5,067 research outputs found
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 the phonon frequency in the
vicinity of the Kohn anomaly, , 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 CuCoCu heterostructures
The effects of local electronic interactions and finite temperatures upon the
transmission across the CuCoCu 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
-electrons contribution, as compared to the non-correlated case in which the
transport is dominated by and electrons.Comment: 29 pages, 7 figures, submited to PR
On the superconducting nature of the Bi-II phase of elemental Bismuth
The superconductivity in the Bi-II phase of elemental Bismuth (transition
temperature K at pressure GPa) was studied
experimentally by means of the muon-spin rotation as well as theoretically by
using the Eliashberg theory in combination with Density Functional Theory
calculations. Experiments reveal that Bi-II is a type-I superconductor with a
zero temperature value of the thermodynamic critical field ~mT. The Eliashberg theory approach provides a good agreement
with the experimental and the temperature evolution of .
The estimated value for the retardation (coupling) parameter ( is the logarithmically
averaged phonon frequency) suggests that Bi-II is an intermediately-coupled
superconductor.Comment: 6 pages, 2 figure
Differential expression of E-cadherin, N-cadherin and beta-catenin in proximal and distal segments of the rat nephron.
BACKGROUND: The classical cadherins such as E- and N-cadherin are Ca(2+)-dependent cell adhesion molecules that play important roles in the development and maintenance of renal epithelial polarity. Recent studies have shown that a variety of cadherins are present in the kidney and are differentially expressed in various segments of the nephron. However, the interpretation of these findings has been complicated by the fact that the various studies focused on different panels of cadherins and utilized different species. Moreover, since only a few of the previous studies focused on the rat, information regarding the expression and localization of renal cadherins in this important species is lacking. In the present study, we have employed dual immunofluorescent labeling procedures that utilized specific antibodies against either E- or N-cadherin, along with antibodies that target markers for specific nephron segments, to characterize the patterns of cadherin expression in frozen sections of adult rat kidney. RESULTS: The results showed that N-cadherin is the predominant cadherin in the proximal tubule, but is essentially absent in other nephron segments. By contrast, E-cadherin is abundant in the distal tubule, collecting duct and most medullary segments, but is present only at very low levels in the proximal tubule. Additional results revealed different patterns of N-cadherin labeling along various segments of the proximal tubule. The S1 and S2 segments exhibit a fine threadlike pattern of labeling at the apical cell surface, whereas the S3 segment show intense labeling at the lateral cell-cell contacts. CONCLUSIONS: These results indicate that E- and N-cadherin are differentially expressed in the proximal and distal tubules of rat kidney and they raise the possibility that differences in cadherin expression and localization may contribute to the differences in the susceptibility of various nephron segments to renal pathology or nephrotoxic injury
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
Infection of neuronal cells by Chlamydia pneumoniae and Herpes simplex virus type 1 alters expression of genes associated with Alzheimer’s disease
Several studies have suggested an infectious etiology for Alzheimer’s disease (AD). We have been investigating a potential role for both Chlamydia pneumoniae and Herpes simplex virus type 1 (HSV1) in the initiation of sporadic late-onset AD. Our current study focuses on investigation of gene expression using Alzheimer-specific Real-Time PCR microarrays on RNA derived from SKNMC human neuronal cells infected with C. pneumoniae and/or HSV1. There are distinct differences in the patterns of gene regulation by the two pathogens. For example, C. pneumoniae induces expression of genes involved in amyloid production and processing, such as β-amyloid precursor protein (APP), β-site APP-cleaving enzyme 1 (BACE1), a γ-secretase complex protein (nicastrin [NCSTN]), NEDD8 activating enzyme E1 (NAE1), as well as a mitochondria-associated protein (hydroxysteroid (17-β) dehydrogenase 10 [HSD17B10]), α-2-macroglobulin (A2M) and the metallopeptidase ADAM9. Conversely, HSV1 tends to down-regulate expression of many genes, including those encoding a component of the γ-secretase complex (anterior pharynx defective 1 homolog A [APH1A]), low density lipoprotein related proteins (LRP1, LRP6, and LRP8), β-synuclein (SNCB) and ubiquinols (UQCRC1, UQCRC2). Co-infection with C. pneumoniae and HSV-1 produced a greater down-regulation of gene expression than that seen with HSV1 alone for several genes, including APP-like proteins (APLP1, APLP2) and kinases (cell division cycle 2 protein [CDC2], cyclin-dependent kinase [CDK5] and CDC2-related kinase [CDKL1]). Our data indicate that both C. pneumoniae and HSV1 can modulate expression of genes associated with AD, and thus could contribute to AD pathology, however these two pathogens likely act via different pathways. Furthermore, for several genes, co-infection with both C. pneumoniae and HSV1 appears to exacerbate the changes in gene expression seen with HSV1 alone.https://digitalcommons.pcom.edu/posters/1007/thumbnail.jp
