Automatic differentiation accelerated shape optimization approaches to photonic inverse design on rectilinear simulation grids

Shape optimization approaches to inverse design offer low-dimensional, physically-guided parameterizations of structures by representing them as combinations of shape primitives. However, on discretized rectilinear simulation grids, computing the gradient of a user objective via the adjoint variables method requires a sum reduction of the forward/adjoint field solutions and the Jacobian of the simulation material distribution with respect to the structural shape parameters. These shape parameters often perturb large or global parts of the simulation grid resulting in many non-zero Jacobian entries, which are typically computed by finite-difference in practice. Consequently, the gradient calculation can be non-trivial. In this work we propose to accelerate the gradient calculation by invoking automatic differentiation (AutoDiff) in instantiations of structural material distributions. In doing so, we develop extensible differentiable mappings from shape parameters to shape primitives and differentiable effective logic operations (denoted AutoDiffGeo). These AutoDiffGeo definitions may introduce some additional discretization error into the field solutions because they relax notions of sub-pixel smoothing along shape boundaries. However, we show that some mappings (e.g. simple cuboids) can achieve zero error with respect to volumetric averaging strategies. We demonstrate AutoDiff enhanced shape optimization using three integrated photonic examples: a multi-etch blazed grating coupler, a non-adiabatic waveguide transition taper, and a polarization-splitting grating coupler. We find accelerations of the gradient calculation by AutoDiff relative to finite-difference often exceed 50x, resulting in total wall time accelerations of 4x or more on the same hardware with little or no compromise to final device performance. Our code is available open source at https://github.com/smhooten/emoptComment: 29 pages, 15 figure

Autocrine CSF-1R activation promotes Src-dependent disruption of mammary epithelial architecture

Elevated coexpression of colony-stimulating factor receptor (CSF-1R) and its ligand, CSF-1, correlates with invasiveness and poor prognosis of a variety of epithelial tumors (Kacinski, B.M. 1995. Ann. Med. 27:79–85). Apart from recruitment of macrophages to the tumor site, the mechanisms by which CSF-1 may potentiate invasion are poorly understood. We show that autocrine CSF-1R activation induces hyperproliferation and a profound, progressive disruption of junctional integrity in acinar structures formed by human mammary epithelial cells in three-dimensional culture. Acini coexpressing receptor and ligand exhibit a dramatic relocalization of E-cadherin from the plasma membrane to punctate intracellular vesicles, accompanied by its loss from the Triton-insoluble fraction. Interfering with Src kinase activity, either by pharmacological inhibition or mutation of the Y561 docking site on CSF-1R, prevents E-cadherin translocation, suggesting that CSF-1R disrupts cell adhesion by uncoupling adherens junction complexes from the cytoskeleton and promoting cadherin internalization through a Src-dependent mechanism. These findings provide a mechanistic basis whereby CSF-1R could contribute to invasive progression in epithelial cancers

Coupling Single NV Centers in Diamond to Optical Microcavities

Coupling of the NV^- ZPL to a silica microcavity and tapered fiber is demonstrated at cryogenic temperatures. Coupling to a high-Q cavity should enhance the usefulness of the NV^-for quantum information applications

Science results from the imaging Fourier transform spectrometer SpIOMM

SpIOMM is an imaging Fourier transform spectrometer designed to obtain the visible range (350 to 850 nm) spectrum of every light source in a circular field of view of 12 arcminutes in diameter. It is attached to the 1.6-m telescope of the Observatoire du Mont Megantic in southern Quebec. We present here some results of three successful observing runs in 2007, which highlight SpIOMMs capabilities to map emission line objects over a very wide field of view and a broad spectral range. In particular, we discuss data cubes from the planetary nebula M27, the supernova remnants NGC 6992 and M1, the barred spiral galaxy NGC7479, as well as Stephans quintet, an interacting group of galaxies.Comment: 10 pages, 7 figures, to appear in "Ground-based and Airborne Instrumentation for Astronomy II", SPIE conference, Marseille, 23-28 June 200

Prevalence and antibiotic resistance of Staphylococcus aureus associated with a college-aged cohort: life-style factors that contribute to nasal carriage

Staphylococcus aureus is an opportunistic human pathogen that can frequently be found at various body locations, such as the upper respiratory tract, nostrils, skin, and perineum. S. aureus is responsible for causing a variety of conditions, which range from minor skin infections and food poisoning to life-threatening sepsis and endocarditis. Furthermore, S. aureus has developed resistance to numerous antimicrobial agents, which has made treatment of S. aureus infections difficult. In the present study, we examined lifestyle factors that could increase the likelihood of S. aureus carriage, the overall prevalence of S. aureus, as well as assessed the antibiotic resistance profiles of the S. aureus isolates among a population of college students. Five hundred nasal samples were collected and analyzed via selective growth media, coagulase and protein A testing, as well as polymerase chain reaction and DNA sequencing. One hundred four out of the 500 samples collected (21%) were identified as containing S. aureus. The S. aureus isolates were resistant to penicillin (74%), azithromycin (34%), cefoxitin (5%), ciprofloxacin (5%), tetracycline (4%), and trimethoprim (1%), but sensitive to gentamicin and rifampin. Lastly, we identified several lifestyle factors (i.e., pet exposure, time spent at the university recreational facility, musical instrument usage, and tobacco usage) positively correlated with S. aureus nasal colonization

Survey of Activated FLT3 Signaling in Leukemia

Activating mutations of FMS-like tyrosine kinase-3 (FLT3) are found in approximately 30% of patients with acute myeloid leukemia (AML). FLT3 is therefore an attractive drug target. However, the molecular mechanisms by which FLT3 mutations lead to cell transformation in AML remain unclear. To develop a better understanding of FLT3 signaling as well as its downstream effectors, we performed detailed phosphoproteomic analysis of FLT3 signaling in human leukemia cells. We identified over 1000 tyrosine phosphorylation sites from about 750 proteins in both AML (wild type and mutant FLT3) and B cell acute lymphoblastic leukemia (normal and amplification of FLT3) cell lines. Furthermore, using stable isotope labeling by amino acids in cell culture (SILAC), we were able to quantified over 400 phosphorylation sites (pTyr, pSer, and pThr) that were responsive to FLT3 inhibition in FLT3 driven human leukemia cell lines. We also extended this phosphoproteomic analysis on bone marrow from primary AML patient samples, and identify over 200 tyrosine and 800 serine/threonine phosphorylation sites in vivo. This study showed that oncogenic FLT3 regulates proteins involving diverse cellular processes and affects multiple signaling pathways in human leukemia that we previously appreciated, such as Fc epsilon RI-mediated signaling, BCR, and CD40 signaling pathways. It provides a valuable resource for investigation of oncogenic FLT3 signaling in human leukemia