Tidal Effects in Clusters of Galaxies

High-redshift clusters of galaxies show an over-abundance of spirals by a factor of 2-3, and the corresponding under-abundance of S0 galaxies, relative to the nearby clusters. This morphological evolution can be explained by tidal interactions with neighboring galaxies and with the hierarchically growing cluster halo. The efficiency of tidal interactions depends on the size and structure of the cluster, as well as on the epoch of its formation. I simulate the formation and evolution of Virgo-type clusters in three cosmologies: a critical density model Omega_0=1, an open model Omega_0=0.4, and a flat model Omega_0=0.4 with a cosmological constant. The orbits of identified halos are traced with a high temporal resolution (~10^7 yr). Halos with low relative velocities merge only shortly after entering the cluster; after virialization mergers are suppressed. The dynamical evolution of galaxies is determined by the tidal field along their trajectories. The maxima of the tidal force do not always correspond to closest approach to the cluster center. They are produced to a large extent by the local density structures, such as the massive galaxies and the unvirialized remnants of infalling groups of galaxies. Collisions of galaxies are intensified by the substructure, with about 10 encounters within 10 kpc per galaxy in the Hubble time. These very close encounters add an important amount (10-50%) of the total heating rate. The integrated effect of tidal interactions is insufficient to transform a spiral galaxy into an elliptical, but can produce an S0 galaxy. Overall, tidal heating is stronger in the low Omega_0 clusters

Detailed Mass Map of CL0024+1654 from Strong Lensing

We construct a high resolution mass map of the z=0.39 cluster 0024+1654, based on parametric inversion of the associated gravitational lens. The lens creates eight well-resolved sub-images of a background galaxy, seen in deep imaging with HST. Excluding mass concentrations centered on visible galaxies, more than 98% of the remaining mass is represented by a smooth concentration of dark matter centered near the brightest cluster galaxies, with a 35 h^{-1} kpc soft core. The asymmetry in the mass distribution is <3% inside 107 ~h^{-1} kpc radius. The dark matter distribution we observe in CL0024 is far more smooth, symmetric, and nonsingular than in typical simulated clusters in either Omega=1 or Omega=0.3 CDM cosmologies. Integrated to 107 h^{-1} kpc radius, the rest-frame mass to light ratio is M/L_V = 276\pm 40 h (M/L_V)_solar.Comment: 16 pages, 4 figures (3 .jpg, 1 .ps), minor changes to make consistent with the final ApJL article. To appear in ApJL, May 8 199

In-Situ Infrared Transmission Study of Rb- and K-Doped Fullerenes

We have measured the four IR active $C_{60}$ molecular vibrations in $M_{x}C_{60}$ $(M = K, Rb)$ as a function of doping $x$. We observe discontinuous changes in the vibrational spectra showing four distinct phases (presumably $x = 0, 3, 4$, and 6). The $1427cm^{-1}$ and $576cm^{-1}$ modes show the largest changes shifting downward in frequency in four steps as the doping increases. Several new very weak modes are visible in the $x=6$ phase and are possibly Raman modes becoming weakly optically active. We present quantitative fits of the data and calculate the electron-phonon coupling of the $1427cm^{-1}$ IR mode.Comment: 3 pages, Figure 1 included, 3 more figures available by request. REVTEX v3.0 IRC60DO

Density-functional study of hydrogen chemisorption on vicinal Si(001) surfaces

Relaxed atomic geometries and chemisorption energies have been calculated for the dissociative adsorption of molecular hydrogen on vicinal Si(001) surfaces. We employ density-functional theory, together with a pseudopotential for Si, and apply the generalized gradient approximation by Perdew and Wang to the exchange-correlation functional. We find the double-atomic-height rebonded D_B step, which is known to be stable on the clean surface, to remain stable on partially hydrogen-covered surfaces. The H atoms preferentially bind to the Si atoms at the rebonded step edge, with a chemisorption energy difference with respect to the terrace sites of >sim 0.1 eV. A surface with rebonded single atomic height S_A and S_B steps gives very similar results. The interaction between H-Si-Si-H mono-hydride units is shown to be unimportant for the calculation of the step-edge hydrogen-occupation. Our results confirm the interpretation and results of the recent H_2 adsorption experiments on vicinal Si surfaces by Raschke and Hoefer described in the preceding paper.Comment: 13 pages, 8 figures, submitted to Phys. Rev. B. Other related publications can be found at http://www.rz-berlin.mpg.de/th/paper.htm

Time of arrival through interacting environments: Tunneling processes

We discuss the propagation of wave packets through interacting environments. Such environments generally modify the dispersion relation or shape of the wave function. To study such effects in detail, we define the distribution function P_{X}(T), which describes the arrival time T of a packet at a detector located at point X. We calculate P_{X}(T) for wave packets traveling through a tunneling barrier and find that our results actually explain recent experiments. We compare our results with Nelson's stochastic interpretation of quantum mechanics and resolve a paradox previously apparent in Nelson's viewpoint about the tunneling time.Comment: Latex 19 pages, 11 eps figures, title modified, comments and references added, final versio

