Effects of large disorder on the Hofstadter butterfly

Motivated by the recent experiments on periodically modulated, two dimensional electron systems placed in large transversal magnetic fields, we investigate the interplay between the effects of disorder and periodic potentials in the integer quantum Hall regime. In particular, we study the case where disorder is larger than the periodic modulation, but both are small enough that Landau level mixing is negligible. In this limit, the self-consistent Born approximation is inadequate. We carry extensive numerical calculations to understand the relevant physics in the lowest Landau level, such as the spectrum and nature (localized or extended) of the wave functions. Based on our results, we propose a qualitative explanation of the new features uncovered recently in transport measurements.Comment: 15 pages, 13 figures, several pictures have been shrunk to comply with the size requirement

Monte Carlo simulations of Rb2MnF4{\rm Rb_2MnF_4}, a classical Heisenberg antiferromagnet in two-dimensions with dipolar interaction

We study the phase diagram of a quasi-two dimensional magnetic system ${\rm Rb_2MnF_4}$ with Monte Carlo simulations of a classical Heisenberg spin Hamiltonian which includes the dipolar interactions between ${\rm Mn}^{2+}$ spins. Our simulations reveal an Ising-like antiferromagnetic phase at low magnetic fields and an XY phase at high magnetic fields. The boundary between Ising and XY phases is analyzed with a recently proposed finite size scaling technique and found to be consistent with a bicritical point at T=0. We discuss the computational techniques used to handle the weak dipolar interaction and the difference between our phase diagram and the experimental results.Comment: 13 pages 18 figure

Hidden zero-temperature bicritical point in the two-dimensional anisotropic Heisenberg model: Monte Carlo simulations and proper finite-size scaling

By considering the appropriate finite-size effect, we explain the connection between Monte Carlo simulations of two-dimensional anisotropic Heisenberg antiferromagnet in a field and the early renormalization group calculation for the bicritical point in $2+\epsilon$ dimensions. We found that the long length scale physics of the Monte Carlo simulations is indeed captured by the anisotropic nonlinear $\sigma$ model. Our Monte Carlo data and analysis confirm that the bicritical point in two dimensions is Heisenberg-like and occurs at T=0, therefore the uncertainty in the phase diagram of this model is removed.Comment: 10 pages, 11 figure

The longitudinal conductance of mesoscopic Hall samples with arbitrary disorder and periodic modulations

We use the Kubo-Landauer formalism to compute the longitudinal (two-terminal) conductance of a two dimensional electron system placed in a strong perpendicular magnetic field, and subjected to periodic modulations and/or disorder potentials. The scattering problem is recast as a set of inhomogeneous, coupled linear equations, allowing us to find the transmission probabilities from a finite-size system computation; the results are exact for non-interacting electrons. Our method fully accounts for the effects of the disorder and the periodic modulation, irrespective of their relative strength, as long as Landau level mixing is negligible. In particular, we focus on the interplay between the effects of the periodic modulation and those of the disorder. This appears to be the relevant regime to understand recent experiments [S. Melinte {\em et al}, Phys. Rev. Lett. {\bf 92}, 036802 (2004)], and our numerical results are in qualitative agreement with these experimental results. The numerical techniques we develop can be generalized straightforwardly to many-terminal geometries, as well as other multi-channel scattering problems.Comment: 13 pages, 11 figure

Experimentally Engineering the Edge Termination of Graphene Nanoribbons

The edges of graphene nanoribbons (GNRs) have attracted much interest due to their potentially strong influence on GNR electronic and magnetic properties. Here we report the ability to engineer the microscopic edge termination of high quality GNRs via hydrogen plasma etching. Using a combination of high-resolution scanning tunneling microscopy and first-principles calculations, we have determined the exact atomic structure of plasma-etched GNR edges and established the chemical nature of terminating functional groups for zigzag, armchair and chiral edge orientations. We find that the edges of hydrogen-plasma-etched GNRs are generally flat, free of structural reconstructions and are terminated by hydrogen atoms with no rehybridization of the outermost carbon edge atoms. Both zigzag and chiral edges show the presence of edge states.Comment: 16+9 pages, 3+4 figure

Estradiol and mTORC2 cooperate to enhance prostaglandin biosynthesis and tumorigenesis in TSC2-deficient LAM cells

