Stellar properties of z ~ 1 Lyman-break galaxies from ACS slitless grism spectra

Lyman-break galaxies are now regularly found in the high redshift Universe by searching for the break in the galaxy spectrum caused by the Lyman-limit redshifted into the optical or even near-IR. At lower redshift, this break is covered by the GALEX UV channels and small samples of z ~ 1 LBGs have been presented in the literature. Here we give results from fitting the spectral energy distributions of a small sub-set of low redshift LBGs and demonstrate the advantage of including photometric points derived from HST ACS slitless grism observations. The results show these galaxies to have very young, star forming populations, while still being massive and dusty. LBGs at low and high redshift show remarkable similarities in their properties, indicating that the LBG selection method picks similar galaxies throughout the Universe.Comment: 7 pages, 3 figures, 2 tables, accepted in A&

The star formation history of mass-selected galaxies in the COSMOS field

We explore the evolution of the specific star formation rate (SSFR) for 3.6um-selected galaxies of different M_* in the COSMOS field. The average SFR for sub-sets of these galaxies is estimated with stacked 1.4GHz radio continuum emission. We separately consider the total sample and a subset of galaxies (SF) that shows evidence for substantive recent star formation in the rest-frame optical SED. At 0.2<z<3 both populations show a strong and M_*-independent decrease in their SSFR towards z=0.2, best described by a power- law (1+z)^n, where n~4.3 for all galaxies and n~3.5 for SF sources. The decrease appears to have started at z>2, at least above 4x10^10M_Sun where our conclusions are most robust. We find a tight correlation with power-law dependence, SSFR (M_*)^beta, between SSFR and M_* at all z. It tends to flatten below ~10^10M_Sun if quiescent galaxies are included; if they are excluded a shallow index beta_SFG -0.4 fits the correlation. On average, higher M_* objects always have lower SSFRs, also among SF galaxies. At z>1.5 there is tentative evidence for an upper SSFR-limit that an average galaxy cannot exceed. It is suggested by a flattening of the SSFR-M_* relation (also for SF sources), but affects massive (>10^10M_Sun) galaxies only at the highest z. Below z=1.5 there thus is no direct evidence that galaxies of higher M_* experience a more rapid waning of their SSFR than lower M_* SF systems. In this sense, the data rule out any strong 'downsizing'. We combine our results with recent measurements of the galaxy (stellar) mass function in order to determine the characteristic mass of a SF galaxy (M_*=10^(10.6\pm0.4)M_Sun). In this sense, too, there is no 'downsizing'. Our analysis constitutes the most extensive SFR density determination with a single technique to z=3. Recent Herschel results are consistent with our results, but rely on far smaller samples.Comment: 37 pages, 14 figures, 7 tables; accepted for publication in the Astrophysical Journal; High resolution versions of all figures available at www.mpia-hd.mpg.de/homes/karim/research.htm

The Hyper Suprime-Cam SSP Survey: Overview and Survey Design

Hyper Suprime-Cam (HSC) is a wide-field imaging camera on the prime focus of the 8.2m Subaru telescope on the summit of Maunakea in Hawaii. A team of scientists from Japan, Taiwan and Princeton University is using HSC to carry out a 300-night multi-band imaging survey of the high-latitude sky. The survey includes three layers: the Wide layer will cover 1400 deg$^2$ in five broad bands ($grizy$), with a $5\,\sigma$ point-source depth of $r \approx 26$. The Deep layer covers a total of 26~deg$^2$ in four fields, going roughly a magnitude fainter, while the UltraDeep layer goes almost a magnitude fainter still in two pointings of HSC (a total of 3.5 deg$^2$). Here we describe the instrument, the science goals of the survey, and the survey strategy and data processing. This paper serves as an introduction to a special issue of the Publications of the Astronomical Society of Japan, which includes a large number of technical and scientific papers describing results from the early phases of this survey.Comment: 14 pages, 7 figures, 5 tables. Corrected for a typo in the coordinates of HSC-Wide spring equatorial field in Table

Detecting violations of temporal regularities in waking and sleeping two-month-old infants

Correctly processing rapid sequences of sounds is essential for developmental milestones, such as language acquisition. We investigated the sensitivity of two-month-old infants to violations of a temporal regularity, by recording event-related brain potentials (ERP) in an auditory oddball paradigm from 36 waking and 40 sleeping infants. Standard tones were presented at a regular 300 ms inter-stimulus interval (ISI). One deviant, otherwise identical to the standard, was preceded by a 100 ms ISI. Two other deviants, presented with the standard ISI, differed from the standard in their spectral makeup. We found significant differences between ERP responses elicited by the standard and each of the deviant sounds. The results suggest that the ability to extract both temporal and spectral regularities from a sound sequence is already functional within the first few months of life. The scalp distribution of all three deviant-stimulus responses was influenced by the infants‟ state of alertness

Obesity resistant mechanisms in the Lean polygenic mouse model as indicated by liver transcriptome and expression of selected genes in skeletal muscle

