Evaluating the Capability of OpenStreetMap for Estimating Vehicle Localization Error

Accurate localization is an important part of successful autonomous driving. Recent studies suggest that when using map-based localization methods, the representation and layout of real-world phenomena within the prebuilt map is a source of error. To date, the investigations have been limited to 3D point clouds and normal distribution (ND) maps. This paper explores the potential of using OpenStreetMap (OSM) as a proxy to estimate vehicle localization error. Specifically, the experiment uses random forest regression to estimate mean 3D localization error from map matching using LiDAR scans and ND maps. Six map evaluation factors were defined for 2D geographic information in a vector format. Initial results for a 1.2 km path in Shinjuku, Tokyo, show that vehicle localization error can be estimated with 56.3% model prediction accuracy with two existing OSM data layers only. When OSM data quality issues (inconsistency and completeness) were addressed, the model prediction accuracy was improved to 73.1%

Peroxisome proliferator-activated receptor α-independent peroxisome proliferation

Hepatic peroxisome proliferation, increases in the numerical and volume density of peroxisomes, is believed to be closely related to peroxisome proliferator-activated receptor α (PPARα) activation; however, it remains unknown whether peroxisome proliferation depends absolutely on this activation. To verify occurrence of PPARα-independent peroxisome proliferation, fenofibrate treatment was used, which was expected to significantly enhance PPARα dependence in the assay system. Surprisingly, a novel type of PPARα-independent peroxisome proliferation and enlargement was uncovered in PPARα-null mice. The increased expression of dynamin-like protein 1, but not peroxisome biogenesis factor 11α, might be associated with the PPARα-independent peroxisome proliferation at least in part.ArticleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 346(4): 1307-1311(2006)journal articl

RANKL directly induces bone morphogenetic protein-2 expression in RANK-expressing POS-1 osteosarcoma cells

International audienceThe POS-1 murine model of osteolytic osteosarcoma was used to elucidate the molecular and cellular mechanisms involved in the development of primary bone tumors and associated lung metastasis. The POS-1 cell line is derived from an osteosarcoma tumor which develops spontaneously in C3H mice. The POS-1 cell line was characterized in vitro by mineralization capacity and expression of bone markers by semi-quantitative RT-PCR, compared to primary osteoblasts and bone marrow cells. POS-1 cells showed no mineralization capacity and exhibited an undifferentiated phenotype, expressing both osteoblastic and unexpected osteoclastic markers (TRAP, cathepsin K and RANK). Thereby, experiments were performed to determine whether RANK was functional, by studying the biological activity of murine RANKL through the receptor RANK expressed on POS-1 cells. Results revealed a RANKL-induced increase in ERK phosphorylation, as well as BMP-2 induction at the mRNA and protein levels, and a decrease of POS-1 cell proliferation in the presence of 10 ng/ml RANKL. BMP-2 induction is dependent on the ERK 1/2 signal transduction pathway, as its expression is abolished in the presence of UO126, a specific synthetic inhibitor of the ERK 1/2 pathway. Moreover, a 2-fold molar excess of soluble RANK blocks the RANKL-induced BMP-2 expression, demonstrating that the biological effects of RANKL observed in POS-1 cells are mediated by RANK. This is the first report describing a functional RANK expressed on osteosarcoma cells, as shown by its ability to induce signal transduction pathways and biological activity when stimulated by RANKL

Significance of chemokine receptor expression in aggressive NK cell leukemia

ArticleLEUKEMIA. 19(7): 1169-1174 (2005)journal articl

Compensation of hologram distortion by controlling defocus component in reference beam wavefront for angle multiplexed holograms

Holographic memory has the potential to function as a recording system with a large capacity and high data-transfer-rate. Photopolymer materials are typically used as a write-once recording medium. When holograms are recorded on this medium, they can distort due to shrinkage or expansion of the materials, which degrades the reconstructed image and causes a higher bit error rate (bER) of the reproduced data. We propose optically compensating for hologram distortion by controlling aberration components in the reference beam wavefront while reproducing data, thereby improving the reproduced data quality. First, we investigated the relation between each aberration component of the reference beam and the signal to noise ratio (SNR) of the reproduced data using numerical simulation and found that horizontal tilt and the defocus component affect the SNR. Next, we experimentally evaluated the reproduced data by controlling the defocus component in the reference beam and found that the bER of the reproduced data could be decreased by controlling the defocus center with respect to the hologram position and phase modulation depth of the defocus component. Then, we investigated a practical control method of the defocus component using an evaluation value similar to the definition of the SNR for actual data reproduction from holograms. Using a defocus controlled wavefront enabled us to decrease the bER from 3.54 x 10^-3 with a plane wave to 3.14 x 10^-4. We also investigated how to reduce the bERs of reproduced data in angle multiplexed holograms. By using a defocus controlled wavefront to compensate for hologram distortion on the 40th data page in 80-page angle multiplexed holograms, the bERs of all pages could be decreased to less than 1x10^-3. We showed that controlling the defocus component is an effective way to compensate for hologram distortion and to decrease the bER of reproduced data in holographic memory

Possible Relationship between Helicobacter pylori Infection and Cap Polyposis of the Colon

The definitive version is available at www.blackwell-synergy.com.ArticleHELICOBACTER. 9(6): 651-656 (2004)journal articl