Classical Analysis of Phenomenological Potentials for Metallic Clusters

The classical trajectories of single particle motion in a Wodds-Saxon and a modified Nilsson potential are studied for axial quadrupole deformation. Both cases give rise to chaotic behaviour when the deformation in the Woods-Saxon and the l**2 term in the modified Nilsson potential are turned on. Important similarities, in particular with regard to the shortest periodic orbits, have been found.Comment: 9 pages LaTex + 4 figures available via e-mail requests from the authors, to appear in Phys.Rev.Let

Rough droplet model for spherical metal clusters

We study the thermally activated oscillations, or capillary waves, of a neutral metal cluster within the liquid drop model. These deformations correspond to a surface roughness which we characterize by a single parameter $\Delta$. We derive a simple analytic approximate expression determining $\Delta$ as a function of temperature and cluster size. We then estimate the induced effects on shell structure by means of a periodic orbit analysis and compare with recent data for shell energy of sodium clusters in the size range $50 < N < 250$. A small surface roughness $\Delta\simeq 0.6$ \AA~ is seen to give a reasonable account of the decrease of amplitude of the shell structure observed in experiment. Moreover -- contrary to usual Jahn-Teller type of deformations -- roughness correctly reproduces the shape of the shell energy in the domain of sizes considered in experiment.Comment: 20 pages, 4 figures, important modifications of the presentation, to appear in Phys. Rev.

Periodic orbit theory for realistic cluster potentials: The leptodermous expansion

The formation of supershells observed in large metal clusters can be qualitatively understood from a periodic-orbit-expansion for a spherical cavity. To describe the changes in the supershell structure for different materials, one has, however, to go beyond that simple model. We show how periodic-orbit-expansions for realistic cluster potentials can be derived by expanding only the classical radial action around the limiting case of a spherical potential well. We give analytical results for the leptodermous expansion of Woods-Saxon potentials and show that it describes the shift of the supershells as the surface of a cluster potential gets softer. As a byproduct of our work, we find that the electronic shell and supershell structure is not affected by a lattice contraction, which might be present in small clusters.Comment: 15 pages RevTex, 11 eps figures, additional information at http://www.mpi-stuttgart.mpg.de/docs/ANDERSEN/users/koch/Diss

Fluticasone/formoterol combination therapy is as effective as fluticasone/salmeterol in the treatment of asthma, but has a more rapid onset of action: an open-label, randomized study

<p>Abstract</p> <p>Background</p> <p>The inhaled corticosteroid (ICS) fluticasone propionate (fluticasone) and the long-acting β₂-agonist (LABA) formoterol fumarate (formoterol) are being made available as a combination product (fluticasone/formoterol, <b><it>flutiform</it></b>^®) in a single aerosol inhaler. This 12-week, open-label, randomized, active-controlled, parallel-group, multicentre, phase 3 study compared the efficacy and safety of fluticasone/formoterol with the commercially available combination product fluticasone/salmeterol.</p> <p>Methods</p> <p>Patients aged ≥ 18 years (N = 202) with mild-to-moderate–severe, persistent asthma for ≥ 6 months prior to screening were included in the study. After a screening phase (4–10 days), eligible patients were randomized 1:1 to receive fluticasone/formoterol or fluticasone/salmeterol during the 12-week treatment period. The primary objective was to demonstrate non-inferiority of fluticasone/formoterol versus fluticasone/salmeterol, measured by pre-dose forced expiratory volume in the first second (FEV₁), at week 12.</p> <p>Results</p> <p>Fluticasone/formoterol was comparable to fluticasone/salmeterol for the primary efficacy endpoint, mean pre-dose FEV₁at week 12. The new combination was also comparable to fluticasone/salmeterol for change from baseline to week 12 in pre-dose FEV₁, change from pre-dose FEV₁at baseline to 2-hour post-dose FEV₁at week 12 and discontinuations due to lack of efficacy. Importantly, fluticasone/formoterol was superior to fluticasone/salmeterol in time to onset of action throughout the duration of the study. The two treatments demonstrated similar results for various other secondary efficacy parameters, including other lung function tests, patient-reported outcomes, rescue medication use, asthma exacerbations and Asthma Quality of Life Questionnaire scores. Fluticasone/formoterol was well tolerated and had a good safety profile that was similar to fluticasone/salmeterol.</p> <p>Conclusions</p> <p>The results of this study indicate that fluticasone/formoterol is as effective as fluticasone/salmeterol, and has a more rapid onset of action, reflecting the faster bronchodilatory effects of formoterol compared with those of salmeterol. If patients perceive the benefits of therapy with fluticasone/formoterol more rapidly than with fluticasone/salmeterol, this could have a positive impact on preference and adherence.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT00476073">NCT00476073</a></p

Mutation analysis of the ATR gene in breast and ovarian cancer families

INTRODUCTION: Mutations in BRCA1, BRCA2, ATM, TP53, CHK2 and PTEN account for only 20–30% of the familial aggregation of breast cancer, which suggests the involvement of additional susceptibility genes. The ATR (ataxia-telangiectasia- and Rad3-related) kinase is essential for the maintenance of genomic integrity. It functions both in parallel and cooperatively with ATM, but whereas ATM is primarily activated by DNA double-strand breaks induced by ionizing radiation, ATR has been shown to respond to a much broader range of DNA damage. Upon activation, ATR phosphorylates several important tumor suppressors, including p53, BRCA1 and CHK1. Based on its central function in the DNA damage response, ATR is a plausible candidate gene for susceptibility to cancer. METHODS: We screened the entire coding region of the ATR gene for mutations in affected index cases from 126 Finnish families with breast and/or ovarian cancer, 75 of which were classified as high-risk and 51 as moderate-risk families, by using conformation sensitive gel electrophoresis and direct sequencing. RESULTS: A large number of novel sequence variants were identified, four of which – Glu254Gly, Ser1142Gly, IVS24-48G>A and IVS26+15C>T – were absent from the tested control individuals (n = 300). However, the segregation of these mutations with the cancer phenotype could not be confirmed, partly because of the lack of suitable DNA samples. CONCLUSION: The present study does not support a major role for ATR mutations in hereditary susceptibility to breast and ovarian cancer