Chlamydophila (Chlamydia) pneumoniae promotes Ab 1-42 amyloid processing in Neuronal Cells: A Pathogenic Trigger for Alzheimer\u27s Disease
Background: Previously, our laboratory identified Chlamydophila (Chlamydia) pneumoniae (Cpn) in autopsied sporadic AD brains. Furthermore, we have developed a BALB/c mouse model that demonstrated infection-induced amyloid plaques similar to those found in AD, and demonstrated that Cpn infection of neuronal cells inhibited apoptotic pathways of cell death. Hypothesis: Our current studies address whether infection with Cpn in neuronal cells triggers abnormal cleavage of the beta amyloid precursor protein (bAPP) into Ab1-42, thereby contributing to amyloid plaque formation characteristic of the pathology identified in AD. Materials and Methods: Human neuroblastoma cells were infected with the respiratory strain AR39 Cpn in vitro, then amyloid processing was analyzed and quantitated using immunocytochemistry, Western blotting and ELISA assays. Results: Cpn was shown to infect neuronal cells and induce intracellular amyloid processing. Cpn infection yielded cytoplasmic labeling of Ab 1-42 that was increased relative to uninfected cells. The ELISA assay revealed that in neuronal cell lysates, Ab 1-42 in the infected cells was increased 3 to 16-fold over the uninfected cells, from 24 to 72hr post infection. Western blot analysis confirmed an increase in Ab 1-42 in the infected neuronal cell lysates. Conclusions: These data suggest that infection of neuronal cells with Chlamydophila (Chlamydia) pneumoniae alters the processing of bAPP, thereby producing Ab1-42. Therefore, these studies and previous research reported by our laboratory support the implication of Cpn as a pathogenic agent in perpetuating the hallmark amyloid plaque formations observed in AD. This concept holds major therapeutic considerations for future studies.https://digitalcommons.pcom.edu/posters/1004/thumbnail.jp
Autophagy and apoptotic genes implicated in Alzheimer’s disease are modulated following infection of neuronal cells with Chlamydia pneumoniae
Background: The focus of the current studies was to determine the relationship between the molecular mechanisms interconnecting autophagy and apoptosis following Chlamydia pneumoniae infection in neuronal cells. Dysfunctions in apoptosis and autophagy have been implicated in the neurodegeneration associated with Alzheimer’s disease (AD). Autophagy in AD pathogenesis has been shown to play a role in amyloid processing through the endosomal-lysosomal system. Apoptosis may contribute to the neuronal cell loss observed in AD; however, there is limited evidence of the apoptotic process proceeding to terminal completion. Although Aβ1-42 has been shown to induce apoptosis in neurons and may be an early factor in AD, our previous investigations demonstrated that neurons infected with Chlamydia pneumoniae are resistant to apoptosis, and that Aβ1-42 is induced following this infection. Thus, these studies address infection as an initiator/trigger or inhibitor for the processes of autophagy and apoptosis observed in Alzheimer’s disease. Methods: SKNMC neuronal cells obtained from ATCC were infected with the AR39 strain of Chlamydia pneumoniae at an MOI=1 for 24, 48, and 72hrs and were analyzed using Real-time PCR arrays from SABiosciences specific for autophagy and apoptosis genetic markers. Results: Some major genes associated with apoptosis such as BID, DAPK1, TP53, TP73 were down regulated by 72hrs post-infection. Genes associated with the regulation of autophagic vacuole formation such as ATG3, ATG4B, ATG4C, ATG9A, ATG9B, ATG12, IRGM, and BECN1 were up-regulated within 72hrs post-infection. With regards to genes involved with co-regulation of autophagy and apoptosis, BNIP3 was significantly up-regulated within 48-72hrs post-infection. Of the genes linking autophagosomes to lysosomes, FAM176A was up-regulated throughout 24-72hrs post-infection. Conclusions: Modulation of autophagy and apoptosis genes occurs in neuronal cells at 24, 48, and 72hrs post- infection with Chlamydia pneumoniae. These genetic changes lead to dysfunction in these basic cellular processes; dysfunction in these processes has been shown to contribute to the neuropathology of late-onset Alzheimer’s disease. This work will allow future studies to further focus on the apoptotic and autophagic pathways to better understand how a pathogen such as Chlamydia pneumoniae plays a role in the development of late-onset Alzheimer’s disease.https://digitalcommons.pcom.edu/posters/1009/thumbnail.jp
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