61 research outputs found
Evidence for Kinetic Limitations as a Controlling Factor of Ge Pyramid Formation: a Study of Structural Features of Ge/Si(001) Wetting Layer Formed by Ge Deposition at Room Temperature Followed by Annealing at 600 {\deg}C
The article presents an experimental study of an issue of whether the
formation of arrays of Ge quantum dots on the Si(001) surface is an equilibrium
process or it is kinetically controlled. We deposited Ge on Si(001) at the room
temperature and explored crystallization of the disordered Ge film as a result
of annealing at 600 {\deg}C. The experiment has demonstrated that the
Ge/Si(001) film formed in the conditions of an isolated system consists of the
standard patched wetting layer and large droplike clusters of Ge rather than of
huts or domes which appear when a film is grown in a flux of Ge atoms arriving
on its surface. We conclude that the growth of the pyramids appearing at
temperatures greater than 600 {\deg}C is controlled by kinetics rather than
thermodynamic equilibrium whereas the wetting layer is an equilibrium
structure.Comment: Accepted for publication in Nanoscale Research Letter
Metal silicide/poly-Si Schottky diodes for uncooled microbolometers
Nickel silicide Schottky diodes formed on polycrystalline Si films are
proposed as temperature sensors of monolithic uncooled microbolometer IR focal
plane arrays. Structure and composition of nickel silicide/polycrystalline
silicon films synthesized in a low-temperature process are examined by means of
transmission electron microscopy. The Ni silicide is identified as multi-phase
compound composed by 20 to 40% of Ni3Si, 30 to 60% of Ni2Si and 10 to 30% of
NiSi with probable minor content of NiSi2 at the silicide/poly-Si interface.
Rectification ratios of the Schottky diodes vary from ~100 to ~20 for the
temperature increasing from 22 to 70C; they exceed 1000 at 80K. A barrier of
~0.95 eV is found to control the photovoltage spectra at room temperature. A
set of barriers is observed in photo-emf spectra at 80K and attributed to the
Ni-silicide/poly-Si interface. Absolute values of temperature coefficients of
voltage and current are found to vary from 0.3 to 0.6%/K for forward biasing
and around 2.5%/K for reverse biasing of the diodes.Comment: 18 pages, 7 figure
Li+ protects nerve cells against destabilization of Ca2+ homeostasis and delayed death caused by removal of external Na+
AbstractIn experiments with fura-2 loaded cultured rat cerebellar granule cells we have compared the changes in [Ca2+]i homeostasis produced by replacement of external Na+ with the organic cation N-methyl-d-glucamine (NMDG) or Li+. The Na+/NMDG replacement caused an increase in baseline [Ca2+]i and a considerable delay in [Ca2+]i recovery following a glutamate (Glu) pulse in almost all the cells. In contrast Na+/Li+ replacement usually did not change baseline [Ca2+]i and produced only a small (if any) delay in the post-glutamate [Ca2+]i recovery. Previously [Storozhevykh et al. (1998) FEBS Lett. 431, 215–218] we revealed that perturbation of [Ca2+]i homeostasis caused by Na+/NMDG replacement cannot be explained by a reversal of the Na+/Ca2+ exchange but is mainly due to Ca2+ influx through NMDA channels activated by Na+ dependent release of endogenous excitatory amino acids (`reversed Glu uptake'). In the present work we confirmed this conclusion and obtained evidence suggesting that in contrast to NMDG Li+ interferes with the `reversed Glu uptake' triggered by removal of external Na+. Thus it has been shown that the addition of Li+ (20 mM) to a Na+-free NMDGcontaining solution suppressed both the perturbation of [Ca2+]i homeostasis and delayed neuronal death caused by Na+/NMDG replacement. Li+ is also able to abolish the [Ca2+]i response induced by PDC which at high concentrations (>200 μM) is shown to stimulate the release of endogenous Glu. In contrast to Na+/Li+, Na+/NMDG replacement greatly enhances [Ca2+]i increase caused by PDC. Control experiments showed that Na+/Li+ replacement does not decrease the [Ca2+]i response to the Glu pulse. Therefore we concluded that a considerable quantitative difference between the effects of Na+/NMDG and Na+/Li+ replacements on both [Ca2+]i homeostasis and cell viability resulted mainly from the ability of Li+ to attenuate the release of endogenous Glu in response to the removal of external Na+
Evolution of Ge wetting layers growing on smooth and rough Si (001) surfaces: isolated {105} facets as a kinetic factor of stress relaxation
The results of STM and RHEED studies of a thin Ge film grown on the
Si/Si(001) epitaxial layers with different surface relief are presented.
