478 research outputs found

    An Embedding of the BSS Model of Computation in Light Affine Lambda-Calculus

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    This paper brings together two lines of research: implicit characterization of complexity classes by Linear Logic (LL) on the one hand, and computation over an arbitrary ring in the Blum-Shub-Smale (BSS) model on the other. Given a fixed ring structure K we define an extension of Terui's light affine lambda-calculus typed in LAL (Light Affine Logic) with a basic type for K. We show that this calculus captures the polynomial time function class FP(K): every typed term can be evaluated in polynomial time and conversely every polynomial time BSS machine over K can be simulated in this calculus.Comment: 11 pages. A preliminary version appeared as Research Report IAC CNR Roma, N.57 (11/2004), november 200

    Quantum entanglement and the Bell Matrix

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    We present a class of maximally entangled states generated by a high-dimensional generalisation of the \textsc{cnot} gate. The advantage of our approach is the simple algebraic structure of both entangling operator and resulting entangled states. In order to show that the method can be applied to any dimension, we introduce new sufficient conditions for global and maximal entanglement with respect to Meyer and Wallach's measure.Comment: 11 pages, 3 figure

    Functions and mechanisms of Rab46 in endothelial cells

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    Endothelial cells maintain vascular integrity by regulating a number of physiological and pathophysiological processes, including haemostasis, thrombosis and inflammation. A pivotal contribution to these processes is the exocytosis of cargo from specialized endothelial storage organelles, namely Weibel-Palade bodies (WPBs). WPBs provide an intracellular storage pool of pro-thrombotic and pro-inflammatory mediators which can be differentially released in response to different stimuli. Ca2+ raising agonists such as thrombin and histamine, respectively released following vascular injury or an immunogenic insult, evoke WPB exocytosis. However, inappropriate and untimely exocytosis of WPBs can promote the pro-thrombotic and pro-inflammatory environment evident in cardiovascular diseases. The mechanisms underlying differential cargo release in order to produce physiologically distinct responses are poorly understood. Some Rab GTPase family members, have been reported to be implicated in regulating the exocytosis of WPBs. Here, we describe a novel Rab GTPase (Rab46) in endothelial cells that is located on WPBs. Super-resolution microscopy confirmed that Rab46 is juxtaposed to von Willebrand Factor (vWF), on the cytosolic side of individual WPBs, whilst quantitative imaging analysis suggested that Rab46 may regulate a subpopulation of WPBs. Interestingly, Rab46 was necessary for acute histamine, but not thrombin, WPB trafficking towards the perinuclear area identified as the Microtubule Organizing Centre (MTOC). Biochemical analysis and mass spectrometry was used to investigate the molecular mechanisms underlying Rab46-dependent retrograde trafficking and the dynein heavy chain was identified as a candidate effector protein. Further biochemical experiments suggested a direct interaction between endogenous Rab46 and the dynein motor complex. Taken together, these results suggest that after acute histamine stimulation, dynein-bound Rab46 mediates retrograde transport of a subset of WPBs along microtubules to the MTOC. These observations indicate Rab46 as a key regulator of differential WPB cargo secretion, allowing an appropriate acute pro-inflammatory response whilst avoiding release of excessive pro-thrombotic mediators. Characterization of in vivo model of Rab46 represents the beginning of understanding the physiological contribution of Rab46 as well as its response to pathological conditions. Understanding the Rab46/WPB signalling axis, both in vitro and in vivo, could be important for achieving better appreciation of how the endothelial cell fine-tunes it’s secretory response and thereby providing novel therapeutic targets for the prevention of endothelial dysfunction, which is often the trigger for cardiovascular diseases

    Investigations into structure and properties of atomically-precise transition metal-chalcogenide clusters of CrTe and ligated Cr6Te8(PEt3)6

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    The complete understanding of a clusters electronic structure, the primary mechanisms for its properties and stabilization is necessary in order to functionalize them for use as building blocks within novel materials. First principle theoretical studies have been carried out upon the electronic properties of CrxTey (x = 1 – 6, y = 0 – 8, x + y ≤ 14), as well as for the larger triethylphosphine (PEt3) ligated cluster system of Cr6Te8(PEt3)6. Together, we aim to use the information garnered from the smaller clusters to address the underlying behavior of the ligated Cr6Te8(PEt3)6. Additionally, the properties of this larger cluster will be used to further understand its role when paired with C60 within the binary cluster assembled material. The stability and macroscopic properties of the Cr6Te8(PEt3)6 cluster, have been found to be sensitive to type of passivating ligand. As will be shown, the ground state structures of Crn atoms are sensitive to both the number and position of bonded Te atoms. Moreover, that this sensitivity carries over into larger cluster sizes, and at several size intervals produces clusters with high magnetization. To this, we add the investigation into the manipulation of the Cr6Te8 cluster geometry and its properties through various ligands, such as PH3, CO, and CN. It will show, that in altering these ligands there is a modification to the clusters valence shell count, which in turn alters its ionization potential and electron affinity. Additionally, although the ionization potential and electron affinity have changed for the Cr6Te8(PEt3)6 cluster, it has been found that its high magnetization does not

    Implementation of a regulatory gene network to simulate the TH1/2 differentiation in an agent-based model of hypersensitivity reactions

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    Abstract Motivation: An unbalanced differentiation of T helper cells from precursor type TH0 to the TH1 or TH2 phenotype in immune responses often leads to a pathological condition. In general, immune reactions biased toward TH1 responses may result in auto-immune diseases, while enhanced TH2 responses may cause allergic reactions. The aim of this work is to integrate a gene network of the TH differentiation in an agent-based model of the hyper-sensitivity reaction. The implementation of such a system introduces a second level of description beyond the mesoscopic level of the inter-cellular interaction of the agent-based model. The intra-cellular level consists in the cell internal dynamics of gene activation and transcription. The gene regulatory network includes genes-related molecules that have been found to be involved in the differentiation process in TH cells. Results: The simulator reproduces the hallmarks of an IgE-mediated hypersensitive reaction and provides an example of how to combine the mesoscopic level description of immune cells with the microscopic gene-level dynamics. Availability: The basic version of the simulator of the immune response can be downloaded here: http://www.iac.cnr.it/~filippo/C-ImmSim.html Contact: [email protected] Supplementary information: Supplementary data are available at Bioinformatics online
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