Malpositioned endoscopically inserted biliary stent causing massive hematemesis managed with vascular plug and stenting

A 46-year-old man with a history of hepatitis B cirrhosis and hepatocellular carcinoma (HCC) status post liver transplantation two years ago complicated by HCC recurrence and biliary stenosis presented with hypovolemic shock and melena one month after endoscopic exchange of plastic biliary stents. During endoscopic retrograde cholangiopancreatography, patient was found to have hemobilia and developed uncontrollable bleeding after a common bile duct (CBD) sweep managed by insertion of a stent-graft across major papilla into presumed CBD. The bleeding continued with subsequent negative angiography, and a computed tomography angiography showed malpositioned stent-graft between major papilla and inferior vena cava (IVC). This was successfully managed by the deployment of a vascular plug inside the stent graft and excluding it by deploying a stent across the affected area in IVC

Subhaloes gone Notts: subhaloes as tracers of the dark matter halo shape

We study the shapes of subhalo distributions from four dark-matter-only simulations of Milky Way-type haloes. Comparing the shapes derived from the subhalo distributions at high resolution to those of the underlying dark matter fields, we find the former to be more triaxial if the analysis is restricted to massive subhaloes. For three of the four analysed haloes, the increased triaxiality of the distributions of massive subhaloes can be explained by a systematic effect caused by the low number of objects. Subhaloes of the fourth halo show indications for anisotropic accretion via their strong triaxial distribution and orbit alignment with respect to the dark matter field. These results are independent of the employed subhalo finder. Comparing the shape of the observed Milky Way satellite distribution to those of high-resolution subhalo samples from simulations, we find agreement for samples of bright satellites, but significant deviations if faint satellites are included in the analysis. These deviations might result from observational incompleteness

Resolve and eco: the halo mass-dependent shape of galaxy stellar and baryonic mass functions

In this work, we present galaxy stellar and baryonic (stars plus cold gas) mass functions (SMF and BMF) and their halo mass dependence for two volume-limited data sets. The first, RESOLVE-B, coincides with the Stripe 82 footprint and is extremely complete down to baryonic mass Mbary ∼ 10^9.1 M⊙, probing the gas-rich dwarf regime below Mbary ∼ 10^10 M⊙. The second, ECO, covers a ~40× larger volume (containing RESOLVE-A) and is complete to Mbary ~10^9.4 M⊙. To construct the SMF and BMF we implement a new “cross-bin sampling” technique with Monte Carlo sampling from the full likelihood distributions of stellar or baryonic mass. Our SMFs exhibit the “plateau” feature starting below Mstar ~10^10 M⊙ that has been described in prior work. However, the BMF fills in this feature and rises as a straight power law below ~10^10 M⊙, as gas-dominated galaxies become the majority of the population. Nonetheless, the low-mass slope of the BMF is not as steep as that of the theoretical dark matter halo MF. Moreover, we assign group halo masses by abundance matching, finding that the SMF and BMF separated into four physically motivated halo mass regimes reveal complex structure underlying the simple shape of the overall MFs. In particular, the satellite MFs are depressed below the central galaxy MF “humps” in groups with mass < 10^13.5 M⊙ yet rise steeply in clusters. Our results suggest that satellite destruction and/or stripping are active from the point of nascent group formation. We show that the key role of groups in shaping MFs enables reconstruction of a given survey’s SMF or BMF based on its group halo mass distribution

Spontaneous Mutagenesis Is Enhanced in Apex Heterozygous Mice

Germ line DNA directs the development of the next generation and, as such, is profoundly different from somatic cell DNA. Spermatogenic cells obtained from young adult lacI transgenic mice display a lower spontaneous mutant frequency and greater in vitro base excision repair activity than somatic cells and tissues obtained from the same mice. However, spermatogenic cells from old lacI mice display a 10-fold higher mutant frequency. This increased spontaneous mutant frequency occurs coincidentally with decreased in vitro base excision repair activity for germ cell and testicular extracts that in turn corresponds to a decreased abundance of AP endonuclease. To directly test whether a genetic diminution of AP endonuclease results in increased spontaneous mutant frequencies in spermatogenic cell types, AP endonuclease heterozygous (Apex(+/−)) knockout mice were crossed with lacI transgenic mice. Spontaneous mutant frequencies were significantly elevated (approximately twofold) for liver and spleen obtained from 3-month-old Apex(+/−) lacI(+) mice compared to frequencies from Apex(+/+) lacI(+) littermates and were additionally elevated for somatic tissues from 9-month-old mice. Spermatogenic cells from 9-month-old Apex(+/−) lacI(+) mice were significantly elevated twofold compared to levels for 9-month-old Apex(+/+) lacI(+) control mice. These data indicate that diminution of AP endonuclease has a significant effect on spontaneous mutagenesis in somatic and germ line cells

Age-Related Macular Degeneration: A High-Resolution Genome Scan for Susceptibility Loci in a Population Enriched for Late-Stage Disease

Age-related macular degeneration (AMD) is a complex multifactorial disease that affects the central region of the retina. AMD is clinically heterogeneous, leading to geographic atrophy (GA) and/or choroidal neovascularization (CNV) at advanced stages. Considerable data exists in support of a genetic predisposition for AMD. Recent linkage studies have provided evidence in favor of several AMD susceptibility loci. We have performed a high-resolution (5-cM) genome scan of 412 affected relative pairs that were enriched for late-stage disease (GA and/or CNV). Nonparametric linkage analysis was performed using two different diagnostic criteria and also by dividing the affected individuals according to GA or CNV phenotype. Our results demonstrate evidence of linkage in regions that were suggested in at least one previous study at chromosomes 1q (236–240 cM in the Marshfield genetic map), 5p (40–50 cM), and 9q (111 cM). Multipoint analysis of affected relatives with CNV provided evidence of additional susceptibility loci on chromosomes 2p (10 cM) and 22q (25 cM). A recently identified Gln5345Arg change in HEMICENTIN-1 on chromosome 1q25 was not detected in 274 affected members in the restricted group with AMD, 346 additional patients with AMD, and 237 unaffected controls. Our results consolidate the chromosomal locations of several AMD susceptibility loci and, together with previous reports, should facilitate the search for disease-associated sequence variants