Genetic spectrum of hereditary neuropathies with onset in the first year of life

Early onset hereditary motor and sensory neuropathies are rare disorders encompassing congenital hypomyelinating neuropathy with disease onset in the direct post-natal period and Dejerine–Sottas neuropathy starting in infancy. The clinical spectrum, however, reaches beyond the boundaries of these two historically defined disease entities. De novo dominant mutations in PMP22, MPZ and EGR2 are known to be a typical cause of very early onset hereditary neuropathies. In addition, mutations in several other dominant and recessive genes for Charcot–Marie–Tooth disease may lead to similar phenotypes. To estimate mutation frequencies and to gain detailed insights into the genetic and phenotypic heterogeneity of early onset hereditary neuropathies, we selected a heterogeneous cohort of 77 unrelated patients who presented with symptoms of peripheral neuropathy within the first year of life. The majority of these patients were isolated in their family. We performed systematic mutation screening by means of direct sequencing of the coding regions of 11 genes: MFN2, PMP22, MPZ, EGR2, GDAP1, NEFL, FGD4, MTMR2, PRX, SBF2 and SH3TC2. In addition, screening for the Charcot–Marie–Tooth type 1A duplication on chromosome 17p11.2-12 was performed. In 35 patients (45%), mutations were identified. Mutations in MPZ, PMP22 and EGR2 were found most frequently in patients presenting with early hypotonia and breathing difficulties. The recessive genes FGD4, PRX, MTMR2, SBF2, SH3TC2 and GDAP1 were mutated in patients presenting with early foot deformities and variable delay in motor milestones after an uneventful neonatal period. Several patients displaying congenital foot deformities but an otherwise normal early development carried the Charcot–Marie–Tooth type 1A duplication. This study clearly illustrates the genetic heterogeneity underlying hereditary neuropathies with infantile onset

Logopenic and nonfluent variants of primary progressive aphasia are differentiated by acoustic measures of speech production

Differentiation of logopenic (lvPPA) and nonfluent/agrammatic (nfvPPA) variants of Primary Progressive Aphasia is important yet remains challenging since it hinges on expert based evaluation of speech and language production. In this study acoustic measures of speech in conjunction with voxel-based morphometry were used to determine the success of the measures as an adjunct to diagnosis and to explore the neural basis of apraxia of speech in nfvPPA. Forty-one patients (21 lvPPA, 20 nfvPPA) were recruited from a consecutive sample with suspected frontotemporal dementia. Patients were diagnosed using the current gold-standard of expert perceptual judgment, based on presence/absence of particular speech features during speaking tasks. Seventeen healthy age-matched adults served as controls. MRI scans were available for 11 control and 37 PPA cases; 23 of the PPA cases underwent amyloid ligand PET imaging. Measures, corresponding to perceptual features of apraxia of speech, were periods of silence during reading and relative vowel duration and intensity in polysyllable word repetition. Discriminant function analyses revealed that a measure of relative vowel duration differentiated nfvPPA cases from both control and lvPPA cases (r2 = 0.47) with 88% agreement with expert judgment of presence of apraxia of speech in nfvPPA cases. VBM analysis showed that relative vowel duration covaried with grey matter intensity in areas critical for speech motor planning and programming: precentral gyrus, supplementary motor area and inferior frontal gyrus bilaterally, only affected in the nfvPPA group. This bilateral involvement of frontal speech networks in nfvPPA potentially affects access to compensatory mechanisms involving right hemisphere homologues. Measures of silences during reading also discriminated the PPA and control groups, but did not increase predictive accuracy. Findings suggest that a measure of relative vowel duration from of a polysyllable word repetition task may be sufficient for detecting most cases of apraxia of speech and distinguishing between nfvPPA and lvPPA

Two novel missense mutations in the myelin protein zero gene causes Charcot-Marie-Tooth type 2 and Déjérine-Sottas syndrome

<p>Abstract</p> <p>Background</p> <p>The Charcot-Marie-Tooth (CMT) phenotype caused by mutation in the <it>myelin protein zero (MPZ) </it>gene varies considerably, from early onset and severe forms to late onset and milder forms. The mechanism is not well understood. The myelin protein zero (P₀) mediates adhesion in the spiral wraps of the Schwann cell's myelin sheath. The crystalline structure of the extracellular domain of the myelin protein zero (P₀ex) is known, while the transmembrane and intracellular structure is unknown.</p> <p>Findings</p> <p>One novel missense mutation caused a milder late onset CMT type 2, while the second missense mutation caused a severe early onset phenotype compatible with Déjérine-Sottas syndrome.</p> <p>Conclusions</p> <p>The phenotypic variation caused by different missense mutations in the <it>MPZ </it>gene is likely caused by different conformational changes of the MPZ protein which affects the functional tetramers. Severe changes of the MPZ protein cause dysfunctional tetramers and predominantly uncompacted myelin, i.e. the severe phenotypes congenital hypomyelinating neuropathy and Déjérine-Sottas syndrome, while milder changes cause the phenotypes CMT type 1 and 2.</p