232 research outputs found
sj-pdf-1-inv-10.1177_15569845221143420 – Supplemental material for Coronary Revascularization in Patients With Diabetes: A Meta-analysis of Randomized Controlled Trials and Propensity-Matched Studies
No full textSupplemental material, sj-pdf-1-inv-10.1177_15569845221143420 for Coronary Revascularization in Patients With Diabetes: A Meta-analysis of Randomized Controlled Trials and Propensity-Matched Studies by Adham Ahmed, Kathryn S. Varghese, Peter J. Fusco, Dave M. Mathew, Serena M. Mathew, Sarah Ahmed, Dillon O. Rogando, Stephanie A. Salazar, Roshan Pandey, Ahmed K. Awad, Kenneth H. Levy, Marisol Hernandez and Rose Calixte in Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery</p
sj-pdf-3-inv-10.1177_15569845221143420 – Supplemental material for Coronary Revascularization in Patients With Diabetes: A Meta-analysis of Randomized Controlled Trials and Propensity-Matched Studies
No full textSupplemental material, sj-pdf-3-inv-10.1177_15569845221143420 for Coronary Revascularization in Patients With Diabetes: A Meta-analysis of Randomized Controlled Trials and Propensity-Matched Studies by Adham Ahmed, Kathryn S. Varghese, Peter J. Fusco, Dave M. Mathew, Serena M. Mathew, Sarah Ahmed, Dillon O. Rogando, Stephanie A. Salazar, Roshan Pandey, Ahmed K. Awad, Kenneth H. Levy, Marisol Hernandez and Rose Calixte in Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery</p
sj-pdf-2-inv-10.1177_15569845221143420 – Supplemental material for Coronary Revascularization in Patients With Diabetes: A Meta-analysis of Randomized Controlled Trials and Propensity-Matched Studies
No full textSupplemental material, sj-pdf-2-inv-10.1177_15569845221143420 for Coronary Revascularization in Patients With Diabetes: A Meta-analysis of Randomized Controlled Trials and Propensity-Matched Studies by Adham Ahmed, Kathryn S. Varghese, Peter J. Fusco, Dave M. Mathew, Serena M. Mathew, Sarah Ahmed, Dillon O. Rogando, Stephanie A. Salazar, Roshan Pandey, Ahmed K. Awad, Kenneth H. Levy, Marisol Hernandez and Rose Calixte in Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery</p
*Corresponding author
No full textAbstract: Accurate reconstruction of phylogenetic trees often involves solving hard optimisation problems, particularly the Maximum Parsimony (MP) and Maximum Likelihood (ML) problems. Various heuristics yield good results for these problems within reasonable time only on small datasets. This is a major impediment for large-scale phylogeny reconstruction. Roshan et al. introduced Rec-I-DCM3, an efficient and accurate meta-method for solving the MP problem on large datasets of up to 14,000 taxa. We improve the performance of Rec-I-DCM3 via parallelisation. The experiments demonstrate that our parallel method, PRec-I-DCM3, achieves significant improvements, both in speed and accuracy, over its sequential counterpart
Rapid coordinate system creation and mapping using Crickets
No full textThesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2004.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.Includes bibliographical references (leaves 55-56).In this thesis, I describe a system that lays the foundation for context-aware applications. This system allows a user to set up a reference coordinate system in a room, using three Cricket listeners attached to a wooden frame. The system then assigns coordinates to Cricket beacons, which are placed on the ceiling. Finally, by using the frame in conjunction with a laser range finder, the user can generate a map of the room in the reference coordinate system, complete with features including doors, walls, and windows. This thesis also describes necessary changes we implemented that made the Cricket positioning system much more accurate.by Roshan Bantwal Baliga.M.Eng
Mechanism of N-Type Inactivation in Shaker Potassium Channels
No full textHyperexcitabilité est l'un des changements les plus importants observés dans de nombreuses maladies neuro-dégénératives telles que la sclérose latérale amyotrophique (SLA) et la maladie d'Alzheimer. De nombreuses recherches études se sont concentrées sur la réduction de l'hyperexcitabilité, soit en inactivant les canaux sodiques ce qui va réduire la génération de potentiels d'action, soit en prolongeant l'ouverture des canaux potassiques ce qui va qui ramener la membrane à son état de repos et réduire l’activité des neurones. Ainsi, pour cibler l'hyperexcitabilité, il faut tout d’abord comprendre les différents aspects de la fonction des canaux ioniques au niveau.
