149,696 research outputs found
Ron Lee photograph, Doncaster St Leger Fair, 1990.
No full textD. Tucker's Foden flat lorry - registration YWT544G - circa 1990
Understanding Ron Rash
No full textThe first book-length study of the work to date by the award-winning poet, novelist, and short story writer.Cover -- Title -- Copyright -- Contents -- Series Editor's Preface -- Acknowledgments -- Chapter 1 Understanding Ron Rash -- Chapter 2 The Night the New Jesus Fell to Earth, Casualties, and Chemistry -- Chapter 3 Eureka Mill, Among the Believers, Raising the Dead, and Waking -- Chapter 4 One Foot in Eden, Saints at the River, and The World Made Straight -- Chapter 5 Serena and The Cove -- Chapter 6 Burning Bright and Nothing Gold Can Stay -- Notes -- Bibliography -- Index -- A -- B -- C -- D -- E -- F -- G -- H -- I -- J -- K -- L -- M -- N -- O -- P -- R -- S -- T -- U -- V -- W -- YThe first book-length study of the work to date by the award-winning poet, novelist, and short story writer.Description based on publisher supplied metadata and other sources.Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, YYYY. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries
Ron Kinder photograph, Nottinghamshire -- Nottingham Goose Fair, 1986.
No full textM. and D. Taylor's Flying Carpet - FP2 - photographed 1986
Identification of the splice variants of Recepteur d'Origine nantais (RON) in lung cancer cell lines
No full textRON receptor tyrosine kinase is a transmembrane protein directly involved in suppression of inflammation and its aberrant expression linked to cancers and metastasis. Efforts to block deregulated RON signaling in tumors using small molecule kinase inhibitors or antibodies have been complicated by the presence of unknown number/types of isoforms of RON, which, despite being structurally similar, localize differently and mediate varied functions. Current study was designed to identify the splice variants of RON transcripts formed by skipping of sequences between exons 9 and 14 for better understanding of isoform specific RON signaling in cancers. PCR amplification and bi-directional sequencing of a 901 bp cDNA sequence located between exons 9 to 14 of RON from lung cancer cell lines revealed the presence of two splicing variants formed by skipping of exons 11 and 11–13. Each of these transcripts was found in more than one cell line. Expressed sequence tag (EST) database search indicated that the splicing variant lacking exons 11–13 was a novel one. Here we conclude that the splice variants of RON lacking exon 11 and exons 11–13 were detected in several lung cancer cell lines. Novel variant formed by skipping exons 11–13, the sequence of which code for transmembrane region, is predicted to code for a truncated isoform that may be secreted out. Tumors may antagonize the ligand dependent anti-inflammatory function of wild-type RON by secreting out the ligand binding isoforms
Titan: The Life of John D. Rockefeller, Sr.
No full textRon Chernov. Titan: the life of John D. Rockefeller, Sr.
Random House reviewhttps://digitalcommons.rockefeller.edu/the-rockefellers/1017/thumbnail.jp
Efficient Interactive Proofs for Non-Deterministic Bounded Space
No full textThe celebrated IP = PSPACE Theorem gives an efficient interactive proof for any bounded-space algorithm. In this work we study interactive proofs for non-deterministic bounded space computations. While Savitch’s Theorem shows that nondeterministic bounded-space algorithms can be simulated by deterministic bounded-space algorithms, this simulation has a quadratic overhead. We give interactive protocols for nondeterministic algorithms directly to get faster verifiers.
More specifically, for any non-deterministic space S algorithm, we construct an interactive proof in which the verifier runs in time Õ(n+S²). This improves on the best previous bound of Õ(n+S³) and matches the result for deterministic space bounded algorithms, up to polylog(S) factors.
We further generalize to alternating bounded space algorithms. For any language L decided by a time T, space S algorithm that uses d alternations, we construct an interactive proof in which the verifier runs in time Õ(n + S log(T) + S d) and the prover runs in time 2^O(S). For d = O(log(T)), this matches the best known interactive proofs for deterministic algorithms, up to polylog(S) factors, and improves on the previous best verifier time for nondeterministic algorithms by a factor of log(T). We also improve the best prior verifier time for unbounded alternations by a factor of S.
Using known connections of bounded alternation algorithms to bounded depth circuits, we also obtain faster verifiers for bounded depth circuits with unbounded fan-in
Plan to Restore the Vote: Ron Paul and the Third-Party Voting Dilemma
No full textTexas Congressman and Republican presidential candidate Ron Paul has been a figure in American politics for more than 40 years. While Paul has commanded a dedicated support base composed of both liberals and conservatives, he remains well behind in the 2012 Republican primary race. This article examines the hypothetical case of a Ron Paul third-party presidential run, and the dilemma that voters face between voting conscientiously for Paul and voting strategically for the most electable and ideologically similar candidate.\u
Novel splicing variants of recepteur d'origine nantais (RON) tyrosine kinase involving exons 15–19 in lung cancer
No full textBackground
Altered expressions of receptor tyrosine kinases drive the growth and metastasis of several cancers. RON is a single pass transmembrane receptor tyrosine kinase (RTK) shown to be aberrantly expressed in various cancer types. However, target validation and successful therapeutic targeting of RON in cancers is hampered by the co-existence of unknown number/types of isoforms, which are structurally similar but functionally diverse.
