Distant star-forming galaxies show a correlation between their star formation rates (SFR) and stellar masses, and this has deep implications for galaxy formation. Here, we present a study on the evolution of the slope and scatter of the SFR-stellar mass relation for galaxies at 3.5 ≤ z ≤ 6.5 using multiwavelength photometry in GOODS-S from the Cosmic Assembly Near-infrared Deep Extragalactic Legacy Survey (CANDELS) and Spitzer Extended Deep Survey. We describe an updated, Bayesian spectral-energy distribution fitting method that incorporates effects of nebular line emission, star formation histories that are constant or rising with time, and different dust attenuation prescriptions (starburst and Small Magellanic Cloud). From z=6.5 to z=3.5 star-forming galaxies in CANDELS follow a nearly unevolving correlation between stellar mass and SFR that follows SFR ∼ M a with a= 0.54 ± 0.16 at z ∼ 6 and 0.70 ± 0.21 at z ∼ 4. This evolution requires a star formation history that increases with decreasing redshift (on average, the SFRs of individual galaxies rise with time). The observed scatter in the SFR-stellar mass relation is tight, σ(log SFR/M yr −1 ) < 0.3 − 0.4 dex, for galaxies with log M /M > 9 dex. Assuming that the SFR is tied to the net gas inflow rate (SFR ∼Ṁ gas ), then the scatter in the gas inflow rate is also smaller than 0.3−0.4 dex for star-forming galaxies in these stellar mass and redshift ranges, at least when averaged over the timescale of star formation. We further show that the implied star formation history of objects selected on the basis of their co-moving number densities is consistent with the evolution in the SFR-stellar mass relation.

The mechanisms responsible for the virulence of the highly pathogenic avian influenza (HPAI) and of the 1918 pandemic influenza virus in humans remain poorly understood. To identify crucial components of the early host response during these infections by using both conventional and functional genomics tools, we studied 34 cynomolgus macaques (Macaca fascicularis) to compare a 2004 human H5N1 Vietnam isolate with 2 reassortant viruses possessing the 1918 hemagglutinin (HA) and neuraminidase (NA) surface proteins, known conveyors of virulence. One of the reassortants also contained the 1918 nonstructural (NS1) protein, an inhibitor of the host interferon response. Among these viruses, HPAI H5N1 was the most virulent. Within 24 h, the H5N1 virus produced severe bronchiolar and alveolar lesions. Notably, the H5N1 virus targeted type II pneumocytes throughout the 7-day infection, and induced the most dramatic and sustained expression of type I interferons and inflammatory and innate immune genes, as measured by genomic and protein assays. The H5N1 infection also resulted in prolonged margination of circulating T lymphocytes and notable apoptosis of activated dendritic cells in the lungs and draining lymph nodes early during infection. While both 1918 reassortant viruses also were highly pathogenic, the H5N1 virus was exceptional for the extent of tissue damage, cytokinemia, and interference with immune regulatory mechanisms, which may help explain the extreme virulence of HPAI viruses in humans.1918 pandemic ͉ functional genomics ͉ H5N1

The observed deficit of strongly Lyman-α emitting galaxies at z > 6.5 is attributed to either increasing neutral hydrogen in the intergalactic medium (IGM) and/or to the evolving galaxy properties. To investigate this, we have performed very deep near-IR spectroscopy of z 7 galaxies using MOSFIRE on the Keck-I Telescope. We measure the Lyman-α fraction at z ∼ 8 using two methods. First, we derived N Lyα /N tot directly using extensive simulations to correct for incompleteness. Second, we used a Bayesian formalism (introduced by Treu et al. 2012) that compares the z > 7 galaxy spectra to models of the Lyman-α equivalent width (W Lyα ) distribution at z ∼ 6. We explored two simple evolutionary scenarios: pure number evolution where Lyman-α is blocked in some fraction of galaxies (perhaps due to the IGM being opaque along only some fraction of sightlines) and uniform dimming evolution where Lyman-α is attenuated in all galaxies by a constant factor (perhaps owing to processes from galaxy evolution or a slowly increasing IGM opacity). The Bayesian formalism places stronger constraints compared with the direct method. Combining our data with that in the literature we find that at z ∼ 8 the Lyman-α fraction has dropped by a factor >3 (84% confidence interval) using both the dimming and number evolution scenarios, compared to the z ∼ 6 values. Furthermore, we find a tentative "positive" Bayesian evidence favoring the number evolution scenario over dimming evolution, extending trends observed at z 7 to higher redshift. Comparison of our results with theoretical models imply the IGM volume averaged neutral hydrogen fraction 0.3 suggesting that we are likely witnessing reionization in progress at z ∼ 8.

Dust attenuation affects nearly all observational aspects of galaxy evolution, yet very little is known about the form of the dust-attenuation law in the distant Universe. Here, we model the spectral energy distributions (SEDs) of galaxies at z ∼ 1.5-3 from CANDELS with rest-frame UV to near-IR imaging under different assumptions about the dust law, and compare the amount of inferred attenuated light with the observed infrared (IR) luminosities. Some individual galaxies show strong Bayesian evidence in preference of one dust law over another, and this preference agrees with their observed location on the plane of infrared excess (IRX, L TIR /L UV ) and UV slope (β). We generalize the shape of the dust law with an empirical model, Calzetti et al. (2000), and show that there exists a correlation between the color excess E(B − V ) and tilt δ with δ = (0.62 ± 0.05) log(E(B − V ))+(0.26 ± 0.02). Galaxies with high color excess have a shallower, starburst-like law, and those with low color excess have a steeper, SMC-like law. Surprisingly, the galaxies in our sample show no correlation between the shape of the dust law and stellar mass, star-formation rate, or β. The change in the dust law with color excess is consistent with a model where attenuation is caused by by scattering, a mixed star-dust geometry, and/or trends with stellar population age, metallicity, and dust grain size. This rest-frame UV-to-near-IR method shows potential to constrain the dust law at even higher (z > 3) redshifts.

Advanced prostate cancer can progress to systemic metastatic tumors, which are generally androgen insensitive and ultimately lethal. Here, we report a comprehensive genomic survey for somatic events in systemic metastatic prostate tumors using both high-resolution copy number analysis and targeted mutational survey of 3508 exons from 577 cancerrelated genes using next generation sequencing. Focal homozygous deletions were detected at 8p22, 10q23.31, 13q13.1, 13q14.11, and 13q14.12. Key genes mapping within these deleted regions include PTEN, BRCA2, C13ORF15, and SIAH3. Focal high-level amplifications were detected at 5p13.2-p12, 14q21.1, 7q22.1, and Xq12. Key amplified genes mapping within these regions include SKP2, FOXA1, and AR. Furthermore, targeted mutational analysis of normal-tumor pairs has identified somatic mutations in genes known to be associated with prostate cancer including AR and TP53, but has also revealed novel somatic point mutations in genes including MTOR, BRCA2, ARHGEF12, and CHD5. Finally, in one patient where multiple independent metastatic tumors were available, we show common and divergent somatic alterations that occur at both the copy number and point mutation level, supporting a model for a common clonal progenitor with metastatic tumor-specific divergence. Our study represents a deep genomic analysis of advanced metastatic prostate tumors and has revealed candidate somatic alterations, possibly contributing to lethal prostate cancer.