Lymphangioleiomyomatosis (LAM) is a progressive neoplastic disorder that leads to lung destruction and respiratory failure primarily in women. LAM is typically caused by tuberous sclerosis complex 2 (TSC2) mutations resulting in mTORC1 activation in proliferative smooth muscle–like cells in the lung. The female predominance of LAM suggests that estradiol contributes to disease development. Metabolomic profiling identified an estradiol-enhanced prostaglandin biosynthesis signature in Tsc2-deficient (TSC−) cells, both in vitro and in vivo. Estradiol increased the expression of cyclooxygenase-2 (COX-2), a rate-limiting enzyme in prostaglandin biosynthesis, which was also increased at baseline in TSC-deficient cells and was not affected by rapamycin treatment. However, both Torin 1 treatment and Rictor knockdown led to reduced COX-2 expression and phospho-Akt-S473. Prostaglandin production was also increased in TSC-deficient cells. In preclinical models, both Celecoxib and aspirin reduced tumor development. LAM patients had significantly higher serum prostaglandin levels than healthy women. 15-epi-lipoxin-A4 was identified in exhaled breath condensate from LAM subjects and was increased by aspirin treatment, indicative of functional COX-2 expression in the LAM airway. In vitro, 15-epi-lipoxin-A4 reduced the proliferation of LAM patient–derived cells in a dose-dependent manner. Targeting COX-2 and prostaglandin pathways may have therapeutic value in LAM and TSC-related diseases, and possibly in other conditions associated with mTOR hyperactivation

Rosiglitazone Inhibits Transforming Growth Factor-β1 Mediated Fibrogenesis in ADPKD Cyst-Lining Epithelial Cells

BACKGROUND: Interstitial fibrosis plays an important role in progressive renal dysfunction in autosomal dominant polycystic kidney disease (ADPKD). In our previous studies, we confirmed that PPAR-γ agonist, rosiglitazone could protect renal function and prolong the survival of a slowly progressive ADPKD animal model by reducing renal fibrosis. However, the mechanism remains unknown. METHODS: Primary culture epithelial cells pretreated with TGF-β1 were incubated with rosiglitazone. Extracellular matrix proteins were detected using real-time PCR and Western blotting. MAPK and Smad2 phosphorylation were measured with western blot. ERK1/2 pathway and P38 pathway were inhibited with the specific inhibitors PD98059 and SB203580. The Smad2 pathway was blocked with the siRNA. To address whether PPAR-γ agonist-mediated inhibition of TGF-β1-induced collagen type I expression was mediated through a PPAR-γ dependent mechanism, genetic and pharmaceutical approaches were used to block the activity of endogenous PPARγ. RESULTS: TGF-β1-stimulated collagen type I and fibronectin expression of ADPKD cyst-lining epithelia were inhibited by rosiglitazone in a dosage-dependent manner. Smad2, ERK1/2 and P38 pathways were activated in response to TGF-β1; however, TGF-β1 had little effect on JNK pathway. Rosiglitazone suppressed TGF-β1 induced Smad2 activation, while ERK1/2 and P38MAPK signals remained unaffected. Rosiglitazone could also attenuate TGF-β1-stimulated collagen type I and fibronectin expression in primary renal tubular epithelial cells, but had no effect on TGF-β1-induced activation of Smad2, ERK1/2 and P38 pathways. There was no crosstalk between the Smad2 and MAPK pathways in ADPKD cyst-lining epithelial cells. These inhibitory effects of rosiglitazone were reversed by the PPARγ specific antagonist GW9662 and PPARγ siRNA. CONCLUSION: ADPKD cyst-lining epithelial cells participate in TGF-β1 mediated fibrogenesis. Rosiglitazone could suppress TGF-β1-induced collagen type I and fibronectin expression in ADPKD cyst-lining epithelia through modulation of the Smad2 pathway. Our study may provide therapeutic basis for clinical applications of rosiglitazone in retarding the progression of ADPKD

Genomic and Proteomic Analyses of the Fungus Arthrobotrys oligospora Provide Insights into Nematode-Trap Formation

Nematode-trapping fungi are “carnivorous” and attack their hosts using specialized trapping devices. The morphological development of these traps is the key indicator of their switch from saprophytic to predacious lifestyles. Here, the genome of the nematode-trapping fungus Arthrobotrys oligospora Fres. (ATCC24927) was reported. The genome contains 40.07 Mb assembled sequence with 11,479 predicted genes. Comparative analysis showed that A. oligospora shared many more genes with pathogenic fungi than with non-pathogenic fungi. Specifically, compared to several sequenced ascomycete fungi, the A. oligospora genome has a larger number of pathogenicity-related genes in the subtilisin, cellulase, cellobiohydrolase, and pectinesterase gene families. Searching against the pathogen-host interaction gene database identified 398 homologous genes involved in pathogenicity in other fungi. The analysis of repetitive sequences provided evidence for repeat-induced point mutations in A. oligospora. Proteomic and quantitative PCR (qPCR) analyses revealed that 90 genes were significantly up-regulated at the early stage of trap-formation by nematode extracts and most of these genes were involved in translation, amino acid metabolism, carbohydrate metabolism, cell wall and membrane biogenesis. Based on the combined genomic, proteomic and qPCR data, a model for the formation of nematode trapping device in this fungus was proposed. In this model, multiple fungal signal transduction pathways are activated by its nematode prey to further regulate downstream genes associated with diverse cellular processes such as energy metabolism, biosynthesis of the cell wall and adhesive proteins, cell division, glycerol accumulation and peroxisome biogenesis. This study will facilitate the identification of pathogenicity-related genes and provide a broad foundation for understanding the molecular and evolutionary mechanisms underlying fungi-nematodes interactions