The coherent artifact in modern pulse measurements

We simulate multi-shot intensity-and-phase measurements of unstable ultrashort-pulse trains using frequency-resolved-optical-gating (FROG) and spectral phase interferometry for direct electric-field reconstruction (SPIDER). Both techniques fail to reveal the pulse structure. FROG yields the average pulse duration and suggests the instability by exhibiting disagreement between measured and retrieved traces. SPIDER under-estimates the average pulse duration but retrieves the correct average pulse spectral phase. An analytical calculation confirms this behavior.Comment: submission to Opt. Let

Morphology of Graphene on SiC(000-1) Surfaces

Graphene is formed on SiC(000-1) surfaces (the so-called C-face of the crystal) by annealing in vacuum, with the resulting films characterized by atomic force microscopy, Auger electron spectroscopy, scanning Auger microscopy and Raman spectroscopy. Morphology of these films is compared with the graphene films grown on SiC(0001) surfaces (the Si-face). Graphene forms a terraced morphology on the C-face, whereas it forms with a flatter morphology on the Si-face. It is argued that this difference occurs because of differing interface structures in the two cases. For certain SiC wafers, nanocrystalline graphite is found to form on top of the graphene.Comment: Submitted to Applied Physics Letters; 9 pages, 3 figures; corrected the stated location of Raman G line for NCG spectrum, to 1596 cm^-

Phases of a polar spin-1 Bose gas in a magnetic field

The two Bose--Einstein condensed phases of a polar spin-1 gas at nonzero magnetizations and temperatures are investigated. The Hugenholtz--Pines theorem is generalized to this system. Crossover to a quantum phase transition is also studied. Results are discussed in a mean field approximation.Comment: 6 pages, 3 figures, revised versio

Quantum Critical Behavior of Two Coupled Bose-Einstein Condensates

The quantum critical behavior of the Bose-Hubbard model for a description of two coupled Bose-Einstein condensates is studied within the framework of an algebraic theory. Energy levels, wavefunction overlaps with those of the Rabi and Fock regimes, and the entanglement are calculated exactly as functions of the phase parameter and the number of bosons. The results show that the system goes though a phase transition and that the critical behavior is enhanced in the thermodynamic limit.Comment: 6 pages, LaTex, 3 figure

Potential Mechanisms Underlying TGF-β-mediated Complement Activation in Lung Fibrosis

While our previous studies suggest that limiting bleomycin-induced complement activation suppresses TGF-β signaling, the specific hierarchical interactions between TGF-β and complement in lung fibrosis are unclear. Herein, we investigated the mechanisms underlying TGF-β-induced complement activation in the pathogenesis of lung fibrosis. C57-BL6 mice were given intratracheal instillations of adenoviral vectors overexpressing TGF-β (Ad-TGFβ) or the firefly gene-luciferase (Ad-Luc; control). Two weeks later, mice with fibrotic lungs were instilled RNAi specific to receptors for C3a or C5a-C3ar or C5ar, and sacrificed at day 28. Histopathological analyses revealed that genetic silencing of C3ar or C5ar arrested the progression of TGF-β-induced lung fibrosis, collagen deposition and content (hydroxyproline, col1a1/2); and significantly suppressed local complement activation. With genetic silencing of either C3ar or C5ar, in Ad-TGFβ-injured lungs: we detected the recovery of Smad7 (TGF-β inhibitor) and diminished local release of DAF (membrane-bound complement inhibitor); in vitro: TGF-β-mediated loss of DAF was prevented. Conversely, blockade of the TGF-β receptor prevented C3a-mediated loss of DAF in both normal primary human alveolar and small airway epithelial cells. Of the 52 miRNAs analyzed as part of the Affymetrix array, normal primary human SAECs exposed to C3a, C5a or TGF-β caused discrete and overlapping miRNA regulation related to epithelial proliferation or apoptosis (miR-891A, miR-4442, miR-548, miR-4633), cellular contractility (miR-1197) and lung fibrosis (miR-21, miR-200C, miR-31HG, miR-503). Our studies present potential mechanisms by which TGF-β activates complement and promotes lung fibrosis

