2,892 research outputs found
Letter from Ralph H. Cameron to Carl Hayden
No full textLetter from Ralph H. Cameron asking to speak to Carl Hayden concerning a matter relevant to the bill granting National Park status to the Grand Canyon
Letter from Carl Hayden to Ralph H. Cameron
No full textLetter from Carl Hayden to Ralph H. Cameron responding favorably to a request to meet in regards to the bill granting National Park status to the Grand Canyon
Letter from Ralph H. Cameron to Carl Hayden
No full textLetter from Ralph H. Cameron to Carl Hayden thanking him for forwarding Senate Bill No. 390 with the report of March 31st, 1918, and expressing interest in their upcoming meeting in Washington
Letter from Ralph H. Cameron to Carl Hayden
No full textLetter from Ralph H. Cameron to Carl Hayden requesting a delay on the introduction of the Grand Canyon bill until he can meet with himself and Senator Ashurst in Washington
Native drama entitled The panting patriot of the pattern parliament, or The palmy parient of the peerless prodigies : in five acts / by the author.
No full textAttributed to Ralph Delaney. Refer to Morris Miller's Australian literature 1795-1938, p. 377.; Electronic reproduction. Canberra, A.C.T. : National Library of Australia, 2013.; ANL's copy lacks cover and is slightly damaged.Panting patriot of the pattern parliament.Palmy parient of the peerless prodigies
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Life History of Ralph W. Spitzer
No full textA detailed biographical sketch of Ralph W. Spitzer (b. 1918), a graduate student of Linus Pauling's and promising academic who joined the Oregon State College chemistry department in 1946. Promoted to Assistant Professor in 1947, Spitzer was nonetheless fired from the OSC faculty in 1949 by President August L. Strand, almost certainly because of progressive political views espoused by Spitzer and his wife Teresa. Spitzer eventually matriculated to Canada where he earned an M.D. specializing in chemical pathology and co-founded a successful diagnostic laboratory firm, C.J. Coady Associates.
The paper is based upon a series of oral history interviews conducted by the author with Ralph Spitzer, his daughter Eloise Spitzer, and his wife Hisako Kurotaki
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Effect of Macrophage Activity and Age on Periodontal Disease in a Mouse Model
No full textBackground: Periodontal disease is an inflammatory disease that increases in prevalence with increasing age. The elderly demonstrate an elevated and dysregulated inflammatory response. Macrophages act as a key regulator of inflammation. The study aim was to evaluate the extent to which age-related changes and chemical inhibition in the macrophage affect periodontal disease in a mouse model. Methods: Old (24 month) and young (3 month) mice were utilized for this study. Periodontal status was examined in mice at baseline. Periodontal disease was induced via Porphyromonas gingivalis (P. gingivalis) inoculated ligatures in old and young mice for 7 days. A second cohort had disease induced for 7 days, followed by ligature removal, and recovery for 7 additional days. Half the mice in each induction or recovery group were treated with Pexidartinib (PLX), which inhibits macrophage recruitment. Linear bone loss, alveolar bone volume, and macrophage quantification were examined by t test.Results: PLX successfully inhibited macrophage numbers in all treatment groups. The young periodontal disease group had significantly more vertical bone loss (0.234±0.024mm) compared to the young periodontal disease PLX group (0.140±0.023mm)(p≤0.001) and less alveolar bone volume (0.460±0.016BV/TV) compared to the young periodontal disease PLX group (0.586±0.004BV/TV)(p≤0.001). The old periodontal disease group exhibited no difference in vertical bone loss (0.242±0.025mm) compared to the old periodontal disease PLX group (0.238±0.032mm)(p=0.825) and significantly less alveolar bone volume (0.536±0.030BV/TV) compared to the old periodontal disease PLX group (0.614±0.030BV/TV)(p≤0.01). The young recovery control group trended towards less vertical bone loss (0.170±0.020mm) compared to the young recovery + PLX group (0.190±0.011mm)(p=0.055) and had no difference in alveolar bone volume (0.557±0.015 BV/TV) compared to the young recovery PLX group (0.545±0.011 BV/TV)(p=0.131). The old recovery control group exhibited no difference in vertical bone loss (0.241±0.019mm) compared to the old recovery PLX group (0.218±0.035mm)(p=0.187) and had significantly less alveolar bone volume (0.567±0.021BV/TV) compared to the old recovery PLX group (0.617±0.023BV/TV)(p≤0.01).Conclusion:PLX prevents periodontal disease induction in old and young groups and improves recovery in older age groups. The difference in response during recovery could suggest that there are age related changes in the macrophage that affect disease progression
