Wetting layer states of InAs/GaAs self-assembled quantum dot structures. Effect of intermixing and capping layer

The authors present a modulated reflectivity study of the wetting layer (WL) states in mol. beam epitaxy grown InAs/GaAs quantum dot (QD) structures designed to emit light in the 1.3-1.5 micro m range. A high sensitivity of the technique has allowed the observation of all optical transitions in the QD system, including low oscillator strength transitions related to QD ground and excited states, and the ones connected with the WL quantum well (QW). The support of WL content profiles, detd. by transmission electron microscopy, has made it possible to analyze in detail the real WL QW confinement potential which was then used for calcg. the optical transition energies. In spite of a very effective WL QW intermixing, mainly due to the Ga-In exchange process (causing the redn. of the max. indium content in the WL layer to about 35% from nominally deposited InAs), the transition energies remain almost unaffected. The latter effect could be explained in effective mass envelope function calcns. taking into account the intermixing of the QW interfaces described within the diffusion model. We have followed the WL-related transitions of 2 closely spaced QD layers grown at different temps., as a function of the In content in the capping layer. Changing the capping layer from pure GaAs to In0.236Ga0.764As has no significant influence on the compn. profile of the WL itself and the WL QW transitions can be usually interpreted properly when based on the cap-induced modification of the confinement potential within a squarelike QW shape approxn. However, some of the obsd. features could be explained only after taking into consideration the effects of intermixing and InGaAs cap layer decompn. [on SciFinder (R)

Epigenetic Regulation of Histone H3 Serine 10 Phosphorylation Status by HCF-1 Proteins in C. elegans and Mammalian Cells

BACKGROUND: The human herpes simplex virus (HSV) host cell factor HCF-1 is a transcriptional coregulator that associates with both histone methyl- and acetyltransferases, and a histone deacetylase and regulates cell proliferation and division. In HSV-infected cells, HCF-1 associates with the viral protein VP16 to promote formation of a multiprotein-DNA transcriptional activator complex. The ability of HCF proteins to stabilize this VP16-induced complex has been conserved in diverse animal species including Drosophila melanogaster and Caenorhabditis elegans suggesting that VP16 targets a conserved cellular function of HCF-1. METHODOLOGY/PRINCIPAL FINDINGS: To investigate the role of HCF proteins in animal development, we have characterized the effects of loss of the HCF-1 homolog in C. elegans, called Ce HCF-1. Two large hcf-1 deletion mutants (pk924 and ok559) are viable but display reduced fertility. Loss of Ce HCF-1 protein at reduced temperatures (e.g., 12 degrees C), however, leads to a high incidence of embryonic lethality and early embryonic mitotic and cytokinetic defects reminiscent of mammalian cell-division defects upon loss of HCF-1 function. Even when viable, however, at normal temperature, mutant embryos display reduced levels of phospho-histone H3 serine 10 (H3S10P), a modification implicated in both transcriptional and mitotic regulation. Mammalian cells with defective HCF-1 also display defects in mitotic H3S10P status. CONCLUSIONS/SIGNIFICANCE: These results suggest that HCF-1 proteins possess conserved roles in the regulation of cell division and mitotic histone phosphorylation

Classification and Prediction of Survival in Patients with the Leukemic Phase of Cutaneous T Cell Lymphoma

We have used cDNA arrays to investigate gene expression patterns in peripheral blood mononuclear cells from patients with leukemic forms of cutaneous T cell lymphoma, primarily Sezary syndrome (SS). When expression data for patients with high blood tumor burden (Sezary cells >60% of the lymphocytes) and healthy controls are compared by Student's t test, at P < 0.01, we find 385 genes to be differentially expressed. Highly overexpressed genes include Th2 cells–specific transcription factors Gata-3 and Jun B, as well as integrin β1, proteoglycan 2, the RhoB oncogene, and dual specificity phosphatase 1. Highly underexpressed genes include CD26, Stat-4, and the IL-1 receptors. Message for plastin-T, not normally expressed in lymphoid tissue, is detected only in patient samples and may provide a new marker for diagnosis. Using penalized discriminant analysis, we have identified a panel of eight genes that can distinguish SS in patients with as few as 5% circulating tumor cells. This suggests that, even in early disease, Sezary cells produce chemokines and cytokines that induce an expression profile in the peripheral blood distinctive to SS. Finally, we show that using 10 genes, we can identify a class of patients who will succumb within six months of sampling regardless of their tumor burden