422 research outputs found

    Observation of coherent transients in ultrashort chirped excitation of an undamped two-level system

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    The effects of Coherent excitation of a two level system with a linearly chirped pulse are studied theoretically and experimentally (in Rb (5s - 5p)) in the low field regime. The Coherent Transients are measured directly on the excited state population on an ultrashort time scale. A sharp step corresponds to the passage through resonance. It is followed by oscillations resulting from interferences between off-resonant and resonant contributions. We finally show the equivalence between this experiment and Fresnel diffraction by a sharp edge.Comment: 4 pages, 4 figures, to appear in PR

    Nucleoplasmic LAP2 alpha-lamin A complexes are required to maintain a proliferative state in human fibroblasts

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    In human diploid fibroblasts (HDFs), expression of lamina-associated polypeptide 2 (LAP2) upon entry and exit from G0 is tightly correlated with phosphorylation and subnuclear localization of retinoblastoma protein (Rb). Phosphoisoforms of Rb and LAP2 are down-regulated in G0. Although RbS780 phosphoform and LAP2 are up-regulated upon reentry into G1 and colocalize in the nucleoplasm, RbS795 migrates between nucleoplasmic and speckle compartments. In HDFs, which are null for lamins A/C, LAP2 is mislocalized within nuclear aggregates, and this is correlated with cell cycle arrest and accumulation of Rb within speckles. Nuclear retention of nucleoplasmic Rb during G1 phase but not of speckle-associated Rb depends on lamin A/C. siRNA knock down of LAP2 or lamin A/C in HDFs leads to accumulation of Rb in speckles and G1 arrest, probably because of activation of a cell cycle checkpoint. Our results suggest that LAP2 and lamin A/C are involved in controlling Rb localization and phosphorylation, and a lack or mislocalization of either protein leads to cell cycle arrest in HDFs

    Long-Term Evolution and Revival Structure of Rydberg Wave Packets for Hydrogen and Alkali-Metal Atoms

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    This paper begins with an examination of the revival structure and long-term evolution of Rydberg wave packets for hydrogen. We show that after the initial cycle of collapse and fractional/full revivals, which occurs on the time scale trevt_{\rm rev}, a new sequence of revivals begins. We find that the structure of the new revivals is different from that of the fractional revivals. The new revivals are characterized by periodicities in the motion of the wave packet with periods that are fractions of the revival time scale trevt_{\rm rev}. These long-term periodicities result in the autocorrelation function at times greater than trevt_{\rm rev} having a self-similar resemblance to its structure for times less than trevt_{\rm rev}. The new sequence of revivals culminates with the formation of a single wave packet that more closely resembles the initial wave packet than does the full revival at time trevt_{\rm rev}, i.e., a superrevival forms. Explicit examples of the superrevival structure for both circular and radial wave packets are given. We then study wave packets in alkali-metal atoms, which are typically used in experiments. The behavior of these packets is affected by the presence of quantum defects that modify the hydrogenic revival time scales and periodicities. Their behavior can be treated analytically using supersymmetry-based quantum-defect theory. We illustrate our results for alkali-metal atoms with explicit examples of the revival structure for radial wave packets in rubidium.Comment: To appear in Physical Review A, vol. 51, June 199

    A rare missense mutation in <i>GJB3</i> (Cx31G45E) is associated with a unique cellular phenotype resulting in necrotic cell death

