scholarly journals Intent Understanding Using an Activation Spreading Architecture

Robotics ◽  
2015 ◽  
Vol 4 (3) ◽  
pp. 284-315
Author(s):  
Mohammad Saffar ◽  
Mircea Nicolescu ◽  
Monica Nicolescu ◽  
Banafsheh Rekabdar
Keyword(s):  
Activation Spreading

Collaborative Human-Robot Hierarchical Task Execution with an Activation Spreading Architecture

2019 ◽  
pp. 301-310
Author(s):  
Bashira Akter Anima ◽  
Janelle Blankenburg ◽  
Mariya Zagainova ◽  
S. Pourya Hoseini A. ◽  
Muhammed Tawfiq Chowdhury ◽  
...  
Keyword(s):  
Task Execution ◽  
Activation Spreading

scholarly journals Semantic Clustering of Search Engine Results

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Sara Saad Soliman ◽  
Maged F. El-Sayed ◽  
Yasser F. Hassan
Keyword(s):  
Search Engine ◽  
Semantic Clustering ◽  
Novel Approach ◽  
Activation Spreading

This paper presents a novel approach for search engine results clustering that relies on the semantics of the retrieved documents rather than the terms in those documents. The proposed approach takes into consideration both lexical and semantics similarities among documents and applies activation spreading technique in order to generate semantically meaningful clusters. This approach allows documents that are semantically similar to be clustered together rather than clustering documents based on similar terms. A prototype is implemented and several experiments are conducted to test the prospered solution. The result of the experiment confirmed that the proposed solution achieves remarkable results in terms of precision.

Language and Brain – Facts, Problems, Mysteries

2008 ◽  
Vol 16 (4) ◽  
pp. 467-481 ◽  
Author(s):  
Manfred Bierwisch
Keyword(s):  
Language Production ◽  
Long Term Memory ◽  
Language Faculty ◽  
Term Memory ◽  
Activated State ◽  
Cognitive Neurosciences ◽  
Standard Models ◽  
Activation Spreading ◽  
The Brain

The representation of language in the brain is one of the lively topics in recent cognitive neurosciences. The present paper argues that standard models of structures and mechanisms of the brain, which are essentially based on principles of activation spreading in neuronal nets and learning by synaptic strengthening through coincidental activation, cannot account for crucial properties of the Language Faculty and are misguided in central respects. In particular, the apparently elegant notion that working memory is just the activated state of long-term memory is shown to be incapable of accounting for structures and processes of language production and comprehension. Four types of problems are sketched that illustrate the impasses encountered by standard models of activation spreading.

scholarly journals Lysophosphatidylcholine is a Major Component of Platelet Microvesicles Promoting Platelet Activation and Reporting Atherosclerotic Plaque Instability

2019 ◽  
Vol 119 (08) ◽  
pp. 1295-1310 ◽  
Author(s):  
Philipp Diehl ◽  
Frederik Nienaber ◽  
Maria T. K. Zaldivia ◽  
Johannes Stamm ◽  
Patrick M. Siegel ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Atherosclerotic Plaque ◽  
Vascular Inflammation ◽  
Surrogate Marker ◽  
The Body ◽  
Lipid Profiling ◽  
Plaque Instability ◽  
Major Interest ◽  
Activation Spreading ◽  
Inflammatory Molecules

Background Microvesicles (MVs) are small cell-derived vesicles, which are mainly released by activated cells. They are part of a communication network delivering biomolecules, for example, inflammatory molecules, via the blood circulation to remote cells in the body. Platelet-derived MVs are known to induce vascular inflammation. Research on the mediators and mechanisms of their inflammatory effects has attracted major interest. We hypothesize that specific lipids are the mediators of vascular inflammation caused by platelet-derived MVs. Methods and Results Liquid chromatography electrospray ionization–tandem mass spectrometry was used for lipid profiling of platelet-derived MVs. Lysophosphatidylcholine (LPC) was found to be a major component of platelet-derived MVs. Investigating the direct effects of LPC, we found that it induces platelet activation, spreading, migration and aggregation as well as formation of inflammatory platelet–monocyte aggregates. We show for the first time that platelets express the LPC receptor G2AR, which mediates LPC-induced platelet activation. In a mouse model of atherosclerotic plaque instability/rupture, circulating LPC was detected as a surrogate marker of plaque instability. These findings were confirmed by matrix-assisted laser desorption ionization imaging, which showed that the LPC concentration of human plaques was highest in vulnerable plaque regions. Conclusion LPC is a major component of platelet-derived MVs and via its interaction with G2AR on platelets contributes to platelet activation, spreading, migration and aggregation and ultimately to vascular inflammation. Circulating LPC reports on atherosclerotic plaque instability in mice and is significantly increased in unstable areas of atherosclerotic plaques in both mice and humans, linking LPC to plaque instability.

scholarly journals Oral administration of Bruton's tyrosine kinase inhibitors impairs GPVI-mediated platelet function

2016 ◽  
Vol 310 (5) ◽  
pp. C373-C380 ◽  
Author(s):  
Rachel A. Rigg ◽  
Joseph E. Aslan ◽  
Laura D. Healy ◽  
Michael Wallisch ◽  
Marisa L. D. Thierheimer ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Platelet Activation ◽  
Platelet Function ◽  
Lymphocytic Leukemia ◽  
Bruton’S Tyrosine Kinase ◽  
Bruton's Tyrosine Kinase ◽  
Glycoprotein Vi ◽  
Activation Spreading

The Tec family kinase Bruton's tyrosine kinase (Btk) plays an important signaling role downstream of immunoreceptor tyrosine-based activation motifs in hematopoietic cells. Mutations in Btk are involved in impaired B-cell maturation in X-linked agammaglobulinemia, and Btk has been investigated for its role in platelet activation via activation of the effector protein phospholipase Cγ2 downstream of the platelet membrane glycoprotein VI (GPVI). Because of its role in hematopoietic cell signaling, Btk has become a target in the treatment of chronic lymphocytic leukemia and mantle cell lymphoma; the covalent Btk inhibitor ibrutinib was recently approved by the US Food and Drug Administration for treatment of these conditions. Antihemostatic events have been reported in some patients taking ibrutinib, although the mechanism of these events remains unknown. We sought to determine the effects of Btk inhibition on platelet function in a series of in vitro studies of platelet activation, spreading, and aggregation. Our results show that irreversible inhibition of Btk with two ibrutinib analogs in vitro decreased human platelet activation, phosphorylation of Btk, P-selectin exposure, spreading on fibrinogen, and aggregation under shear flow conditions. Short-term studies of ibrutinib analogs administered in vivo also showed abrogation of platelet aggregation in vitro, but without measurable effects on plasma clotting times or on bleeding in vivo. Taken together, our results suggest that inhibition of Btk significantly decreased GPVI-mediated platelet activation, spreading, and aggregation in vitro; however, prolonged bleeding was not observed in a model of bleeding.

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