DefSLAM: Tracking and Mapping of Deforming Scenes from Monocular Sequences

Monocular simultaneous localization and mapping (SLAM) algorithms perform robustly when observing rigid scenes; however, they fail when the observed scene deforms, for example, in medical endoscopy applications. In this article, we present DefSLAM, the first monocular SLAM capable of operating in deforming scenes in real time. Our approach intertwines Shape-from-Template (SfT) and Non-Rigid Structure-from-Motion (NRSfM) techniques to deal with the exploratory sequences typical of SLAM. A deformation tracking thread recovers the pose of the camera and the deformation of the observed map, at frame rate, by means of SfT processing a template that models the scene shape-at-rest. A deformation mapping thread runs in parallel with the tracking to update the template, at keyframe rate, by means of an isometric NRSfM processing a batch of full perspective keyframes. In our experiments, DefSLAM processes close-up sequences of deforming scenes, both in a laboratory-controlled experiment and in medical endoscopy sequences, producing accurate 3-D models of the scene with respect to the moving camera

Reconfigurable Network for Quantum Transport Simulation

In 1981, Richard Feynman discussed the possibility of performing quantum mechanical simulations of nature. Ever since, there has been an enormous interest in using quantum mechanical systems, known as quantum simulators, to mimic specific physical systems. Hitherto, these controllable systems have been implemented on different platforms that rely on trapped atoms, superconducting circuits and photonic arrays. Unfortunately, these platforms do not seem to satisfy, at once, all desirable features of an universal simulator, namely long-lived coherence, full control of system parameters, low losses, and scalability. Here, we overcome these challenges and demonstrate robust simulation of quantum transport phenomena using a state-of-art reconfigurable electronic network. To test the robustness and precise control of our platform, we explore the ballistic propagation of a single-excitation wavefunction in an ordered lattice, and its localization due to disorder. We implement the Su-Schrieffer-Heeger model to directly observe the emergence of topologically-protected one-dimensional edge states. Furthermore, we present the realization of the so-called perfect transport protocol, a key milestone for the development of scalable quantum computing and communication. Finally, we show the first simulation of the exciton dynamics in the B800 ring of the purple bacteria LH2 complex. The high fidelity of our simulations together with the low decoherence of our device make it a robust, versatile and promising platform for the simulation of quantum transport phenomena

Role of AGAP2 in the profibrogenic effects induced by TGFβ in LX-2 hepatic stellate cells

Liver damage induces hepatic stellate cells (HSC) activation, characterised by a fibrogenic, proliferative and migratory phenotype. Activated HSC are mainly regulated by transforming growth factor β 1 (TGFβ1), which increases the production of extracellular matrix proteins (e.g. collagen-I) promoting the progression of hepatic fibrosis. AGAP2 (ArfGAP with GTPase domain, ankyrin repeat and PH domain 2) is a GTPase/GTP-activating protein involved in the actin remodelling system and receptor recycling. In the present work the role of AGAP2 in human HSC in response to TGFβ1 was investigated. LX-2 HSC were transfected with AGAP2 siRNA and treated with TGFβ1. AGAP2 knockdown prevented to some extent the proliferative and migratory TGFβ1-induced capacities of LX-2 cells. An array focused on human fibrosis revealed that AGAP2 knockdown partially prevented TGFβ1-mediated gene expression of the fibrogenic genes ACTA2, COL1A2, EDN1, INHBE, LOX, PDGFB, TGFΒ12, while favored the expression of CXCR4, IL1A, MMP1, MMP3 and MMP9 genes. Furthermore, TGFβ1 induced AGAP2 promoter activation and its protein expression in LX-2. In addition, AGAP2 silencing affected TGFβ1-receptor 2 (TGFR2) trafficking in U2OS cells, blocking its effective recycling to the membrane. AGAP2 silencing in LX-2 cells prevented the TGFβ1-induced increase of collagen-I protein levels, while its over-expression enhanced collagen I protein expression in the presence or absence of the cytokine. AGAP2 overexpression also increased focal adhesion kinase (FAK) phosphorylated levels in LX-2 cells. FAK and MEK1 inhibitors prevented the increase of collagen-I expression caused by TGFβ1 in LX-2 overexpressing AGAP2. In summary, the present work shows for the first time, that AGAP2 is a potential new target involved in TGFβ1 signalling, contributing to the progression of hepatic fibrosis

Whole sequence of the mitochondrial DNA genome of Kearns Sayre Syndrome patients: Identification of deletions and variants

Mitochondria both produce the energy of the cell as ATP via respiration and regulate cellular metabolism. Accordingly, any deletion or mutation in the mitochondrial DNA (mtDNA) may result in a disease. One of these diseases is Kearns Sayre syndrome (KSS), described for the first time in 1958, where different large-scale deletions of different sizes and at different positions have been reported in the mitochondrial genome of patients with similar clinical symptoms. In this study, sequences of the mitochondrial genome of three patients with clinic features of KSS were analyzed. Our results revealed the position, heteroplasmy percentage, size of deletions, and their haplogroups. Two patients contained deletions reported previously and one patient showed a new deletion not reported previously. These results display for the first time a systematic analysis of mtDNA variants in the whole mtDNA genome of patients with KSS to help to understand their association with the disease

DD04107-Derived neuronal exocytosis inhibitor peptides: Evidences for synaptotagmin-1 as a putative target

The analgesic peptide DD04107 (Pal-EEMQRR-NH2) and its acetylated analogue inhibit a-calcitonin gene-related peptide (a-CGRP) exocytotic release from primary sensory neurons. Examining the crystal structure of the SNARE-Synaptotagmin-1(Syt1) complex, we hypothesized that these peptides could inhibit neuronal exocytosis by binding to Syt1, hampering at least partially its interaction with the SNARE complex. To address this hypothesis, we first interrogate the role of individual side-chains on the inhibition of a-CGRP release, finding that E1, M3, Q4 and R6 residues were crucial for activity. CD and NMR conformational analysis showed that linear peptides have tendency to adopt a-helical conformations, but the results with cyclic analogues indicated that this secondary structure is not needed for activity. Isothermal titration calorimetry (ITC) measurements demonstrate a direct interaction of some of these peptides with Syt1-C2B domain, but not with Syt7-C2B region, indicating selectivity. As expected for a compound able to inhibit a-CGRP release, cyclic peptide derivative Pal-E-cyclo[EMQK]R-NH2 showed potent in vivo analgesic activity, in a model of inflammatory pain. Molecular dynamics simulations provided a model consistent with KD values for the interaction of peptides with Syt1-C2B domain, and with their biological activity. Altogether, these results identify Syt1 as a potential new analgesic target. © 202

Spanish ATLAS tier-2: Facing up to LHC Run 2

The goal of this work is to describe the way of addressing the main challenges of Run 2 by the Spanish ATLAS Tier-2. The considerable increase of energy and luminosity for the upcoming Run 2 with respect to Run 1 has led to a revision of the ATLAS computing model as well as some of the main ATLAS computing tools. In this paper, the adaptation to these changes will be described. The Spanish ATLAS Tier-2 is a R&D project which consists of a distributed infrastructure composed of three sites and its members are involved in ATLAS computing progress, namely the work in different tasks and the development of new tools (e.g. Event Index)This work has been supported by MINECO, Spain (Proj. Ref. FPA2010-21919-C03-01,02,03 & FPA2013-47424-C3,01,02,03), which include FEDER funds from the European Unio