A Chandra study of the large-scale shock and cool filaments in Hydra A: Evidence for substantial gas dredge-up by the central outburst

We present the results of a Chandra study of the Hydra A galaxy cluster, where a powerful AGN outburst created a large-scale cocoon shock. We investigated possible azimuthal variations in shock strength and shape, finding indications for a weak shock with a Mach number in the range ~1.2-1.3. We measured the temperature change across the shock front. However, the detection of a temperature rise in the regions immediately inside of the front is complicated by the underlying temperature profile of the cluster atmosphere. We measured the global temperature profile of the cluster up to 700 kpc, which represents the farthest measurement obtained with Chandra for this cluster. A "plateau" in the temperature profile in the range ~70-150 kpc indicates the presence of cool gas, which is likely the result of uplift of material by the AGN outburst. After masking the cool filaments visible in the hardness ratio map, the plateau disappears and the temperature profile recovers a typical shape with a peak around 190 kpc, just inside the shock front. However, it is unlikely that such a temperature feature is produced by the shock as it is consistent with the general shape of the temperature profiles observed for relaxed galaxy clusters. We studied the spectral properties of the cool filaments finding evidence that ~10^11 M_sun of low-entropy material has been dredged up by the rising lobes from the central 30 kpc to the observed current position of 75-150 kpc. The energy required to lift the cool gas is >~2.2 x 10^60 erg, which is comparable to the work required to inflate the cavities and is ~25% of the total energy of the large-scale shock. Our results show that the AGN feedback in Hydra A is acting not only by directly heating the gas, but also by removing a substantial amount of potential fuel for the SMBH.Comment: 11 pages, 9 figures, accepted for publication in ApJ (version with full resolution figures available at http://www.bo.astro.it/~myriam/files/papers/gitti-hydra.pdf

Identification of pathologic features associated with “ulcerative colitis-like” Crohn’s disease

AIM: To identify pathologic features associated with this “ulcerative colitis (UC)-like” subgroup of Crohn’s disease (CD). METHODS: Seventeen subjects diagnosed as having UC who underwent proctocolectomy (RPC) from 2003-2007 and subsequently developed CD of the ileal pouch were identified. UC was diagnosed based on pre-operative clinical, endoscopic, and pathologic studies. Eighteen patients who underwent RPC for UC within the same time period without subsequently developing CD were randomly selected and used as controls. Pathology reports and histological slides were reviewed for a wide range of gross and microscopic pathological features, as well as extent of disease. The demographics, gross description and histopathology of the resection specimens were reviewed and compared between the two groups. RESULTS: Patients with “UC-like” CD were on average 13 years younger than those with “true” UC (P < 0.01). More severe disease in the proximal involved region and active ileitis with/without architectural distortion were observed in 6 of 17 (35%) and 7 of 17 (41%) “UC-like” CD cases, respectively, but in none of the “true” UC cases (P < 0.05). Active appendicitis occurred in 8 of 16 (50%) “UC-like” CD cases but in only two (11%) “true” UC cases (P < 0.05). Conspicuous lamina propria neutrophils were more specific for “UC-like” CD (76% vs 22%, P < 0.05). In addition, prominent lymphoid aggregates tended to be more common in “UC-like” CD (P = 0.07). The “true” UC group contained a greater number of cases with severe activity (78% vs 47%). Therefore, the features more commonly seen in “UC-like” CD were not due to a more severe disease process. Crohn’s granulomas and transmural inflammation in non-ulcerated areas were absent in both groups. CONCLUSION: More severe disease in the proximal involved region, terminal ileum involvement, active appendicitis, and prominent lamina propria neutrophils may be morphological factors associated with “UC-like” CD

Women and children living in areas of armed conflict in Africa: a geospatial analysis of mortality and orphanhood

