Dynamics and Origin of the 2:1 Orbital Resonances of the GJ 876 Planets

(Abridged) A dynamical fit has placed the two planets about the star GJ 876 in coplanar orbits deep in 3 resonances at the 2:1 mean-motion commensurability with small libration amplitudes. The libration of both lowest order mean-motion resonance variables, theta_1 and theta_2, and the secular resonance variable, theta_3, about 0 deg. differs from the familiar geometry of the Io-Europa pair, where theta_2 and theta_3 librate about 180 deg. By considering a condition for stable simultaneous librations of theta_1 and theta_2, we show that the GJ 876 geometry results because of the large orbital eccentricities e_i, whereas the very small e_i in the Io-Europa system lead to the latter's geometry. Surprisingly, the GJ 876 resonance configuration remains stable for e_1 up to 0.86 and for amplitude of libration of theta_1 approaching 45 deg. with the current e_i. We find that inward migration of the outer planet of the GJ 876 system results in certain capture into the observed resonances if initially e_1 <0.06 and e_2<0.03 and the migration rate |(da_2/dt)/a_2| < 0.03(a_2/AU)^{-3/2} yr^{-1}. The bound on the migration rate is easily satisfied by migration due to planet-nebula interaction. If there is no eccentricity damping, eccentricity growth is rapid with continued migration within the resonance, with e_i exceeding the observed values after a further reduction in the semi-major axes a_i of only 7%. With eccentricity damping (de_i/dt)/e_i = -K|(da_i/dt)/a_i|, the e_i reach equilibrium values that remain constant for arbitrarily long migration within the resonances. The equilibrium e_i are close to the observed e_i for K=100 (K=10) if there is migration and damping of the outer planet only (of both planets). It is as yet unclear that planet-nebula interaction can produce the large value of K required to obtain the observed eccentricities.Comment: 23 pages, including 8 figures; uses AASTeX v5.0; minor additions; accepted for publication in Ap

Enabling Hyper-Personalisation: Automated Ad Creative Generation and Ranking for Fashion e-Commerce

Homepage is the first touch point in the customer's journey and is one of the prominent channels of revenue for many e-commerce companies. A user's attention is mostly captured by homepage banner images (also called Ads/Creatives). The set of banners shown and their design, influence the customer's interest and plays a key role in optimizing the click through rates of the banners. Presently, massive and repetitive effort is put in, to manually create aesthetically pleasing banner images. Due to the large amount of time and effort involved in this process, only a small set of banners are made live at any point. This reduces the number of banners created as well as the degree of personalization that can be achieved. This paper thus presents a method to generate creatives automatically on a large scale in a short duration. The availability of diverse banners generated helps in improving personalization as they can cater to the taste of larger audience. The focus of our paper is on generating wide variety of homepage banners that can be made as an input for user level personalization engine. Following are the main contributions of this paper: 1) We introduce and explain the need for large scale banner generation for e-commerce 2) We present on how we utilize existing deep learning based detectors which can automatically annotate the required objects/tags from the image. 3) We also propose a Genetic Algorithm based method to generate an optimal banner layout for the given image content, input components and other design constraints. 4) Further, to aid the process of picking the right set of banners, we designed a ranking method and evaluated multiple models. All our experiments have been performed on data from Myntra (http://www.myntra.com), one of the top fashion e-commerce players in India.Comment: Workshop on Recommender Systems in Fashion, 13th ACM Conference on Recommender Systems, 201

The Response Phase - The First Six Hours After Acute Airway Injury by SO2 Inhalation: An in vivo and in vitro Study

