Variational Approaches for Motion and Structure from Monocular Video

Motion and structure estimation are elementary problems of computer vision. These are active areas of research, even though the first methods were proposed several decades ago. We develop new approaches for motion and structure estimation for autonomous driving. An autonomous vehicle requires an accurate model of its environment, wrong decisions made by an autonomous car can have severe consequences. We assume the monocular setup, where only a single camera is mounted on the car. Outdoor traffic sequences are challenging for optical flow estimation. The high speed of the car causes large displacements in the optical flow field, the lighting conditions are unstable and there can be strong distortions due to reflections and difficult weather conditions. We propose new discrete methods, which determine optical flow as optimal configuration of probabilistic graphical models. The first approach selects sparse locations in the reference frame, and matches them across the second image. The best correspondences, which match constraints from a multiple view configuration, are considered motion vectors in a graphical model. In a second approach, we solve for dense optical flow by approximating the original infeasible graphical model with a sequence of reduced models. The monocular configuration poses challenges to the estimation of scene structure, camera positions and scene parameters need to be estimated jointly. The geometry of multiple views creates blind spots in the images, and adds a scale ambiguity, which both to not exist in a setup with multiple cameras. We propose two methods for structure estimation. The first approach determines the energy optimal camera track, given optical flow and depth observations. A further approach estimates camera motion and a piecewise planar scene description jointly from a single optical flow field. The scene description contains depth and plane normal information. We evaluate our approaches for motion and structure estimation on different real world and rendered datasets. In addition to evaluation on publicly available evaluation data, we evaluate on a new rendered dataset with ground truth plane normals

A Genetic Screen in Drosophila Reveals Novel Cytoprotective Functions of the Autophagy-Lysosome Pathway

The highly conserved autophagy-lysosome pathway is the primary mechanism for breakdown and recycling of macromolecular and organellar cargo in the eukaryotic cell. Autophagy has recently been implicated in protection against cancer, neurodegeneration, and infection, and interest is increasing in additional roles of autophagy in human health, disease, and aging. To search for novel cytoprotective features of this pathway, we carried out a genetic mosaic screen for mutations causing increased lysosomal and/or autophagic activity in the Drosophila melanogaster larval fat body. By combining Drosophila genetics with live-cell imaging of the fluorescent dye LysoTracker Red and fixed-cell imaging of autophagy-specific fluorescent protein markers, the screen was designed to identify essential metazoan genes whose disruption causes increased flux through the autophagy-lysosome pathway. The screen identified a large number of genes associated with the protein synthesis and ER-secretory pathways (e.g. aminoacyl tRNA synthetases, Oligosaccharyl transferase, Sec61α), and with mitochondrial function and dynamics (e.g. Rieske iron-sulfur protein, Dynamin-related protein 1). We also observed that increased lysosomal and autophagic activity were consistently associated with decreased cell size. Our work demonstrates that disruption of the synthesis, transport, folding, or glycosylation of ER-targeted proteins at any of multiple steps leads to autophagy induction. In addition to illuminating cytoprotective features of autophagy in response to cellular damage, this screen establishes a genetic methodology for investigating cell biological phenotypes in live cells, in the context of viable wild type organisms

SAR distribution in human beings when using body-worn RF transmitters

This study analyzes the exposure of the human torso to electromagnetic fields caused by wireless body-mounted or handheld devices. Because of the frequency and distance ranges from 30-5800 MHz and 10 to 200 mm, respectively, both near-field and far-field effects are considered. A generic body model and simulations of anatomical models are used to evaluate the worst case tissue composition with respect to the absorption of electromagnetic energy. Both standing wave effects and enhanced coupling of reactive near-field components can lead to a specific absorption rate (SAR) increase in comparison to homogeneous tissue. In addition, the exposure and temperature increase of different inner organs is assessed. With respect to compliance testing, the observed SAR enhancement may require the introduction of a multiplication factor for the spatial peak SAR measured in the liquid-filled phantom in order to obtain a conservative exposure assessment. The observed tissue heating at the body surface under adiabatic conditions can be significant, whereas the temperature increase in the inner organs turned out to be negligible for the cases investigate

Gauge-invariant Green's functions for the bosonic sector of the standard model

There are many applications in gauge theories where the usually employed framework involving gauge-dependent Green's functions leads to considerable problems. In order to overcome the difficulties invariably tied to gauge dependence, we present a manifestly gauge-invariant approach. We propose a generating functional of appropriately chosen gauge-invariant Green's functions for the bosonic sector of the standard model. Since the corresponding external sources emit one-particle states, these functions yield the same S-matrix elements as those obtained in the usual framework. We evaluate the generating functional for the bosonic sector of the standard model up to the one-loop level and carry out its renormalization in the on-shell scheme. Explicit results for some two-point functions are given. Gauge invariance is manifest at any step of our calculation.Comment: 29 pages, Revtex. v2: Discussions improved, conclusions unchanged. Some references added. v3: Published versio

Drug-induced trafficking of p-glycoprotein in human brain capillary endothelial cells as demonstrated by exposure to mitomycin C.

