Investigation of the Burning Properties of Slow-Propagation Tungsten Type Delay Compositions

2008 ◽  
Vol 33 (3) ◽  
pp. 219-226 ◽  
Author(s):  
Kai-Tai Lu ◽  
Ching-Chyuan Yang ◽  
Yang-Hsiung Ko
Keyword(s):  
Slow Propagation

scholarly journals Anti-aging treatments slow propagation of synucleinopathy by restoring lysosomal function

Autophagy ◽  
2016 ◽  
Vol 12 (10) ◽  
pp. 1849-1863 ◽  
Author(s):  
Dong-Kyu Kim ◽  
Hee-Sun Lim ◽  
Ichiro Kawasaki ◽  
Yhong-Hee Shim ◽  
Nishant N. Vaikath ◽  
...  
Keyword(s):  
Lysosomal Function ◽  
Slow Propagation

scholarly journals Slow propagation of 2 GHz acoustical waves in a suspended GaAs phononic waveguide on insulator

2020 ◽  
Vol 117 (19) ◽  
pp. 193501
Author(s):  
Giuseppe Modica ◽  
Rui Zhu ◽  
Robert Horvath ◽  
Gregoire Beaudoin ◽  
Isabelle Sagnes ◽  
...  
Keyword(s):  
Slow Propagation

scholarly journals Computational Approaches to Understanding the Role of Fibroblast-Myocyte Interactions in Cardiac Arrhythmogenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Tashalee R. Brown ◽  
Trine Krogh-Madsen ◽  
David J. Christini
Keyword(s):  
Gap Junctions ◽  
Potential Role ◽  
Cardiac Tissue ◽  
Cardiac Fibroblasts ◽  
Cardiac Arrhythmogenesis ◽  
Voltage Dependent ◽  
Underlying Mechanisms ◽  
Slow Propagation

The adult heart is composed of a dense network of cardiomyocytes surrounded by nonmyocytes, the most abundant of which are cardiac fibroblasts. Several cardiac diseases, such as myocardial infarction or dilated cardiomyopathy, are associated with an increased density of fibroblasts, that is, fibrosis. Fibroblasts play a significant role in the development of electrical and mechanical dysfunction of the heart; however the underlying mechanisms are only partially understood. One widely studied mechanism suggests that fibroblasts produce excess extracellular matrix, resulting in collagenous septa. These collagenous septa slow propagation, cause zig-zag conduction paths, and decouple cardiomyocytes resulting in a substrate for arrhythmia. Another emerging mechanism suggests that fibroblasts promote arrhythmogenesis through direct electrical interactions with cardiomyocytes via gap junctions. Due to the challenges of investigating fibroblast-myocyte coupling in native cardiac tissue, computational modeling andin vitroexperiments have facilitated the investigation into the mechanisms underlying fibroblast-mediated changes in cardiomyocyte action potential morphology, conduction velocity, spontaneous excitability, and vulnerability to reentry. In this paper, we summarize the major findings of the existing computational studies investigating the implications of fibroblast-myocyte interactions in the normal and diseased heart. We then present investigations from our group into the potential role of voltage-dependent gap junctions in fibroblast-myocyte interactions.

Secondary faulting, a consequence of a single continuous bifurcation process

1980 ◽  
Vol 117 (4) ◽  
pp. 373-380 ◽  
Author(s):  
Dov Bahat
Keyword(s):  
New Zealand ◽  
Continuous Process ◽  
Fracture Propagation ◽  
Critical Conditions ◽  
Rapid Propagation ◽  
Branching Angle ◽  
Regional Stresses ◽  
Bifurcation Process ◽  
Slow Propagation

SummaryFracture propagation in the crust under post-critical conditions (rapid propagation), and possibly in some instances even under sub-critical conditions (slow propagation) can produce fracture-branching in a single continuous process. Later local or regional stresses result in displacements along the fractures and secondary faulting develops. This concept can explain various secondary features like conditions of branching, branching-angle and shallow secondary faults. The splaying of the Hope Fault in New Zealand is primarily a result of early fracture bifurcation and later minor displacements.

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