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Ware, K.

Publications and source records attributed to Ware, K..

4 recordsLinked to original sources

Passive Acoustic Monitoring within the Northwest Forest Plan Area: 2024 Annual Report

Passive acoustic monitoring (PAM) has become the primary framework for assessing the status, distribution, and habitat associations of forest-dependent wildlife under the Northwest Forest Plan (NWFP). In 2024, the NWFP PAM program continued to operate as a fully integrated, range-wide monitoring network, building on deployments initiated in 2018 and now conducting surveys across approximately 24 million acres of federal land. Using a randomized 2+20% sampling design, more than 4,000 autonomous recording units generated over 2 million hours of acoustic data analyzed with convolutional neural networks, enabling statistically rigorous inference at regional and range-wide scales. This report summarizes 2024 field efforts and analytical advancements in the context of recent peer-reviewed and in-progress studies. Updated analyses confirm persistent, low occupancy of northern spotted owls (Strix occidentalis caurina), with detections concentrated in the Klamath Mountains and southern Cascades, consistent with long-term demographic declines. Range-wide models of barred owl (Strix varia) landscape use continue to show high occupancy across much of the NWFP area, reinforcing competitive displacement as the dominant driver of spotted owl range contraction. The PAM network also advanced monitoring of marbled murrelets (Brachyramphus marmoratus), with 2024 results supporting PAM as a cost-efficient alternative to traditional audio-visual surveys for assessing inland nesting habitat use in coastal forests. Beyond focal species, the program increasingly supports multi-taxa biodiversity monitoring through bioacoustic bycatch and soundscape analyses, linking species occurrence, habitat condition, and disturbance dynamics. Collectively, 2024 results demonstrate that PAM has reached operational maturity as the cornerstone of Phase II NWFP effectiveness monitoring. Sustaining adequate sampling effort and field capacity remains a challenge but essential, as reduced deployment intensity would increase uncertainty and weaken inference. Continued investment in PAM infrastructure and expertise is critical for informing adaptive management, supporting sustainable timber harvest, and evaluating ecosystem resilience under changing disturbance regimes.

ecology↗

Finding the right tool: a comprehensive evaluation of microglial inducible cre mouse models

The recent proliferation of new Cre and CreER recombinase lines provides researchers with a diverse toolkit to study microglial gene function. To determine how best to apply these lines in studies of microglial gene function, a thorough and detailed comparison of their properties is needed. Here, we examined four different microglial CreER lines (Cx3cr1CreER(Litt), Cx3cr1CreER(Jung), P2ry12CreER, Tmem119CreER), focusing on (1) recombination specificity; (2) leakiness - degree of non-tamoxifen recombination in microglia and other cells; (3) efficiency of tamoxifen-induced recombination; (4) extra-neural recombination -the degree of recombination in cells outside the CNS, particularly myelo/monocyte lineages (5) off-target effects in the context of neonatal brain development. We identify important caveats and strengths for these lines which will provide broad significance for researchers interested in performing conditional gene deletion in microglia. We also provide data emphasizing the potential of these lines for injury models that result in the recruitment of splenic immune cells.

neuroscience↗

Emergent dynamics of underlying regulatory network links EMT and androgen receptor-dependent resistance in prostate cancer

Advanced prostate cancer patients initially respond to hormone therapy, be it in the form of androgen deprivation therapy or second-generation hormone therapies, such as abiraterone acetate or enzalutamide. However, most men with prostate cancer eventually develop hormone therapy resistance. This resistance emerges in several ways, such as through genetic mutations, epigenetic mechanisms, or through non-genetic pathways, such as lineage plasticity along epithelial-mesenchymal or neuroendocrine-like axes. These mechanisms of hormone therapy resistance often co-exist within a single patients tumor and can overlap within a single cell. There exists a growing need to better understand how phenotypic heterogeneity and plasticity results from emergent dynamics of the regulatory networks governing androgen independence. Here, we investigated the dynamics of a regulatory network connecting the drivers of androgen receptor (AR) splice variant-mediated androgen independence and those of epithelial-mesenchymal transition. Model simulations for this network revealed four possible phenotypes: epithelial-sensitive (ES), epithelial-resistant (ER), mesenchymal-resistant (MR) and mesenchymal-sensitive (MS), with the latter phenotype occurring rarely. We observed that well-coordinated "teams" of regulators working antagonistically within the network enable these phenotypes. These model predictions are supported by multiple transcriptomic datasets both at single-cell and bulk levels, including in vitro EMT induction models and clinical samples. Further, our simulations reveal spontaneous stochastic switching between the ES and MR states. Addition of the immune checkpoint molecule, PD-L1, to the network was able to capture the interactions between AR, PD-L1, and the mesenchymal marker SNAIL, which was also confirmed through quantitative experiments. This systems-level understanding of the driver of androgen independence and EMT could aid in understanding non-genetic transitions and progression of such cancers and help in identifying novel therapeutic strategies or targets.

cancer biology↗

A cross-species drug discovery pipeline to identify and validate new treatments for osteosarcoma

PurposeOsteosarcoma is a rare but aggressive bone cancer that occurs primarily in children. Like other rare cancers, treatment advances for osteosarcoma have stagnated, with little improvement in survival for the past several decades. Developing new treatments has been hampered by extensive genomic heterogeneity and limited access to patient samples to study the biology of this complex disease. Experimental designTo overcome these barriers, we combined the power of comparative oncology with patient-derived models of cancer and high-throughput chemical screens in a cross-species drug discovery pipeline. ResultsCoupling in vitro high-throughput drug screens on low-passage and established cell lines with in vivo validation in patient-derived xenografts we identify the proteasome and CRM1 nuclear export pathways as therapeutic sensitivities in osteosarcoma, with dual inhibition of these pathways inducing synergistic cytotoxicity. ConclusionsThese collective efforts provide an experimental framework and set of new tools for osteosarcoma and other rare cancers to identify and study new therapeutic vulnerabilities.

cancer biology↗