Relevant bibliographies by topics / Nogood repairs

Academic literature on the topic 'Nogood repairs'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Nogood repairs"

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Yu, Bo, Hongmei Zhang, Jun Hong, Yonggang Lu, and Yajun Zhang. "Promoting Axonal Extension and Repair After Spinal Cord Injury by Inhibiting the Expression of Rho Gene Based on RNA Interference." Journal of Biomaterials and Tissue Engineering 10, no. 7 (July 1, 2020): 1046–51. http://dx.doi.org/10.1166/jbt.2020.2349.

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Spinal cord injury causes central nervous system damage. Rho inhibits axonal regeneration. This study is intended to analyze the effect of inhibition of Rho expression on axonal repair. The oligodendrocytes were isolated and divided into NC group and shRNA-RhoA group followed by analysis of the average length of axon growth and average microtubule fluorescence density by immunofluorescence, Nogo, MAG and RhoA expression were by Real time PCR. Wistar rats were separated into control group; SCI group and shRNA-RhoA group followed by analysis of the BBB scores and the Reuter score of sensory function, RhoA expression by Real time PCR and Western blot, Caspase3 activity as well as Nogo and MAG expression by Real time PCR. Compared with NC group, shRNA-RhoA group showed significantly increased average length of axon growth and average microtubule fluorescence density at the distal axon and reduced expression of RhoA, Nogo and MAG (P < 0 05). In comparison to control group, SCI group presented significantly increased RhoA expression, decreased BBB score, increased Reuter score and Caspase3 activity as well as elevated Nogo and MAG expression (P < 0 05). The shRNA-RhoA group significantly decreased RhoA expression, increased BBB score, decreased Reuter score and Caspase3 activity, and reduced Nogo and MAG expression compared with SCI group (P < 0 05). Inhibiting RhoA expression can promote axon extension and regenerative repair. Targeting RhoA reduces axon growth inhibitory factor expression, inhibits apoptosis and effectively alleviates SCI.
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Rust, Ruslan, Lisa Grönnert, Christina Gantner, Alinda Enzler, Geertje Mulders, Rebecca Z. Weber, Arthur Siewert, et al. "Nogo-A targeted therapy promotes vascular repair and functional recovery following stroke." Proceedings of the National Academy of Sciences 116, no. 28 (June 24, 2019): 14270–79. http://dx.doi.org/10.1073/pnas.1905309116.

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Stroke is a major cause of serious disability due to the brain’s limited capacity to regenerate damaged tissue and neuronal circuits. After ischemic injury, a multiphasic degenerative and inflammatory response is coupled with severely restricted vascular and neuronal repair, resulting in permanent functional deficits. Although clinical evidence indicates that revascularization of the ischemic brain regions is crucial for functional recovery, no therapeutics that promote angiogenesis after cerebral stroke are currently available. Besides vascular growth factors, guidance molecules have been identified to regulate aspects of angiogenesis in the central nervous system (CNS) and may provide targets for therapeutic angiogenesis. In this study, we demonstrate that genetic deletion of the neurite outgrowth inhibitor Nogo-A or one of its corresponding receptors, S1PR2, improves vascular sprouting and repair and reduces neurological deficits after cerebral ischemia in mice. These findings were reproduced in a therapeutic approach using intrathecal anti–Nogo-A antibodies; such a therapy is currently in clinical testing for spinal cord injury. These results provide a basis for a therapeutic blockage of inhibitory guidance molecules to improve vascular and neural repair after ischemic CNS injuries.
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Li, Hengyu, Zhuo Cheng, Pinghua Yang, Wei Huang, Xizhou Li, Daimin Xiang, and Xiaojun Wu. "Endothelial Nogo-B Suppresses Cancer Cell Proliferation via a Paracrine TGF-β/Smad Signaling." Cells 11, no. 19 (September 30, 2022): 3084. http://dx.doi.org/10.3390/cells11193084.

