Investigation of Size-Dependent Plasmonic and Catalytic Properties of Metallic Nanocrystals Enabled by Size Control with HCl Oxidative Etching

Small ◽  
2012 ◽  
Vol 8 (11) ◽  
pp. 1710-1716 ◽  
Author(s):  
Bo Li ◽  
Ran Long ◽  
Xiaolan Zhong ◽  
Yu Bai ◽  
Zijie Zhu ◽  
...  
Keyword(s):  
Catalytic Properties ◽  
Size Control ◽  
Size Dependent ◽  
Oxidative Etching

Synthesis and size control of Si nanocrystals by SiO/SiO2 superlattices and Er doping

2002 ◽  
Vol 737 ◽  
Author(s):  
J. Heitmann ◽  
D. Kovalev ◽  
M. Schmidt ◽  
L.X. Yi ◽  
R. Scholz ◽  
...  
Keyword(s):  
Phase Separation ◽  
Crystal Size ◽  
Radiative Lifetime ◽  
Size Control ◽  
Luminescence Signal ◽  
Er Doping ◽  
Size Dependent ◽  
Transmission Electron ◽  
Si Nanocrystals ◽  
Ultrathin Layers

ABSTRACTThe synthesis of nc-Si by reactive evaporation of SiO and subsequent thermal induced phase separation is reported. The size control of nc-Si is realized by evaporation of SiO/SiO2 superlattices. By this method an independent control of crystal size and density is possible. The phase separation of SiO into SiO2 and nc-Si in the limit of ultrathin layers is investigated. Different steps of this phase separation are characterized by photoluminescence, infrared absorption and transmission electron microscopy measurements. The strong room temperature luminescence of nc-Si shows a strong blueshift of the photoluminescence signal from 850 to 750 nm with decreasing crystal size. Several size dependent properties of this luminescence signal, like decreasing radiative lifetime and increasing no-phonon transition properties with decreasing crystal size are in good agreement with the quantum confinement model. Er doping of the nc-Si shows an enhancement of the Er luminescence at 1.54 μm by a factor of 5000 compared to doped SiO2 layers. The decreasing transfer time for the nc-Si to Er transition with decreasing crystal size can be understood as additional proof of increasing recombination probability within the nc-Si for decreasing crystal size.

scholarly journals Size-Controlled Synthesis of CoFe2O4Nanoparticles Potential Contrast Agent for MRI and Investigation on Their Size-Dependent Magnetic Properties

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Fujun Liu ◽  
Sophie Laurent ◽  
Alain Roch ◽  
Luce Vander Elst ◽  
Robert N. Muller
Keyword(s):  
Magnetic Layer ◽  
Size Control ◽  
Correlation Spectroscopy ◽  
Local Concentration ◽  
Long Term Stability ◽  
Size Dependent ◽  
Transmission Electron ◽  
Size Controlled ◽  
Size Of Nuclei

Cobalt ferrite nanoparticles (CoFe2O4NPs) were synthesized by coprecipitation followed by treatments with diluted nitric acid and sodium citrate. Transmission electron microscope (TEM) and photon correlation spectroscopy (PCS) characterization showed that the size distributions of these nanoparticles were monodisperse and that no aggregation occurred. This colloid showed a long-term stability. Through adjustment of the concentrations of reactants and reaction temperature, the size of the NPs can be tuned from 6 to 80 nm. The size-control mechanism is explained by a nucleation-growth model, where the local concentration of monomers is assumed to decide the size of nuclei, and reaction temperatures influence the growth of nuclei. Magnetization and relaxivityr1,2measurements showed that the NPs revealed size-dependent magnetization and relaxivity properties, which are explained via a “dead magnetic layer” theory where reductions of saturation magnetization (Ms) andr1,2are assumed to be caused by the demagnetization of surface spins.

scholarly journals Cell size-dependent regulation of Wee1 localization by Cdr2 cortical nodes

2017 ◽  
Author(s):  
Corey A. H. Allard ◽  
Hannah E. Opalko ◽  
Ko-Wei Liu ◽  
Uche Medoh ◽  
James B. Moseley
Keyword(s):  
Cell Growth ◽  
Fission Yeast ◽  
Cell Size ◽  
Kinase Activity ◽  
Size Control ◽  
Small Cells ◽  
Mitotic Entry ◽  
Size Dependent ◽  
Biochemical Fractionation ◽  
Mitotic Inhibitor

AbstractCell size control requires mechanisms that link cell growth with Cdk1 activity. In fission yeast, the protein kinase Cdr2 forms cortical nodes that include the Cdk1 inhibitor Wee1, along with the Wee1-inhibitory kinase Cdr1. We investigated how nodes inhibit Wee1 during cell growth. Biochemical fractionation revealed that Cdr2 nodes were megadalton structures enriched for activated Cdr2, which increases in level during interphase growth. In live-cell TIRF movies, Cdr2 and Cdr1 remained constant at nodes over time, but Wee1 localized to nodes in short bursts. Recruitment of Wee1 to nodes required Cdr2 kinase activity and the noncatalytic N-terminus of Wee1. Bursts of Wee1 localization to nodes increased 20-fold as cells doubled in size throughout G2. Size-dependent signaling was due in part to the Cdr2 inhibitor Pom1, which suppressed Wee1 node bursts in small cells. Thus, increasing Cdr2 activity during cell growth promotes Wee1 localization to nodes, where inhibitory phosphorylation of Wee1 by Cdr1 and Cdr2 kinases promotes mitotic entry.SummaryCells turn off the mitotic inhibitor Wee1 to enter into mitosis. This study shows how cell growth progressively inhibits fission yeast Wee1 through dynamic bursts of localization to cortical node structures that contain Wee1 inhibitory kinases.

