Molecular Processes for Surface Selective Growth on Patterned Substrates; An Investigation of CBE ALAS Deposition

Author(s):  
J. S. Foord ◽  
C. L. Levoguer ◽  
G. J. Davies
1998 ◽  
Vol 535 ◽  
Author(s):  
E. Gil-Lafon ◽  
J. Napierala ◽  
D. Castelluci ◽  
A. Pimpinelli ◽  
B. Gérard ◽  
...  

AbstractThe selective growth of GaAs by HVPE was studied on (001), (110), (111)Ga and (111)As, GaAs patterned substrates by varying the I1I/V ratio. A kinetic modelling of the growth was developed, based upon the SEM observations of the growth morphologies as well as on experimental curve synthesis. The growth rate is written as a function of the diffusion fluxes of the adsorbed AsGa and AsGaCI molecules and takes into account the chlorine desorption by H2. 1.5 μm thick GaAs films were then fabricated on Si (001) by a confined epitaxial lateral overgrowth technique. These conformal films exhibit intense and uniform luminescence signals, showing that the dislocation densities of GaAs are lower than 105 cm−2. SEM analyses reveal that conformal growth fronts consist in (110) and (111)As A planes under the III/V ratios (superior to 1) which were tested.


1994 ◽  
Vol 340 ◽  
Author(s):  
F. Peiro ◽  
A. Cornet ◽  
J.R. Morante ◽  
K. Zekentes ◽  
A. Georgakilas

ABSTRACTIn this work we present structural characterization by both Scanning and Transmission Electron Microscopy of InAlAs/InGaAs heterostructures grown on InP substrates. Our attention is devoted to study the two main problems limiting the application of these structures as devices: the presence of defects on the epilayer and the growth habit at theedges of the well. Our results show that a different faceting between the two <110> orthogonal directions develops during the growth and that a high density of defects is observed just at the intersection between the layers grown inside the windows and on the walls. Moreover, the presence of a polycrystalline layer developing over the mask indicates that a selective growth occurs.


2007 ◽  
Vol 301-302 ◽  
pp. 744-747 ◽  
Author(s):  
S. Ohkouchi ◽  
Y. Nakamura ◽  
N. Ikeda ◽  
Y. Sugimoto ◽  
K. Asakawa

1995 ◽  
Vol 146 (1-4) ◽  
pp. 475-481 ◽  
Author(s):  
Takuya Fujii ◽  
Mitsuru Ekawa ◽  
Susumu Yamazaki

2014 ◽  
Vol E97.C (5) ◽  
pp. 393-396
Author(s):  
Katsunori MAKIHARA ◽  
Mitsuhisa IKEDA ◽  
Seiichi MIYAZAKI

2012 ◽  
Vol 14 (3) ◽  
pp. 239-252

In this review, we outline critical molecular processes that have been implicated by discovery of genetic mutations in autism. These mechanisms need to be mapped onto the neurodevelopment step(s) gone awry that may be associated with cause in autism. Molecular mechanisms include: (i) regulation of gene expression; (ii) pre-mRNA splicing; (iii) protein localization, translation, and turnover; (iv) synaptic transmission; (v) cell signaling; (vi) the functions of cytoskeletal and scaffolding proteins; and (vii) the function of neuronal cell adhesion molecules. While the molecular mechanisms appear broad, they may converge on only one of a few steps during neurodevelopment that perturbs the structure, function, and/or plasticity of neuronal circuitry. While there are many genetic mutations involved, novel treatments may need to target only one of few developmental mechanisms.


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