We have identified an airway epithelial response following acute injury that cannot be termed \u27repair\u27 or regeneration. It precedes these well characterized events and it is termed the \u27response phase\u27. We tested the hypothesis that for the first 6 h following acute injury to the tracheal mucosa, the initial cellular events of the response phase will continue as in vivo even if the tissue is maintained in vitro in an Ussing chamber. The tracheal mucosa of anesthetized, intubated mongrel dogs was injured by the inhalation of SO2 500 ppm for 1 h (7 dogs); controls (3 dogs) breathed filtered, compressed air for 1 h. 4 dogs were killed, in pairs, at 1 and 6 h after 500ppm of SO2; their tracheas were removed and fixed for microscopic examination. 3 dogs were killed immediately after the SO2 exposure, their tracheas were removed and epithelium isolated from the posterior-membranous sheath was mounted in Ussing chambers in oxygenated, Krebs-Henseleit buffer (8 per dog with aperature area of 1.5 cm2). These tissues (and those from control dogs prepared identically) were fixed after 1 and 6 h incubation for microscopic examination. Epithelial damage was not observed in any controls but was in all tissues exposed to SO2. A wide spectrum of mucosal cell injury during the response phase was observed. The patterns of exfoliation noted were: individual cells, rows (several cells wide) of mucosal cells and entire regions (several hundred μm2). At 1 h after exposure, in some lesions, the injury is difficult to assess because the tracheal surface was either blanketed in exfoliated cells or appeared in total disarray. By 6 h, the lesions were well defined and large flattened cells (130 μm2 in surface area) covered the basement membrane in areas where mucosal cells had exfoliated. Some ciliated cells still remained attached at their base in these areas. These were the findings whether the tissues were taken fresh from the animal or have been maintained in Ussing chambers for up to 6 h. These results show that cellular repair of the tracheal epithelium can be studied in vitro during the first 6 h after injury, even if the injury has occurred in situ

Statistics of Gravitational Microlensing Magnification. I. Two-Dimensional Lens Distribution

(Abridged) In this paper we refine the theory of microlensing for a planar distribution of point masses. We derive the macroimage magnification distribution P(A) at high magnification (A-1 >> tau^2) for a low optical depth (tau << 1) lens distribution by modeling the illumination pattern as a superposition of the patterns due to individual ``point mass plus weak shear'' lenses. We show that a point mass plus weak shear lens produces an astroid- shaped caustic and that the magnification cross-section obeys a simple scaling property. By convolving this cross-section with the shear distribution, we obtain a caustic-induced feature in P(A) which also exhibits a simple scaling property. This feature results in a 20% enhancement in P(A) at A approx 2/tau. In the low magnification (A-1 << 1) limit, the macroimage consists of a bright primary image and a large number of faint secondary images formed close to each of the point masses. Taking into account the correlations between the primary and secondary images, we derive P(A) for low A. The low-A distribution has a peak of amplitude ~ 1/tau^2 at A-1 ~ tau^2 and matches smoothly to the high-A distribution. We combine the high- and low-A results and obtain a practical semi-analytic expression for P(A). This semi-analytic distribution is in qualitative agreement with previous numerical results, but the latter show stronger caustic-induced features at moderate A for tau as small as 0.1. We resolve this discrepancy by re-examining the criterion for low optical depth. A simple argument shows that the fraction of caustics of individual lenses that merge with those of their neighbors is approx 1-exp(-8 tau). For tau=0.1, the fraction is surprisingly high: approx 55%. For the purpose of computing P(A) in the manner we did, low optical depth corresponds to tau << 1/8.Comment: 35 pages, including 6 figures; uses AASTeX v4.0 macros; submitted to Ap

Permutation symmetry for the tomographic probability distribution of a system of identical particles

The symmetry properties under permutation of tomograms representing the states of a system of identical particles are studied. Starting from the action of the permutation group on the density matrix we define its action on the tomographic probability distribution. Explicit calculations are performed in the case of the two-dimensional harmonic oscillator.Comment: 13 pages, latex, no figure

Nonlinear Decoherence in Quantum State Preparation of a Trapped Ion

We present a nonlinear decoherence model which models decoherence effect caused by various decohereing sources in a quantum system through a nonlinear coupling between the system and its environment, and apply it to investigating decoherence in nonclassical motional states of a single trapped ion. We obtain an exactly analytic solution of the model and find very good agreement with experimental results for the population decay rate of a single trapped ion observed in the NIST experiments by Meekhof and coworkers (D. M. Meekhof, {\it et al.}, Phys. Rev. Lett. {\bf 76}, 1796 (1996)).Comment: 5 pages, Revte

