Snapshot navigation in the wavelet domain

Many animals rely on robust visual navigation which can be explained by snapshot models, where an agent is assumed to store egocentric panoramic images and subsequently use them to recover a heading by comparing current views to the stored snapshots. Long-range route navigation can also be explained by such models, by storing multiple snapshots along a training route and comparing the current image to these. For such models, memory capacity and comparison time increase dramatically with route length, rendering them unfeasible for small-brained insects and low-power robots where computation and storage are limited. One way to reduce the requirements is to use a compressed image representation. Inspired by the filter bank-like arrangement of the visual system, we here investigate how a frequency-based image representation influences the performance of a typical snapshot model. By decomposing views into wavelet coefficients at different levels and orientations, we achieve a compressed visual representation that remains robust when used for navigation. Our results indicate that route following based on wavelet coefficients is not only possible but gives increased performance over a range of other models

Gamma Interferon-Induced Guanylate Binding Protein 1 Is a Novel Actin Cytoskeleton Remodeling Factor

Gamma interferon (IFN-gamma) regulates immune defenses against viruses, intracellular pathogens, and tumors by modulating cell proliferation, migration, invasion, and vesicle trafficking processes. The large GTPase guanylate binding protein 1 (GBP-1) is among the cellular proteins that is the most abundantly induced by IFN-gamma and mediates its cell biologic effects. As yet, the molecular mechanisms of action of GBP-1 remain unknown. Applying an interaction proteomics approach, we identified actin as a strong and specific binding partner of GBP-1. Furthermore, GBP-1 colocalized with actin at the subcellular level and was both necessary and sufficient for the extensive remodeling of the fibrous actin structure observed in IFN-gamma -exposed cells. These effects were dependent on the oligomerization and the GTPase activity of GBP-1. Purified GBP-1 and actin bound to each other, and this interaction was sufficient to impair the formation of actin filaments in vitro, as demonstrated by atomic force microscopy, dynamic light scattering, and fluorescence-monitored polymerization. Cosedimentation and band shift analyses demonstrated that GBP-1 binds robustly to globular actin and slightly to filamentous actin. This indicated that GBP-1 may induce actin remodeling via globular actin sequestering and/or filament capping. These results establish GBP-1 as a novel member within the family of actin-remodeling proteins specifically mediating IFN-gamma -dependent defense strategies

PU.1 controls fibroblast polarization and tissue fibrosis

Fibroblasts are polymorphic cells with pleiotropic roles in organ morphogenesis, tissue homeostasis and immune responses. In fibrotic diseases, fibroblasts synthesize abundant amounts of extracellular matrix, which induces scarring and organ failure. By contrast, a hallmark feature of fibroblasts in arthritis is degradation of the extracellular matrix because of the release of metalloproteinases and degrading enzymes, and subsequent tissue destruction. The mechanisms that drive these functionally opposing pro-fibrotic and pro-inflammatory phenotypes of fibroblasts remain unknown. Here we identify the transcription factor PU.1 as an essential regulator of the pro-fibrotic gene expression program. The interplay between transcriptional and post-transcriptional mechanisms that normally control the expression of PU.1 expression is perturbed in various fibrotic diseases, resulting in the upregulation of PU.1, induction of fibrosis-associated gene sets and a phenotypic switch in extracellular matrix-producing pro-fibrotic fibroblasts. By contrast, pharmacological and genetic inactivation of PU.1 disrupts the fibrotic network and enables reprogramming of fibrotic fibroblasts into resting fibroblasts, leading to regression of fibrosis in several organs

Diffusion Limited Photoluminescence Quantum Yields in 1-D Semiconductors: Single-Wall Carbon Nanotubes

Photoluminescence quantum yields and nonradiative decay of the excitonic S-1, state in length fractionated (6,5) single-wall carbon nanotubes (SWNTs) are studied by continuous wave and time-resolved fluorescence spectroscopy. The experimental data are modeled by diffusion limited contact quenching of excitons at stationary quenching sites including tube ends. A combined analysis of the time-resolved photoluminescence decay and the length dependence of photoluminescence quantum yields (PL QYs) from SWNTs in sodium cholate suspensions allows to determine the exciton diffusion coefficient D = 10.7 +/- 0.4 cm(2)s(-1) and lifetime T-pL for long tubes of 20 +/- 1 ps. PL quantum yields Phi(pL) are found to scale with the inverse diffusion coefficient and the square of the mean quenching site distance, here I-d = 120 +/- 25 nm. The results suggest that low PL QYs of SWNTs are due to the combination of high-diffusive exciton mobility with the presence of only a few quenching sites