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    Erythrokeratodermia variabilis et progressiva (EKV-P) is caused by mutations in either the GJB3 (Cx31) or GJB4 genes (Cx30.3). We identified a rare GJB3 missense mutation, c.134G>A (p.G45E), in two unrelated patients and investigated its cellular characteristics. Expression of Cx31G45E-GFP caused previously undescribed changes within HeLa cells and HaCaT cells, a model human keratinocyte cell line. Cx31WT-GFP localised to the plasma membrane, but expression of Cx31G45E-GFP caused vacuolar expansion of the endoplasmic reticulum (ER), the mutant protein accumulated within the ER membrane and disassembly of the microtubular network occurred. No ER stress responses were evoked. Cx31WT-myc-myc-6xHis and Cx31G45E-GFP co-immunoprecipitated, indicative of heteromeric interaction, but co-expression with Cx31WT-mCherry, Cx26 or Cx30.3 did not mitigate the phenotype. Cx31 and Cx31G45E both co-immunoprecipitated with Cx43, indicating the ability to form heteromeric connexons. WT-Cx31 and Cx43 assembled into large gap junction plaques at points of cell-to-cell contact; Cx31G45E restricted the ability of Cx43 to reach the plasma membrane in both HaCaT cells and HeLa cells stably expressing Cx43 where the proteins strongly co-localised with the vacolourised ER. Cell viability assays identified an increase in cell death in cells expressing Cx31G45E-GFP, which FACS analysis determined was necrotic. Blocking connexin channel function with 18α-glycyrrhetinic acid did not completely rescue necrosis or prevent propidium iodide uptake, suggesting that expression of Cx31G45E-GFP damages the cellular membrane independent of its channel function. Our data suggest that entrapment of Cx43 and necrotic cell death in the epidermis could underlie the EKV skin phenotype

    'The Germans are Hydrophobes': Germany and the Germans in the Shaping of French Identity

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    This article addresses issues of national identity and nationalism in the age of the French Revolution by looking at French attitudes towards the Germans. It engages with theories of nationalism while presenting empirical evidence gleaned from archival research. This material, sometimes grimly, sometimes rather amusingly, reveals much about French ideas and prejudices about the Germans and how it reflected back on the revolutionary and Napoleonic sense of what it meant to be French

    Edge-Magnetoplasmon Wave-Packet Revivals in the Quantum Hall Effect

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    The quantum Hall effect is necessarily accompanied by low-energy excitations localized at the edge of a two-dimensional electron system. For the case of electrons interacting via the long-range Coulomb interaction, these excitations are edge magnetoplasmons. We address the time evolution of localized edge-magnetoplasmon wave packets. On short times the wave packets move along the edge with classical E cross B drift. We show that on longer times the wave packets can have properties similar to those of the Rydberg wave packets that are produced in atoms using short-pulsed lasers. In particular, we show that edge-magnetoplasmon wave packets can exhibit periodic revivals in which a dispersed wave packet reassembles into a localized one. We propose the study of edge-magnetoplasmon wave packets as a tool to investigate dynamical properties of integer and fractional quantum-Hall edges. Various scenarios are discussed for preparing the initial wave packet and for detecting it at a later time. We comment on the importance of magnetoplasmon-phonon coupling and on quantum and thermal fluctuations.Comment: 18 pages, RevTex, 7 figures and 2 tables included, Fig. 5 was originally 3Mbyte and had to be bitmapped for submission to archive; in the process it acquired distracting artifacts, to upload the better version, see http://physics.indiana.edu/~uli/publ/projects.htm

    Personality traits, ventricular tachyarrhythmias, and mortality in patients with an implantable cardioverter defibrillator: 6 years follow-up of the WEBCARE cohort

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    Objective: Risk stratification within the ICD population warrants the examining of the role of protective- and risk factors. Current study examines the association between Type D personality, pessimism, and optimism and risk of ventricular tachyarrhythmias (VTa's) and mortality in patients with a first-time ICD 6 years post implantation. Methods: A total of 221 first-implant ICD patients completed questionnaires on optimism and pessimism (Life Orientation Test) and Type D personality (Type D scale DS14) 10 to 14 days after implantation. VTa's and all-cause mortality 6 years post implant comprised the study endpoints. Results: Ninety (40.7%) patients had experienced VTa's and 37 (16.7%) patients died, 12 (5.4%) due to a cardiac cause. Adjusted logistic regression analysis showed that pessimism was significantly associated with increased risk of VTa's (OR = 1.09; 95% CI = 1.00–1.19; p =.05). Type D personality (OR = 1.05; 95% CI = 0.47–2.32; p =.91) and optimism (OR = 1.00; 95% CI = 0.90–1.12; p =.98) were not associated with VTa's. None of the personality types were associated with mortality. Conclusion: Pessimism was associated with VTa's but not with mortality. No significant association with either of the endpoints was observed for Type D personality and optimism. Future research should focus on the coexistent psychosocial factors that possibly lead to adverse cardiac prognosis in this patient population

