163 research outputs found

    Wintering cows on hay: Eastern Oklahoma winter feeding demonstration

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    The Oklahoma Cooperative Extension Service periodically issues revisions to its publications. The most current edition is made available. For access to an earlier edition, if available for this title, please contact the Oklahoma State University Library Archives by email at [email protected] or by phone at 405-744-6311

    Site-Specific Metal Chelation Facilitates the Unveiling of Hidden Coordination Sites in an Fe II/Fe III -Seamed Pyrogallol[4]arene Nanocapsule

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    Under suitable conditions, C-alkylpyrogallol­[4]­arenes (PgCs) arrange into spherical metal–organic nanocapsules (MONCs) upon coordination to appropriate metal ions. Herein we present the synthesis and structural characterization of a novel FeII/FeIII-seamed MONC, as well as studies related to its electrochemical and magnetic behaviors. Unlike other MONCs that are assembled through 24 metal ions, this nanocapsule comprises 32 Fe ions, uncovering 8 additional coordination sites situated between the constituent PgC subunits. The FeII ions are likely formed by the reducing ability of DMF used in the synthesis, representing a novel synthetic route toward polynuclear mixed-valence MONCs

    Knockout and transgenic mice of Trp53: what have we learned about p53 in breast cancer?

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    The human p53 tumor suppressor gene TP53 is mutated at a high frequency in sporadic breast cancer, and Li-Fraumeni syndrome patients who carry germline mutations in one TP53 allele have a high incidence of breast cancer. In the 10 years since the first knockout of the mouse p53 tumor suppressor gene (designated Trp53) was published, much has been learned about the contribution of p53 to biology and tumor suppression in the breast through the use of p53 transgenic and knockout mice. The original mice deficient in p53 showed no mammary gland phenotype. However, studies using BALB/c-Trp53-deficient mice have demonstrated a delayed involution phenotype and a mammary tumor phenotype. Together with other studies of mutant p53 transgenes and p53 bitransgenics, a greater understanding has been gained of the role of p53 in involution, of the regulation of p53 activity by hormones, of the effect of mouse strain and modifier genes on tumor phenotype, and of the cooperation between p53 and other oncogenic pathways, chemical carcinogens and hormonal stimulation in mammary tumorigenesis. Both p53 transgenic and knockout mice are important in vivo tools for understanding breast cancer, and are yet to be exploited for developing therapeutic strategies in breast cancer

    De novo design of potent and resilient hACE2 decoys to neutralize SARS-CoV-2

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    We developed a de novo protein design strategy to swiftly engineer decoys for neutralizing pathogens that exploit extracellular host proteins to infect the cell. Our pipeline allowed the design, validation, and optimization of de novo hACE2 decoys to neutralize SARS-CoV-2. The best decoy, CTC-445.2, binds with low nanomolar affinity and high specificity to the RBD of the spike protein. Cryo-EM shows that the design is accurate and can simultaneously bind to all three RBDs of a single spike protein. Because the decoy replicates the spike protein target interface in hACE2, it is intrinsically resilient to viral mutational escape. A bivalent decoy, CTC-445.2d, shows ~10-fold improvement in binding. CTC-445.2d potently neutralizes SARS-CoV-2 infection of cells in vitro and a single intranasal prophylactic dose of decoy protected Syrian hamsters from a subsequent lethal SARS-CoV-2 challenge

    Lower export production during glacial periods in the equatorial Pacific derived from (231Pa/230Th)xs,0 measurements in deep-sea sediments