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Nogo-B has been reported to play a critical role in angiogenesis and the repair of damaged blood vessels; however, its role in the tumor microenvironment remains unclear. Here, we observed the differential expression of Nogo-B in endothelial cells from hepatocellular carcinoma (HCC) and glioma samples. Downregulation of Nogo-B expression correlated with the malignant phenotype of cancer and a poor prognosis for patients. In subsequent studies, endothelial Nogo-B inhibition robustly promoted the growth of HCC or glioma xenografts in nude mice. Intriguingly, endothelial Nogo-B silencing dramatically suppressed endothelial cell expansion and tumor angiogenesis, but potently enhanced the proliferation of neighboring HCC and glioma cells. Based on the results of the ELISA assay, Nogo-B silencing reduced TGF-β production in endothelial cells, which attenuated the phosphorylation and nuclear translocation of Smad in neighboring cancer cells. The endothelial Nogo-B silencing-mediated increase in cancer cell proliferation was abolished by either a TGF-β neutralizing antibody or TGF-β receptor inhibitor, indicating the essential role for TGF-β in endothelial Nogo-B-mediated suppression of cancer growth. These findings not only broaden our understanding of the crosstalk between cancer cells and endothelial cells but also provide a novel prognostic biomarker and a therapeutic target for cancer treatments.
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Soto, Altea, Manuel Nieto-Díaz, David Reigada, María Asunción Barreda-Manso, Teresa Muñoz-Galdeano, and Rodrigo M. Maza. "miR-182-5p Regulates Nogo-A Expression and Promotes Neurite Outgrowth of Hippocampal Neurons In Vitro." Pharmaceuticals 15, no. 5 (April 25, 2022): 529. http://dx.doi.org/10.3390/ph15050529.

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Nogo-A protein is a key myelin-associated inhibitor of axonal growth, regeneration, and plasticity in the central nervous system (CNS). Regulation of the Nogo-A/NgR1 pathway facilitates functional recovery and neural repair after spinal cord trauma and ischemic stroke. MicroRNAs are described as effective tools for the regulation of important processes in the CNS, such as neuronal differentiation, neuritogenesis, and plasticity. Our results show that miR-182-5p mimic specifically downregulates the expression of the luciferase reporter gene fused to the mouse Nogo-A 3′UTR, and Nogo-A protein expression in Neuro-2a and C6 cells. Finally, we observed that when rat primary hippocampal neurons are co-cultured with C6 cells transfected with miR-182-5p mimic, there is a promotion of the outgrowth of neuronal neurites in length. From all these data, we suggest that miR-182-5p may be a potential therapeutic tool for the promotion of axonal regeneration in different diseases of the CNS.
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Soto, Altea, Manuel Nieto-Díaz, David Reigada, María Asunción Barreda-Manso, Teresa Muñoz-Galdeano, and Rodrigo M. Maza. "miR-182-5p Regulates Nogo-A Expression and Promotes Neurite Outgrowth of Hippocampal Neurons In Vitro." Pharmaceuticals 15, no. 5 (April 25, 2022): 529. http://dx.doi.org/10.3390/ph15050529.

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Nogo-A protein is a key myelin-associated inhibitor of axonal growth, regeneration, and plasticity in the central nervous system (CNS). Regulation of the Nogo-A/NgR1 pathway facilitates functional recovery and neural repair after spinal cord trauma and ischemic stroke. MicroRNAs are described as effective tools for the regulation of important processes in the CNS, such as neuronal differentiation, neuritogenesis, and plasticity. Our results show that miR-182-5p mimic specifically downregulates the expression of the luciferase reporter gene fused to the mouse Nogo-A 3′UTR, and Nogo-A protein expression in Neuro-2a and C6 cells. Finally, we observed that when rat primary hippocampal neurons are co-cultured with C6 cells transfected with miR-182-5p mimic, there is a promotion of the outgrowth of neuronal neurites in length. From all these data, we suggest that miR-182-5p may be a potential therapeutic tool for the promotion of axonal regeneration in different diseases of the CNS.
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Kim, Min, Jung Kang, Paschalis Theotokis, Nikolaos Grigoriadis, and Steven Petratos. "Can We Design a Nogo Receptor-Dependent Cellular Therapy to Target MS?" Cells 8, no. 1 (December 20, 2018): 1. http://dx.doi.org/10.3390/cells8010001.