Process of the partial stress relaxation was accompanied by changes in the
surface structure of the Ge wetting layer. Besides the well-known sequence of
surface reconstructions ( patches) and hut clusters faceted with {105} planes, the formation of
isolated {105} planes, which faceted the edges of patches, has
been observed owing to the deposition of Ge on a rough Si/Si (001) surface. A
model of the isolated {105} facet formation has been proposed based on the
assumption that the mutual arrangement of the monoatomic steps on the initial
Si surface promotes the wetting layer formation with the inhomogeneously
distributed thickness that results in the appearance of patches
partially surrounded by deeper trenches than those observed in the usual Ge
wetting layer grown on the smooth Si(001) surface. Isolated {105} facets are an
inherent part of the Ge wetting layer structure and their formation decreases
the surface energy of the Ge wetting layer.Comment: 27 pages, 8 figure
Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
<p>Abstract</p> <p>Background</p> <p>Accumulated evidence suggests that hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub>2</sub>O<sub>2 </sub>in neuronal insulin receptor activation and the origin of insulin-induced H<sub>2</sub>O<sub>2 </sub>in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub>2</sub>O<sub>2 </sub>is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub>2</sub>O<sub>2 </sub>production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p> <p>Results</p> <p>Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub>2</sub>O<sub>2 </sub>release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub>2</sub>O<sub>2 </sub>scavenger, inhibited both insulin-stimulated H<sub>2</sub>O<sub>2 </sub>release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub>2</sub>O<sub>2 </sub>production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub>2</sub>O<sub>2 </sub>release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p> <p>Conclusion</p> <p>Results of the present study suggest that insulin-induced H<sub>2</sub>O<sub>2 </sub>is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub>2</sub>O<sub>2 </sub>production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p
Peculiarities and evolution of Raman spectra of multilayer Ge/Si(001) heterostructures containing arrays of low-temperature MBE-grown Ge quantum dots of different size and number density: Experimental studies and numerical simulations
Ge/Si(001) multilayer heterostructures containing arrays of low-temperature
self-assembled Ge quantum dots and very thin SiGe layers of varying
composition and complex geometry have been studied using Raman spectroscopy and
scanning tunneling microscopy. The dependence of Raman spectra on the effective
thickness of deposited Ge layers has been investigated in detail in the range
from 4 to 18 \r{A}. The position and shape of both Ge and SiGe vibrational
modes are of great interest since they are closely related to the strain and
composition of the material that plays a role of active component in
perspective optoelectronic devices based on such structures. In this work, we
present an explanation for some peculiar features of Raman spectra, which makes
it possible to control the quality of the grown heterostructures more
effectively. A dramatic increase of intensity of both the GeGe and SiGe
bands for the structure containing Ge layers of 10 \r{A} and anomalous shift
and broadening of the SiGe band for structures comprising Ge layers of 8 and
9 \r{A} thick were observed. In our model, the anomalous behavior of the Raman
spectra with the change of thickness of deposited Ge is connected with the
flatness of Ge layers as well as transitional SiGe domains formed via the
stress-induced diffusion from {105} facets of quantum dots. The conclusions are
supported by the STM studies and the numerical calculations.Comment: 17 pages, 11 figure
Hypothalamic Reactive Oxygen Species Are Required for Insulin-Induced Food Intake Inhibition: An NADPH Oxidase–Dependent Mechanism
1939-327X (Electronic) Journal Article Research Support, Non-U.S. Gov'tOBJECTIVE: Insulin plays an important role in the hypothalamic control of energy balance, especially by reducing food intake. Emerging data point to a pivotal role of reactive oxygen species (ROS) in energy homeostasis regulation, but their involvement in the anorexigenic effect of insulin is unknown. Furthermore, ROS signal derived from NADPH oxidase activation is required for physiological insulin effects in peripheral cells. In this study, we investigated the involvement of hypothalamic ROS and NADPH oxidase in the feeding behavior regulation by insulin. RESEARCH DESIGN AND METHODS: We first measured hypothalamic ROS levels and food intake after acute intracerebroventricular injection of insulin. Second, effect of pretreatment with a ROS scavenger or an NADPH oxidase inhibitor was evaluated. Third, we examined the consequences of two nutritional conditions of central insulin unresponsiveness (fasting or short-term high-fat diet) on the ability of insulin to modify ROS level and food intake. RESULTS: In normal chow-fed mice, insulin inhibited food intake. At the same dose, insulin rapidly and transiently increased hypothalamic ROS levels by 36%. The pharmacological suppression of this insulin-stimulated ROS elevation, either by antioxidant or by an NADPH oxidase inhibitor, abolished the anorexigenic effect of insulin. Finally, in fasted and short-term high-fat diet-fed mice, insulin did not promote elevation of ROS level and food intake inhibition, likely because of an increase in hypothalamic diet-induced antioxidant defense systems. CONCLUSIONS: A hypothalamic ROS increase through NADPH oxidase is required for the anorexigenic effect of insulin
- …