Estrogen activation of microglia underlies the sexually dimorphic differences in Nf1 optic glioma-induced retinal pathology

Children with neurofibromatosis type 1 (NF1) develop low-grade brain tumors throughout the optic pathway. Nearly 50% of children with optic pathway gliomas (OPGs) experience visual impairment, and few regain their vision after chemotherapy. Recent studies have revealed that girls with optic nerve gliomas are five times more likely to lose vision and require treatment than boys. To determine the mechanism underlying this sexually dimorphic difference in clinical outcome, we leveraged Nf1 optic glioma (Nf1-OPG) mice. We demonstrate that female Nf1-OPG mice exhibit greater retinal ganglion cell (RGC) loss and only females have retinal nerve fiber layer (RNFL) thinning, despite mice of both sexes harboring tumors of identical volumes and proliferation. Female gonadal sex hormones are responsible for this sexual dimorphism, as ovariectomy, but not castration, of Nf1-OPG mice normalizes RGC survival and RNFL thickness. In addition, female Nf1-OPG mice have threefold more microglia than their male counterparts, and minocycline inhibition of microglia corrects the retinal pathology. Moreover, pharmacologic inhibition of microglial estrogen receptor-β (ERβ) function corrects the retinal abnormalities in female Nf1-OPG mice. Collectively, these studies establish that female gonadal sex hormones underlie the sexual dimorphic differences in Nf1 optic glioma–induced retinal dysfunction by operating at the level of tumor-associated microglial activation

Ferromagnetic phase transition and Bose-Einstein condensation in spinor Bose gases

Phase transitions in spinor Bose gases with ferromagnetic (FM) couplings are studied via mean-field theory. We show that an infinitesimal value of the coupling can induce a FM phase transition at a finite temperature always above the critical temperature of Bose-Einstein condensation. This contrasts sharply with the case of Fermi gases, in which the Stoner coupling $I_s$ can not lead to a FM phase transition unless it is larger than a threshold value $I_0$. The FM coupling also increases the critical temperatures of both the ferromagnetic transition and the Bose-Einstein condensation.Comment: 4 pages, 4 figure

Repeated Randomization and Matching in Multi‐Arm Trials

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/102047/1/biom12077.pd

Orbital Elements of Comet C/1490 Y1 and the Quadrantid shower

The Quadrantid shower, one of the most intense showers, has been observed at the beginning of January each year. However, the origin of the meteors is still unknown. It was Hasegawa (1979) who first suggested comet C/1490 Y1 to be the likely origin of the shower based on the historical records of East Asia. We analyse the records of Jo-Seon-Wang-Jo-Sil-Lok (the Annals of the Joseon Dynasty in ancient Korea) and calculate the preliminary orbital elements of comet C/1490 Y1 using a modified Gauss method. We find that comet C/1490 Y1 was a periodic one and its orbital path was very similar to that of the Quadrantid meteor stream. The determined orbital elements are perifocal passage time Tp=2265652.2983 days (7.8 Jan. 1491 in UT), perifocal distance q=0.769 AU, eccentricity e=0.747, semimajor axis a=3.04 AU, argument of the perifocus omega=164.03 degrees, longitude of ascending node Omega=283.00 degrees, and inclination i=70.22 degrees for the epoch of J2000.0. We, therefore, conclude that our result verifies the suggestion that the comet C/1490 Y1 is the origin of the Quandrantid meteor shower, but was a periodic comet. We dicuss a possible link between this comet and the asteroid 2003 EH1 as well.Comment: 7 pages, 2 figures, accepted for publication in MNRA

Mathematizing Darwin

Ernst Mayr called the first part of the evolutionary synthesis the ‘Fisherian synthesis’ on account of the dominant role played by R.A. Fisher in forging a mathematical theory of natural selection together with J.B.S. Haldane and Sewall Wright in the decade 1922–1932. It is here argued that Fisher’s contribution relied on a close reading of Darwin’s work to a much greater extent than did the contributions of Haldane and Wright, that it was synthetic in contrast to their analytic approach and that it was greatly influenced by his friendship with the Darwin family, particularly with Charles’s son Leonard