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The current landscape of therapeutics designed to treat multiple sclerosis (MS) and its pathological sequelae is saturated with drugs that modify disease course and limit relapse rates. While these small molecules and biologicals are producing profound benefits to patients with reductions in annualized relapse rates, the repair or reversal of demyelinated lesions with or without axonal damage, remains the principle unmet need for progressive forms of the disease. Targeting the extracellular pathological milieu and the signaling mechanisms that drive neurodegeneration are potential means to achieve neuroprotection and/or repair in the central nervous system of progressive MS patients. The Nogo-A receptor-dependent signaling mechanism has raised considerable interest in neurological disease paradigms since it can promulgate axonal transport deficits, further demyelination, and extant axonal dystrophy, thereby limiting remyelination. If specific therapeutic regimes could be devised to directly clear the Nogo-A-enriched myelin debris in an expedited manner, it may provide the necessary CNS environment for neurorepair to become a clinical reality. The current review outlines novel means to achieve neurorepair with biologicals that may be directed to sites of active demyelination.
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Sozmen, Elif G., Shira Rosenzweig, Irene L. Llorente, David J. DiTullio, Michal Machnicki, Harry V. Vinters, Lief A. Havton, Roman J. Giger, Jason D. Hinman, and S. Thomas Carmichael. "Nogo receptor blockade overcomes remyelination failure after white matter stroke and stimulates functional recovery in aged mice." Proceedings of the National Academy of Sciences 113, no. 52 (December 12, 2016): E8453—E8462. http://dx.doi.org/10.1073/pnas.1615322113.

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White matter stroke is a distinct stroke subtype, accounting for up to 25% of stroke and constituting the second leading cause of dementia. The biology of possible tissue repair after white matter stroke has not been determined. In a mouse stroke model, white matter ischemia causes focal damage and adjacent areas of axonal myelin disruption and gliosis. In these areas of only partial damage, local white matter progenitors respond to injury, as oligodendrocyte progenitors (OPCs) proliferate. However, OPCs fail to mature into oligodendrocytes (OLs) even in regions of demyelination with intact axons and instead divert into an astrocytic fate. Local axonal sprouting occurs, producing an increase in unmyelinated fibers in the corpus callosum. The OPC maturation block after white matter stroke is in part mediated via Nogo receptor 1 (NgR1) signaling. In both aged and young adult mice, stroke induces NgR1 ligands and down-regulates NgR1 inhibitors during the peak OPC maturation block. Nogo ligands are also induced adjacent to human white matter stroke in humans. A Nogo signaling blockade with an NgR1 antagonist administered after stroke reduces the OPC astrocytic transformation and improves poststroke oligodendrogenesis in mice. Notably, increased white matter repair in aged mice is translated into significant poststroke motor recovery, even when NgR1 blockade is provided during the chronic time points of injury. These data provide a perspective on the role of NgR1 ligand function in OPC fate in the context of a specific and common type of stroke and show that it is amenable to systemic intervention to promote recovery.
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Pernet, Vincent, and Martin E. Schwab. "The role of Nogo-A in axonal plasticity, regrowth and repair." Cell and Tissue Research 349, no. 1 (May 17, 2012): 97–104. http://dx.doi.org/10.1007/s00441-012-1432-6.

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Elliott Donaghue, Irja, Charles H. Tator, and Molly S. Shoichet. "Local Delivery of Neurotrophin-3 and Anti-NogoA Promotes Repair After Spinal Cord Injury." Tissue Engineering Part A 22, no. 9-10 (May 2016): 733–41. http://dx.doi.org/10.1089/ten.tea.2015.0471.

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Yu, J., C. Fernandez-Hernando, Y. Suarez, M. Schleicher, Z. Hao, P. L. Wright, A. DiLorenzo, T. R. Kyriakides, and W. C. Sessa. "Reticulon 4B (Nogo-B) is necessary for macrophage infiltration and tissue repair." Proceedings of the National Academy of Sciences 106, no. 41 (September 25, 2009): 17511–16. http://dx.doi.org/10.1073/pnas.0907359106.

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Dissertations / Theses on the topic "Nogood repairs"

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Zhou, Lingzhong, and n/a. "Agent Ordering and Nogood Repairs in Distributed Constraint Solving." Griffith University. School of Information and Communication Technology, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070713.162515.