William E. Hoy, letter to Mr. Ralph Elliot Lin Weber, July 8, 1943, with envelope and newspaper articles
No full textThis letter was sent from William E. Hoy to Mr. Ralph Elliot Lin Weber and is dated July 8, 1943. The letter recounts information about the only baseball game where Hoy, a deaf athlete, was at-bat against Taylor, also a deaf athlete. Mentioned in the letter is a typewritten play by play of the same game, copied from the Enquirer of May 17, 1902. Also included is an envelope and newspaper articles. The envelope, from International League Information, is addressed to Ralph E Lin Weber and has handwritten lists of players of N.Y. and Cincinnati. The newspaper articles are from the Dayton Daily News and the Cincinnati Enquirer and feature pictures of William E. Hoy, the author of the letter
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The New Face of Cilia: How the Cell's Antenna Coordinates Midfacial Development
No full textPrimary cilia are ubiquitous microtubule-based organelles that coordinate multiple signaling pathways critical for craniofacial development including Hedgehog, Wnt, and PDGF. Ciliary dysfunction causes a range of human disorders, collectively referred to as ciliopathies, many of which display craniofacial defects such as cleft lip/palate, micrognathia, midface dysplasia, and craniosynostosis. This dissertation explores how defects in the transition zone complex- a ciliary gatekeeper- results in a narrowing or collapse of the midface utilizing transgenic and knockout mouse models. Developmental analysis uncovered that the first molecular defects occur in the prechordal plate, a central organizing center in the developing midface. These early prechordal plate defects were transmitted to the adjacent developing forebrain resulting in a massive increase in cell death and culminating in collapse of the midface. Surprisingly, we could fully rescue the midface defects in multiple transition zone mutants by decreasing Ptch1 gene dosage. These results have uncovered the molecular underpinnings underlying craniofacial dysmorphology in a group of poorly characterized ciliopathies and hold powerful clinical implications for future strategies aimed at treatment and prevention of these defects
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Deficiency in immunoadaptor protein DAP12 leads to altered fracture repair
No full textPurpose: To determine if genetically deficient DAP12 mice demonstrate impaired fracture healing responses. Methods: All studies were performed under IACUC approval. Genetically deficient DAP12 and age-matched C57BL/(6) (B6) control mice were used. The right tibia was cleaned and prepped for surgery and a closed, mid-diaphysis fracture was created. The fractures remained unstabilized to promote healing through the formation of a cartilage intermediate. Mice were sacrificed at 7, 10, 14, 21, and 28 days post fracture and processed for histology by decalcifying the tibia and embedding the samples into paraffin wax. Serial sections were collected through the callus and every tenth slide was stained with Milligan’s Trichrome, which stains for bone tissue. Using stereology, the volume of the fracture callus, cartilage, bone, bone marrow, and fibrous tissue was determined.Results: Histological and stereological analysis demonstrated less trabecular bone percentage and volume, increased and delayed cartilage resorption, decreased bone marrow volume, and decreased overall callus volume in the DAP12-/-. Furthermore, DAP12-/- mice displayed elevated levels of fibrous tissue within the callus. Statistical significance was not observed in the callus volume between the DAP12-/- and control B6 mice. Conclusion: Our data indicates that DAP12 deficiency disrupts the fracture healing process. Enhancing the understanding behind the mechanism of fracture repair can lead to improve healing strategies and potential therapeutics
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