"Neither from nor towards; at the still point, there the dance is". Recensione alla mostra di Bill Viola "Rinascimento elettronico" (dal 10 marzo al 23 luglio 2017, Palazzo Strozzi, Firenze 2017)

Focus on "Rinascimento elettronico" \u2013 exhibition displayed in Palazzo Strozzi, Firenze (May/July 2017). Bill Viola uses videos to explore the phenomena of sense perception as paths to self-acknowledgement. His works target universal human experiences\u2014birth, death, and the unfolding of consciousness\u2014and have roots in both Eastern and Western art, as well as spiritual traditions, including Zen Buddhism, Islamic Sufism, and Christian mysticism. Using the inner language of subjective thoughts and collective memories, his videos communicate to a wide audience, allowing viewers to experience the work directly, and in their own personal way

Estimation of hail damage using crop models and remote sensing

Insurance agents often provide crop hail damage estimates based on their personal experience and field samples, which are not always representative of the investigated field\u2019s spatial variability. For these reasons, farmers and the insurance market ask for a reliable, objective, and less labor-intensive method to determine crop hail losses. Integrating remote sensing and crop modeling provides a unique opportunity for the crop insurance market for a reliable, objective, and less labor-intensive method to estimate hail damage. To this end, a study was conducted on eight distinct maize fields for a total of 90 hectares. Five fields were damaged by the hailstorm that occurred on 13 July 2019 and three were not damaged. Soil and plant samples were collected to characterize the experimental areas. The Surface Energy Balance Algorithm for Land (SEBAL) was deployed to determine the total aboveground biomass and obtainable yield at harvest, using Landsat 7 and 8 satellite images. Modeled hail damages (HDDSSAT1, coupling SEBAL estimates of obtainable yield and DSSAT-based potential yield; HDDSSAT2, coupling yield map at harvest and the Decision Support System for Agrotechnology Transfer (DSSAT)-based potential yield) were calculated and compared to the estimates of the insurance company (HDinsurance). SEBAL-based biomass and yield estimates agreed with in-season measurements ( 124% and +0.5%, respectively). While some under and overestimations were observed, HDinsurance and HDDSSAT1 averaged similar values ( 124.9% and +3.4%) compared to the reference approach (HDDSSAT2)

Increased age is associated with epigenetic and structural changes in chromatin from neuronal nuclei

FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOChromatin organization has been considered to play a major role on aging, by regulating DNA accessibility to transcription and repair machinery. Such organization can be modulated by epigenetic events, such as DNA methylation and histone post-translational modifications. Since changes on gene expression profiles have been described in aged neurons, our aim was to study the age-dependent relationship between structural and epigenetic alterations on chromatin of cortical neurons from mice. For this purpose, isolated neuronal nuclei from mice of two ages were studied by image analysis after cytochemistry, or assessed for chromatin accessibility by enzymatic digestion. Additionally, two epigenetic marks, for open and for densely packed chromatin fibers were quantified. Results indicate epigenetically driven alterations on chromatin organization of cortical neurons with advancing age, whose fibers seem to undergo redistribution and unpackaging. Since increased transcriptional activity is not characteristic of aged neurons, these loosened chromatin fibers may be associated with impaired genome stability, as well as with increased accessibility of repair machinery to a life span damaged DNA. J. Cell. Biochem. 115: 659-665, 2014. © 2013 Wiley Periodicals, Inc. © 2013 Wiley Periodicals, Inc.Chromatin organization has been considered to play a major role on aging, by regulating DNA accessibility to transcription and repair machinery. Such organization can be modulated by epigenetic events, such as DNA methylation and histone post-translational modifications. Since changes on gene expression profiles have been described in aged neurons, our aim was to study the age-dependent relationship between structural and epigenetic alterations on chromatin of cortical neurons from mice. For this purpose, isolated neuronal nuclei from mice of two ages were studied by image analysis after cytochemistry, or assessed for chromatin accessibility by enzymatic digestion. Additionally, two epigenetic marks, for open and for densely packed chromatin fibers were quantified. Results indicate epigenetically driven alterations on chromatin organization of cortical neurons with advancing age, whose fibers seem to undergo redistribution and unpackaging. Since increased transcriptional activity is not characteristic of aged neurons, these loosened chromatin fibers may be associated with impaired genome stability, as well as with increased accessibility of repair machinery to a life span damaged DNA.Chromatin organization has been considered to play a major role on aging, by regulating DNA accessibility to transcription and repair machinery. Such organization can be modulated by epigenetic events, such as DNA methylation and histone post-translational modifications. Since changes on gene expression profiles have been described in aged neurons, our aim was to study the age-dependent relationship between structural and epigenetic alterations on chromatin of cortical neurons from mice. For this purpose, isolated neuronal nuclei from mice of two ages were studied by image analysis after cytochemistry, or assessed for chromatin accessibility by enzymatic digestion. Additionally, two epigenetic marks, for open and for densely packed chromatin fibers were quantified. Results indicate epigenetically driven alterations on chromatin organization of cortical neurons with advancing age, whose fibers seem to undergo redistribution and unpackaging. Since increased transcriptional activity is not characteristic of aged neurons, these loosened chromatin fibers may be associated with impaired genome stability, as well as with increased accessibility of repair machinery to a life span damaged DNA.1154659665FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO2008/58067‐2; 2010/50015‐6471303/2009‐7; 301943/2009‐5; 506463/2010‐

ATRX binds to atypical chromatin domains at the 3′ exons of zinc finger genes to preserve H3K9me3 enrichment

<p>ATRX is a SWI/SNF chromatin remodeler proposed to govern genomic stability through the regulation of repetitive sequences, such as rDNA, retrotransposons, and pericentromeric and telomeric repeats. However, few direct ATRX target genes have been identified and high-throughput genomic approaches are currently lacking for ATRX. Here we present a comprehensive ChIP-sequencing study of ATRX in multiple human cell lines, in which we identify the 3′ exons of zinc finger genes (ZNFs) as a new class of ATRX targets. These 3′ exonic regions encode the zinc finger motifs, which can range from 1–40 copies per ZNF gene and share large stretches of sequence similarity. These regions often contain an atypical chromatin signature: they are transcriptionally active, contain high levels of H3K36me3, and are paradoxically enriched in H3K9me3. We find that these ZNF 3′ exons are co-occupied by SETDB1, TRIM28, and ZNF274, which form a complex with ATRX. CRISPR/Cas9-mediated loss-of-function studies demonstrate (i) a reduction of H3K9me3 at the ZNF 3′ exons in the absence of ATRX and ZNF274 and, (ii) H3K9me3 levels at atypical chromatin regions are particularly sensitive to ATRX loss compared to other H3K9me3-occupied regions. As a consequence of ATRX or ZNF274 depletion, cells with reduced levels of H3K9me3 show increased levels of DNA damage, suggesting that ATRX binds to the 3′ exons of ZNFs to maintain their genomic stability through preservation of H3K9me3.</p