A Laboratory for Collaboration: Where, Why and Why Not?

12 pages

White-light flares on cool stars in the Kepler Quarter 1 Data

We present the results of a search for white light flares on the ~23,000 cool dwarfs in the Kepler Quarter 1 long cadence data. We have identified 373 flaring stars, some of which flare multiple times during the observation period. We calculate relative flare energies, flare rates and durations, and compare these with the quiescent photometric variability of our sample. We find that M dwarfs tend to flare more frequently but for shorter durations than K dwarfs, and that they emit more energy relative to their quiescent luminosity in a given flare than K dwarfs. Stars that are more photometrically variable in quiescence tend to emit relatively more energy during flares, but variability is only weakly correlated with flare frequency. We estimate distances for our sample of flare stars and find that the flaring fraction agrees well with other observations of flare statistics for stars within 300 pc above the Galactic Plane. These observations provide a more rounded view of stellar flares by sampling stars that have not been pre-selected by their activity, and are informative for understanding the influence of these flares on planetary habitability.Comment: 42 pages, 10 figures, 2 tables; Accepted for publication in the Astronomical Journa

Learning to be an insider agent of change in a Brazilian rural university

The “University” is under pressure to address both local and general requirements from society towards a phenomenon called globalisation. In Brazil, the Ministry of Education has tried, without success, to promote institutional change. Confronted by this situation a process initiated by an internal change agent and based upon the introduction of Action Research was itself the subject of this AR Study by the change agent. This thesis draws upon the findings of that AR and uses it to critically examine the potential to foster change within the higher education context in Brazil using AR. The research was designed in two synchronous processes taking place at two different levels. The first is the facilitation of the uptake of Action Research by a group of academic staff, and the second is the research into that process as a piece of Action Research in its own right by the change agent/facilitator. Facilitation of change has been described as taking place in three phases: a) Mobilization; b) Implementation; and c) Continuation. Throughout such phases in this case data were systematically gathered by the use of five instruments of data collection: 1) Observation; 2) Diary; 3) Questionnaires; 4) Interviews; and 5) Sociogram. Results show my personal learning in facilitating this process of change and two main contributions to knowledge. The first is one which, though local and specific, may nevertheless speak to the challenges faced by other practitioners. Exemplified in this study by the critical exploration of the ‘Daisy Model’ of introducing AR that led to its modification into the ‘Flower Model’. The second is that new knowledge which appears to be more generalisable and for which a case can be made for its wider applicability. Again exemplified in the continuous and disruptive process of change that unfolded to reveal a suitable framework for the use of Action Research as a vehicle of change in a rural university in Brazil where all actions were based on four central principles that emerged from the research: neutrality, voluntary participation, time and motivation. The future success and sustainability of the change processes begun are contingent upon the reaction of the current management of the institution. Five scenarios are examined and a second phase for this AR project is suggested that attempts to address the issues raised.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Hematopoietic Cell–Restricted Deletion of CD36 Reduces High-Fat Diet–Induced Macrophage Infiltration and Improves Insulin Signaling in Adipose Tissue

OBJECTIVE: The fatty acid translocase and scavenger receptor CD36 is important in the recognition and uptake of lipids. Accordingly, we hypothesized that it plays a role in saturated fatty acid-induced macrophage lipid accumulation and proinflammatory activation. RESEARCH DESIGN AND METHODS: In vitro, the effect of CD36 inhibition and deletion in lipid-induced macrophage inflammation was assessed using the putative CD36 inhibitor, sulfosuccinimidyl oleate (SSO), and bone marrow-derived macrophages from mice with (CD36KO) or without (wild-type) global deletion of CD36. To investigate whether deletion of macrophage CD36 would improve insulin sensitivity in vivo, wild-type mice were transplanted with bone marrow from CD36KO or wild-type mice and then fed a standard or high-fat diet (HFD) for 20 weeks. RESULTS: SSO treatment markedly reduced saturated fatty acid-induced lipid accumulation and inflammation in RAW264.7 macrophages. Mice harboring CD36-specific deletion in hematopoietic-derived cells (HSC CD36KO) fed an HFD displayed improved insulin signaling and reduced macrophage infiltration in adipose tissue compared with wild-type mice, but this did not translate into protection against HFD-induced whole-body insulin resistance. Contrary to our hypothesis and our results using SSO in RAW264.7 macrophages, neither saturated fatty acid-induced lipid accumulation nor inflammation was reduced when comparing CD36KO with wild-type bone marrow-derived macrophages. CONCLUSIONS: Although CD36 does not appear important in saturated fatty acid-induced macrophage lipid accumulation, our study uncovers a novel role for CD36 in the migration of proinflammatory phagocytes to adipose tissue in obesity, with a concomitant improvement in insulin action

