Distribution and Kinematics of O VI in the Galactic Halo

FUSE spectra of 100 extragalactic objects are analyzed to obtain measures of O VI absorption along paths through the Milky Way thick disk/halo. Strong O VI absorption over the approximate velocity range from -100 to 100 km/s reveals a widespread but highly irregular distribution of thick disk O VI, implying the existence of substantial amounts of hot gas with T ~ 3x10^5 K in the Milky Way halo. Large irregularities in the distribution of the absorbing gas are found to be similar over angular scales extending from less than one to 180 degrees, indicating a considerable amount of small and large scale structure in the gas. The overall distribution of Galactic O VI is not well described by a symmetrical plane-parallel layer of patchy O VI absorption. The simplest departure from such a model that provides a reasonable fit to the observations is a plane-parallel patchy absorbing layer with a scale height of 2.3 kpc, and a 0.25 dex excess of O VI in the northern Galactic polar region. The O VI absorption has a Doppler parameter b = 30 to 99 km/s, with an average value of 60 km/s . Thermal broadening alone cannot explain the large observed profile widths. The average O VI absorption velocities toward high latitude objects range from -46 to 82 km/s, with a sample average of 0 km/s and a standard deviation of 21 km/s. O VI associated with the thick disk moves both toward and away from the plane with roughly equal frequency. A combination of models involving the radiative cooling of hot fountain gas, the cooling of supernova bubbles in the halo, and the turbulent mixing of warm and hot halo gases is required to explain the presence of O VI and other highly ionized atoms found in the halo. (abbreviated)Comment: 70 pages, single-spaced, PDF format. Bound copies of this manuscript and two accompanying articles are available upon request. Submitted to ApJ

Self-regulation: differences by year and area in college students

Neste estudo procura-se analisar a existência de diferenças nas estratégias auto-regulatórias de alunos universitários em áreas de formação distintas. Participaram 518 alunos de três níveis (inicial, intermédio e final) das áreas de ciências e humanidades. Aplicou-se a escala “CHE – Comportamentos e hábitos de estudo e aprendizagem”, que avalia cinco dimensões: estratégias cognitivas de transformação e manipulação da informação, organização e planeamento de rotinas, gestão e monitorização, aquisição e selecção da informação, e reforço motivacional. Verificou-se uma maior utilização das estratégias cognitivas e metacognitivas de gestão e monitorização apesar dos resultados não indicarem diferenças substantivas entre os alunos diferenciados por nível e área. Os resultados podem indicar estabilidade nos comportamentos ou limitações no tipo de instrumento e amostra utilizada. O estudo de mudanças nestas estratégias deverá ser conduzido com recurso a delineamentos longitudinais. O impacto da estabilidade deverá ser ponderado na elaboração de projectos de intervenção.In this study we seek to analyze the existence of differences in self-regulating strategies of university students in distinct graduation areas. 518 students of three levels (initial, intermediate and final) of science and humanities fields participated. We used the scale “Behavior and study skill”, which evaluates five dimensions: cognitive strategies of transformation and manipulation of information, organization and planning of routines, management and monitoring, information acquisition and selection, and motivational reinforcement. A higher use of cognitive and metacognitive strategies of management and monitoring was noted although the results do not indicate major differences between students in different levels and graduation areas. The results can indicate stability in the behaviors or limitations in the type of instrument and in the sample used. The study of changes in these strategies must be carried out having in mind longitudinal outlines. The impact of the stability should be taken into account while elaborating intervention projects.(undefined

CD8+ T-Cell Interleukin-7 Receptor Alpha Expression as a Potential Indicator of Disease Status in HIV-Infected Children

Background: Initiation and modification of antiretroviral therapy in HIV-infected children depend on viral load and CD4+ T-cell count. However, these surrogates have limitations, and complementary immunological markers to assess therapeutic response are needed. Our aim was to evaluate CD8+ T-cell expression of CD127 as a marker of disease status in HIV-infected children, based on adult data suggesting its usefulness. We hypothesized that CD127 expression on CD8+ T-cells is lower in children with more advanced disease. Methods: In a cross-sectional evaluation, we used flow cytometry to measure CD127+ expression on CD8+ T-cells in whole blood from HIV-infected children with varying disease status. This was compared with expression of CD38 on this subset, currently used in clinical practice as a marker of disease status. Results: 51 HIV-infected children were enrolled. There was a strong positive correlation between CD127 expression on CD8+ T-cells and CD4+ T-cell count, and height and weight z-scores, and a strong negative correlation between CD127 expression and viral load. In contrast, we found no association between CD38 expression and these disease status markers. Conclusions: CD8+ T-cell CD127 expression is significantly higher in children with better HIV disease control, and may have a role as an immunologic indicator of disease status. Longitudinal studies are needed to determine the utility of this marker as a potential indicator of HIV disease progression

