17,810 research outputs found
STAT4 AND BLK BUT NOT BANK1 OR IRF5 ARE ASSOCIATED WITH THE PRIMARY ANTIPHOSPHOLIPID SYNDROME
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The Story of "Me" Contemporary American Autofiction
No full textCover -- Title Page -- Copyright Page -- Contents -- Acknowledgments -- Introduction -- 1. Masculinity, Whiteness, and Postmodern Self-Consciousness -- 2. Rage against the Dying of the Author -- 3. The New Journalism as the New Fiction -- 4. Trauma Autofiction, Dissociation, and the Authenticity of "Real" Experience -- 5. Memoir vs. Autofiction as the Story of Me vs. the Story of "Me" -- Coda -- Appendix -- Notes -- References -- IndexDescription 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
IRF5 is associated with primary antiphospholipid syndrome,but is not a major risk factor
No full textAssociation of STAT4 and BLK, but not BANK1 or IRF5, with primary antiphospholipid syndrome.
No full textEndpoint Sobolev bounds for fractional Hardy–Littlewood maximal operators
No full textFunding Information: I would like to thank my supervisor, Juha Kinnunen, for all of his support. I would like to thank Olli Saari for introducing me to this problem. I am also thankful for the discussions with Juha Kinnunen, Panu Lahti and Olli Saari who made me aware of a version of the coarea formula [, Theorem 3.11], which was used in the first draft of the proof, and for discussions with David Beltran, Cristian González-Riquelme and Jose Madrid, in particular about the centered fractional maximal operator. The author has been supported by the Vilho, Yrjö and Kalle Väisälä Foundation of the Finnish Academy of Science and Letters. Publisher Copyright: © 2022, The Author(s).Let 0 0 the fractional maximal function does not use certain small balls. For α= 0 the proof collapses.Peer reviewe
New Attempts to Define and Clarify Lupus
No full textThe purpose is to discuss the advances that genetics and genomics have provided to better understand the molecular mechanisms behind SLE and how to solve its heterogeneity. I propose new ideas that can help us stratify lupus in order to find the best therapies for each patient, and the idea of substituting clinical diagnosis with molecular diagnosis according to their molecular patterns, an idea that may not only include lupus but also other diseases. The study of rare mutations may provide insight into groups of lupus patients where type I interferon signature is important and help understand those with an atypical clinical presentation. Recent papers used longitudinal blood transcriptome data correlating with disease activity scores to stratify lupus into molecular clusters. The implication of neutrophils in the risk to develop nephritis was established, but also that neutrophils and lymphocytes may correlate with activity differentiating the mechanisms of flares and separating patients into clinically separate groups. The role of type I interferon signature is important; however, the stratification of SLE patients according to the genes and cellular compartments being modulated during disease activity may be even more important to define those patients who may benefit the most with new anti-type I IFN receptor therapies
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