Les objectifs des travaux présentés dans cette thèse consistent à déterminer le mécanisme d'inactivation dans les canaux potassiques Shaker. Les canaux Shaker Kv s'inactivent rapidement pour culminer le potentiel d'action et maintenir l'homéostasie des cellules excitables. L'inactivation de type N est causée par les 46 premiers acides aminés situés de l'extrémité N-terminale du canal, encore appelé, peptide d'inactivation (IP). De nombreuses études mutationnelles ont caractérisé l'inactivation de type N au niveau fonctionnel, cependant, la position de l'IP à l'état de repos et leur transition lors de l'inactivation est encore débattue. L'objectif de la première étude consiste à évaluer le mouvement des IP pendant leur inactivation à l'aide de la fluorométrie en voltage imposé. En insérant un acide aminé non naturel, la 3-[(6-acétyl-2-naphtalényl) amino]-L-alanine (Anap), qui est sensible aux changements d'environnement, nous avons identifié séparément les mouvements de la boule et de la chaîne. Nos données suggèrent que l'inactivation de type N se produit dans un mouvement biphasique en libérant d'abord le IP, ce qui va bloquer le pore du côté cytoplasmique. Pour affiner davantage la position de repos des IP, nous avons utilisé le transfert d'énergie de résonance à base de lanthanide et le métal de transition FRET. Nous proposons que le IP se situe dans la fenêtre formée par le canal et le domaine T1, interagissant avec les résidus acides-aminés du domaine T1.
Dans notre deuxième étude, nous avons montré que le ralentissement de l'inactivation de type N observé dans la première étude est causée par une expression élevée des canaux Shaker. En effet, l'extrémité C-terminale du canal interagit avec les protéines d'échafaudage associées à la membrane pour la formation d'amas. Nous avons aussi montré qu'en tronquant les quatre derniers résidus C-terminaux impliqués dans la formation des amas, nous empêchons également le ralentissement de la cinétique d'inactivation dans les canaux Shaker. Nous avons également démontré que l'inactivation lente de type N n'est pas affectée par l'accumulation des cations potassiques [K+] externe ou toute diaphonie entre les sous-unités voisines. Cette étude élucide non seulement la cause du ralentissement de l'inactivation, mais montre également que les canaux modifient leur comportement en fonction des conditions d'expression. Les résultats trouvés au niveau moléculaire ne peuvent donc pas toujours être extrapolés au niveau cellulaire.Hyperexcitability of neurons is a major symptom observed in many degenerative diseases such as ALS and Alzheimer’s disease. A lot of research is focused on reducing hyperexcitability, either by inactivating sodium channels that will reduce the generation of action potentials, or by prolonging the opening of potassium channels which will help to bring the membrane back to resting state and thus, reduce firing frequency of neurons. At the molecular level, it is important to understand different aspects of ion channel function to target hyperexcitability.
The aim of this thesis was to investigate in two projects the inactivation mechanism in Shaker potassium channels. Shaker Kv channels inactivate rapidly to culminate the action potential and maintain the homeostasis of excitable cells. The so-called N-type inactivation is caused by the first 46 amino acids of the N-terminus of the channel, known as the inactivation peptide (IP). Numerous mutational studies have characterized N-type inactivation functionally, however, the position of the IP in the resting state and its transition during inactivation is still debated. The aim of the first project was to track the movement of IP during inactivation using voltage clamp fluorometry. By inserting an unnatural amino acid, 3-[(6-acetyl-2-naphthalenyl) amino]-L-alanine (Anap), which is sensitive to changes in environment, we identified the movements of ball and chain separately. Our data suggests that N-type inactivation occurs in a biphasic movement by first releasing the IP, which then blocks the pore from the cytoplasmic side. To further narrow down the resting position of the inactivation peptide, we used Lanthanide-based Resonance Energy transfer and transition metal FRET. We propose that the inactivation peptide is located in the window formed by the channel and the T1 domain, interacting with the acidic residues of the T1 domain.
