An ALMA survey of the S2CLS UDS field: optically invisible submillimetre galaxies

We analyse a robust sample of 30 near-infrared-faint (KAB > 25.3, 5σ) submillimetre galaxies (SMGs) selected from a 0.96 deg2 field to investigate their properties and the cause of their faintness in optical/near-infrared wavebands. Our analysis exploits precise identifications based on Atacama Large Millimeter Array (ALMA) 870-μm continuum imaging, combined with very deep near-infrared imaging from the UKIDSS Ultra Deep Survey. We estimate that SMGs with KAB > 25.3 mag represent 15 ± 2 per cent of the total population brighter than S870 = 3.6 mJy, with a potential surface density of ∼450 deg−2 above S870 ≥ 1 mJy. As such, they pose a source of contamination in surveys for both high-redshift ‘quiescent’ galaxies and very high redshift Lyman-break galaxies. We show that these K-faint SMGs represent the tail of the broader submillimetre population, with comparable dust and stellar masses to KAB ≤ 25.3 mag SMGs, but lying at significantly higher redshifts (z = 3.44 ± 0.06 versus z = 2.36 ± 0.11) and having higher dust attenuation (AV = 5.2 ± 0.3 versus AV = 2.9 ± 0.1). We investigate the origin of the strong dust attenuation and find indications that these K-faint galaxies have smaller dust continuum sizes than the KAB ≤ 25.3 mag galaxies, as measured by ALMA, which suggests their high attenuation is related to their compact sizes. We identify a correlation of dust attenuation with star formation rate surface density (SFR), with the K-faint SMGs representing the higher SFR and highest AV galaxies. The concentrated, intense star formation activity in these systems is likely to be associated with the formation of spheroids in compact galaxies at high redshifts, but as a result of their high obscuration these galaxies are completely missed in ultraviolet, optical, and even near-infrared surveys

Millimeter imaging of submillimeter galaxies in the COSMOS field: Redshift distribution

We present new IRAM PdBI 1.3mm continuum observations at ~1.5" resolution of 28 SMGs previously discovered with the 870um bolometer LABOCA at APEX within the central 0.7deg2 of the COSMOS field. 19 out of the 28 LABOCA sources were detected with the PdBI at a >~3sigma level of ~1.4mJy/b. A combined analysis of this new sample with existing interferometrically identified SMGs in the COSMOS field yields the following results: 1) >~15%, and possibly up to ~40% of single-dish detected SMGs consist of multiple sources, 2) statistical identifications of multi-wavelength counterparts to the single-dish SMGs yield that only ~50% of these single-dish SMGs have real radio or IR counterparts, 3) ~18% of interferometric SMGs have only radio or even no multi-wavelength counterpart at all, and 4) ~50-70% of z>~3 SMGs have no radio counterparts down to an rms of 7-12uJy at 1.4GHz. Using the exact interferometric positions to identify proper multi-wavelength counterparts allows us to determine accurate photometric redshifts for these sources. The redshift distributions of the combined and the individual 1.1mm and 870um selected samples have a higher mean and broader width than the redshift distributions derived in previous studies. Our sample supports the previous tentative trend that on average brighter and/or mm-selected SMGs are located at higher redshifts. There is a tentative offset between the mean redshift for the 1.1mm (=3.1+/-0.4) and 870um (=2.6+/-0.4) selected samples, with the 1.1mm sources lying on average at higher redshifts. Based on our nearly complete sample of AzTEC 1.1mm SMGs within a uniform 0.15deg2 area we infer a higher surface density of z>~4 SMGs than predicted by current cosmological models. In summary, our findings imply that (sub-)millimeter interferometric identifications are crucial to build statistically complete and unbiased samples of SMGs.Comment: 35 pages, 18 figures, 10 tables; accepted for publication in A&

An ALMA/NOEMA survey of the molecular gas properties of high-redshift star-forming galaxies