Background: The population effects of armed conflict on non-combatant vulnerable populations are incompletely understood. We aimed to study the effects of conflict on mortality among women of childbearing age (15–49 years) and on orphanhood among children younger than 15 years in Africa. Methods: We tested the extent to which mortality among women aged 15–49 years, and orphanhood among children younger than 15 years, increased in response to nearby armed conflict in Africa. Data on location, timing, and intensity of armed conflicts were obtained from the Uppsala Conflict Data Program, and data on the location, timing, and outcomes of women and children from Demographic and Health Surveys done in 35 African countries from 1990 to 2016. Mortality among women was obtained from sibling survival data. We used cluster-area fixed-effects regression models to compare survival of women during periods of nearby conflict (within 50 km) to survival of women in the same area during times without conflict. We used similar methods to examine the extent to which children living near armed conflicts are at increased risk of becoming orphans. We examined the effects of varying conflict intensity using number of direct battle deaths and duration of consecutive conflict exposure. Findings: We analysed data on 1 629 352 women (19286387 person-years), of which 103011 (6·3%) died (534·1 deaths per 100000 women-years), and 2 354 041 children younger than 15 years, of which 204276 (8·7%) had lost a parent. On average, conflict within 50 km increased women’s mortality by 112 deaths per 100 000 person-years (95% CI 97–128; a 21% increase above baseline), and the probability that a child has lost at least one parent by 6·0% (95% CI 3–8). This effect was driven by high-intensity conflicts: exposure to the highest (tenth) decile conflict in terms of conflict-related deaths increased the probability of female mortality by 202% (187–218) and increased the likelihood of orphanhood by 42% compared with a conflict-free period. Among the conflict-attributed deaths, 10% were due to maternal mortality. Interpretation: African women of childbearing age are at a substantially increased risk of death from nearby highintensity armed conflicts. Children exposed to conflict are analogously at increased risk of becoming orphans. This work fills gaps in literature on the harmful effects of armed conflict on non-combatants and highlights the need for humanitarian interventions to protect vulnerable populations. Funding: Bill & Melinda Gates Foundation to the BRANCH Consortium

An Elusive Z' Coupled to Beauty

By extending the standard gauge group to SU(3)_c \times SU(2)_L \times U(1)_Y \times U(1)_X with X charges carried only by the third family we accommodate the LEP measurement of R_b and predict a potentially measurable discrepancy in A_{FB}^{b} in e^+e^- scattering and that D^0\bar{D}^0 mixing may be near its experimental limit. The Z', which explicitly violates the GIM mechanism, can nevertheless be naturally consistent with FCNC constraints. Direct detection of the Z' is possible but challenging.Comment: 12 pages, plus 1 Postscript figure, uses revtex, Discussion of FCNC extende

Permissive and Restricted Virus Infection of Murine Embryonic Stem Cells

Recent RNA interference (RNAi) studies have identified many host proteins that modulate virus infection, but small interfering RNA 'off-target' effects and the use of transformed cell lines limit their conclusiveness. As murine embryonic stem (mES) cells can be genetically modified and resources exist where many and eventually all known mouse genes are insertionally inactivated, it was reasoned that mES cells would provide a useful alternative to RNAi screens. Beyond allowing investigation of host-pathogen interactions in vitro, mES cells have the potential to differentiate into other primary cell types, as well as being used to generate knockout mice for in vivo studies. However, mES cells are poorly characterized for virus infection. To investigate whether ES cells can be used to explore host-virus interactions, this study characterized the responses of mES cells following infection by herpes simplex virus type 1 (HSV-1) and influenza A virus. HSV-1 replicated lytically in mES cells, although mES cells were less permissive than most other cell types tested. Influenza virus was able to enter mES cells and express some viral proteins, but the replication cycle was incomplete and no infectious virus was produced. Knockdown of the host protein AHCYL1 in mES cells reduced HSV-1 replication, showing the potential for using mES cells to study host-virus interactions. Transcriptional profiling, however, indicated the lack of an efficient innate immune response in these cells. mES cells may thus be useful to identify host proteins that play a role in virus replication, but they are not suitable to determine factors that are involved in innate host defence