56 research outputs found

    Attosecond electron spectroscopy using a novel interferometric pump-probe technique

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    We present an interferometric pump-probe technique for the characterization of attosecond electron wave packets (WPs) that uses a free WP as a reference to measure a bound WP. We demonstrate our method by exciting helium atoms using an attosecond pulse with a bandwidth centered near the ionization threshold, thus creating both a bound and a free WP simultaneously. After a variable delay, the bound WP is ionized by a few-cycle infrared laser precisely synchronized to the original attosecond pulse. By measuring the delay-dependent photoelectron spectrum we obtain an interferogram that contains both quantum beats as well as multi-path interference. Analysis of the interferogram allows us to determine the bound WP components with a spectral resolution much better than the inverse of the attosecond pulse duration.Comment: 5 pages, 4 figure

    Attosecond streaking of photoelectron emission from disordered solids

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    Attosecond streaking of photoelectrons emitted by extreme ultraviolet light has begun to reveal how electrons behave during their transport within simple crystalline solids. Many sample types within nanoplasmonics, thin-film physics, and semiconductor physics, however, do not have a simple single crystal structure. The electron dynamics which underpin the optical response of plasmonic nanostructures and wide-bandgap semiconductors happen on an attosecond timescale. Measuring these dynamics using attosecond streaking will enable such systems to be specially tailored for applications in areas such as ultrafast opto-electronics. We show that streaking can be extended to this very general type of sample by presenting streaking measurements on an amorphous film of the wide-bandgap semiconductor tungsten trioxide, and on polycrystalline gold, a material that forms the basis of many nanoplasmonic devices. Our measurements reveal the near-field temporal structure at the sample surface, and photoelectron wavepacket temporal broadening consistent with a spread of electron transport times to the surface

    Temporal broadening of attosecond photoelectron wavepackets from solid surfaces

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    The response of solids to electromagnetic fields is of crucial importance in many areas of science and technology. Many fundamental questions remain to be answered about the dynamics of the photoexcited electrons that underpin this response, which can evolve on timescales of tens to hundreds of attoseconds. How, for example, is the photoexcited electron affected by the periodic potential as it travels in the solid, and how do the other electrons respond in these strongly correlated systems? Furthermore, control of electronic motion in solids with attosecond precision would pave the way for the development of ultrafast optoelectronics. Attosecond electron dynamics can be traced using streaking, a technique in which a strong near-infrared laser field accelerates an attosecond electron wavepacket photoemitted by an extreme ultraviolet light pulse, imprinting timing information onto it. We present attosecond streaking measurements on the wide-bandgap semiconductor tungsten trioxide, and on gold, a metal used in many nanoplasmonic devices. Information about electronic motion in the solid is encoded on the temporal properties of the photoemitted electron wavepackets, which are consistent with a spread of electron transport times to the surface following photoexcitation

    LKB1 and AMPK differentially regulate pancreatic β-cell identity.

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    Fully differentiated pancreatic β cells are essential for normal glucose homeostasis in mammals. Dedifferentiation of these cells has been suggested to occur in type 2 diabetes, impairing insulin production. Since chronic fuel excess ("glucotoxicity") is implicated in this process, we sought here to identify the potential roles in β-cell identity of the tumor suppressor liver kinase B1 (LKB1/STK11) and the downstream fuel-sensitive kinase, AMP-activated protein kinase (AMPK). Highly β-cell-restricted deletion of each kinase in mice, using an Ins1-controlled Cre, was therefore followed by physiological, morphometric, and massive parallel sequencing analysis. Loss of LKB1 strikingly (2.0-12-fold, E<0.01) increased the expression of subsets of hepatic (Alb, Iyd, Elovl2) and neuronal (Nptx2, Dlgap2, Cartpt, Pdyn) genes, enhancing glutamate signaling. These changes were partially recapitulated by the loss of AMPK, which also up-regulated β-cell "disallowed" genes (Slc16a1, Ldha, Mgst1, Pdgfra) 1.8- to 3.4-fold (E<0.01). Correspondingly, targeted promoters were enriched for neuronal (Zfp206; P=1.3×10(-33)) and hypoxia-regulated (HIF1; P=2.5×10(-16)) transcription factors. In summary, LKB1 and AMPK, through only partly overlapping mechanisms, maintain β-cell identity by suppressing alternate pathways leading to neuronal, hepatic, and other characteristics. Selective targeting of these enzymes may provide a new approach to maintaining β-cell function in some forms of diabetes.-Kone, M., Pullen, T. J., Sun, G., Ibberson, M., Martinez-Sanchez, A., Sayers, S., Nguyen-Tu, M.-S., Kantor, C., Swisa, A., Dor, Y., Gorman, T., Ferrer, J., Thorens, B., Reimann, F., Gribble, F., McGinty, J. A., Chen, L., French, P. M., Birzele, F., Hildebrandt, T., Uphues, I., Rutter, G. A. LKB1 and AMPK differentially regulate pancreatic β-cell identity

    Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers a role for <i>Elovl2</i> in glucose-induced insulin secretion.

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    In type 2 diabetes (T2D), pancreatic β cells become progressively dysfunctional, leading to a decline in insulin secretion over time. In this study, we aimed to identify key genes involved in pancreatic beta cell dysfunction by analyzing multiple mouse strains in parallel under metabolic stress. Male mice from six commonly used non-diabetic mouse strains were fed a high fat or regular chow diet for three months. Pancreatic islets were extracted and phenotypic measurements were recorded at 2 days, 10 days, 30 days, and 90 days to assess diabetes progression. RNA-Seq was performed on islet tissue at each time-point and integrated with the phenotypic data in a network-based analysis. A module of co-expressed genes was selected for further investigation as it showed the strongest correlation to insulin secretion and oral glucose tolerance phenotypes. One of the predicted network hub genes was &lt;i&gt;Elovl2&lt;/i&gt; , encoding Elongase of very long chain fatty acids 2. &lt;i&gt;Elovl2&lt;/i&gt; silencing decreased glucose-stimulated insulin secretion in mouse and human β cell lines. Our results suggest a role for &lt;i&gt;Elovl2&lt;/i&gt; in ensuring normal insulin secretory responses to glucose. Moreover, the large comprehensive dataset and integrative network-based approach provides a new resource to dissect the molecular etiology of β cell failure under metabolic stress
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