<p>Abstract</p> <p>Background</p> <p>Divergently selected Lean and Fat mouse lines represent unique models for a polygenic form of resistance and susceptibility to obesity development. Previous research on these lines focused mainly on obesity-susceptible factors in the Fat line. This study aimed to examine the molecular basis of obesity-resistant mechanisms in the Lean line by analyzing various fat depots and organs, the liver transcriptome of selected metabolic pathways, plasma and lipid homeostasis and expression of selected skeletal muscle genes.</p> <p>Results</p> <p>Expression profiling using our custom Steroltalk v2 microarray demonstrated that Lean mice exhibit a higher hepatic expression of cholesterol biosynthesis genes compared to the Fat line, although this was not reflected in elevation of total plasma or liver cholesterol. However, FPLC analysis showed that protective HDL cholesterol was elevated in Lean mice. A significant difference between the strains was also found in bile acid metabolism. Lean mice had a higher expression of <it>Cyp8b1</it>, a regulatory enzyme of bile acid synthesis, and the <it>Abcb11 </it>bile acid transporter gene responsible for export of acids to the bile. Additionally, a higher content of blood circulating bile acids was observed in Lean mice. Elevated HDL and upregulation of some bile acids synthesis and transport genes suggests enhanced reverse cholesterol transport in the Lean line - the flux of cholesterol out of the body is higher which is compensated by upregulation of endogenous cholesterol biosynthesis. Increased skeletal muscle <it>Il6 </it>and <it>Dio2 </it>mRNA levels as well as increased activity of muscle succinic acid dehydrogenase (SDH) in the Lean mice demonstrates for the first time that changes in muscle energy metabolism play important role in the Lean line phenotype determination and corroborate our previous findings of increased physical activity and thermogenesis in this line. Finally, differential expression of <it>Abcb11 </it>and <it>Dio2 </it>identifies novel strong positional candidate genes as they map within the quantitative trait loci (QTL) regions detected previously in crosses between the Lean and Fat mice.</p> <p>Conclusion</p> <p>We identified novel candidate molecular targets and metabolic changes which can at least in part explain resistance to obesity development in the Lean line. The major difference between the Lean and Fat mice was in increased liver cholesterol biosynthesis gene mRNA expression, bile acid metabolism and changes in selected muscle genes' expression in the Lean line. The liver <it>Abcb11 </it>and muscle <it>Dio2 </it>were identified as novel positional candidate genes to explain part of the phenotypic difference between the Lean and Fat lines.</p

Association between the -455T>C promoter polymorphism of the APOC3 gene and the metabolic syndrome in a multi-ethnic sample

<p>Abstract</p> <p>Background</p> <p>Common polymorphisms in the promoter of the <it>APOC3 </it>gene have been associated with hypertriglyceridemia and may impact on phenotypic expression of the metabolic syndrome (MetS). The rs7566605 marker, located near the <it>INSIG2 </it>gene, has been found to be associated with obesity, making it also a potential genetic determinant for MetS. The objective of this study is to examine the <it>APOC3 </it>-455T>C and the <it>INSIG2 </it>rs7566605 polymorphisms as potential genetic determinants for MetS in a multi-ethnic sample.</p> <p>Methods</p> <p>Subjects were genotyped for both the <it>APOC3 </it>-455T>C and <it>INSIG2 </it>rs7566605 polymorphisms, and classified for the presence or absence of MetS (NCEP ATP III and IDF definitions). The total study population included 2675 subjects (≥18 years of age) from six different geographical ancestries.</p> <p>Results</p> <p>For the overall study population, the prevalence of MetS was 22.6% (NCEP ATP III definition). Carriers of ≥1 copy of <it>APOC3 </it>-455C were more likely to have MetS (NCEP ATP III definition) than noncarriers (carrier odds ratio 1.73, 95% CI 1.40 to 2.14, adjusting for age and study group). The basis of the association was related not only to a higher proportion of -455C carriers meeting the triglyceride and high-density lipoprotein cholesterol criteria, but also the blood pressure criteria compared with wild-type homozygotes. Plasma apo C-III concentrations were not associated with <it>APOC3 </it>-455T>C genotype. The <it>INSIG2 </it>rs7566605 polymorphism was not associated with MetS or measures of obesity.</p> <p>Conclusion</p> <p>Meta-analysis of the sample of multiple geographic ancestries indicated that the functional -455T>C promoter polymorphism in <it>APOC3 </it>was associated with an approximately 2-fold increased risk of MetS, whereas the <it>INSIG2 </it>rs7566605 polymorphism was not associated with MetS.</p

TRIM16 acts as a tumour suppressor by inhibitory effects on cytoplasmic vimentin and nuclear E2F1 in neuroblastoma cells

The family of tripartite-motif (TRIM) proteins are involved in diverse cellular processes, but are often characterized by critical protein–protein interactions necessary for their function. TRIM16 is induced in different cancer types, when the cancer cell is forced to proceed down a differentiation pathway. We have identified TRIM16 as a DNA-binding protein with histone acetylase activity, which is required for the retinoic acid receptor β2 transcriptional response in retinoid-treated cancer cells. In this study, we show that overexpressed TRIM16 reduced neuroblastoma cell growth, enhanced retinoid-induced differentiation and reduced tumourigenicity in vivo. TRIM16 was only expressed in the differentiated ganglion cell component of primary human neuroblastoma tumour tissues. TRIM16 bound directly to cytoplasmic vimentin and nuclear E2F1 in neuroblastoma cells. TRIM16 reduced cell motility and this required downregulation of vimentin. Retinoid treatment and enforced overexpression caused TRIM16 to translocate to the nucleus, and bind to and downregulate nuclear E2F1, required for cell replication. This study, for the first time, demonstrates that TRIM16 acts as a tumour suppressor, affecting neuritic differentiation, cell migration and replication through interactions with cytoplasmic vimentin and nuclear E2F1 in neuroblastoma cells