The galaxy mass-size relation in CARLA clusters and proto-clusters at 1.4 < z < 2.8: larger cluster galaxy sizes

(Abridged) We study the galaxy mass-size relation in CARLA spectroscopically confirmed clusters at $1.4<z<2.8$, which span a total stellar mass $11.3<\mathrm{log}(M^c_*/M_{\odot})<12.6$ (halo mass $13.5 \lesssim \mathrm{log}(M^c_h/M_{\odot}) \lesssim 14.5$). Our main finding is that cluster passive ETG at $z \gtrsim 1.5$ with ${\rm log}(M/M_{\odot})>10.5$ are systematically $\gtrsim 0.2-0.3~{\rm dex}$ larger than field ETGs. The passive ETG average size evolution is slower at $1<z<2$ when compared to the field. This could be explained by differences in the formation and early evolution of galaxies in haloes of a different mass. Strong compaction and gas dissipation in field galaxies, followed by a sequence of mergers may have also played a significant role in the field ETG evolution, but not in the evolution of cluster galaxies. Our passive ETG mass-size relation shows a tendency to flatten at $9.6<{\rm log}(M/M_{\odot})<10.5$, where the average size is $\mathrm{log}(R_e/\mathrm{kpc}) = 0.05 \pm 0.22$. This implies that galaxies in the low end of the mass-size relation do not evolve much from $z\sim 2$ to the present, and that their sizes evolve in a similar way in clusters and in the field. BCGs lie on the same mass-size relation as satellites, suggesting that their size evolution is not different at redshift z $\gtrsim$ 2. Half of the active ETGs ($\sim 30\%$ of the ETGs) follow the field passive galaxy mass-size relation, and the other half follow the field active galaxy mass-size relation. These galaxies likely went through a recent merger or neighbor galaxy interaction, and would most probably quench at a later epoch and increase the fraction of passive ETGs in clusters. We do not observe a large population of compact galaxies, as is observed in the field at these redshifts, implying that the galaxies in our clusters are not observed in an epoch close to their compaction.Comment: 15 pages, 10 figures, accepted for publication in Astronomy & Astrophysic

HST grism confirmation of two z ~ 2 structures from the clusters around radio-loud AGN (CARLA) survey

Using Hubble Space Telescope slitless grism data, we report the spectroscopic confirmation of two distant structures at z ~ 2 associated with powerful high-redshift radio-loud active galactic nuclei (AGNs). These rich structures, likely (forming) clusters, are among the most distant structures currently known, and were identified on the basis of Spitzer/IRAC [3.6]–[4.5] color. We spectroscopically confirm nine members in the field of MRC 2036−254, comprising eight star-forming galaxies and the targeted radio galaxy. The median redshift is z=2.000. We spectroscopically confirm 10 members in the field of B3 0756+406, comprising 8 star-forming galaxies and 2 AGNs, including the targeted radio-loud quasar. The median redshift is z=1.986. All confirmed members are within 500 kpc (1 arcmin) of the targeted AGNs. We derive median (mean) star-formation rates of ~35 Mʘ yr‾¹ (~50 M yr‾¹) for the confirmed star-forming members of both structures based on their [O III]ʎ5007 luminosities, and estimate average galaxy stellar masses ≲1 x 10¹¹ Mʘ based on mid-infrared fluxes and spectral energy distribution modeling. Most of our confirmed members are located above the star-forming main sequence toward starburst galaxies, consistent with clusters at these early epochs being the sites of significant levels of star formation. The structure around MRC 2036−254 shows an overdensity of IRAC-selected candidate galaxy cluster members consistent with being quiescent galaxies, while the structure around B3 0756+406 shows field values, albeit with many lower limits to colors that could allow an overdensity of faint red quiescent galaxies. The structure around MRC 2036−254 shows a red sequence of passive galaxy candidates

Three Linked Vasculopathic Processes Characterize Kawasaki Disease: A Light and Transmission Electron Microscopic Study

