1 (nombre)

Résumé

1 (un) est l'entier naturel représentant une entité seule — définition qui n'est autre qu'une pétition de principe. « Un » fait quelquefois référence à l'unité, et « unitaire » est quelquefois utilisé comme un adjectif dans ce sens (par exemple, un segment de longueur unitaire est un segment de longueur 1). Écriture Tous les systèmes de numération possèdent un chiffre pour signifier le nombre un. Chiffre arabe Un (chiffre) Le chiffre « un », symbolisé « 1 », est le chiffre arabe servant notamment à signifier le nombre un. Autres chiffres actuels Le chiffre « 1 » n'est pas le seul utilisé dans le monde ; un certain nombre d'alphabets — particulièrement ceux des langues du sous-continent indien et du sud-est asiatique — utilisent des chiffres différents, même au sein de la numération indo-arabe. En mathématiques Le nombre 1 est défini comme le successeur du nombre 0. C'est le plus petit ordinal successeur et le premier nombre impa

Source officielle

https://fr.wikipedia.org/wiki/1_(nombre)

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Publications associées (19)

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Cours associés (220)

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Séances de cours associées (398)

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Chargement

AiiDA 1.0, a scalable computational infrastructure for automated reproducible workflows and data provenance

Casper Welzel Andersen, Andrea Cepellotti, Fernando Gargiulo, Sebastiaan Philippe Huber, Conrad Johnston, Leonid Kahle, Boris Kozinsky, Snehal Pramod Kumbhar, Nicola Marzari, Andrius Merkys, Nicolas Frank Mounet, Elsa Passaro, Giovanni Pizzi, Christoph Leopold Talirz, Martin Uhrin, Aliaksandr Yakutovich, Spyros Zoupanos

The ever-growing availability of computing power and the sustained development of advanced computational methods have contributed much to recent scientific progress. These developments present new challenges driven by the sheer amount of calculations and data to manage. Next-generation exascale supercomputers will harden these challenges, such that automated and scalable solutions become crucial. In recent years, we have been developing AiiDA (aiida.net), a robust open-source high-throughput infrastructure addressing the challenges arising from the needs of automated workflow management and data provenance recording. Here, we introduce developments and capabilities required to reach sustained performance, with AiiDA supporting throughputs of tens of thousands processes/hour, while automatically preserving and storing the full data provenance in a relational database making it queryable and traversable, thus enabling high-performance data analytics. AiiDA's workflow language provides advanced automation, error handling features and a flexible plugin model to allow interfacing with external simulation software. The associated plugin registry enables seamless sharing of extensions, empowering a vibrant user community dedicated to making simulations more robust, user-friendly and reproducible.

2020

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The Nt17 Domain and its Helical Conformation Regulate the Aggregation, Cellular Properties and Neurotoxicity of Mutant Huntingtin Exon 1

Urszula Beata Cendrowska, Anass Chiki, Sean Michael Deguire, Giovanni Dietler, Hilal Lashuel, Anne-Laure Mahul Mellier, Nathan Alain Denis Riguet, Francesco Simone Ruggeri, Sophie Vieweg

Converging evidence points to the N-terminal domain comprising the first 17 amino acids of the Huntingtin protein (Nt17) as a key regulator of its aggregation, cellular properties and toxicity. In this study, we further investigated the interplay between Nt17 and the polyQ domain repeat length in regulating the aggregation and inclusion formation of exon 1 of the Huntingtin protein (Httex1). In addition, we investigated the effect of removing Nt17 or modulating its local structure on the membrane interactions, neuronal uptake, and toxicity of monomeric or fibrillar Httex1. Our results show that the polyQ and Nt17 domains synergistically modulate the aggregation propensity of Httex1 and that the Nt17 domain plays important roles in shaping the surface properties of mutant Httex1 fibrils and regulating their poly-Q-dependent growth, lateral association and neuronal uptake. Removal of Nt17 or disruption of its transient helical conformations slowed the aggregation of monomeric Httex1 in vitro, reduced inclusion formation in cells, enhanced the neuronal uptake and nuclear accumulation of monomeric Httex1 proteins, and was sufficient to prevent cell death induced by Httex1 72Q overexpression. Finally, we demonstrate that the uptake of Httex1 fibrils into primary neurons and the resulting toxicity are strongly influenced by mutations and phosphorylation events that influence the local helical propensity of Nt17. Altogether, our results demonstrate that the Nt17 domain serves as one of the key master regulators of Htt aggregation, internalization, and toxicity and represents an attractive target for inhibiting Htt aggregate formation, inclusion formation, and neuronal toxicity.

2021

Chargement

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AMP-activated protein kinase (AMPK) plays diverse roles and coordinates complex metabolic pathways for maintenance of energy homeostasis. This could be explained by the fact that AMPK exists as multiple heterotrimer complexes comprising a catalytic alpha-subunit (alpha 1 and alpha 2) and regulatory beta (beta 1 and beta 2)- and gamma (gamma 1, gamma 2, gamma 3)-subunits, which are uniquely distributed across different cell types. There has been keen interest in developing specific and isoform-selective AMPK-activating drugs for therapeutic use and also as research tools. Moreover, establishing ways of enhancing cellular AMPK activity would be beneficial for both purposes. Here, we investigated if a recently described potent AMPK activator called 991, in combination with the commonly used activator 5-aminoimidazole-4-carboxamide riboside or contraction, further enhances AMPK activity and glucose transport in mouse skeletal muscle ex vivo. Given that the gamma 3-subunit is exclusively expressed in skeletal muscle and has been implicated in contraction-induced glucose transport, we measured the activity of AMPK gamma 3 as well as ubiquitously expressed gamma 1-containing complexes. We initially validated the specificity of the antibodies for the assessment of isoform-specific AMPK activity using AMPK-deficient mouse models. We observed that a low dose of 991 (5 mu M) stimulated a modest or negligible activity of both gamma 1- and gamma 3-containing AMPK complexes. Strikingly, dual treatment with 991 and 5-aminoimidazole-4-carboxamide riboside or 991 and contraction profoundly enhanced AMPK gamma 1/gamma 3 complex activation and glucose transport compared with any of the single treatments. The study demonstrates the utility of a dual activator approach to achieve a greater activation of AMPK and downstream physiological responses in various cell types, including skeletal muscle.

Amer Physiological Soc2016

Chargement

The Nt17 Domain and its Helical Conformation Regulate the Aggregation, Cellular Properties and Neurotoxicity of Mutant Huntingtin Exon 1

Urszula Beata Cendrowska, Anass Chiki, Sean Michael Deguire, Giovanni Dietler, Hilal Lashuel, Anne-Laure Mahul Mellier, Nathan Alain Denis Riguet, Francesco Simone Ruggeri, Sophie Vieweg

2021