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The distributed constraint satisfaction problem is a general formalization used to represent problems in distributed multi-agent systems. A large body of problems in artificial intelligence and computer science can be easily formulated as distributed constraint satisfaction problems. In this thesis we study agent ordering, effects of no-goods, search efficiency and threshold repairing in distributed constraint satisfaction problems and its variants. A summary of contributions is as follows: 1. We present a new algorithm, Dynamic Agent Ordering. A distinctive feature of this algorithm is that it uses the degree of unsatisfiability as a guiding parameter to dynamically determine agent ordering during the search. We show through an empirical study that our algorithm performs better than the existing approaches. In our approach, the independence of agents is guaranteed and agents without neighbouring relationships can run concurrently and asynchronously. (Part of this work was published in the Australian Al Conference (80)). 2. We extend the Dynamic Agent Ordering algorithm by incorporating a novel technique called nogood repairing. This results in a dramatic reduction in the nogoods being stored, and communication costs. In an empirical study, we11 show that this approach outperforms an equivalent static ordering algorithm and a current state-of-the-art technique in terms of execution time, memory usage and communication cost. (Part of this work was published at FLAIRS Conference (81)). Further, we introduce a new algorithm, Over-constrained Dynamic Agent Ordering, that breaks new ground in handling multiple variables per agent in distributed over-constrained satisfaction problems. The algorithm also uses the degree of unsatisfiability as a measure for relaxing constraints, and hence as a way to guide the search toward the best optimal solution(s). By applying our Threshold Repair method, we can solve a distributed constraint satisfaction problem without knowing whether the problem is under- or over-constrained. In an experimental study, we show that the new algorithm compares favourably to an implementation of asynchronous weak commitment search adapted to handle over-constrained problems. (Part of this work was published at the Canadian AI conference (79)).
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Zhou, Lingzhong. "Agent Ordering and Nogood Repairs in Distributed Constraint Solving." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365303.

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The distributed constraint satisfaction problem is a general formalization used to represent problems in distributed multi-agent systems. A large body of problems in artificial intelligence and computer science can be easily formulated as distributed constraint satisfaction problems. In this thesis we study agent ordering, effects of no-goods, search efficiency and threshold repairing in distributed constraint satisfaction problems and its variants. A summary of contributions is as follows: 1. We present a new algorithm, Dynamic Agent Ordering. A distinctive feature of this algorithm is that it uses the degree of unsatisfiability as a guiding parameter to dynamically determine agent ordering during the search. We show through an empirical study that our algorithm performs better than the existing approaches. In our approach, the independence of agents is guaranteed and agents without neighbouring relationships can run concurrently and asynchronously. (Part of this work was published in the Australian Al Conference (80)). 2. We extend the Dynamic Agent Ordering algorithm by incorporating a novel technique called nogood repairing. This results in a dramatic reduction in the nogoods being stored, and communication costs. In an empirical study, we11 show that this approach outperforms an equivalent static ordering algorithm and a current state-of-the-art technique in terms of execution time, memory usage and communication cost. (Part of this work was published at FLAIRS Conference (81)). Further, we introduce a new algorithm, Over-constrained Dynamic Agent Ordering, that breaks new ground in handling multiple variables per agent in distributed over-constrained satisfaction problems. The algorithm also uses the degree of unsatisfiability as a measure for relaxing constraints, and hence as a way to guide the search toward the best optimal solution(s). By applying our Threshold Repair method, we can solve a distributed constraint satisfaction problem without knowing whether the problem is under- or over-constrained. In an experimental study, we show that the new algorithm compares favourably to an implementation of asynchronous weak commitment search adapted to handle over-constrained problems. (Part of this work was published at the Canadian AI conference (79)).
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Information and Communication Technology
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Book chapters on the topic "Nogood repairs"

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Jiang, Yuejun, Thomas Richards, and Barry Richards. "Nogood backmarking with min-conflict repair in constraint satisfaction and optimization." In Lecture Notes in Computer Science, 21–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/3-540-58601-6_87.

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Roman, Willi, and Schwab Martin E. "Suppression of Nogo-A to Enhance CNS Repair." In Cerebral Plasticity, 367–82. The MIT Press, 2011. http://dx.doi.org/10.7551/mitpress/9780262015233.003.0029.

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