ORCA-SPOT: An Automatic Killer Whale Sound Detection Toolkit Using Deep Learning

Large bioacoustic archives of wild animals are an important source to identify reappearing communication patterns, which can then be related to recurring behavioral patterns to advance the current understanding of intra-specific communication of non-human animals. A main challenge remains that most large-scale bioacoustic archives contain only a small percentage of animal vocalizations and a large amount of environmental noise, which makes it extremely difficult to manually retrieve sufficient vocalizations for further analysis – particularly important for species with advanced social systems and complex vocalizations. In this study deep neural networks were trained on 11,509 killer whale (Orcinus orca) signals and 34,848 noise segments. The resulting toolkit ORCA-SPOT was tested on a large-scale bioacoustic repository – the Orchive – comprising roughly 19,000 hours of killer whale underwater recordings. An automated segmentation of the entire Orchive recordings (about 2.2 years) took approximately 8 days. It achieved a time-based precision or positive-predictive-value (PPV) of 93.2% and an area-under-the-curve (AUC) of 0.9523. This approach enables an automated annotation procedure of large bioacoustics databases to extract killer whale sounds, which are essential for subsequent identification of significant communication patterns. The code will be publicly available in October 2019 to support the application of deep learning to bioaoucstic research. ORCA-SPOT can be adapted to other animal species

ORCA-SPY enables killer whale sound source simulation, detection, classification and localization using an integrated deep learning-based segmentation

Acoustic identification of vocalizing individuals opens up new and deeper insights into animal communications, such as individual-/group-specific dialects, turn-taking events, and dialogs. However, establishing an association between an individual animal and its emitted signal is usually non-trivial, especially for animals underwater. Consequently, a collection of marine species-, array-, and position-specific ground truth localization data is extremely challenging, which strongly limits possibilities to evaluate localization methods beforehand or at all. This study presents ORCA-SPY, a fully-automated sound source simulation, classification and localization framework for passive killer whale (Orcinus orca) acoustic monitoring that is embedded into PAMGuard, a widely used bioacoustic software toolkit. ORCA-SPY enables array- and position-specific multichannel audio stream generation to simulate real-world ground truth killer whale localization data and provides a hybrid sound source identification approach integrating ANIMAL-SPOT, a state-of-the-art deep learning-based orca detection network, followed by downstream Time-Difference-Of-Arrival localization. ORCA-SPY was evaluated on simulated multichannel underwater audio streams including various killer whale vocalization events within a large-scale experimental setup benefiting from previous real-world fieldwork experience. Across all 58,320 embedded vocalizing killer whale events, subject to various hydrophone array geometries, call types, distances, and noise conditions responsible for a signal-to-noise ratio varying from −14.2 dB to 3 dB, a detection rate of 94.0 % was achieved with an average localization error of 7.01∘. ORCA-SPY was field-tested on Lake Stechlin in Brandenburg Germany under laboratory conditions with a focus on localization. During the field test, 3889 localization events were observed with an average error of 29.19∘ and a median error of 17.54∘. ORCA-SPY was deployed successfully during the DeepAL fieldwork 2022 expedition (DLFW22) in Northern British Columbia, with a mean average error of 20.01∘ and a median error of 11.01∘ across 503 localization events. ORCA-SPY is an open-source and publicly available software framework, which can be adapted to various recording conditions as well as animal species

Activation of NF-κB and p300/CBP potentiates cancer chemoimmunotherapy through induction of MHC-I antigen presentation

Many cancers evade immune rejection by suppressing major histocompatibility class I (MHC-I) antigen processing and presentation (AgPP). Such cancers do not respond to immune checkpoint inhibitor therapies (ICIT) such as PD-1/PD-L1 [PD-(L)1] blockade. Certain chemotherapeutic drugs augment tumor control by PD-(L)1 inhibitors through potentiation of T-cell priming but whether and how chemotherapy enhances MHC-I-dependent cancer cell recognition by cytotoxic T cells (CTLs) is not entirely clear. We now show that the lysine acetyl transferases p300/CREB binding protein (CBP) control MHC-I AgPPM expression and neoantigen amounts in human cancers. Moreover, we found that two distinct DNA damaging drugs, the platinoid oxaliplatin and the topoisomerase inhibitor mitoxantrone, strongly up-regulate MHC-I AgPP in a manner dependent on activation of nuclear factor kappa B (NF-κB), p300/CBP, and other transcription factors, but independently of autocrine IFNγ signaling. Accordingly, NF-κB and p300 ablations prevent chemotherapy-induced MHC-I AgPP and abrogate rejection of low MHC-I-expressing tumors by reinvigorated CD8+ CTLs. Drugs like oxaliplatin and mitoxantrone may be used to overcome resistance to PD-(L)1 inhibitors in tumors that had "epigenetically down-regulated," but had not permanently lost MHC-I AgPP activity

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Activation of NF-κB and p300/CBP potentiates cancer chemoimmunotherapy through induction of MHC-I antigen presentation.

Many cancers evade immune rejection by suppressing major histocompatibility class I (MHC-I) antigen processing and presentation (AgPP). Such cancers do not respond to immune checkpoint inhibitor therapies (ICIT) such as PD-1/PD-L1 [PD-(L)1] blockade. Certain chemotherapeutic drugs augment tumor control by PD-(L)1 inhibitors through potentiation of T-cell priming but whether and how chemotherapy enhances MHC-I-dependent cancer cell recognition by cytotoxic T cells (CTLs) is not entirely clear. We now show that the lysine acetyl transferases p300/CREB binding protein (CBP) control MHC-I AgPPM expression and neoantigen amounts in human cancers. Moreover, we found that two distinct DNA damaging drugs, the platinoid oxaliplatin and the topoisomerase inhibitor mitoxantrone, strongly up-regulate MHC-I AgPP in a manner dependent on activation of nuclear factor kappa B (NF-κB), p300/CBP, and other transcription factors, but independently of autocrine IFNγ signaling. Accordingly, NF-κB and p300 ablations prevent chemotherapy-induced MHC-I AgPP and abrogate rejection of low MHC-I-expressing tumors by reinvigorated CD8+ CTLs. Drugs like oxaliplatin and mitoxantrone may be used to overcome resistance to PD-(L)1 inhibitors in tumors that had "epigenetically down-regulated," but had not permanently lost MHC-I AgPP activity