scholarly journals Cell size–dependent regulation of Wee1 localization by Cdr2 cortical nodes

2018 ◽  
Vol 217 (5) ◽  
pp. 1589-1599 ◽  
Author(s):  
Corey A.H. Allard ◽  
Hannah E. Opalko ◽  
Ko-Wei Liu ◽  
Uche Medoh ◽  
James B. Moseley
Keyword(s):  
Cell Growth ◽  
Cell Size ◽  
Total Internal Reflection ◽  
Kinase Activity ◽  
Size Control ◽  
Small Cells ◽  
Mitotic Entry ◽  
Size Dependent ◽  
N Terminus ◽  
Biochemical Fractionation

Cell size control requires mechanisms that link cell growth with Cdk1 activity. In fission yeast, the protein kinase Cdr2 forms cortical nodes that include the Cdk1 inhibitor Wee1 along with the Wee1-inhibitory kinase Cdr1. We investigated how nodes inhibit Wee1 during cell growth. Biochemical fractionation revealed that Cdr2 nodes were megadalton structures enriched for activated Cdr2, which increases in level during interphase growth. In live-cell total internal reflection fluorescence microscopy videos, Cdr2 and Cdr1 remained constant at nodes over time, but Wee1 localized to nodes in short bursts. Recruitment of Wee1 to nodes required Cdr2 kinase activity and the noncatalytic N terminus of Wee1. Bursts of Wee1 localization to nodes increased 20-fold as cells doubled in size throughout G2. Size-dependent signaling was caused in part by the Cdr2 inhibitor Pom1, which suppressed Wee1 node bursts in small cells. Thus, increasing Cdr2 activity during cell growth promotes Wee1 localization to nodes, where inhibitory phosphorylation of Wee1 by Cdr1 and Cdr2 kinases promotes mitotic entry.

scholarly journals Scaling gene expression for cell size control and senescence in Saccharomyces cerevisiae

2020 ◽  
Author(s):  
Yuping Chen ◽  
Bruce Futcher
Keyword(s):  
Gene Expression ◽  
Cell Size ◽  
Size Control ◽  
Gene Expression Program ◽  
Set Point ◽  
Size Dependent ◽  
Large Size ◽  
Mean Size ◽  
Almost All ◽  
Expression Program

Abstract Cells divide with appropriate frequency by coupling division to growth—that is, cells divide only when they have grown sufficiently large. This process is poorly understood, but has been studied using cell size mutants. In principle, mutations affecting cell size could affect the mean size (“set-point” mutants), or they could affect the variability of sizes (“homeostasis” mutants). In practice, almost all known size mutants affect set-point, with little effect on size homeostasis. One model for size-dependent division depends on a size-dependent gene expression program: Activators of cell division are over-expressed at larger and larger sizes, while inhibitors are under-expressed. At sufficiently large size, activators overcome inhibitors, and the cell divides. Amounts of activators and inhibitors determine the set-point, but the gene expression program (the rate at which expression changes with cell size) determines the breadth of the size distribution (homeostasis). In this model, set-point mutants identify cell cycle activators and inhibitors, while homeostasis mutants identify regulators that couple expression of activators and inhibitors to size. We consider recent results suggesting that increased cell size causes senescence, and suggest that at very large sizes, an excess of DNA binding proteins leads to size induced senescence.

scholarly journals Increasing cell size remodels the proteome and promotes senescence

2021 ◽  
Author(s):  
Michael C Lanz ◽  
Evgeny Zatulovskiy ◽  
Matthew P Swaffer ◽  
Lichao Zhang ◽  
Shuyuan Zhang ◽  
...  
Keyword(s):  
Cell Size ◽  
Protein Concentration ◽  
Cell Function ◽  
Size Control ◽  
Cell Physiology ◽  
Proliferating Cells ◽  
Size Dependent ◽  
Large Size ◽  
Concentration Changes ◽  
Proteome Changes

Cell size is tightly controlled in healthy tissues, but it is poorly understood how cell size affects cell physiology. To address this, we measured how the proteome changes with cell size. Protein concentration changes are widespread, depend on the DNA-to-cell size ratio, and are predicted by subcellular localization, size-dependent mRNA concentrations, and protein turnover. As proliferating cells grow larger, concentration changes associated with cellular senescence are increasingly pronounced, suggesting that large size may be a cause rather than just a consequence of cell senescence. Consistent with this hypothesis, larger cells are prone to replicative-, DNA damage-, and CDK4/6i-induced senescence. More broadly, our findings show how cell size could impact many aspects of cell physiology through remodeling the proteome, thereby providing a rationale for cell size control to optimize cell function.

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