291 research outputs found
Single Electrode Heat Effects:I. Peltier Entropies of Gas Electrodes in Carbonate Paste Electrolytes
Long-Term Evolution and Revival Structure of Rydberg Wave Packets for Hydrogen and Alkali-Metal Atoms
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
, 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 . These
long-term periodicities result in the autocorrelation function at times greater
than having a self-similar resemblance to its structure for times
less than . 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 , 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
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
Characterization of a new small cell lung cancer (SCLC) cell line STP54 derived from a metastatic bioptate of a combined type of SCLC with Non-SCLC component.
Edge-Magnetoplasmon Wave-Packet Revivals in the Quantum Hall Effect
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
'The Germans are Hydrophobes': Germany and the Germans in the Shaping of French Identity
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
Experimental investigation of rubidium atoms above the field-ionization limit using a time-resolved wave-packet approach
Patients Enrolled in Large Randomized Clinical Trials of Antiplatelet Treatment for Prevention After Transient Ischemic Attack or Ischemic Stroke Are Not Representative of Patients in Clinical Practice: the Netherlands Stroke Survey
Background and Purpose—Many randomized clinical trials have evaluated the benefit of long-term use of antiplatelet
drugs in reducing the risk of new vascular events in patients with a recent transient ischemic attack or ischemic stroke.
Evidence from these trials forms the basis for national and international guidelines for the management of nearly all such
patients in clinical practice. However, abundant and strict enrollment criteria may limit the validity and the applicability
of results of randomized clinical trials to clinical practice. We estimated the eligibility for participation in landmark trials
of antiplatelet drugs of an unselected group of patients with stroke or transient ischemic attack from a national stroke
survey.
Methods—Nine hundred seventy-two patients with transient ischemic at
Lamin A Rod Domain Mutants Target Heterochromatin Protein 1α and β for Proteasomal Degradation by Activation of F-Box Protein, FBXW10
Lamins are major structural proteins of the nucleus and contribute to the organization of various nuclear functions. Mutations in the human lamin A gene cause a number of highly degenerative diseases, collectively termed as laminopathies. Cells expressing lamin mutations exhibit abnormal nuclear morphology and altered heterochromatin organization; however, the mechanisms responsible for these defects are not well understood.The lamin A rod domain mutants G232E, Q294P and R386K are either diffusely distributed or form large aggregates in the nucleoplasm, resulting in aberrant nuclear morphology in various cell types. We examined the effects of these lamin mutants on the distribution of heterochromatin protein 1 (HP1) isoforms. HeLa cells expressing these mutants showed a heterogeneous pattern of HP1alpha and beta depletion but without altering HP1gamma levels. Changes in HP1alpha and beta were not observed in cells expressing wild-type lamin A or mutant R482L, which assembled normally at the nuclear rim. Treatment with proteasomal inhibitors led to restoration of levels of HP1 isoforms and also resulted in stable association of lamin mutants with the nuclear periphery, rim localization of the inner nuclear membrane lamin-binding protein emerin and partial improvement of nuclear morphology. A comparison of the stability of HP1 isoforms indicated that HP1alpha and beta displayed increased turnover and higher basal levels of ubiquitination than HP1gamma. Transcript analysis of components of the ubiquitination pathway showed that a specific F-box protein, FBXW10 was induced several-fold in cells expressing lamin mutants. Importantly, ectopic expression of FBXW10 in HeLa cells led to depletion of HP1alpha and beta without alteration of HP1gamma levels.Mislocalized lamins can induce ubiquitin-mediated proteasomal degradation of certain HP1 isoforms by activation of FBXW10, a member of the F-box family of proteins that is involved in E3 ubiquitin ligase activity
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