50 research outputs found

    How to bend galaxy disc profiles - II. Stars surfing the bar in Type-III discs

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    The radial profiles of stars in disc galaxies are observed to be either purely exponential (Type-I), truncated (Type-II) or antitruncated (Type-III) exponentials. Controlled formation simulations of isolated galaxies can reproduce all of these profile types by varying a single parameter, the initial halo spin. In this paper, we examine these simulations in more detail in an effort to identify the physical mechanism that leads to the formation of Type-III profiles. The stars in the antitruncated outskirts of such discs are now on eccentric orbits, but were born on near-circular orbits at much smaller radii. We show that, and explain how, they were driven to the outskirts via non-linear interactions with a strong and long-lived central bar, which greatly boosted their semimajor axis but also their eccentricity. While bars have been known to cause radial heating and outward migration to stellar orbits, we link this effect to the formation of Type-III profiles. This predicts that the antitruncated parts of galaxies have unusual kinematics for disc-like stellar configurations: high radial velocity dispersions and slow net rotation. Whether such discs exist in nature, can be tested by future observations

    The stellar orbit distribution in present-day galaxies inferred from the CALIFA survey

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    Galaxy formation entails the hierarchical assembly of mass, along with the condensation of baryons and the ensuing, self-regulating star formation. The stars form a collisionless system whose orbit distribution retains dynamical memory that can constrain a galaxy's formation history. The ordered-rotation dominated orbits with near maximum circularity λz1\lambda_z \simeq1 and the random-motion dominated orbits with low circularity λz0\lambda_z \simeq0 are called kinematically cold and kinematically hot, respectively. The fraction of stars on `cold' orbits, compared to the fraction of stars on `hot' orbits, speaks directly to the quiescence or violence of the galaxies' formation histories. Here we present such orbit distributions, derived from stellar kinematic maps via orbit-based modelling for a well defined, large sample of 300 nearby galaxies. The sample, drawn from the CALIFA survey, includes the main morphological galaxy types and spans the total stellar mass range from 108.710^{8.7} to 1011.910^{11.9} solar masses. Our analysis derives the orbit-circularity distribution as a function of galaxy mass, p(λz  M)p(\lambda_z~|~M_\star), and its volume-averaged total distribution, p(λz)p(\lambda_z). We find that across most of the considered mass range and across morphological types, there are more stars on `warm' orbits defined as 0.25λz0.80.25\le \lambda_z \le 0.8 than on either `cold' or `hot' orbits. This orbit-based "Hubble diagram" provides a benchmark for galaxy formation simulations in a cosmological context

    Factors influencing identification of and response to intimate partner violence: a survey of physicians and nurses

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    BACKGROUND: Intimate partner violence against women (IPV) has been identified as a serious public health problem. Although the health care system is an important site for identification and intervention, there have been challenges in determining how health care professionals can best address this issue in practice. We surveyed nurses and physicians in 2004 regarding their attitudes and behaviours with respect to IPV, including whether they routinely inquire about IPV, as well as potentially relevant barriers, facilitators, experiential, and practice-related factors. METHODS: A modified Dillman Tailored Design approach was used to survey 1000 nurses and 1000 physicians by mail in Ontario, Canada. Respondents were randomly selected from professional directories and represented practice areas pre-identified from the literature as those most likely to care for women at the point of initial IPV disclosure: family practice, obstetrics and gynecology, emergency care, maternal/newborn care, and public health. The survey instrument had a case-based scenario followed by 43 questions asking about behaviours and resources specific to woman abuse. RESULTS: In total, 931 questionnaires were returned; 597 by nurses (59.7% response rate) and 328 by physicians (32.8% response rate). Overall, 32% of nurses and 42% of physicians reported routinely initiating the topic of IPV in practice. Principal components analysis identified eight constructs related to whether routine inquiry was conducted: preparedness, self-confidence, professional supports, abuse inquiry, practitioner consequences of asking, comfort following disclosure, practitioner lack of control, and practice pressures. Each construct was analyzed according to a number of related issues, including clinician training and experience with woman abuse, area of practice, and type of health care provider. Preparedness emerged as a key construct related to whether respondents routinely initiated the topic of IPV. CONCLUSION: The present study provides new insight into the factors that facilitate and impede clinicians' decisions to address the issue of IPV with their female patients. Inadequate preparation, both educational and experiential, emerged as a key barrier to routine inquiry, as did the importance of the "real world" pressures associated with the daily context of primary care practice

    Inhibition of the inositol kinase Itpkb augments calcium signaling in lymphocytes and reveals a novel strategy to treat autoimmune disease

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    Emerging approaches to treat immune disorders target positive regulatory kinases downstream of antigen receptors with small molecule inhibitors. Here we provide evidence for an alternative approach in which inhibition of the negative regulatory inositol kinase Itpkb in mature T lymphocytes results in enhanced intracellular calcium levels following antigen receptor activation leading to T cell death. Using Itpkb conditional knockout mice and LMW Itpkb inhibitors these studies reveal that Itpkb through its product IP4 inhibits the Orai1/Stim1 calcium channel on lymphocytes. Pharmacological inhibition or genetic deletion of Itpkb results in elevated intracellular Ca2+ and induction of FasL and Bim resulting in T cell apoptosis. Deletion of Itpkb or treatment with Itpkb inhibitors blocks T-cell dependent antibody responses in vivo and prevents T cell driven arthritis in rats. These data identify Itpkb as an essential mediator of T cell activation and suggest Itpkb inhibition as a novel approach to treat autoimmune disease

    Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

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    Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
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