2,053 research outputs found

    Space storm measurements of the July 2005 solar extreme events from the low corona to the Earth

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    The Athens Neutron Monitor Data Processing (ANMODAP) Center recorded an unusual Forbush decrease with a sharp enhancement of cosmic ray intensity right after the main phase of the Forbush decrease on 16 July 2005, followed by a second decrease within less than 12 h. This exceptional event is neither a ground level enhancement nor a geomagnetic effect in cosmic rays. It rather appears as the effect of a special structure of interplanetary disturbances originating from a group of coronal mass ejections (CMEs) in the 13-14 July 2005 period. The initiation of the CMEs was accompanied by type IV radio bursts and intense solar flares (SFs) on the west solar limb (AR 786); this group of energetic phenomena appears under the label of Solar Extreme Events of July 2005. We study the characteristics of these events using combined data from Earth (the ARTEMIS IV radioheliograph, the Athens Neutron Monitor (ANMODAP)), space (WIND/WAVES) and data archives. We propose an interpretation of the unusual Forbush profile in terms of a magnetic structure and a succession of interplanetary shocks interacting with the magnetosphere.Comment: Advances in Space Research, Volume 43, Issue 4, p. 600-60

    Regional Transfer Multipliers

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    A series of discontinuities in the allocation mechanism of federal transfers, to municipal governments in Brazil allow us to identify the causal effect of public spending on local labor markets, using a ‘fuzzy’ Regression Discontinuity Design (RDD). Our estimates imply a cost per job of about 8,000 US dollars per year and a local income multiplier around two. The effect comes mostly from employment in services and is more pronounced among less financially developed municipalities

    Oxidative stress dependent microRNA-34a activation via PI3Kα reduces the expression of sirtuin-1 and sirtuin-6 in epithelial cells

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    Sirtuin-1 (SIRT1) and SIRT6, NAD(+)-dependent Class III protein deacetylases, are putative anti-aging enzymes, down-regulated in patients with chronic obstructive pulmonary disease (COPD), which is characterized by the accelerated ageing of the lung and associated with increased oxidative stress. Here, we show that oxidative stress (hydrogen peroxide) selectively elevates microRNA-34a (miR-34a) but not the related miR-34b/c, with concomitant reduction of SIRT1/-6 in bronchial epithelial cells (BEAS2B), which was also observed in peripheral lung samples from patients with COPD. Over-expression of a miR-34a mimic caused a significant reduction in both mRNA and protein of SIRT1/-6, whereas inhibition of miR-34a (antagomir) increased these sirtuins. Induction of miR-34a expression with H2O2 was phosphoinositide-3-kinase (PI3K) dependent as it was associated with PI3Kα activation as well as phosphatase and tensin homolog (PTEN) reduction. Importantly, miR-34a antagomirs increased SIRT1/-6 mRNA levels, whilst decreasing markers of cellular senescence in airway epithelial cells from COPD patients, suggesting that this process is reversible. Other sirtuin isoforms were not affected by miR-34a. Our data indicate that miR-34a is induced by oxidative stress via PI3K signaling, and orchestrates ageing responses under oxidative stress, therefore highlighting miR-34a as a new therapeutic target and biomarker in COPD and other oxidative stress-driven aging diseases

    Lack of Genetic Interaction between Tbx20 and Tbx3 in Early Mouse Heart Development

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    Members of the T-box family of transcription factors are important regulators orchestrating the complex regionalization of the developing mammalian heart. Individual mutations in Tbx20 and Tbx3 cause distinct congenital heart abnormalities in the mouse: Tbx20 mutations result in failure of heart looping, developmental arrest and lack of chamber differentiation, while hearts of Tbx3 mutants progress further, loop normally but show atrioventricular convergence and outflow tract defects. The two genes have overlapping areas of expression in the atrioventricular canal and outflow tract of the heart but their potential genetic interaction has not been previously investigated. In this study we produced compound mutants to investigate potential genetic interactions at the earliest stages of heart development. We find that Tbx20; Tbx3 double heterozygous mice are viable and fertile with no apparent abnormalities, while double homozygous mutants are embryonic lethal by midgestation. Double homozygous mutant embryos display abnormal cardiac morphogenesis, lack of heart looping, expression patterns of cardiac genes and time of death that are indistinguishable from Tbx20 homozygous mutants. Prior to death, the double homozygotes show an overall developmental delay similar to Tbx3 homozygous mutants. Thus the effects of Tbx20 are epistatic to Tbx3 in the heart but Tbx3 is epistatic to Tbx20 with respect to developmental delay
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