scholarly journals Diffusion-reaction model for positron trapping and annihilation at spherical extended defects and in precipitate-matrix composites

2018 ◽  
Vol 97 (22) ◽  
Author(s):  
Roland Würschum ◽  
Laura Resch ◽  
Gregor Klinser
2006 ◽  
Vol 57 (15) ◽  
pp. 4215-4224 ◽  
Author(s):  
Q. T. Ho ◽  
B. E. Verlinden ◽  
P. Verboven ◽  
S. Vandewalle ◽  
B. M. Nicolai

Author(s):  
J Liaudat ◽  
C López ◽  
I Carol

2021 ◽  
pp. 26-26
Author(s):  
Ling Lin ◽  
Yun Qiao

Fractal modifications of Fick?s laws are discussed by taking into account the electrode?s porous structure, and a fractal derivative model for diffusion-reaction process in a thin film of an amperometric enzymatic reaction is established. Particular attention is paid to giving an intuitive grasp for its fractal variational principle and its solution procedure. Extremely fast or extremely slow diffusion process can be achieved by suitable control of the electrode?s surface morphology, a sponge-like surface leads to an extremely fast diffusion, while a lotus-leaf-like uneven surface predicts an extremely slow process. This paper sheds a bright light on an optimal design of an electrode?s surface morphology.


2014 ◽  
Vol 25 (01) ◽  
pp. 79-108 ◽  
Author(s):  
R. Penta ◽  
D. Ambrosi ◽  
A. Quarteroni

A system of differential equations for coupled fluid and drug transport in vascularized (malignant) tissues is derived by a multiscale expansion. We start from mass and momentum balance equations, stated in the physical domain, geometrically characterized by the intercapillary distance (the microscale). The Kedem–Katchalsky equations are used to account for blood and drug exchange across the capillary walls. The multiscale technique (homogenization) is used to formulate continuum equations describing the coupling of fluid and drug transport on the tumor length scale (the macroscale), under the assumption of local periodicity; macroscale variations of the microstructure account for spatial heterogeneities of the angiogenic capillary network. A double porous medium model for the fluid dynamics in the tumor is obtained, where the drug dynamics is represented by a double advection–diffusion–reaction model. The homogenized equations are straightforward to approximate, as the role of the vascular geometry is recovered at an average level by solving standard cell differential problems. Fluid and drug fluxes now read as effective mass sources in the macroscale model, which upscale the interplay between blood and drug dynamics on the tissue scale. We aim to provide a theoretical setting for a better understanding of the design of effective anti-cancer therapies.


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