We have used ALMA and NOEMA to study the molecular gas reservoirs in 61 ALMA-identified submillimetre galaxies (SMGs) in the COSMOS, UDS, and ECDFS fields. We detect 12CO (⁠Jup= 2–5) emission lines in 50 sources, and [C I](3P1 − 3P0) emission in eight, at z= 1.2–4.8 and with a median redshift of 2.9 ± 0.2. By supplementing our data with literature sources, we construct a statistical CO spectral line energy distribution and find that the 12CO line luminosities in SMGs peak at Jup ∼ 6, consistent with similar studies. We also test the correlations of the CO, [C I], and dust as tracers of the gas mass, finding the three to correlate well, although the CO and dust mass as estimated from the 3-mm continuum are preferable. We estimate that SMGs lie mostly on or just above the star-forming main sequence, with a median gas depletion timescale, tdep = Mgas/SFR, of 210 ± 40 Myr for our sample. Additionally, tdep declines with redshift across z ∼ 1–5, while the molecular gas fraction, μgas = Mgas/M*, increases across the same redshift range. Finally, we demonstrate that the distribution of total baryonic mass and dynamical line width, Mbaryon–σ, for our SMGs is consistent with that followed by early-type galaxies in the Coma cluster, providing strong support to the suggestion that SMGs are progenitors of massive local spheroidal galaxies. On the basis of this, we suggest that the SMG populations above and below an 870-μm flux limit of S870 ∼ 5 mJy may correspond to the division between slow and fast rotators seen in local early-type galaxies

Oral Fluid–Based Biomarkers of Alveolar Bone Loss in Periodontitis

Periodontal disease is a bacteria-induced chronic inflammatory disease affecting the soft and hard supporting structures encompassing the teeth. When left untreated, the ultimate outcome is alveolar bone loss and exfoliation of the involved teeth. Traditional periodontal diagnostic methods include assessment of clinical parameters and radiographs. Though efficient, these conventional techniques are inherently limited in that only a historical perspective, not current appraisal, of disease status can be determined. Advances in the use of oral fluids as possible biological samples for objective measures of current disease state, treatment monitoring, and prognostic indicators have boosted saliva and other oral-based fluids to the forefront of technology. Oral fluids contain locally and systemically derived mediators of periodontal disease, including microbial, host-response, and bone-specific resorptive markers. Although most biomarkers in oral fluids represent inflammatory mediators, several specific collagen degradation and bone turnover-related molecules have emerged as possible measures of periodontal disease activity. Pyridinoline cross-linked carboxyterminal telopeptide (ICTP), for example, has been highly correlated with clinical features of the disease and decreases in response to intervention therapies, and has been shown to possess predictive properties for possible future disease activity. One foreseeable benefit of an oral fluid–based periodontal diagnostic would be identification of highly susceptible individuals prior to overt disease. Timely detection and diagnosis of disease may significantly affect the clinical management of periodontal patients by offering earlier, less invasive, and more cost-effective treatment therapies.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73247/1/annals.1384.028.pd

The Dramatic Size and Kinematic Evolution of Massive Early-type Galaxies

We aim to provide a holistic view on the typical size and kinematic evolution of massive early-type galaxies (ETGs) that encompasses their high-z star-forming progenitors, their high-z quiescent counterparts, and their configurations in the local Universe. Our investigation covers the main processes playing a relevant role in the cosmic evolution of ETGs. Specifically, their early fast evolution comprises biased collapse of the low angular momentum gaseous baryons located in the inner regions of the host dark matter halo; cooling, fragmentation, and infall of the gas down to the radius set by the centrifugal barrier; further rapid compaction via clump/gas migration toward the galaxy center, where strong heavily dust-enshrouded star formation takes place and most of the stellar mass is accumulated; and ejection of substantial gas amount from the inner regions by feedback processes, which causes a dramatic puffing-up of the stellar component. In the late slow evolution, passive aging of stellar populations and mass additions by dry merger events occur. We describe these processes relying on prescriptions inspired by basic physical arguments and by numerical simulations to derive new analytical estimates of the relevant sizes, timescales, and kinematic properties for individual galaxies along their evolution. Then we obtain quantitative results as a function of galaxy mass and redshift, and compare them to recent observational constraints on half-light size Re, on the ratio v/\u3c3 between rotation velocity and velocity dispersion (for gas and stars) and on the specific angular momentum j 17of the stellar component; we find good consistency with the available multiband data in average values and dispersion, both for local ETGs and for their z 3c 1-2 star-forming and quiescent progenitors. The outcomes of our analysis can provide hints to gauge sub-grid recipes implemented in simulations, to tune numerical experiments focused on specific processes, and to plan future multiband, high-resolution observations on high-redshift star-forming and quiescent galaxies with next-generation facilities

Exploring the mechanisms of renoprotection against progressive glomerulosclerosis