Tumor Progression Locus 2 (Tpl2) Deficiency Does Not Protect against Obesity-Induced Metabolic Disease

Obesity is associated with a state of chronic low grade inflammation that plays an important role in the development of insulin resistance. Tumor progression locus 2 (Tpl2) is a serine/threonine mitogen activated protein kinase kinase kinase (MAP3K) involved in regulating responses to specific inflammatory stimuli. Here we have used mice lacking Tpl2 to examine its role in obesity-associated insulin resistance. Wild type (wt) and tpl2−/− mice accumulated comparable amounts of fat and lean mass when fed either a standard chow diet or two different high fat (HF) diets containing either 42% or 59% of energy content derived from fat. No differences in glucose tolerance were observed between wt and tpl2−/− mice on any of these diets. Insulin tolerance was similar on both standard chow and 42% HF diets, but was slightly impaired in tpl2−/− mice fed the 59% HFD. While gene expression markers of macrophage recruitment and inflammation were increased in the white adipose tissue of HF fed mice compared with standard chow fed mice, no differences were observed between wt and tpl2−/− mice. Finally, a HF diet did not increase Tpl2 expression nor did it activate Extracellular Signal-Regulated Kinase 1/2 (ERK1/2), the MAPK downstream of Tpl2. These findings argue that Tpl2 does not play a non-redundant role in obesity-associated metabolic dysfunction

The Milky Way Tomography With SDSS. III. Stellar Kinematics

We study Milky Way kinematics using a sample of 18.8 million main-sequence stars with r 20 degrees). We find that in the region defined by 1 kpc < Z < 5 kpc and 3 kpc < R < 13 kpc, the rotational velocity for disk stars smoothly decreases, and all three components of the velocity dispersion increase, with distance from the Galactic plane. In contrast, the velocity ellipsoid for halo stars is aligned with a spherical coordinate system and appears to be spatially invariant within the probed volume. The velocity distribution of nearby (Z < 1 kpc) K/M stars is complex, and cannot be described by a standard Schwarzschild ellipsoid. For stars in a distance-limited subsample of stars (< 100 pc), we detect a multi-modal velocity distribution consistent with that seen by HIPPARCOS. This strong non-Gaussianity significantly affects the measurements of the velocity-ellipsoid tilt and vertex deviation when using the Schwarzschild approximation. We develop and test a simple descriptive model for the overall kinematic behavior that captures these features over most of the probed volume, and can be used to search for substructure in kinematic and metallicity space. We use this model to predict further improvements in kinematic mapping of the Galaxy expected from Gaia and the Large Synoptic Survey Telescope.NSF AST-615991, AST-0707901, AST-0551161, AST-02-38683, AST-06-07634, AST-0807444, PHY05-51164NASA NAG5-13057, NAG5-13147, NNXO-8AH83GPhysics Frontier Center/Joint Institute for Nuclear Astrophysics (JINA) PHY 08-22648U.S. National Science FoundationMarie Curie Research Training Network ELSA (European Leadership in Space Astrometry) MRTN-CT-2006-033481Fermi Research Alliance, LLC, United States Department of Energy DE-AC02-07CH11359Alfred P. Sloan FoundationParticipating InstitutionsJapanese MonbukagakushoMax Planck SocietyHigher Education Funding Council for EnglandMcDonald Observator

The negative cofactor 2 complex is a key regulator of drug resistance in Aspergillus fumigatus

The frequency of antifungal resistance, particularly to the azole class of ergosterol biosynthetic inhibitors, is a growing global health problem. Survival rates for those infected with resistant isolates are exceptionally low. Beyond modification of the drug target, our understanding of the molecular basis of azole resistance in the fungal pathogen Aspergillus fumigatus is limited. We reasoned that clinically relevant antifungal resistance could derive from transcriptional rewiring, promoting drug resistance without concomitant reductions in pathogenicity. Here we report a genome-wide annotation of transcriptional regulators in A. fumigatus and construction of a library of 484 transcription factor null mutants. We identify 12 regulators that have a demonstrable role in itraconazole susceptibility and show that loss of the negative cofactor 2 complex leads to resistance, not only to the azoles but also the salvage therapeutics amphotericin B and terbinafine without significantly affecting pathogenicity