P-glycoprotein (Pgp; ABCB1/MDR1) is a major efflux transporter at the blood-brain barrier (BBB), restricting the penetration of various compounds. In other tissues, trafficking of Pgp from subcellular stores to the cell surface has been demonstrated and may constitute a rapid way of the cell to respond to toxic compounds by functional membrane insertion of the transporter. It is not known whether drug-induced Pgp trafficking also occurs in brain capillary endothelial cells that form the BBB. In this study, trafficking of Pgp was investigated in human brain capillary endothelial cells (hCMEC/D3) that were stably transfected with a doxycycline-inducible MDR1-EGFP fusion plasmid. In the presence of doxycycline, these cells exhibited a 15-fold increase in Pgp-EGFP fusion protein expression, which was associated with an increased efflux of the Pgp substrate rhodamine 123 (Rho123). The chemotherapeutic agent mitomycin C (MMC) was used to study drug-induced trafficking of Pgp. Confocal fluorescence microscopy of single hCMEC/D3-MDR1-EGFP cells revealed that Pgp redistribution from intracellular pools to the cell surface occurred within 2 h of MMC exposure. Pgp-EGFP exhibited a punctuate pattern at the cell surface compatible with concentrated regions of the fusion protein in membrane microdomains, i.e., lipid rafts, which was confirmed by Western blot analysis of biotinylated cell surface proteins in Lubrol-resistant membranes. MMC exposure also increased the functionality of Pgp as assessed in three functional assays with Pgp substrates (Rho123, eFluxx-ID Gold, calcein-AM). However, this increase occurred with some delay after the increased Pgp expression and coincided with the release of Pgp from the Lubrol-resistant membrane complexes. Disrupting rafts by depleting the membrane of cholesterol increased the functionality of Pgp. Our data present the first direct evidence of drug-induced Pgp trafficking at the human BBB and indicate that Pgp has to be released from lipid rafts to gain its full functionality

Corneal Transduction by Intra-Stromal Injection of AAV Vectors In Vivo in the Mouse and Ex Vivo in Human Explants

The cornea is a transparent, avascular tissue that acts as the major refractive surface of the eye. Corneal transparency, assured by the inner stroma, is vital for this role. Disruption in stromal transparency can occur in some inherited or acquired diseases. As a consequence, light entering the eye is blocked or distorted, leading to decreased visual acuity. Possible treatment for restoring transparency could be via viral-based gene therapy. The stroma is particularly amenable to this strategy due to its immunoprivileged nature and low turnover rate. We assayed the potential of AAV vectors to transduce keratocytes following intra-stromal injection in vivo in the mouse cornea and ex vivo in human explants. In murine and human corneas, we transduced the entire stroma using a single injection, preferentially targeted keratocytes and achieved long-term gene transfer (up to 17 months in vivo in mice). Of the serotypes tested, AAV2/8 was the most promising for gene transfer in both mouse and man. Furthermore, transgene expression could be transiently increased following aggression to the cornea

Development of the Epilepsy Risk Awareness scale (ERA scale) for people with epilepsy

Purpose: Quality of life in people with epilepsy depends on balancing protection from risks and avoiding unnecessary restrictions. The Epilepsy Risk Awareness Checklist (ERAC) was developed to summarise an individual’s safety, health care and quality of life and to facilitate communication between professionals. Although effective, the existing Checklist required quantification and shortening to increase its utility, particularly as a longitudinal tool for measuring and communicating changes over time. Methods: 5 clinical experts, 3 people with epilepsy and 5 carers assessed the importance of each item on the ERAC questionnaire in a two-round Delphi survey. The refined Epilepsy Risk Awareness scale (ERA scale) was piloted in 30 patients to obtain an overall and sub-scale score for personal safety, health care, and quality of life domains, and was compared with the validated Seizure Severity Scale and Epilepsy Self-Management Scale. Results: ERAC was shortened from 69 to 48 items to take 15–20 min for completion. Pilot results showed good internal consistency for the overall ERA scale, for the Personal Safety and Health Care subscales, but less for the Quality of Life subscale. There was strong association between ERA scale and the Epilepsy Self- Management Scale, but little relationship with Seizure Severity Scale scores, which focus on individual seizures. User ratings were high. Conclusions: The ERA scale has been shortened and quantified to provide an objective measure of the risks and safety profile in people with epilepsy. The scale will be further tested for intra-rater variability and utility

Early Embryonic Vascular Patterning by Matrix-Mediated Paracrine Signalling: A Mathematical Model Study

During embryonic vasculogenesis, endothelial precursor cells of mesodermal origin known as angioblasts assemble into a characteristic network pattern. Although a considerable amount of markers and signals involved in this process have been identified, the mechanisms underlying the coalescence of angioblasts into this reticular pattern remain unclear. Various recent studies hypothesize that autocrine regulation of the chemoattractant vascular endothelial growth factor (VEGF) is responsible for the formation of vascular networks in vitro. However, the autocrine regulation hypothesis does not fit well with reported data on in vivo early vascular development. In this study, we propose a mathematical model based on the alternative assumption that endodermal VEGF signalling activity, having a paracrine effect on adjacent angioblasts, is mediated by its binding to the extracellular matrix (ECM). Detailed morphometric analysis of simulated networks and images obtained from in vivo quail embryos reveals the model mimics the vascular patterns with high accuracy. These results show that paracrine signalling can result in the formation of fine-grained cellular networks when mediated by angioblast-produced ECM. This lends additional support to the theory that patterning during early vascular development in the vertebrate embryo is regulated by paracrine signalling