The finite spectral line width of an ensemble of CdSe nanocrystals arises from size and shape inhomogeneity and the single-nanocrystal spectrum itself. This line width directly limits the performance of nanocrystal-based devices, yet most optical measurements cannot resolve the underlying contributions. We use two-dimensional electronic spectroscopy (2D ES) to measure the line width of the band-edge exciton of CdSe nanocrystals as a function of radii and surface chemistry. We find that the homogeneous width decreases for increasing nanocrystal radius and that surface chemistry plays a critical role in controlling this line width. To explore the hypothesis that unpassivated trap states serve to broaden the homogeneous line width and to explain its size-dependence, we use 3D ES to identify the spectral signatures of exciton-phonon coupling to optical and acoustic phonons. We find enhanced coupling to optical phonon modes for nanocrystals that lack electron-passivating ligands, suggesting that localized surface charges enhance exciton-phonon coupling via the Fröhlich interaction. Lastly, the data reveal that spectral diffusion contributes negligibly to the homogeneous line width on subnanosecond time scales.

IntroductionMantle cell lymphoma (MCL) is an aggressive and mostly incurable B-cell malignancy accounting for 5% of non-Hodgkin lymphomas (NHLs). MCL arises from naive B cells (NBCs) in the mantle zone of lymph node follicles and is characterized by the t(11,14) chromosomal translocation leading to overexpression of cyclin D1 (CCND1). 1 However, murine models overexpressing CCND1 in the absence of other oncogenes, such as MYC, do not develop lymphoma, 2 implying that additional pathogenic mechanisms are involved in MCL. Cip/Kip proteins have an important role in the formation of active CDK4/cyclin D complexes. In NHLs other than MCL, p27(Kip) protein expression is inversely related to the proliferation activity of the tumors. 3 Apoptosis-related genes such as BCL2 have also been found to be altered in MCL with the use of different approaches. Homozygous deletions of BIM, a member of the BCL2 family, have also been found in MCL. 4 Epigenetic changes, such as methylation of gene promoters, have been shown to contribute to the pathogenesis of both solid and hematologic malignancies. 5 Single-locus studies analyzing methylation in MCL patient samples have shown hypermethylation of key genes, such as cell-cycle regulators p14 ARF and CDKN2A,6,7 protein phosphatase SHP-1 8 and Rho-adenosine triphosphatase PARG-1. 9 However these studies did not compare the methylation to NBCs, the normal counterparts of these malignant cells. 10 Several lines of evidence conclusively show NBCs to be the cell of origin of MCL, including immunoglobulin heavy chain mutation status, t (11,14) chromosomal breakpoint analysis, 11 and gene expression microarrays. 12,13 To develop a more comprehensive understanding of aberrant DNA methylation in MCL, we performed a genomewide analysis of MCL DNA methylation and gene expression with the use of purified normal NBCs as controls. We report that promoter DNA methylation is aberrantly distributed in the MCL genome compared with normal NBCs, and we identified aberrantly hypermethylated and hypomethylated genes that provide a basis for rational targeted therapy in this disease. Methods Patient samplesTissues and blood samples were obtained from patients newly diagnosed with MCL before any treatment after informed consent in accordance with the Declaration of Helsinki. Sample collection and laboratory studies were in compliance with institutional review board and Helsinki protocols. CD19 ϩ cells from 22 patients treated at the National Institutes of Health were purified by magnetic bead sorting from peripheral blood or pheresis products before freezing to ensure greater than 90% purity for HpaII tiny The publisher or recipient acknowledges right of the US government to retain a nonexclusive, royalty-free license in and to any copyright covering the article.The online version of this article contains a data supplement.The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked ''advertisement'' in accorda...

Conical intersections are molecular configurations at which adiabatic potential-energy surfaces touch. They are predicted to be ubiquitous, yet condensed-phase experiments have focused on the few systems with clear spectroscopic signatures of negligible fluorescence, high photoactivity, or femtosecond electronic kinetics. Although rare, these signatures have become diagnostic for conical intersections. Here we detect a coherent surface-crossing event nearly two picoseconds after optical excitation in a highly fluorescent molecule that has no photoactivity and nanosecond electronic kinetics. Time-frequency analysis of high-sensitivity measurements acquired using sub-8 fs pulses reveals phase shifts of the signal due to branching of the wavepacket through a conical intersection. The time-frequency analysis methodology demonstrated here on a model compound will enable studies of conical intersections in molecules that do not exhibit their diagnostic signatures. Improving the ability to detect conical intersections will enrich the understanding of their mechanistic role in molecular photochemistry.

SOX11 (Sex determining region Y-box 11) expression is specific for MCL as compared to other Non-Hodgkin's lymphomas. However, the function and direct binding targets of SOX11 in MCL are largely unknown. We used high-resolution ChIP-Seq to identify the direct target genes of SOX11 in a genome-wide, unbiased manner and elucidate its functional significance. Pathway analysis identified WNT, PKA and TGF-beta signaling pathways as significantly enriched by SOX11 target genes. qCHIP and promoter reporter assays confirmed that SOX11 directly binds to individual genes and modulates their transcription activities in these pathways in MCL. Functional studies using RNA interference demonstrate that SOX11 directly regulates WNT in MCL. We analyzed SOX11 expression in three independent well-annotated tissue microarrays from the University of Wisconsin (UW), Karolinska Institute and British Columbia Cancer Agency (BCCA). Our findings suggest that high SOX11 expression is associated with improved survival in a subset of MCL patients, particularly those treated with intensive chemotherapy. Transcriptional regulation of WNT and other biological pathways affected by SOX11 target genes may help explain the impact of SOX11 expression on patient outcomes.