Scaling behavior of the momentum distribution of a quantum Coulomb system in a confining potential

We calculate the single-particle momentum distribution of a quantum many-particle system in the presence of the Coulomb interaction and a confining potential. The region of intermediate momenta, where the confining potential dominates, marks a crossover from a Gaussian distribution valid at low momenta to a power-law behavior valid at high momenta. We show that for all momenta the momentum distribution can be parametrized by a $q$-Gaussian distribution whose parameters are specified by the confining potential. Furthermore, we find that the functional form of the probability of transitions between the confined ground state and the $n^{th}$ excited state is invariant under scaling of the ratio $Q^2/\nu_n$, where $Q$ is the transferred momentum and $\nu_n$ is the corresponding excitation energy. Using the scaling variable $Q^2/\nu_n$ the maxima of the transition probabilities can also be expressed in terms of a $q$-Gaussian.Comment: 6 pages, 5 figure

Lattice dynamics of palladium in the presence of electronic correlations

We compute the phonon dispersion, density of states, and the Gr\"uneisen parameters of bulk palladium in the combined density functional theory (DFT) and dynamical mean-field theory (DMFT). We find good agreement with experimental results for ground state properties (equilibrium lattice parameter and bulk modulus) and the experimentally measured phonon spectra. We demonstrate that at temperatures $T \lesssim 20~K$ the phonon frequency in the vicinity of the Kohn anomaly, $\omega_{T1}({\bf q}_{K})$, strongly decreases. This is in contrast to DFT where this frequency remains essentially constant in the whole temperature range. Apparently correlation effects reduce the restoring force of the ionic displacements at low temperatures, leading to a mode softening.Comment: minor revision

Transmission through correlated Cun_nCoCun_n heterostructures

The effects of local electronic interactions and finite temperatures upon the transmission across the Cu$_4$CoCu$_4$ metallic heterostructure are studied in a combined density functional and dynamical mean field theory. It is shown that, as the electronic correlations are taken into account via a local but dynamic self-energy, the total transmission at the Fermi level gets reduced (predominantly in the minority spin channel), whereby the spin polarization of the transmission increases. The latter is due to a more significant $d$-electrons contribution, as compared to the non-correlated case in which the transport is dominated by $s$ and $p$ electrons.Comment: 29 pages, 7 figures, submited to PR

Thermo-mechanic-electrical coupling in phospholipid monolayers near the critical point

Lipid monolayers have been shown to represent a powerful tool in studying mechanical and thermodynamic properties of lipid membranes as well as their interaction with proteins. Using Einstein's theory of fluctuations we here demonstrate, that an experimentally derived linear relationship both between transition entropy S and area A as well as between transition entropy and charge q implies a linear relationships between compressibility \kappa_T, heat capacity c_\pi, thermal expansion coefficient \alpha_T and electric capacity CT. We demonstrate that these couplings have strong predictive power as they allow calculating electrical and thermal properties from mechanical measurements. The precision of the prediction increases as the critical point TC is approached

Two Gastropods from the Lower Cretaceous (Albian) of Coahuila, Mexico

14-22http://deepblue.lib.umich.edu/bitstream/2027.42/48381/2/ID226.pd

Herpes Simplex Virus 1 and Chlamydophila (Chlamydia) pneumoniae promote Ab 1-42 amyloid processing in murine astrocytes linking an infectious process to Alzheimer\u27s disease

Background: Several studies have suggested an infectious etiology for Alzheimer\u27s disease (AD). Previously, our laboratory identified Chlamydia pneumoniae (Cpn) from autopsied sporadic AD brains, as well as developed a BALB/c mouse model that demonstrated infection-induced amyloid plaques similar to those found in AD. Hypothesis: We propose that an additional pathogen such as herpes simplex virus type 1 (HSV1), also may be a contributing factor in toin the pathology seen in AD. HSV1, in addition to Cpn, may be triggering the abnormal cleavage of the beta amyloid precursor protein (bAPP) into Ab1-42 , thereby contributing to amyloid plaque formation. Our current study examines amyloid processing following infection of primary and C8-DIA murine astrocytes with Cpn and HSV1. Materials and Methods: Immunocytochemistry and western analysis was used to analyze the outcome of infection by these two pathogens. Results: Cpn infection resulted in an increase in cytoplasmic labeling of Ab 1-42 relative to uninfected cells, while increased nuclear labeling of Ab 1-42 was observed following HSV1 infection. Co-infections with Cpn and HSV1 resulted in amyloid labeling resembling that of HSV1 infection alone, though Ab 1-42 labeling appeared decreased specifically in Cpn-infected cells of the co-infected monolayers. Conclusions: These data suggest that infection of astrocytic cells by HSV1 and (Cpn) alter the processing of bAPP, thereby producing Ab1-42. Therefore, these studies, inaddition to the previous research reported by our laboratory, support an emerging linkage of the infectious processs to the neuropathology characteristic of Alzheimer\u27s disease.https://digitalcommons.pcom.edu/posters/1008/thumbnail.jp

Analysis of Chlamydia pneumoniae and AD-like Pathology in the Brains of BALB/c Mice Following Direct Intra-cranial Infection

Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disorder and the most common form of dementia. The pathology in the central nervous system (CNS) impairs memory and cognition, hindering the capabilities and the quality of life of the individual. This project continues studying the role of infection and Alzheimer’s disease, as previous studies in this laboratory have done, and contributes to the overall understanding of the possible causes of this disease. In this study, BALB/c mice were infected, via direct intracranial injection, with a respiratory isolate (AR-39) of Chlamydia pneumoniae. Their brains were analyzed at 7 and 14 days post-infection, via immunohistochemistry, for the presence of C. pneumoniae, amyloid deposits and activated glial cells. The goal of this project was to measure the location and degree of C. pneumoniae burden, amyloid deposition and glial cell activation in the CNS following direct intracranial injection and to compare this data with results obtained from previous studies in this laboratory. We hypothesized that C. pneumoniae antigen and activated inflammatory cells will be observed in the infected mouse brains following direct intracranial injection and Aβ deposition will be observed in areas where inflammation occurs. C. pneumoniae, amyloid deposits and activated glial cells were detected in the brains following direct intracranial infection with C. pneumoniae. In infected mice there was an approximate 3.5-fold increase of C. pneumoniae antigen burden compared to uninfected mice at day 7 and there was an approximate 5.5-fold increase of C. pneumoniae antigen burden compared to uninfected mice at day 14. The burden of C. pneumoniae antigen, in the infected mice, increased 1.009-fold (no change) from day 7 to day 14 post-infection. The amyloid burden in infected mice increased approximately 3-fold compared to uninfected mice at day 7 and increased greater than10-fold compared to uninfected mice at day 14. The burden of amyloid, in the infected mice, increased 7-fold from day 7 to 14. From 7 to 14 days post-infection the C. pneumoniae and amyloid deposits located near the injection site spread distally from this location to other regions of the brain. Global activation of glia was observed in the CNS of infected mice at both 7 and 14 days post-infection. This data confirms that C. pneumoniae is capable of establishing an infection in the CNS. Although deposits were observed, the lack of a substantial amount of amyloid deposits suggested that the generation of deposits may require longer than 14 days following C. pneumoniae infection. As early as 7 days post-infection, inflammation is observed in response to the presence of C. pneumoniae and/or soluble amyloid in the CNS and the contribution of both infection with C. pneumoniae and the presence of soluble amyloid elicit the inflammatory response that presumably precedes and contributes to amyloid depositionhttps://digitalcommons.pcom.edu/posters/1003/thumbnail.jp