Where's Whaledo: A software toolkit for array localization of animal vocalizations.

Where's Whaledo is a software toolkit that uses a combination of automated processes and user interfaces to greatly accelerate the process of reconstructing animal tracks from arrays of passive acoustic recording devices. Passive acoustic localization is a non-invasive yet powerful way to contribute to species conservation. By tracking animals through their acoustic signals, important information on diving patterns, movement behavior, habitat use, and feeding dynamics can be obtained. This method is useful for helping to understand habitat use, observe behavioral responses to noise, and develop potential mitigation strategies. Animal tracking using passive acoustic localization requires an acoustic array to detect signals of interest, associate detections on various receivers, and estimate the most likely source location by using the time difference of arrival (TDOA) of sounds on multiple receivers. Where's Whaledo combines data from two small-aperture volumetric arrays and a variable number of individual receivers. In a case study conducted in the Tanner Basin off Southern California, we demonstrate the effectiveness of Where's Whaledo in localizing groups of Ziphius cavirostris. We reconstruct the tracks of six individual animals vocalizing concurrently and identify Ziphius cavirostris tracks despite being obscured by a large pod of vocalizing dolphins.

Bayesian detection and tracking of odontocetes in 3-D from their echolocation clicks.

Localization and tracking of marine animals can reveal key insights into their behaviors underwater that would otherwise remain unexplored. A promising nonintrusive approach to obtaining location information of marine animals is to process their bioacoustic signals, which are passively recorded using multiple hydrophones. In this paper, a data processing chain that automatically detects and tracks multiple odontocetes (toothed whales) in three dimensions (3-D) from their echolocation clicks recorded with volumetric hydrophone arrays is proposed. First, the time-difference-of-arrival (TDOA) measurements are extracted with a generalized cross-correlation that whitens the received acoustic signals based on the instrument noise statistics. Subsequently, odontocetes are tracked in the TDOA domain using a graph-based multi-target tracking (MTT) method to reject false TDOA measurements and close gaps of missed detections. The resulting TDOA estimates are then used by another graph-based MTT stage that estimates odontocete tracks in 3-D. The tracking capability of the proposed data processing chain is demonstrated on real acoustic data provided by two volumetric hydrophone arrays that recorded echolocation clicks from Cuvier's beaked whales (Ziphius cavirostris). Simulation results show that the presented MTT method using 3-D can outperform an existing approach that relies on manual annotation.

Tempol protects against oxidative damage and delays epithelial tumor onset in Fanconi anemia mice.

Fanconi anemia (FA) is a genetic disorder characterized by congenital abnormalities, bone marrow failure, and marked cancer susceptibility. FA patients have an elevated risk of developing hematologic malignancies and solid tumors. Using Fancd2(-/-) knockout mice as a model of FA, we examined the potential of tempol, a nitroxide antioxidant and a superoxide dismutase mimetic, as a tumor-delaying agent for solid tumors. Dietary tempol increased the mean tumor-free survival time of Fancd2(-/-) Trp53(+/-) mice by 27% (P < 0.01), from 308 to 390 days, without changing the overall tumor spectrum. More strikingly, tempol delayed the onset of epithelial tumors and increased the mean epithelial tumor-free survival time by 38% (P < 0.0001), from 312 to 432 days, in Fancd2(-/-) Trp53(+/-) mice. These results show that tempol can significantly delay tumor formation in Fancd2(-/-) Trp53(+/-) mice. Furthermore, tempol treatment did not adversely affect the repopulating ability of FA hematopoietic stem cells. The reduction in oxidative DNA damage in tempol-treated FA fibroblasts and mice suggests that its tumor-delaying function may be attributed to its antioxidant activity.

Variation in cisplatinum sensitivity is not associated with Fanconi Anemia/BRCA pathway inactivation in head and neck squamous cell carcinoma cell lines.

Fanconi Anemia has recently been associated with a high risk of head and neck squamous cell carcinoma (HNSCC). Inactivation of the Fanconi Anemia (FANC-BRCA) pathway via promoter methylation of the FANCF gene has been proposed to be responsible for variation in cisplatinum (CDDP) sensitivity seen in ovarian and HNSCCs. Promoter methylation of the FANCF gene has been observed in 15% of HNSCC specimens, but the relationship to FANC pathway activation and CDDP sensitivity has not been reported. In the present study, 10 HNSCC cell lines were examined for expression of nine genes involved in the FANC-BRCA pathway by RT-PCR: FANCA, FANCC, FANCD2, FANCE, FANCF, FANCG, FANCL, BRCA1 and BRCA2. FANC pathway function was evaluated by western blotting for FANCD2 mono-ubiquitination. All of the cell lines were also analyzed for variation in CDDP cytotoxicity. While significant differences were found in CDDP cytotoxicity, Fanconi pathway defects are an infrequent cause, as no evidence of transcriptional down-regulation of FANCF or other FANC mRNAs, or functional FANC-BRCA pathway defects were observed. These findings suggest that the variation in CDDP sensitivity of many HNSCCs is most frequently due to factors other than FANC-BRCA pathway inactivation.