    Reorganization of the nuclear lamina and cytoskeleton in adipogenesis

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    A thorough understanding of fat cell biology is necessary to counter the epidemic of obesity. Although molecular pathways governing adipogenesis are well delineated, the structure of the nuclear lamina and nuclear-cytoskeleton junction in this process are not. The identification of the ‘linker of nucleus and cytoskeleton’ (LINC) complex made us consider a role for the nuclear lamina in adipose conversion. We herein focused on the structure of the nuclear lamina and its coupling to the vimentin network, which forms a cage-like structure surrounding individual lipid droplets in mature adipocytes. Analysis of a mouse and human model system for fat cell differentiation showed fragmentation of the nuclear lamina and subsequent loss of lamins A, C, B1 and emerin at the nuclear rim, which coincides with reorganization of the nesprin-3/plectin/vimentin complex into a network lining lipid droplets. Upon 18 days of fat cell differentiation, the fraction of adipocytes expressing lamins A, C and B1 at the nuclear rim increased, though overall lamin A/C protein levels were low. Lamin B2 remained at the nuclear rim throughout fat cell differentiation. Light and electron microscopy of a subcutaneous adipose tissue specimen showed striking indentations of the nucleus by lipid droplets, suggestive for an increased plasticity of the nucleus due to profound reorganization of the cellular infrastructure. This dynamic reorganization of the nuclear lamina in adipogenesis is an important finding that may open up new venues for research in and treatment of obesity and nuclear lamina-associated lipodystrophy

    Nuclear rupture at sites of high curvature compromises retention of DNA repair factors.

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    The nucleus is physically linked to the cytoskeleton, adhesions, and extracellular matrix-all of which sustain forces, but their relationships to DNA damage are obscure. We show that nuclear rupture with cytoplasmic mislocalization of multiple DNA repair factors correlates with high nuclear curvature imposed by an external probe or by cell attachment to either aligned collagen fibers or stiff matrix. Mislocalization is greatly enhanced by lamin A depletion, requires hours for nuclear reentry, and correlates with an increase in pan-nucleoplasmic foci of the DNA damage marker γH2AX. Excess DNA damage is rescued in ruptured nuclei by cooverexpression of multiple DNA repair factors as well as by soft matrix or inhibition of actomyosin tension. Increased contractility has the opposite effect, and stiff tumors with low lamin A indeed exhibit increased nuclear curvature, more frequent nuclear rupture, and excess DNA damage. Additional stresses likely play a role, but the data suggest high curvature promotes nuclear rupture, which compromises retention of DNA repair factors and favors sustained damage

    The Different Function of Single Phosphorylation Sites of Drosophila melanogaster Lamin Dm and Lamin C

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    Lamins' functions are regulated by phosphorylation at specific sites but our understanding of the role of such modifications is practically limited to the function of cdc 2 (cdk1) kinase sites in depolymerization of the nuclear lamina during mitosis. In our study we used Drosophila lamin Dm (B-type) to examine the function of particular phosphorylation sites using pseudophosphorylated mutants mimicking single phosphorylation at experimentally confirmed in vivo phosphosites (S25E, S45E, T435E, S595E). We also analyzed lamin C (A-type) and its mutant S37E representing the N-terminal cdc2 (mitotic) site as well as lamin Dm R64H mutant as a control, non-polymerizing lamin. In the polymerization assay we could observe different effects of N-terminal cdc2 site pseudophosphorylation on A- and B-type lamins: lamin Dm S45E mutant was insoluble, in contrast to lamin C S37E. Lamin Dm T435E (C-terminal cdc2 site) and R64H were soluble in vitro. We also confirmed that none of the single phosphorylation site modifications affected the chromatin binding of lamin Dm, in contrast to the lamin C N-terminal cdc2 site. In vivo, all lamin Dm mutants were incorporated efficiently into the nuclear lamina in transfected Drosophila S2 and HeLa cells, although significant amounts of S45E and T435E were also located in cytoplasm. When farnesylation incompetent mutants were expressed in HeLa cells, lamin Dm T435E was cytoplasmic and showed higher mobility in FRAP assay
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