1,721,308 research outputs found

    The Studio Reader: On the Space of Artists

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    Book Review of The Studio Reader: On the Space of Artists, ed. by Mary Jane Jacob and Michelle Grabner. ISBN 9780226389615. Reviewed by Carolyn Caizzi

    Anna Treves, Le nascite e la politica nell’Italia del Novecento

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    Caizzi Andréa. Anna Treves, Le nascite e la politica nell’Italia del Novecento. In: Recherches et Prévisions, n°80, 2005. Acteurs et politiques de la petite enfance. Permanences et mutations. pp. 152-154

    La modernisation et le service : un mariage de sentiments ou de raison ?

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    Caizzi Andréa. La modernisation et le service : un mariage de sentiments ou de raison ?. In: Recherches et Prévisions, n°87, 2007. La nouvelle administration. Le social administré. pp. 51-56

    Caizzi (B.) - Industria, Commercio e Banca in Lombardia nel XVIII secolo.

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    Bousquet G.-H. Caizzi (B.) - Industria, Commercio e Banca in Lombardia nel XVIII secolo.. In: Revue économique, volume 21, n°3, 1970. p. 506

    Alien Registration- Caizzi, Mauro (Portland, Cumberland County)

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    https://digitalmaine.com/alien_docs/22903/thumbnail.jp

    Recensione di F. Decleva Caizzi, Pirroniana, Led, Milano 2020 (319 pp.)

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    Recensione di F. Decleva Caizzi, Pirroniana, Led, Milano 2020 (319 pp.

    Caizzi (B.) - Industria, Commercio e Banca in Lombardia nel XVIII secolo.

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    Bousquet G.-H. Caizzi (B.) - Industria, Commercio e Banca in Lombardia nel XVIII secolo.. In: Revue économique, volume 21, n°3, 1970. p. 506

    Global donor and acceptor splicing site kinetics in human cells

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    RNA splicing is an essential part of eukaryotic gene expression. Although the mechanism of splicing has been extensively studied in vitro, in vivo kinetics for the two-step splicing reaction remain poorly understood. Here, we combine transient transcriptome sequencing (TT-seq) and mathematical modeling to quantify RNA metabolic rates at donor and acceptor splice sites across the human genome. Splicing occurs in the range of minutes and is limited by the speed of RNA polymerase elongation. Splicing kinetics strongly depends on the position and nature of nucleotides flanking splice sites, and on structural interactions between unspliced RNA and small nuclear RNAs in spliceosomal intermediates. Finally, we introduce the \‘yield\’ of splicing as the efficiency of converting unspliced to spliced RNA and show that it is highest for mRNAs and independent of splicing kinetics. These results lead to quantitative models describing how splicing rates and yield are encoded in the human genome.Genes are portions of DNA that carry the instructions to build proteins. In particular, they are formed of segments called exons, which contain the protein-building information, and of non-coding segments known as introns. Exons and introns alternate within a gene. To create a given protein, the cell first uses an enzyme, Polymerase II, to copy the entire related gene – including introns and exons – into a molecule of ribonucleic acid, or RNA. As the gene is copied, a machine called the spliceosome comes onto the RNA molecule to remove the introns and create the final RNA template used to produce proteins. The spliceosome works by recognizing specific sequences that signal the border between introns and exons. Once the machine is bound to these ‘splice sites’ on each side of an intron, it brings the two neighboring exons close together and cuts out the intron. The two ends of the exons are then attached together. Previous studies have measured how fast introns are removed, but it remained unclear how long it takes to cut individual splice sites genome-wide. To address this question, Wachutka, Caizzi et al. combined a mathematical approach with a biochemical method that purifies newly made RNA in human cells. The experiments showed that it only took a few minutes to cut most splice sites. Cutting splice sites that bordered very long introns was slower, presumably because the Polymerase II took longer to produce these introns. In addition, the genetic sequences of the splice sites affected the time it took to remove the introns: some made it harder for the spliceosome to recognize where to cut, but others made it easier. Mistakes in removing introns from RNA can lead to producing abnormal proteins, and many diseases such as cystic fibrosis and Duchenne muscular dystrophy can be caused by such errors. In particular, small changes in the sequences at the splice sites or in the surrounding areas can create problems when it comes to eliminating introns. Decrypting the dynamics of intron cutting and removal may give scientists new insight into the molecular causes of cystic fibrosis and many other genetic disorders.RNA splicing is an essential part of eukaryotic gene expression. Although the mechanism of splicing has been extensively studied in vitro, in vivo kinetics for the two-step splicing reaction remain poorly understood. Here, we combine transient transcriptome sequencing (TT-seq) and mathematical modeling to quantify RNA metabolic rates at donor and acceptor splice sites across the human genome. Splicing occurs in the range of minutes and is limited by the speed of RNA polymerase elongation. Splicing kinetics strongly depends on the position and nature of nucleotides flanking splice sites, and on structural interactions between unspliced RNA and small nuclear RNAs in spliceosomal intermediates. Finally, we introduce the ‘yield’ of splicing as the efficiency of converting unspliced to spliced RNA and show that it is highest for mRNAs and independent of splicing kinetics. These results lead to quantitative models describing how splicing rates and yield are encoded in the human genome.Genes are portions of DNA that carry the instructions to build proteins. In particular, they are formed of segments called exons, which contain the protein-building information, and of non-coding segments known as introns. Exons and introns alternate within a gene. To create a given protein, the cell first uses an enzyme, Polymerase II, to copy the entire related gene – including introns and exons – into a molecule of ribonucleic acid, or RNA. As the gene is copied, a machine called the spliceosome comes onto the RNA molecule to remove the introns and create the final RNA template used to produce proteins. The spliceosome works by recognizing specific sequences that signal the border between introns and exons. Once the machine is bound to these ‘splice sites’ on each side of an intron, it brings the two neighboring exons close together and cuts out the intron. The two ends of the exons are then attached together. Previous studies have measured how fast introns are removed, but it remained unclear how long it takes to cut individual splice sites genome-wide. To address this question, Wachutka, Caizzi et al. combined a mathematical approach with a biochemical method that purifies newly made RNA in human cells. The experiments showed that it only took a few minutes to cut most splice sites. Cutting splice sites that bordered very long introns was slower, presumably because the Polymerase II took longer to produce these introns. In addition, the genetic sequences of the splice sites affected the time it took to remove the introns: some made it harder for the spliceosome to recognize where to cut, but others made it easier. Mistakes in removing introns from RNA can lead to producing abnormal proteins, and many diseases such as cystic fibrosis and Duchenne muscular dystrophy can be caused by such errors. In particular, small changes in the sequences at the splice sites or in the surrounding areas can create problems when it comes to eliminating introns. Decrypting the dynamics of intron cutting and removal may give scientists new insight into the molecular causes of cystic fibrosis and many other genetic disorders

    Fernanda Decleva Caizzi, Maria Serena Funghi, Marcello Gigante, François Lasserre, Anna Santoni (Ed.), Varia Papyrologica

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    Heilporn Paul. Fernanda Decleva Caizzi, Maria Serena Funghi, Marcello Gigante, François Lasserre, Anna Santoni (Ed.), Varia Papyrologica. In: L'antiquité classique, Tome 62, 1993. pp. 443-444
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