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    Author Posting. © American Geophysical Union, 2004. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Paleoceanography 19 (2004): PA4023, doi:10.1029/2003PA000994.The (231Pa/230Th)xs,0 records obtained from two cores from the western (MD97-2138; 1°25′S, 146°24′E, 1900 m) and eastern (Ocean Drilling Program Leg 138 Site 849, 0°11.59′N, 110°31.18′W, 3851 m) equatorial Pacific display similar variability over the last 85,000 years, i.e., from isotopic stages 1 to 5a, with systematically higher values during the Holocene, isotopic stage 3, and isotopic stage 5a, and lower values, approaching the production rate ratio of the two isotopes (0.093), during the colder periods corresponding to isotopic stages 2 and 4. We have also measured the 230Th-normalized biogenic preserved and terrigenous fluxes, as well as major and trace elements concentrations, in both cores. The (231Pa/230Th)xs,0 results combined with the changes in preserved carbonate and opal fluxes at the eastern site indicate lower productivity in the eastern equatorial Pacific during glacial periods. The (231Pa/230Th)xs,0 variations in the western equatorial Pacific also seem to be controlled by productivity (carbonate and/or opal). The generally high (231Pa/230Th)xs,0 ratios (>0.093) of the profile could be due to opal and/or MnO2 in the sinking particles. The profiles of (231Pa/230Th)xs,0 and 230Th-normalized fluxes indicate a decrease in exported carbonate, and possibly opal, during isotopic stages 2 and 4 in MD97-2138. Using 230Th-normalized flux, we also show that sediments from the two cores were strongly affected by sediment redistribution by bottom currents suggesting a control of mass accumulation rates by sediment focusing variability.SP funding for this research was provided by grants from the French Minister of Research and a EURODOC grant of the Re´gion Rhoˆne-Alpes (SAFIR-980065327). SP also gratefully acknowledges the financial support of the WHOI Geology and Geophysics Dept. This work was also supported by a CNRS-NSF grant (SP and KWWS). The contribution of JFM to this study was supported in part by the US NSF and by WHOI OCCI and Mellon awards

    Repression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) but not its receptors during oral cancer progression

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    BACKGROUND: TRAIL plays an important role in host immunosurveillance against tumor progression, as it induces apoptosis of tumor cells but not normal cells, and thus has great therapeutic potential for cancer treatment. TRAIL binds to two cell-death-inducing (DR4 and DR5) and two decoy (DcR1, and DcR2) receptors. Here, we compare the expression levels of TRAIL and its receptors in normal oral mucosa (NOM), oral premalignancies (OPM), and primary and metastatic oral squamous cell carcinomas (OSCC) in order to characterize the changes in their expression patterns during OSCC initiation and progression. METHODS: DNA microarray, immunoblotting and immunohistochemical analyses were used to examine the expression levels of TRAIL and its receptors in oral epithelial cell lines and in archival tissues of NOM, OPM, primary and metastatic OSCC. Apoptotic rates of tumor cells and tumor-infiltrating lymphocytes (TIL) in OSCC specimens were determined by cleaved caspase 3 immunohistochemistry. RESULTS: Normal oral epithelia constitutively expressed TRAIL, but expression was progressively lost in OPM and OSCC. Reduction in DcR2 expression levels was noted frequently in OPM and OSCC compared to respective patient-matched uninvolved oral mucosa. OSCC frequently expressed DR4, DR5 and DcR1 but less frequently DcR2. Expression levels of DR4, DR5 and DcR1 receptors were not significantly altered in OPM, primary OSCC and metastatic OSCC compared to patient-matched normal oral mucosa. Expression of proapoptotic TRAIL-receptors DR4 and DR5 in OSCC seemed to depend, at least in part, on whether or not these receptors were expressed in their parental oral epithelia. High DR5 expression in primary OSCC correlated significantly with larger tumor size. There was no significant association between TRAIL-R expression and OSSC histology grade, nodal status or apoptosis rates of tumor cells and TIL. CONCLUSION: Loss of TRAIL expression is an early event during oral carcinogenesis and may be involved in dysregulation of apoptosis and contribute to the molecular carcinogenesis of OSCC. Differential expressions of TRAIL receptors in OSCC do not appear to play a crucial role in their apoptotic rate or metastatic progression
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