In a follow-up study, we explored the reason underlying slow inactivation kinetics observed during the study of N-type inactivation in the first project. High expression of Shaker channels results in slowing of the N-type inactivation. The C-terminus of the channel interacts with membrane associated scaffold proteins for cluster formation. In this study, we have shown that by truncating the last four C-terminal residues involved in cluster formation, and hence preventing channel clustering, we also prevent slowing of the inactivation kinetics in Shaker channels. We also showed that slow N-type inactivation is not affected by accumulation of external [K+] or any crosstalk between the neighboring subunits. The second project not only elucidates the cause of the inactivation slow-down but illustrates that the channels alter their behavior dependent on the expression conditions. Results found on the molecular level can thus not always be extrapolated to the cellular level
Mongolian spot
No full textColorful skin spots on a pediatric patient can easily be mistaken as signs of child abuse. Professionals should therefore gain knowledge about Mongolian spots; also known as Mongolian blue spots. These are flat, congenital and benign birthmarks, commonly located in sacro-coccygeal or lumbar area of an infant. Child abuse is a major public health problem across the world. The most common manifestations of physical child abuse are cutaneous, and their recognition and differential diagnosis are of great importance. Mongolian spots may appear as signs of child abuse; however, Mongolian spots are harmless
Mongolian spot
No full textColorful skin spots on a pediatric patient can easily be mistaken as signs of child abuse. Professionals should therefore gain knowledge about Mongolian spots; also known as Mongolian blue spots. These are flat, congenital and benign birthmarks, commonly located in sacro-coccygeal or lumbar area of an infant. Child abuse is a major public health problem across the world. The most common manifestations of physical child abuse are cutaneous, and their recognition and differential diagnosis are of great importance. Mongolian spots may appear as signs of child abuse; however, Mongolian spots are harmless
Challenges in Virtual Testing of Autonomous Vehicles
No full textThe worldwide development of Autonomous Vehicles (AVs) has also encouraged the use of software simulators for virtual testing of AVs. However, the effectiveness of the AV simulators is constrained by numerous challenges, such as their computational cost and lack of fidelity in specific areas. In this paper, we describe the modality of virtual testing and its benefits for AV development and validation. Moreover, we summarize and provide an overview of the state-of-the-art AV simulators, their limitations, and the current directions toward improvement.Green Open Access added to TU Delft Institutional Repository 'You share, we take care!' - Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Signal Processing System
Combinatory actions of CP29 phosphorylation by STN7 and stability regulate leaf age-dependent disassembly of photosynthetic complexes
No full text© 2020, The Author(s). A predominant physiological change that occurs during leaf senescence is a decrease in photosynthetic
efciency. An optimal organization of photosynthesis complexes in plant leaves is critical for efcient
photosynthesis. However, molecular mechanisms for regulating photosynthesis complexes during leaf
senescence remain largely unknown. Here we tracked photosynthesis complexes alterations during
leaf senescence in Arabidopsis thaliana. Grana stack is signifcantly thickened and photosynthesis
complexes were disassembled in senescing leaves. Defects in STN7 and CP29 led to an altered
chloroplast ultrastructure and a malformation of photosynthesis complex organization in stroma
lamella. Both CP29 phosphorylation by STN7 and CP29 fragmentation are highly associated with the
photosynthesis complex disassembly. In turn, CP29 functions as a molecular glue to facilitate protein
complex formation leading phosphorylation cascade and to maintain photosynthetic efciency during
leaf senescence. These data suggest a novel molecular mechanism to modulate leaf senescence via
CP29 phosphorylation and fragmentation, serving as an efcient strategy to control photosynthesis
complexes.11Nsciescopu
- …
