A Gaussian Theory of Superfluid--Bose-Glass Phase Transition

We show that gaussian quantum fluctuations, even if infinitesimal, are sufficient to destroy the superfluidity of a disordered boson system in 1D and 2D. The critical disorder is thus finite no matter how small the repulsion is between particles. Within the gaussian approximation, we study the nature of the elementary excitations, including their density of states and mobility edge transition. We give the gaussian exponent $\eta$ at criticality in 1D and show that its ratio to $\eta$ of the pure system is universal.Comment: Revtex 3.0, 11 pages (4 figures will be sent through airmail upon request

Disordered Boson Systems: A Perturbative Study

A hard-core disordered boson system is mapped onto a quantum spin 1/2 XY-model with transverse random fields. It is then generalized to a system of spins with an arbitrary magnitude S and studied through a 1/S expansion. The first order 1/S expansion corresponds to a spin-wave theory. The effect of weak disorder is studied perturbatively within such a first order 1/S scheme. We compute the reduction of the speed of sound and the life time of the Bloch phonons in the regime of weak disorder. Generalizations of the present study to the strong disordered regime are discussed.Comment: 27 pages, revte

Ground State and Excitations of Disordered Boson Systems

After an introduction to the dirty bosons problem, we present a gaussian theory for the ground state and excitations. This approach is physically equivalent to the Bogoliubov approximation. We find that ODLRO can be destroyed with sufficient disorder. The density of states and localization of the elementary excitations are discussed. (To appear in JLTP Proceedings of the Conference on Condensed Bose Systems at the University of Minnesota, 1993.)Comment: 13 pages. (postscript file because of the figures inserted in the text.

Oblique Parameter Constraints on Large Extra Dimensions

We consider the Kaluza-Klein scenario in which gravity propagates in the $4+n$ dimensional bulk of spacetime and the Standard Model particles are confined to a 3-brane. We calculate the gauge boson self-energy corrections arising from the exchange of virtual gravitons and present our results in the $STU$-formalism. We find that the new physics contributions to $S$, $T$ and $U$ decouple in the limit that the string scale $M_S$ goes to infinity. The oblique parameters constrain the lower limit on $M_S$. Taking the quantum gravity cutoff to be $M_S$, $S$-parameter constraints impose $M_S>1.55$ TeV for $n=2$ at the 1$\sigma$ level. $T$-parameter constraints impose $M_S>1.25 (0.75)$ TeV for $n=3 (6)$.Comment: Version to appear in PR

Senescent mouse cells fail to overtly regulate the HIRA histone chaperone and do not form robust Senescence Associated Heterochromatin Foci

<p>Abstract</p> <p>Background</p> <p>Cellular senescence is a permanent growth arrest that occurs in response to cellular stressors, such as telomere shortening or activation of oncogenes. Although the process of senescence growth arrest is somewhat conserved between mouse and human cells, there are some critical differences in the molecular pathways of senescence between these two species. Recent studies in human fibroblasts have defined a cell signaling pathway that is initiated by repression of a specific Wnt ligand, Wnt2. This, in turn, activates a histone chaperone HIRA, and culminates in formation of specialized punctate domains of facultative heterochromatin, called Senescence-Associated Heterochromatin Foci (SAHF), that are enriched in the histone variant, macroH2A. SAHF are thought to repress expression of proliferation-promoting genes, thereby contributing to senescence-associated proliferation arrest. We asked whether this Wnt2-HIRA-SAHF pathway is conserved in mouse fibroblasts.</p> <p>Results</p> <p>We show that mouse embryo fibroblasts (MEFs) and mouse skin fibroblasts, do not form robust punctate SAHF in response to an activated Ras oncogene or shortened telomeres. However, senescent MEFs do exhibit elevated levels of macroH2A staining throughout the nucleus as a whole. Consistent with their failure to fully activate the SAHF assembly pathway, the Wnt2-HIRA signaling axis is not overtly regulated between proliferating and senescent mouse cells.</p> <p>Conclusions</p> <p>In addition to the previously defined differences between mouse and human cells in the mechanisms and phenotypes associated with senescence, we conclude that senescent mouse and human fibroblasts also differ at the level of chromatin and the signaling pathways used to regulate chromatin. These differences between human and mouse senescence may contribute to the increased propensity of mouse fibroblasts (and perhaps other mouse cell types) to become immortalized and transformed, compared to human cells.</p

Structure and phase transition in BaThO3: A combined neutron and synchrotron X-ray diffraction study