Kawasaki disease is recognized as the most common cause of acquired heart disease in children in the developed world. Clinical, epidemiologic, and pathologic evidence supports an infectious agent, likely entering through the lung. Pathologic studies proposing an acute coronary arteritis followed by healing fail to account for the complex vasculopathy and clinical course.Specimens from 32 autopsies, 8 cardiac transplants, and an excised coronary aneurysm were studied by light (n=41) and transmission electron microscopy (n=7). Three characteristic vasculopathic processes were identified in coronary (CA) and non-coronary arteries: acute self-limited necrotizing arteritis (NA), subacute/chronic (SA/C) vasculitis, and luminal myofibroblastic proliferation (LMP). NA is a synchronous neutrophilic process of the endothelium, beginning and ending within the first two weeks of fever onset, and progressively destroying the wall into the adventitia causing saccular aneurysms, which can thrombose or rupture. SA/C vasculitis is an asynchronous process that can commence within the first two weeks onward, starting in the adventitia/perivascular tissue and variably inflaming/damaging the wall during progression to the lumen. Besides fusiform and saccular aneurysms that can thrombose, SA/C vasculitis likely causes the transition of medial and adventitial smooth muscle cells (SMC) into classic myofibroblasts, which combined with their matrix products and inflammation create progressive stenosing luminal lesions (SA/C-LMP). Remote LMP apparently results from circulating factors. Veins, pulmonary arteries, and aorta can develop subclinical SA/C vasculitis and SA/C-LMP, but not NA. The earliest death (day 10) had both CA SA/C vasculitis and SA/C-LMP, and an "eosinophilic-type" myocarditis.NA is the only self-limiting process of the three, is responsible for the earliest morbidity/mortality, and is consistent with acute viral infection. SA/C vasculitis can begin as early as NA, but can occur/persist for months to years; LMP causes progressive arterial stenosis and thrombosis and is composed of unique SMC-derived pathologic myofibroblasts

Patient Safety in the Cardiac Operating Room: Human Factors and Teamwork: A Scientific Study from the American Heart Association

The cardiac surgical operating room (OR) is a complex environment in which highly trained subspecialists interact with each other using sophisticated equipment to care for patients with severe cardiac disease and significant comorbidities. Thousands of patient lives have been saved or significantly improved with the advent of modern cardiac surgery. Indeed, both mortality and morbidity for coronary artery bypass surgery have decreased during the past decade. Nonetheless, the highly skilled and dedicated personnel in cardiac ORs are human and will make errors. Refined techniques, advanced technologies, and enhanced coordination of care have led to significant improvements in cardiac surgery outcomes

The mammalian gene function resource: the International Knockout Mouse Consortium.

In 2007, the International Knockout Mouse Consortium (IKMC) made the ambitious promise to generate mutations in virtually every protein-coding gene of the mouse genome in a concerted worldwide action. Now, 5 years later, the IKMC members have developed high-throughput gene trapping and, in particular, gene-targeting pipelines and generated more than 17,400 mutant murine embryonic stem (ES) cell clones and more than 1,700 mutant mouse strains, most of them conditional. A common IKMC web portal (www.knockoutmouse.org) has been established, allowing easy access to this unparalleled biological resource. The IKMC materials considerably enhance functional gene annotation of the mammalian genome and will have a major impact on future biomedical research

The mammalian gene function resource: The International Knockout Mouse Consortium

In 2007, the International Knockout Mouse Consortium (IKMC) made the ambitious promise to generate mutations in virtually every protein-coding gene of the mouse genome in a concerted worldwide action. Now, 5 years later, the IKMC members have developed highthroughput gene trapping and, in particular, gene-targeting pipelines and generated more than 17,400 mutant murine embryonic stem (ES) cell clones and more than 1,700 mutant mouse strains, most of them conditional. A common IKMC web portal (www.knockoutmouse.org) has been established, allowing easy access to this unparalleled biological resource. The IKMC materials considerably enhance functional gene annotation of the mammalian genome and will have a major impact on future biomedical research

Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction.

Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction