Robust Wheel Detection for Vehicle Re-Identification.

Vehicle re-identification is a demanding and challenging task in automated surveillance systems. The goal of vehicle re-identification is to associate images of the same vehicle to identify re-occurrences of the same vehicle. Robust re-identification of individual vehicles requires reliable and discriminative features extracted from specific parts of the vehicle. In this work, we construct an efficient and robust wheel detector that precisely locates and selects vehicular wheels from vehicle images. The associated hubcap geometry can hence be utilized to extract fundamental signatures from vehicle images and exploit them for vehicle re-identification. Wheels pattern information can yield additional information about vehicles in questions. To that end, we utilized a vehicle imagery dataset that has thousands of side-view vehicle collected under different illumination conditions and elevation angles. The collected dataset was used for training and testing the wheel detector. Experiments show that our approach could detect vehicular wheels accurately for 99.41% of the vehicles in the dataset.

Decision-Based Fusion for Vehicle Matching.

In this work, a framework is proposed for decision fusion utilizing features extracted from vehicle images and their detected wheels. Siamese networks are exploited to extract key signatures from pairs of vehicle images. Our approach then examines the extent of reliance between signatures generated from vehicle images to robustly integrate different similarity scores and provide a more informed decision for vehicle matching. To that end, a dataset was collected that contains hundreds of thousands of side-view vehicle images under different illumination conditions and elevation angles. Experiments show that our approach could achieve better matching accuracy by taking into account the decisions made by a whole-vehicle or wheels-only matching network.

Correction to: Imaging features of immune-mediated genitourinary disease.

The authors regret that they neglected to cite their conference report on the technical part of a 'preliminary study' presented at, and published in, the Biomedical Sciences and Engineering Conference (BSEC), 2010, May 25-26 (Fully automated segmentation and characterization of the dendritic trees of retinal horizontal neurons -DOI: 10.1109/BSEC.2010.5510843 ), as it related to the larger dataset presented as validation of the method in the Neurochemical Research article (Automated Tracing of Horizontal Neuron Processes During Retinal Development- Neurochem Res. 2011 Apr;36(4):583-93). This resulted in the lack of transparency on the re-use and duplication of introductory text, which should have been cited. No figures or tables were reproduced, but rather larger confirmatory data and different set of results were reported. Appropriate authors were cited in both papers.

Automated tracing of horizontal neuron processes during retinal development.

In the developing mammalian retina, horizontal neurons undergo a dramatic reorganization of their processes shortly after they migrate to their appropriate laminar position. This is an important process because it is now understood that the apical processes are important for establishing the regular mosaic of horizontal cells in the retina and proper reorganization during lamination is required for synaptogenesis with photoreceptors and bipolar neurons. However, this process is difficult to study because the analysis of horizontal neuron anatomy is labor intensive and time-consuming. In this paper, we present a computational method for automatically tracing the three-dimensional (3-D) dendritic structure of horizontal retinal neurons in two-photon laser scanning microscope (TPLSM) imagery. Our method is based on 3-D skeletonization and is thus able to preserve the complex structure of the dendritic arbor of these cells. We demonstrate the effectiveness of our approach by comparing our tracing results against two sets of semi-automated traces over a set of 10 horizontal neurons ranging in age from P1 to P5. We observe an average agreement level of 81% between our automated trace and the manual traces. This automated method will serve as an important starting point for further refinement and optimization.

Drebrin-mediated microtubule-actomyosin coupling steers cerebellar granule neuron nucleokinesis and migration pathway selection.

Neuronal migration from a germinal zone to a final laminar position is essential for the morphogenesis of neuronal circuits. While it is hypothesized that microtubule-actomyosin crosstalk is required for a neuron's 'two-stroke' nucleokinesis cycle, the molecular mechanisms controlling such crosstalk are not defined. By using the drebrin microtubule-actin crosslinking protein as an entry point into the cerebellar granule neuron system in combination with super-resolution microscopy, we investigate how these cytoskeletal systems interface during migration. Lattice light-sheet and structured illumination microscopy reveal a proximal leading process nanoscale architecture wherein f-actin and drebrin intervene between microtubules and the plasma membrane. Functional perturbations of drebrin demonstrate that proximal leading process microtubule-actomyosin coupling steers the direction of centrosome and somal migration, as well as the switch from tangential to radial migration. Finally, the Siah2 E3 ubiquitin ligase antagonizes drebrin function, suggesting a model for control of the microtubule-actomyosin interfaces during neuronal differentiation.

Restoring auditory cortex plasticity in adult mice by restricting thalamic adenosine signaling.

Circuits in the auditory cortex are highly susceptible to acoustic influences during an early postnatal critical period. The auditory cortex selectively expands neural representations of enriched acoustic stimuli, a process important for human language acquisition. Adults lack this plasticity. Here we show in the murine auditory cortex that juvenile plasticity can be reestablished in adulthood if acoustic stimuli are paired with disruption of ecto-5'-nucleotidase-dependent adenosine production or A1-adenosine receptor signaling in the auditory thalamus. This plasticity occurs at the level of cortical maps and individual neurons in the auditory cortex of awake adult mice and is associated with long-term improvement of tone-discrimination abilities. We conclude that, in adult mice, disrupting adenosine signaling in the thalamus rejuvenates plasticity in the auditory cortex and improves auditory perception.

Correlation filters with controlled scale response.

Correlation filtering methods are becoming increasingly popular for image recognition and location. The recent introduction of optimal tradeoff circular harmonic function filters allowed the user to specify the response of a correlation filter to in-plane rotation distortion. In this paper we introduce a new correlation filter design that can provide a user-specified response to in-plane scale distortion. The design is based on the Mellin radial harmonic (MRH) transform and incorporates multiple harmonics into the correlation filter for improved discrimination capability. Additionally, the filter design minimizes the average correlation energy in order to achieve sharp correlation peaks, and thus we refer to these filters as minimum average correlation energy Mellin radial harmonic (MACE-MRH) filters. We present underlying theory, a MACE-MRH filter design method, and numerical simulation results.

Leading-process actomyosin coordinates organelle positioning and adhesion receptor dynamics in radially migrating cerebellar granule neurons.

BACKGROUND: During brain development, neurons migrate from germinal zones to their final positions to assemble neural circuits. A unique saltatory cadence involving cyclical organelle movement (e.g., centrosome motility) and leading-process actomyosin enrichment prior to nucleokinesis organizes neuronal migration. While functional evidence suggests that leading-process actomyosin is essential for centrosome motility, the role of the actin-enriched leading process in globally organizing organelle transport or traction forces remains unexplored. RESULTS: We show that myosin ii motors and F-actin dynamics are required for Golgi apparatus positioning before nucleokinesis in cerebellar granule neurons (CGNs) migrating along glial fibers. Moreover, we show that primary cilia are motile organelles, localized to the leading-process F-actin-rich domain and immobilized by pharmacological inhibition of myosin ii and F-actin dynamics. Finally, leading process adhesion dynamics are dependent on myosin ii and F-actin. CONCLUSIONS: We propose that actomyosin coordinates the overall polarity of migrating CGNs by controlling asymmetric organelle positioning and cell-cell contacts as these cells move along their glial guides.

Analysis of tight junction formation and integrity.

In this paper, we study segmentation of tight junctions and analyze the formation and integrity of tight junctions in large-scale confocal image stacks, a challenging biological problem because of the low spatial resolution images and the presence of breaks in tight junction structure. We present an automated, three-step processing approach for tight junction analysis. In our approach, we first localize each individual nucleus in the image by using thresholding, morphological filters and active contours. By using each nucleus position as a seed point, we automatically segment the cell body based on the active contour. We then use an intensity-based skeletonization algorithm to generate the boundary regions for each cell, and features are extracted from tight junctions associated with each cell to assess tight junction continuity. Based on qualitative results and quantitative comparisons, we show that we are able to automatically segment tight junctions and compute relevant features that provide a quantitative measure of tight junction formation to which the permeability of the cell monolayer can ultimately be correlated.

Automated 3-D tracking of centrosomes in sequences of confocal image stacks.

In order to facilitate the study of neuron migration, we propose a method for 3-D detection and tracking of centrosomes in time-lapse confocal image stacks of live neuron cells. We combine Laplacian-based blob detection, adaptive thresholding, and the extraction of scale and roundness features to find centrosome-like objects in each frame. We link these detections using the joint probabilistic data association filter (JPDAF) tracking algorithm with a Newtonian state-space model tailored to the motion characteristics of centrosomes in live neurons. We apply our algorithm to image sequences containing multiple cells, some of which had been treated with motion-inhibiting drugs. We provide qualitative results and quantitative comparisons to manual segmentation and tracking results showing that our average motion estimates agree to within 13% of those computed manually by neurobiologists.

Myosin II motors and F-actin dynamics drive the coordinated movement of the centrosome and soma during CNS glial-guided neuronal migration.

Lamination of cortical regions of the vertebrate brain depends on glial-guided neuronal migration. The conserved polarity protein Par6alpha localizes to the centrosome and coordinates forward movement of the centrosome and soma in migrating neurons. The cytoskeletal components that produce this unique form of cell polarity and their relationship to polarity signaling cascades are unknown. We show that F-actin and Myosin II motors are enriched in the neuronal leading process and that Myosin II activity is necessary for leading process actin dynamics. Inhibition of Myosin II decreased the speed of centrosome and somal movement, whereas Myosin II activation increased coordinated movement. Ectopic expression or silencing of Par6alpha inhibited Myosin II motors by decreasing Myosin light-chain phosphorylation. These findings suggest leading-process Myosin II may function to "pull" the centrosome and soma forward during glial-guided migration by a mechanism involving the conserved polarity protein Par6alpha.