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

On the superconducting nature of the Bi-II phase of elemental Bismuth

The superconductivity in the Bi-II phase of elemental Bismuth (transition temperature $T_{\rm c}\simeq3.92$ K at pressure $p\simeq 2.80$ 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 $B_{\rm c}(0)\simeq31.97$~mT. The Eliashberg theory approach provides a good agreement with the experimental $T_{\rm c}$ and the temperature evolution of $B_{\rm c}$. The estimated value for the retardation (coupling) parameter $k_{\rm B}T_{\rm c}/\omega_{\rm ln} \approx 0.07$ ($\omega_{\rm ln}$ 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

Patient reported upper gastro-intestinal symptoms associated with fractionated image-guided conformal radiotherapy for metastatic spinal cord compression

Background and purpose Palliative radiotherapy is given to sustain or improve quality of life for patients with advanced cancer. Radiotherapy may however result in symptomatic side effects, which may affect the patient negatively. This prospective longitudinal study of 30 patients aimed at investigating the incidence and severity of early toxicity, particularly focusing on dysphagia, esophagitis and mucositis, following fractionated radiotherapy for cervical and thoracic metastatic spinal cord compression (MSCC), as well as determining the relationship between esophageal dose and early upper gastro-intestinal symptoms. Materials and methods Thirty patients receiving radiotherapy of 3Gyx10 for MSCC were included in the study. Patients were assessed for a total of 7 weeks from onset of radiotherapy using the Edmonton Symptom Assessment System (ESAS) questionnaire. Upper gastro-intestinal symptoms and severity were assessed from the tenth and eleventh question section of the ESAS questionnaire of “other problems” and how much this affected them. The relationships between the mean and maximum esophageal doses and incidence of dysphagia, esophagitis or mucositis were estimated and dose response curves determined. Results Eleven patients reported esophageal symptoms (average duration eleven days, range 1–18 days). Incidence of esophageal toxicity in patients treated at Th8 or above was 79 percent, while no patients treated below Th8 reported any symptoms (p < 0.001). Furthermore, 2 out of 3 patients irradiated at the cervical region reported substantial changes in taste sensation. Risk of symptoms correlated with both mean and maximum esophageal dose and may be a useful tool in planning radiotherapy for MSCC, potentially reducing early upper gastro-intestinal toxicity