Objective
The objective of this study was to identify differential splicing in the C-terminal region of RON transcripts to better understand RON signaling in cancers. mRNA transcript sequence between exons 14 and 20 of RON was PCR amplified and sequenced using cDNA from 10 SCLC and 13 NSCLC cell lines. Specific exon deletions were identified by aligning sequencing chromatograms with reference RON cDNA sequence.
Results
We identified the presence of four unique transcript sequence variants of RON formed through skipping of exons 15–19, 16–19, 16–17 and 16. The transcript variants, except the one lacking exons 15–19, were found in more than one cell line. Several cell lines contained two to four of these uniquely spliced transcript variants. dbEST (Expressed Sequence Tags database) or other DNA sequence databases did not contain RON cDNA sequences corresponding to any of the above exon deletions indicating that all these transcript sequence alterations are novel.
Conclusions
Results of our study indicate common occurrence of different types of alternatively spliced transcripts of RON in lung cancer with potential to be translated into proteins lacking active kinase domain. Our findings suggest that tumors produce several dominant negative isoforms which probably inhibit ligand dependent RON signaling, and hence, raise important questions regarding the appropriateness of blocking wild type RON signaling for therapy. Further, presence of transcript variants and their isoform products may interfere with quantitative and functional analysis during target validation.
Abbreviations
MST1R, macrophage stimulating 1 receptor; RTK, receptor tyrosine kinase; MSP, macrophage stimulating protein; SCLC, small cell lung cancer; NSCLC, non-small cell lung cancer; EGFR, epidermal growth factor recepto
Recepteur d'Origine nantais (RON) tyrosine kinase splicing variants lacking exons 18 and 19 occur ubiquitously in lung cancer
No full textBackground: Aberrant expression of RON, a MET family receptor tyrosine kinase, has been correlated to tumor growth and metastasis. Intense research efforts are on to target RON using small molecule tyrosine kinase inhibitors or specific antibodies. However, progress towards specific targeting of RON is hampered by a lack of understanding of the nature and number of isoforms of RON expressed by tumors. We hypothesize that formation of different isoforms via alternative splicing may be fundamental to the tumor promoting functions associated with aberrantly expressed RON in cancers. Methods: In this study, we analyzed the transcript sequence variations caused by alternative splicing in the C-terminal region of RON cDNA by PCR amplification and sequencing of five small cell lung carcinoma (SCLC) and seven non-small cell lung carcinoma (NSCLC) cell lines. Results: Results revealed the presence of two alternatively spliced variants, each caused by unique exon(s) deletion: a previously known transcript variant lacking exon 19 and a novel one lacking exons 18+19. The two alternatively spliced variants together with the wild-type transcript were detected in each of the 12 lung cancer cell lines analyzed. Combined loss of exons 18+19 results in an in-frame deletion of 303 nucleotides corresponding to 101 amino acids of the tyrosine kinase domain. Translation products of transcript variants lacking exons 18 and 19 are expected to dominant negatively inhibit ligand stimulated RON signaling. Conclusions: The ubiquitous presence of alternatively spliced transcripts and their translation products may affect quantitative expression analysis, either by immunological or PCR methods, by interfering with estimation of normal RON, leading to exaggerated values. Besides, RON isoforms with dominant negative activities may interfere with siRNA based functional analysis of wild-type RON
Recepteur d'Origine nantais (RON) tyrosine kinase splicing variants lacking exons 18 and 19 occur ubiquitously in lung cancer
No full textAberrant expression of RON, a MET family receptor tyrosine kinase, has been correlated to tumor growth and metastasis. Intense research efforts are on to target RON using small molecule tyrosine kinase inhibitors or specific antibodies. However, progress towards specific targeting of RON is hampered by a lack of understanding of the nature and number of isoforms of RON expressed by tumors. We hypothesize that formation of different isoforms via alternative splicing may be fundamental to the tumor promoting functions associated with aberrantly expressed RON in cancers. Methods: In this study, we analyzed the transcript sequence variations caused by alternative splicing in the C-terminal region of RON cDNA by PCR amplification and sequencing of five small cell lung carcinoma (SCLC) and seven non-small cell lung carcinoma (NSCLC) cell lines. Results: Results revealed the presence of two alternatively spliced variants, each caused by unique exon(s) deletion: a previously known transcript variant lacking exon 19 and a novel one lacking exons 18+19. The two alternatively spliced variants together with the wild-type transcript were detected in each of the 12 lung cancer cell lines analyzed. Combined loss of exons 18+19 results in an in-frame deletion of 303 nucleotides corresponding to 101 amino acids of the tyrosine kinase domain. Translation products of transcript variants lacking exons 18 and 19 are expected to dominant negatively inhibit ligand stimulated RON signaling. Conclusions: The ubiquitous presence of alternatively spliced transcripts and their translation products may affect quantitative expression analysis, either by immunological or PCR methods, by interfering with estimation of normal RON, leading to exaggerated values. Besides, RON isoforms with dominant negative activities may interfere with siRNA based functional analysis of wild-type RON
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