In this review, I introduce the strategy developed by our laboratory to explore the mechanisms of renoprotection against progressive glomerulosclerosis leading to renal death. First, I describe the experimental rat model in which disturbances of vascular regeneration and glomerular hemodynamics lead to irreversible glomerulosclerosis. Second, I discuss the possible mechanisms determining the progression of glomerulosclerosis and introduce a new imaging system based on intravital confocal laser scanning microscopy. Third, I provide an in-depth review of the regulatory glomerular hemodynamics at the cellular and molecular levels while focusing on the pivotal role of Ca2+-dependent gap junctional intercellular communication in coordinating the behavior of mesangial cells. Last, I show that local delivery of renoprotective agents, in combination with diagnostic imaging of the renal microvasculature, allows the evaluation of the therapeutic effects of angiotensin II receptor and cyclooxygenase activity local blockade on the progression of glomerulosclerosis, which would otherwise lead to renal death

Yokukansan Inhibits Neuronal Death during ER Stress by Regulating the Unfolded Protein Response

Recently, several studies have reported Yokukansan (Tsumura TJ-54), a traditional Japanese medicine, as a potential new drug for the treatment of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress is known to play an important role in the pathogenesis of AD, particularly in neuronal death. Therefore, we examined the effect of Yokukansan on ER stress-induced neurotoxicity and on familial AD-linked presenilin-1 mutation-associated cell death.We employed the WST-1 assay and monitored morphological changes to evaluate cell viability following Yokukansan treatment or treatment with its components. Western blotting and PCR were used to observe the expression levels of GRP78/BiP, caspase-4 and C/EBP homologous protein.Yokukansan inhibited neuronal death during ER stress, with Cnidii Rhizoma (Senkyu), a component of Yokukansan, being particularly effective. We also showed that Yokukansan and Senkyu affect the unfolded protein response following ER stress and that these drugs inhibit the activation of caspase-4, resulting in the inhibition of ER stress-induced neuronal death. Furthermore, we found that the protective effect of Yokukansan and Senkyu against ER stress could be attributed to the ferulic acid content of these two drugs.Our results indicate that Yokukansan, Senkyu and ferulic acid are protective against ER stress-induced neuronal cell death and may provide a possible new treatment for AD

Cell-specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain

BACKGROUND: The complement cascade not only provides protection from infection but can also mediate destructive inflammation. Complement is also involved in elimination of neuronal synapses which is essential for proper development, but can be detrimental during aging and disease. C1q, required for several of these complement-mediated activities, is present in the neuropil, microglia, and a subset of interneurons in the brain. METHODS: To identify the source(s) of C1q in the brain, the C1qa gene was selectively inactivated in the microglia or Thy-1(+) neurons in both wild type mice and a mouse model of Alzheimer’s disease (AD), and C1q synthesis assessed by immunohistochemistry, QPCR, and western blot analysis. RESULTS: While C1q expression in the brain was unaffected after inactivation of C1qa in Thy-1(+) neurons, the brains of C1qa (FL/FL) :Cx3cr1 (CreERT2) mice in which C1qa was ablated in microglia were devoid of C1q with the exception of limited C1q in subsets of interneurons. Surprisingly, this loss of C1q occurred even in the absence of tamoxifen by 1 month of age, demonstrating that Cre activity is tamoxifen-independent in microglia in Cx3cr1 (CreERT2/WganJ) mice. C1q expression in C1qa (FL/FL) : Cx3cr1 (CreERT2/WganJ) mice continued to decline and remained almost completely absent through aging and in AD model mice. No difference in C1q was detected in the liver or kidney from C1qa (FL/FL) : Cx3cr1 (CreERT2/WganJ) mice relative to controls, and C1qa (FL/FL) : Cx3cr1 (CreERT2/WganJ) mice had minimal, if any, reduction in plasma C1q. CONCLUSIONS: Thus, microglia, but not neurons or peripheral sources, are the dominant source of C1q in the brain. While demonstrating that the Cx3cr1 (CreERT2/WganJ) deleter cannot be used for adult-induced deletion of genes in microglia, the model described here enables further investigation of physiological roles of C1q in the brain and identification of therapeutic targets for the selective control of complement-mediated activities contributing to neurodegenerative disorders. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12974-017-0814-9) contains supplementary material, which is available to authorized users