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Block Card 2967 Gracewood Road
No full textThis image was produced by the Auditor's Office in Lucas County, Ohio for tax assessment purposes. Associated dates are approximate. Descriptive terms related to this photograph include: Garrison colonial | Dwelling | 2967 Gracewood Road (Toledo, Ohio) | Gracewood Place Addition (Toledo, Ohio) | Willys Park area (Toledo, Ohio) | West Toledo (Toledo, Ohio
Linked collectors and determiners for: Occurrence of invertebrates from all over Africa in natural history museum collection in Nairobi, Kenya.
No full textNatural history specimen data linked to collectors and determiners held within, "Occurrence of invertebrates from all over Africa in natural history museum collection in Nairobi, Kenya". Claims or attributions were made on Bionomia by volunteer Scribes, <a href="http://bionomia.net/dataset/3b8eb92e-2967-42a7-9027-2351e6956813">https://bionomia.net/dataset/3b8eb92e-2967-42a7-9027-2351e6956813</a> using specimen data from the dataset aggregated by the Global Biodiversity Information Facility, <a href="https://gbif.org/dataset/3b8eb92e-2967-42a7-9027-2351e6956813">https://gbif.org/dataset/3b8eb92e-2967-42a7-9027-2351e6956813</a>. Formatted as a Frictionless Data package
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Abstract 2967: The mammalian 8-oxo-dGTPase, MTH1, as a novel targetable vulnerability in pancreatic ductal adenocarcinoma
No full textAbstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive KRAS-driven cancer that remains one of the most lethal of all human malignancies. Oncogenic KRAS relies on elevated reactive oxygen species (ROS) to support pro-tumorigenic signaling. However, these elevated ROS levels can also evoke tumor suppressive oxidative stress; thus KRAS-driven cancers must evolve protective redox adaptations to mitigate ROS-induced anti-tumor consequences. Here we report a unique adaptation centered on redox maintenance of nucleotide pool integrity, that supports aggressive PDAC tumorigenesis. MTH1 is the main mammalian 8-oxodGTPase that is known to be elevated in various RAS-driven cancers including PDAC. We have previously shown MTH1 is critical for ROS-mediated oncogenic signaling, and promotes escape from oncogene-induced senescence. We therefore hypothesized that MTH1 provides important redox support for aggressive PDAC tumor growth. Consistent with this, we found that elevated MTH1 expression was strongly correlated with poor disease-free survival in PDAC patients. These findings extended to KRAS-driven PDAC cell lines: highly proliferative human PDAC cells strongly expressed MTH1 (MTH1high), and MTH1 deletion was selectively anti-tumorigenic against MTH1high cells. Furthermore, introduction of MTH1-null backgrounds into gold standard genetically engineered PDAC mouse models selectively decreased 8-oxodGTPase activity levels and slowed PDAC growth in aggressive, short latency Ptf1acre/+;LSL-KrasG12D/+;Tgfbr2flox/flox (PKT) mice, but with no effect in longer latency Pdx1Cre; LSL- KrasG12D/+; LSL-Trp53R172H/+ (KPC) mice. These selective anti-tumorigenic effects were accompanied by a reduction in circulating immunosuppressive cytokines in PKT mice, further suggesting that MTH1 potentially supports aggressive tumorigenesis through induction of systemic immunosuppression. Consistent with this, pancreatic-restricted MTH1 conditional deletion fully rescued PDAC growth in PKT mice. Our findings here thus suggest that MTH1-dependent redox protection of the nucleotide pool represents a unique TME adaptation that supports aggressive PDAC tumorigenesis. Further studies will investigate whether this adaptation is maintained through symbiotic tumor/stroma or tumor/immune cell crosstalk, as observed for other KRAS-driven traits. Ultimately, interventions designed to target MTH1-dependent protection of the nucleotide pool could hold promise as novel therapeutic strategies for this untreatable disease. Citation Format: Beatriz Mateo-Victoriano, Ling Zhang, Jaya Samaranayake, Z McGaughey, Cassie Due, Clara Troccoli, Michael G. Mohsen, Nagaraj Nagathihalli, Oliver G. McDonald, Michael VanSaun, Eric T. Kool, Priyamvada Rai. The mammalian 8-oxo-dGTPase, MTH1, as a novel targetable vulnerability in pancreatic ductal adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2967
Morse, Alexander Porter, 1842-1921 (SC 2967)
Full text linkFinding aid and full-text transcription (Click on Additional Files below) of Manuscripts Small Collection 2967. Letter, 9 December 1861, of A. P. Morse, serving with the First Louisiana Cavalry. Writing to his father from camp near Bowling Green, Kentucky, he describes troop numbers, movements and fortifications in the area. He also refers to an outbreak of measles and to dining with an officer involved in the Battle of Belmont near Columbus, Kentucky
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
D-2967-7: 1603 Sunset Drive, Logan, Utah, Glen L. and Alda R. Allan residence
No full textD-2967-7: 1603 Sunset Drive, Logan, Utah, Glen L. and Alda R. Allan residenc
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