The structure of BaThO3, obtained by solid state synthesis, was refined for the first time by the Rietveld method using a combination of synchrotron X-ray and neutron powder diffraction data. BaThO3 has an orthorhombic structure at room temperature, in space group Pbnm with a = 6.3491(5), b = 6.3796(4) and c = 8.9907(7) Å. Heating BaThO3 to above 700 °C results in a continuous transition to a second orthorhombic structure, in space group Ibmm, demonstrated by both in situ neutron and synchrotron X-ray powder diffraction measurements. The coefficient of volumetric thermal expansion for BaThO3 is determined to be 1.04 x 10-5 oC-1 from 50 to 625 oC (Pbnm phase), and 9.43 x 10-6 oC-1 from 800 to 1000 oC (Ibmm phase). BaThO3 was found to decompose upon exposure to atmospheric moisture resulting in the formation of ThO2. The thermal expansion of ThO2, which invariably co-exists with BaThO3, is also described.Australian Synchrotron Australian Research Council2019-12-1

Structure and phase transition in BaThO3: A combined neutron and synchrotron X-ray diffraction study

The structure of BaThO3, obtained by solid state synthesis, was refined for the first time by the Rietveld method using a combination of synchrotron X-ray and neutron powder diffraction data. BaThO3 has an orthorhombic structure at room temperature, in space group Pbnm with a = 6.3491(5), b = 6.3796(4) and c = 8.9907(7) Å. Heating BaThO3 to above 700 °C results in a continuous transition to a second orthorhombic structure, in space group Ibmm, demonstrated by both in situ neutron and synchrotron X-ray powder diffraction measurements. The coefficient of volumetric thermal expansion for BaThO3 is determined to be 1.04 x 10-5 oC-1 from 50 to 625 oC (Pbnm phase), and 9.43 x 10-6 oC-1 from 800 to 1000 oC (Ibmm phase). BaThO3 was found to decompose upon exposure to atmospheric moisture resulting in the formation of ThO2. The thermal expansion of ThO2, which invariably co-exists with BaThO3, is also described.Australian Synchrotron Australian Research Counci

Metformin reduces airway glucose permeability and hyperglycaemia-induced Staphylococcus aureus load independently of effects on blood glucose

Background Diabetes is a risk factor for respiratory infection, and hyperglycaemia is associated with increased glucose in airway surface liquid and risk of Staphylococcus aureus infection. Objectives To investigate whether elevation of basolateral/blood glucose concentration promotes airway Staphylococcus aureus growth and whether pretreatment with the antidiabetic drug metformin affects this relationship. Methods Human airway epithelial cells grown at air–liquid interface (±18 h pre-treatment, 30 μM–1 mM metformin) were inoculated with 5×105 colony-forming units (CFU)/cm2 S aureus 8325-4 or JE2 or Pseudomonas aeruginosa PA01 on the apical surface and incubated for 7 h. Wild-type C57BL/6 or db/db (leptin receptor-deficient) mice, 6–10 weeks old, were treated with intraperitoneal phosphate-buffered saline or 40 mg/kg metformin for 2 days before intranasal inoculation with 1×107 CFU S aureus. Mice were culled 24 h after infection and bronchoalveolar lavage fluid collected. Results Apical S aureus growth increased with basolateral glucose concentration in an in vitro airway epithelia–bacteria co-culture model. S aureus reduced transepithelial electrical resistance (RT) and increased paracellular glucose flux. Metformin inhibited the glucose-induced growth of S aureus, increased RT and decreased glucose flux. Diabetic (db/db) mice infected with S aureus exhibited a higher bacterial load in their airways than control mice after 2 days and metformin treatment reversed this effect. Metformin did not decrease blood glucose but reduced paracellular flux across ex vivo murine tracheas. Conclusions Hyperglycaemia promotes respiratory S aureus infection, and metformin modifies glucose flux across the airway epithelium to limit hyperglycaemia-induced bacterial growth. Metformin might, therefore, be of additional benefit in the prevention and treatment of respiratory infection

Franck-Condon Effect in Central Spin System

We study the quantum transitions of a central spin surrounded by a collective-spin environment. It is found that the influence of the environmental spins on the absorption spectrum of the central spin can be explained with the analog of the Franck-Condon (FC) effect in conventional electron-phonon interaction system. Here, the collective spins of the environment behave as the vibrational mode, which makes the electron to be transitioned mainly with the so-called "vertical transitions" in the conventional FC effect. The "vertical transition" for the central spin in the spin environment manifests as, the certain collective spin states of the environment is favored, which corresponds to the minimal change in the average of the total spin angular momentum.Comment: 8 pages, 8 figure