Interference effects in isolated Josephson junction arrays with geometric symmetries

As the size of a Josephson junction is reduced, charging effects become important and the superconducting phase across the link turns into a periodic quantum variable. Isolated Josephson junction arrays are described in terms of such periodic quantum variables and thus exhibit pronounced quantum interference effects arising from paths with different winding numbers (Aharonov-Casher effects). These interference effects have strong implications for the excitation spectrum of the array which are relevant in applications of superconducting junction arrays for quantum computing. The interference effects are most pronounced in arrays composed of identical junctions and possessing geometric symmetries; they may be controlled by either external gate potentials or by adding/removing charge to/from the array. Here we consider a loop of N identical junctions encircling one half superconducting quantum of magnetic flux. In this system, the ground state is found to be non-degenerate if the total number of Cooper pairs on the array is divisible by N, and doubly degenerate otherwise (after the stray charges are compensated by the gate voltages).Comment: 9 pages, 6 figure

nu=1/2 quantum Hall effect in the Aharonov-Casher geometry in a mesoscopic ring

We study the effect of an electric charge in the middle of a ring of electrons in a magnetic field such as $\nu = 1/2$. In the absence of the central charge, a residual current should appear due to an Aharanov-Bohm effect. As the charge varies, periodic currents should appear in the ring. We evaluate the amplitude of these currents, as well as their period as the central charge varies. The presence of these currents should be a direct signature of the existence of a statistical gauge field in the $\nu=1/2$ quantum Hall effect. Numerical diagonalizations for a small number of electrons on the sphere are also carried out. The numerical results up to 9 electrons are qualitatively consistent with the mean field picture.Comment: 23 pages,14 included postscript figures, submitted to Phys. Rev.

Possible realization of Josephson charge qubits in two coupled Bose-Einstein condensates

We demonstrate that two coupled Bose-Einstein condensates (BEC) at zero temperature can be used to realize a qubit which is the counterpart of Josephson charge qubits. The two BEC are weakly coupled and confined in an asymmetric double-well trap. When the "charging energy" of the system is much larger than the Josephson energy and the system is biased near a degeneracy point, the two BEC represent a qubit with two states differing only by one atom. The realization of the BEC qubits in realistic BEC experiments is briefly discussed.Comment: 4 pages; comments are welcome / Corrected typos in Eq. (16); a note adde

Hsp90 orchestrates transcriptional regulation by Hsf1 and cell wall remodelling by MAPK signalling during thermal adaptation in a pathogenic yeast

Acknowledgments We thank Rebecca Shapiro for creating CaLC1819, CaLC1855 and CaLC1875, Gillian Milne for help with EM, Aaron Mitchell for generously providing the transposon insertion mutant library, Jesus Pla for generously providing the hog1 hst7 mutant, and Cathy Collins for technical assistance.Peer reviewedPublisher PD

The effects of antiviral treatment on breast cancer cell line

Background: Recent studies have revealed the positive antiproliferative and cytotoxic effects of antiviral agents in cancer treatment. The real effect of adjuvant antiviral therapy is still controversial due to the lack of studies in biochemical mechanisms. Here, we studied the effect of the antiviral agent acyclovir on morphometric and migratory features of the MCF7 breast cancer cell line. Molecular levels of various proteins have also been examined. Methods: To evaluate and assess the effect of antiviral treatment on morphometric, migratory and other cellular characteristics of MCF7 breast cancer cells, the following experiments were performed: (i) MTT assay to measure the viability of MCF7 cells; (ii) Colony formation ability by soft agar assay; (iii) Morphometric characterization by immunofluorescent analysis using confocal microscopy; (iv) wound healing and transwell membrane assays to evaluate migration and invasion capacity of the cells; (v) ELISA colorimetric assays to assess expression levels of caspase-3, E-cadherin and enzymatic activity of aldehyde dehydrogenase (ALDH). Results: We demonstrate the suppressive effect of acyclovir on breast cancer cells. Acyclovir treatment decreases the growth and the proliferation rate of cells and correlates with the upregulated levels of apoptosis associated cytokine Caspase-3. Moreover, acyclovir inhibits colony formation ability and cell invasion capacity of the cancer cells while enhancing the expression of E-cadherin protein in MCF7 cells. Breast cancer cells are characterized by high ALDH activity and associated with upregulated proliferation and invasion. According to this study, acyclovir downregulates ALDH activity in MCF7 cells. Conclusions: These results are encouraging and demonstrate the possibility of partial suppression of cancer cell proliferation using an antiviral agent. Acyclovir antiviral agents have a great potential as an adjuvant therapy in the cancer treatment. However, more research is necessary to identify relevant biochemical mechanisms by which acyclovir induces a potent anti-cancer effect

Cdc48 and Cofactors Npl4-Ufd1 Are Important for G1 Progression during Heat Stress by Maintaining Cell Wall Integrity in Saccharomyces cerevisiae

The ubiquitin-selective chaperone Cdc48, a member of the AAA (ATPase Associated with various cellular Activities) ATPase superfamily, is involved in many processes, including endoplasmic reticulum-associated degradation (ERAD), ubiquitin- and proteasome-mediated protein degradation, and mitosis. Although Cdc48 was originally isolated as a cell cycle mutant in the budding yeast Saccharomyces cerevisiae, its cell cycle functions have not been well appreciated. We found that temperature-sensitive cdc48-3 mutant is largely arrested at mitosis at 37°C, whereas the mutant is also delayed in G1 progression at 38.5°C. Reporter assays show that the promoter activity of G1 cyclin CLN1, but not CLN2, is reduced in cdc48-3 at 38.5°C. The cofactor npl4-1 and ufd1-2 mutants also exhibit G1 delay and reduced CLN1 promoter activity at 38.5°C, suggesting that Npl4-Ufd1 complex mediates the function of Cdc48 at G1. The G1 delay of cdc48-3 at 38.5°C is a consequence of cell wall defect that over-activates Mpk1, a MAPK family member important for cell wall integrity in response to stress conditions including heat shock. cdc48-3 is hypersensitive to cell wall perturbing agents and is synthetic-sick with mutations in the cell wall integrity signaling pathway. Our results suggest that the cell wall defect in cdc48-3 is exacerbated by heat shock, which sustains Mpk1 activity to block G1 progression. Thus, Cdc48-Npl4-Ufd1 is important for the maintenance of cell wall integrity in order for normal cell growth and division

Environmental and Genetic Determinants of Colony Morphology in Yeast

Nutrient stresses trigger a variety of developmental switches in the budding yeast Saccharomyces cerevisiae. One of the least understood of such responses is the development of complex colony morphology, characterized by intricate, organized, and strain-specific patterns of colony growth and architecture. The genetic bases of this phenotype and the key environmental signals involved in its induction have heretofore remained poorly understood. By surveying multiple strain backgrounds and a large number of growth conditions, we show that limitation for fermentable carbon sources coupled with a rich nitrogen source is the primary trigger for the colony morphology response in budding yeast. Using knockout mutants and transposon-mediated mutagenesis, we demonstrate that two key signaling networks regulating this response are the filamentous growth MAP kinase cascade and the Ras-cAMP-PKA pathway. We further show synergistic epistasis between Rim15, a kinase involved in integration of nutrient signals, and other genes in these pathways. Ploidy, mating-type, and genotype-by-environment interactions also appear to play a role in the controlling colony morphology. Our study highlights the high degree of network reuse in this model eukaryote; yeast use the same core signaling pathways in multiple contexts to integrate information about environmental and physiological states and generate diverse developmental outputs