Composite Chemically Sensitive Resistors

We describe a method for generating a variety of chemically diverse, broadly responsive, low power vapor sensors. A key to our ability to fabricate chemically diverse sensing elements is the preparation of processable, air stable films of electrically conducting organic polymers. An array of such sensing elements produces a chemically reversible, diagnostic pattern of electrical resistance changes upon exposure to different odorants. Such conducting polymer elements are simply prepared and are readily modified chemically to respond to a broad range of analytes. In addition, these sensors yield a fairly rapid, low power, de electrical signal in response to the vapor of interest, and their signals are readily integrated with software or hardware-based neural networks for purposes of analyte identification. Principle component analysis has demonstrated that such sensors can identify and quantify different airborne organic solvents, and can yield information on the components of gas mixtures

Skimming the Lunar Surface for Science: The LADEE Mission

Presentation on LADEE final work including shipping, final test, launch, operations, impact. Includes preliminary (but published) science results

Evidence That Aberrant Protein Metabolism Contributes To Chemoresistance In Multiple Myeloma Cells

Multiple myeloma (MM) is an incurable B lymphocyte cancer. To date, a comparative analysis of global protein metabolism for the MM cell line CCL-155 (RPMI-8226) and the non-cancerous B lymphocyte cell line CCL-156 (RPMI-1788) has not been published. Here, we report that both global protein synthesis and degradation occur at a higher rate in MM cells and demonstrate that alkylating agents can reduce global protein degradation in both cell lines, but the effect is greater in CCL-156 cells. Treatment with melphalan plus the proteasome inhibitor MG132 reduced global protein degradation for MM cells to roughly 60% of that seen without drugs,, but the reduction was approximately three times greater for CCL-156 cells. This drug combination was growth inhibitory for both cell lines, but CCL-156 inhibition was 2-fold greater than that of the MM cell line. Additionally, treatment with melphalan plus the lysosomal inhibitor chloroquine did not affect growth of MM cells more than melphalan alone, whereas this combination drastically inhibited growth of CCL-156 cells despite protein degradation being maintained at 60% level for both cell lines. This suggests that a lysosomal function other than protein degradation is required for recovery from alkylation damage in CCL-156 cells. In general, CCL-156 cells were affected to a greater extent for both protein degradation and growth inhibition with most drug combinations tested. Statistical analysis of our data (P=0.066) provides evidence that aberrant proteasome-mediated protein degradation correlates with chemoresistance in MM cells, but that lysosome-mediated protein degradation does not

Mechanism of Lysine 48 Selectivity during Polyubiquitin Chain Formation by the Ube2R1/2 Ubiquitin-Conjugating Enzyme

Lysine selectivity is of critical importance during polyubiquitin chain formation because the identity of the lysine controls the biological outcome. Ubiquitins are covalently linked in polyubiquitin chains through one of seven lysine residues on its surface and the C terminus of adjacent protomers. Lys 48-linked polyubiquitin chains signal for protein degradation; however, the structural basis for Lys 48 selectivity remains largely unknown. The ubiquitin-conjugating enzyme Ube2R1/2 has exquisite specificity for Lys 48, and computational docking of Ube2R1/2 and ubiquitin predicts that Lys 48 is guided to the active site through a key electrostatic interaction between Arg 54 on ubiquitin and Asp 143 on Ube2R1/2. The validity of this interaction was confirmed through biochemical experiments. Since structural examples involving Arg 54 in protein-ubiquitin complexes are exceedingly rare, these results provide additional insight into how ubiquitin-protein complexes can be stabilized. We discuss how these findings relate to how other ubiquitin-conjugating enzymes direct the lysine specificity of polyubiquitin chains

The p53R172H Mutant Does Not Enhance Hepatocellular Carcinoma Development and Progression

Hepatocellular carcinoma is a highly deadly malignancy, accounting for approximately 800,000 deaths worldwide every year. Mutation of the p53 tumor suppressor gene is a common genetic change in HCC, present in 30% of cases. p53R175H (corresponding to p53R172H in mice) is a hotspot for mutation that demonstrates prometastatic gain-of-function in other cancer models. Since the frequency of p53 mutation increases with tumor grade in HCC, we hypothesized that p53R172H is a gain-of-function mutation in HCC that contributes to a decrease in tumor-free survival and an increase in metastasis. In an HCC mouse model, we found that p53R172H/flox mice do not have decreased survival, increased tumor incidence, or increased metastasis, relative to p53flox/flox littermates. Analysis of cell lines derived from both genotypes indicated that there are no differences in anchorage-independent growth and cell migration. However, shRNA-mediated knockdown of mutant p53 in p53R172H-expressing HCC cell lines resulted in decreased cell migration and anchorage-independent growth. Thus, although p53 mutant-expressing cells and tumors do not have enhanced properties relative to their p53 null counterparts, p53R172H-expressing HCC cells depend on this mutant for their transformation. p53 mutants have been previously shown to bind and inhibit the p53 family proteins p63 and p73. Interestingly, we find that the levels of p63 and p73 target genes are similar in p53 mutant and p53 null HCC cells. These data suggest that pathways regulated by these p53 family members are similarly impacted by p53R172H in mutant expressing cells, and by alternate mechanisms in p53 null cells, resulting in equivalent phenotypes. Consistent with this, we find that p53 null HCC cell lines display lower levels of the TA isoforms of p63 and p73 and higher levels of DeltaNp63. Taken together these data point to the importance of p63 and p73 in constraining HCC progression