SUMOylation inhibits FOXM1 activity and delays mitotic transition

The forkhead box transcription factor FOXM1 is an essential effector of G2/M-phase transition, mitosis and the DNA damage response. As such, it is frequently deregulated during tumorigenesis. Here we report that FOXM1 is dynamically modified by SUMO1 but not by SUMO2/3 at multiple sites. We show that FOXM1 SUMOylation is enhanced in MCF-7 breast cancer cells in response to treatment with epirubicin and mitotic inhibitors. Mutation of five consensus conjugation motifs yielded a SUMOylation-deficient mutant FOXM1. Conversely, fusion of the E2 ligase Ubc9 to FOXM1 generated an auto-SUMOylating mutant (FOXM1-Ubc9). Analysis of wild-type FOXM1 and mutants revealed that SUMOylation inhibits FOXM1 activity, promotes translocation to the cytoplasm and enhances APC/Cdh1-mediated ubiquitination and degradation. Further, expression of the SUMOylation-deficient mutant enhanced cell proliferation compared with wild-type FOXM1, whereas the FOXM1-Ubc9 fusion protein resulted in persistent cyclin B1 expression and slowed the time from mitotic entry to exit. In summary, our findings suggest that SUMOylation attenuates FOXM1 activity and causes mitotic delay in cytotoxic drug response

Neuroimaging in Leber Hereditary Optic Neuropathy: State-of-the-art and future prospects

Leber Hereditary Optic Neuropathy (LHON) is an inherited mitochondrial retinal disease that causes the degeneration of retinal ganglion cells and leads to drastic loss of visual function. In the last decades, there has been a growing interest in using Magnetic Resonance Imaging (MRI) to better understand mechanisms of LHON beyond the retina. This is partially due to the emergence of gene-therapies for retinal diseases, and the accompanying expanded need for reliably quantifying and monitoring visual processing and treatment efficiency in patient populations. This paper aims to draw a current picture of key findings in this field so far, the challenges of using neuroimaging methods in patients with LHON, and important open questions that MRI can help address about LHON disease mechanisms and prognoses, including how downstream visual brain regions are affected by the disease and treatment and why, and how scope for neural plasticity in these pathways may limit or facilitate recovery

Derivation of continuum stochastic equations for discrete growth models

We present a formalism to derive the stochastic differential equations (SDEs) for several solid-on-solid growth models. Our formalism begins with a mapping of the microscopic dynamics of growth models onto the particle systems with reactions and diffusion. We then write the master equations for these corresponding particle systems and find the SDEs for the particle densities. Finally, by connecting the particle densities with the growth heights, we derive the SDEs for the height variables. Applying this formalism to discrete growth models, we find the Edwards-Wilkinson equation for the symmetric body-centered solid-on-solid (BCSOS) model, the Kardar-Parisi-Zhang equation for the asymmetric BCSOS model and the generalized restricted solid-on-solid (RSOS) model, and the Villain--Lai--Das Sarma equation for the conserved RSOS model. In addition to the consistent forms of equations for growth models, we also obtain the coefficients associated with the SDEs.Comment: 5 pages, no figur

A subset of morphologically distinct mammary myoepithelial cells lacks corresponding immunophenotypic markers

INTRODUCTION: Immunostaining for smooth muscle actin (SMA) is commonly used to elucidate mammary myoepithelial (ME) cells, whose presence or absence is a reliable criterion for differentiating in situ and invasive carcinomas. However, some morphologically distinct ME cells fail to stain for SMA. This study intended to assess whether these SMA-negative cells also lack the expression of other ME cell markers. METHODS: Hematoxylin/eosin and SMA immunostained sections from 175 breast cancer patients were examined. Three cases were found to harbor ducts that showed morphologically distinct ME cell layers, but showed no SMA immunostaining in at least one-third of the layer or the entire layer. Eight additional consecutive sections from each case were stained for SMA, using a black chromogen, and each was then re-stained for one of eight additional markers supposed to exclusively or preferentially stain ME cells, using a red chromogen. SMA-negative ME cells were re-examined for the expression of other markers. RESULTS: SMA-negative ME cells in two cases also failed to display immunoreactivity for other markers, including calponin, CD10, smooth muscle myosin heavy chain, protease inhibitor 5 (maspin), Wilms' tumor-1, and cytokeratins 5, 14, and 17 (CK5, CK14, and CK17). However, in one case SMA-negative ME cells displayed immunoreactivities for maspin, CK5, CK14, and CK17. The distribution of these ME cells is independent of ductal size, length, and architecture. CONCLUSIONS: A subset of morphologically identifiable ME cells lack the expression of nine corresponding immunophenotypic markers, suggesting that ME cells might also be subject to different normal and pathological alterations