Impact of long-term viral suppression in CD4+ recovery of HIV-children on Highly Active Antiretroviral Therapy

BACKGROUND: The effects of HAART may differ between children and adults because children have a developing immune system, and the long-term immunological outcome in HIV-infected children on HAART is not well-known. A major aim of our study was to determine CD4+ evolution associated with long-term VL control during 4 years of observation on HAART. METHODS: We carried out a retrospective study on a cohort of 160 vertically HIV-infected children. It was carried out from 1996 to 2004 in six large Spanish pediatric referral hospitals. We compared 33 children who had long-term VL suppression (VL ≤400 copies/ml) in the first 12 months of follow-up and maintained that level throughout follow-up (Responders-group), and 127 children with persistently detectable VL in spite of ART switches (Non-Responders-group). RESULTS: We observed a quick initial and significant increase in CD4(+ )counts from the baseline to 12 months on HAART in both groups (p < 0.01). The Non-Responders group sustained CD4+ increases and most of these children maintained high CD4(+ )level counts (≥25%). The Non-Responders group reached a plateau between 26% and 27% CD4(+ )at the first 12 months of follow-up that remained stable during the following 3 years. However, the Responders group reached a plateau between 30% and 32% CD4(+ )at 24, 36 and 48 months of follow-up. We found that the Responders group had higher CD4(+ )count values and higher percentages of children with CD4(+ )≥25% than the Non-Responders group (p < 0.05) after month 12. CONCLUSION: Long-term VL suppression in turn induces large beneficial effects in immunological responses. However, it is not indispensable to recover CD4(+ )levels

Structural cerebellar correlates of cognitive functions in spinocerebellar ataxia type 2

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant neurodegenerative disease involving the cerebellum and characterized by a typical motor syndrome. In addition, the presence of cognitive impairment is now widely acknowledged as a feature of SCA2. Given the extensive connections between the cerebellum and associative cerebral areas, it is reasonable to hypothesize that cerebellar neurodegeneration associated with SCA2 may impact on the cerebellar modulation of the cerebral cortex, thus resulting in functional impairment. The aim of the present study was to investigate and quantitatively map the pattern of cerebellar gray matter (GM) atrophy due to SCA2 neurodegeneration and to correlate that with patients' cognitive performances. Cerebellar GM maps were extracted and compared between SCA2 patients (n = 9) and controls (n = 33) by using voxel-based morphometry. Furthermore, the relationship between cerebellar GM atrophy and neuropsychological scores of the patients was assessed. Specific cerebellar GM regions were found to be affected in patients. Additionally, GM loss in cognitive posterior lobules (VI, Crus I, Crus II, VIIB, IX) correlated with visuospatial, verbal memory and executive tasks, while additional correlations with motor anterior (V) and posterior (VIIIA, VIIIB) lobules were found for the tasks engaging motor and planning components. Our results provide evidence that the SCA2 neurodegenerative process affects the cerebellar cortex and that MRI indices of atrophy in different cerebellar subregions may account for the specificity of cognitive symptomatology observed in patients, as result of a cerebello-cerebral dysregulation

Adenosine Deaminase Acting on RNA-1 (ADAR1) Inhibits HIV-1 Replication in Human Alveolar Macrophages

While exploring the effects of aerosol IFN-γ treatment in HIV-1/tuberculosis co-infected patients, we observed A to G mutations in HIV-1 envelope sequences derived from bronchoalveolar lavage (BAL) of aerosol IFN-γ-treated patients and induction of adenosine deaminase acting on RNA 1 (ADAR1) in the BAL cells. IFN-γ induced ADAR1 expression in monocyte-derived macrophages (MDM) but not T cells. ADAR1 siRNA knockdown induced HIV-1 expression in BAL cells of four HIV-1 infected patients on antiretroviral therapy. Similar results were obtained in MDM that were HIV-1 infected in vitro . Over-expression of ADAR1 in transformed macrophages inhibited HIV-1 viral replication but not viral transcription measured by nuclear run-on, suggesting that ADAR1 acts post-transcriptionally. The A to G hyper-mutation pattern observed in ADAR1 over-expressing cells in vitro was similar to that found in the lungs of HIV-1 infected patients treated with aerosol IFN-γ suggesting the model accurately represented alveolar macrophages. Together, these results indicate that ADAR1 restricts HIV-1 replication post-transcriptionally in macrophages harboring HIV-1 provirus. ADAR1 may therefore contribute to viral latency in macrophages