54 research outputs found
CO J=2-1 line emission in cluster galaxies at z~1: fueling star formation in dense environments
We present observations of CO J=2-1 line emission in infrared-luminous
cluster galaxies at z~1 using the IRAM Plateau de Bure Interferometer. Our two
primary targets are optically faint, dust-obscured galaxies (DOGs) found to lie
within 2 Mpc of the centers of two massive (>10^14 Msun) galaxy clusters. CO
line emission is not detected in either DOG. We calculate 3-sigma upper limits
to the CO J=2-1 line luminosities, L'_CO < 6.08x10^9 and < 6.63x10^9 K km/s
pc^2. Assuming a CO-to-H_2 conversion factor derived for ultraluminous infrared
galaxies in the local Universe, this translates to limits on the cold molecular
gas mass of M_H_2 < 4.86x10^9 Msun and M_H_2 < 5.30x10^9 Msun. Both DOGs
exhibit mid-infrared continuum emission that follows a power-law, suggesting
that an AGN contributes to the dust heating. As such, estimates of the star
formation efficiencies in these DOGs are uncertain. A third cluster member with
an infrared luminosity, L_IR < 7.4x10^11 Lsun, is serendipitously detected in
CO J=2-1 line emission in the field of one of the DOGs located roughly two
virial radii away from the cluster center. The optical spectrum of this object
suggests that it is likely an obscured AGN, and the measured CO line luminosity
is L'_CO = (1.94 +/- 0.35)x10^10 K km/s pc^2, which leads to an estimated cold
molecular gas mass M_H_2 = (1.55+/-0.28)x10^10 Msun. A significant reservoir of
molecular gas in a z~1 galaxy located away from the cluster center demonstrates
that the fuel can exist to drive an increase in star-formation and AGN activity
at the outskirts of high-redshift clusters.Comment: 22 pages, 4 figures; accepted for publication in Ap
Zebrafish prox1b Mutants Develop a Lymphatic Vasculature, and prox1b Does Not Specifically Mark Lymphatic Endothelial Cells
Background: The expression of the Prospero homeodomain transcription factor (Prox1) in a subset of cardinal venous cells specifies the lymphatic lineage in mice. Prox1 is also indispensible for the maintenance of lymphatic cell fate, and is therefore considered a master control gene for lymphangiogenesis in mammals. In zebrafish, there are two prox1 paralogues, the previously described prox1 (also known as prox1a) and the newly identified prox1b. Principal Findings: To investigate the role of the prox1b gene in zebrafish lymphangiogenesis, we knocked-down prox1b and found that depletion of prox1b mRNA did not cause lymphatic defects. We also generated two different prox1b mutant alleles, and maternal-zygotic homozygous mutant embryos were viable and did not show any lymphatic defects. Furthermore, the expression of prox1b was not restricted to lymphatic vessels during zebrafish development. Conclusion: We conclude that Prox1b activity is not essential for embryonic lymphatic development in zebrafish
Economic Returns to Investment in AIDS Treatment in Low and Middle Income Countries
Since the early 2000s, aid organizations and developing country governments have invested heavily in AIDS treatment. By 2010, more than five million people began receiving antiretroviral therapy (ART) – yet each year, 2.7 million people are becoming newly infected and another two million are dying without ever having received treatment. As the need for treatment grows without commensurate increase in the amount of available resources, it is critical to assess the health and economic gains being realized from increasingly large investments in ART. This study estimates total program costs and compares them with selected economic benefits of ART, for the current cohort of patients whose treatment is cofinanced by the Global Fund to Fight AIDS, Tuberculosis and Malaria. At end 2011, 3.5 million patients in low and middle income countries will be receiving ART through treatment programs cofinanced by the Global Fund. Using 2009 ART prices and program costs, we estimate that the discounted resource needs required for maintaining this cohort are 12 to $34 billion through increased labor productivity, averted orphan care, and deferred medical treatment for opportunistic infections and end-of-life care. Under alternative assumptions regarding the labor productivity effects of HIV infection, AIDS disease, and ART, the monetary benefits range from 81 percent to 287 percent of program costs over the same period. These results suggest that, in addition to the large health gains generated, the economic benefits of treatment will substantially offset, and likely exceed, program costs within 10 years of investment
Togo: Thorny transition and misguided aid at the roots of economic misery
The parliamentary elections of October 2007, the first free Togolese elections since decades, were meant to correct at least partially the rigged presidential elections of 2005. Western donors considered it as a litmus test of despotic African regimes’ propensity to change towards democratization and economic prosperity. They took Togo as model to test their approach of political conditionality of aid, which had been emphasised also as corner stone of the joint EU-Africa strategy. Empirical findings on the linkage between democratization and economic performance are challenged in this paper because of its basic data deficiencies. It is open to question, whether Togo’s expected economic consolidation and growth will be due to democratization of its institutions or to the improved external environment, notably the growing competition between global players for African natural resources
Geographic and temporal trends in the molecular epidemiology and genetic mechanisms of transmitted HIV-1 drug resistance:an individual-patient- and sequence-level meta-analysis
Regional and subtype-specific mutational patterns of HIV-1 transmitted drug resistance (TDR) are essential for informing first-line antiretroviral (ARV) therapy guidelines and designing diagnostic assays for use in regions where standard genotypic resistance testing is not affordable. We sought to understand the molecular epidemiology of TDR and to identify the HIV-1 drug-resistance mutations responsible for TDR in different regions and virus subtypes.status: publishe
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