5,822 research outputs found
Mr. Melvin J. Collier, RWWL AUC, June 2011
No full textThis video is a conversation with Mr. Melvin J. Collier. Mr. Collier talks about his book, "From Mississippi to Africa: A Journey of Discovery". Daniel Le, AUC Woodruff Library, is the interviewer
Report on Meteorological Research March 1, 1935 (m-1)
No full textThe object of the report was to elucidate in detail the various features of the research program in meteorology being carried on at the Daniel Guggenheim Airship Institute in Akron, Ohio. Mr. L. J. Fangman, of the U.S. Weather Bureau, was collaborating with the author in carrying out work such as a study of autographic records of the various meteorological elements during frontal passages with a view to the possible prediction of the intensity of the accompanying disturbance as it may affect the operation of aircraft and a study of atmospheric gustiness with a view to finding the dependence between frequency end amplitude of velocity fluctuations and the vertical temperature and velocity gradients
Daniel J. Boorstin
No full textPhotograph used for a newspaper owned by the Oklahoma Publishing Company. Caption: "Daniel J. Boorstin, author and keynote speaker.
The Meckel-Gruber syndrome protein TMEM67 controls basal body positioning and epithelial branching morphogenesis in mice via the non-canonical Wnt pathway.
No full textCiliopathies are a group of developmental disorders that manifest with multi-organ anomalies. Mutations in TMEM67 (MKS3) cause a range of human ciliopathies, including Meckel-Gruber and Joubert syndromes. In this study we describe multi-organ developmental abnormalities in the Tmem67(tm1Dgen/H1) knockout mouse that closely resemble those seen in Wnt5a and Ror2 knockout mice. These include pulmonary hypoplasia, ventricular septal defects, shortening of the body longitudinal axis, limb abnormalities, and cochlear hair cell stereociliary bundle orientation and basal body/kinocilium positioning defects. The basal body/kinocilium complex was often uncoupled from the hair bundle, suggesting aberrant basal body migration, although planar cell polarity and apical planar asymmetry in the organ of Corti were normal. TMEM67 (meckelin) is essential for phosphorylation of the non-canonical Wnt receptor ROR2 (receptor-tyrosine-kinase-like orphan receptor 2) upon stimulation with Wnt5a-conditioned medium. ROR2 also colocalises and interacts with TMEM67 at the ciliary transition zone. Additionally, the extracellular N-terminal domain of TMEM67 preferentially binds to Wnt5a in an in vitro binding assay. Cultured lungs of Tmem67 mutant mice failed to respond to stimulation of epithelial branching morphogenesis by Wnt5a. Wnt5a also inhibited both the Shh and canonical Wnt/β-catenin signalling pathways in wild-type embryonic lung. Pulmonary hypoplasia phenotypes, including loss of correct epithelial branching morphogenesis and cell polarity, were rescued by stimulating the non-canonical Wnt pathway downstream of the Wnt5a-TMEM67-ROR2 axis by activating RhoA. We propose that TMEM67 is a receptor that has a main role in non-canonical Wnt signalling, mediated by Wnt5a and ROR2, and normally represses Shh signalling. Downstream therapeutic targeting of the Wnt5a-TMEM67-ROR2 axis might, therefore, reduce or prevent pulmonary hypoplasia in ciliopathies and other congenital conditions
Dr. Daniel J. Boorstin (S2_B32_F3_33)
No full textDr. Daniel J. Boorstin-historian, author and Director of the National Museum of History and Technology at the Smithsonian Institution. He was the guest speaker at Bierce Library's Dedication Ceremony
Author Meets Reader: Not the Marrying Kind: A Feminist Critique of Same-Sex Marriage
No full textThis is an audio recording of an author meets reader session held at the SLSA Annual Conference, University of York, 27 March 2013. Nicola Barker's book, Not the Marrying Kind: A Feminist Critique of Same-Sex Marriage, was the winner of the 2013 Hart SLSA Book Prize. In the session she introduces the book and then engages in discussion about it with Daniel Monk
Defoe's Foes:The Author as Character
No full textThe most famous fictional Defoe features in J. M. Coetzee’s Foe (1986), in which he conjures Robinson Crusoe out of a memoir by a “true” castaway. Harrumphing across the country alongside the modern-day narrator of Stuart Campbell’s Daniel Defoe’s Railway Journey (2017), a surreal iteration quite literally leaps out of the pages of a Penguin Classics edition of his real-life counterpart’s travel writing. Setting aside a long tradition of neo-Georgian novels in which Defoe cameos as a seventeenth-century spy, a Defoe-as-character only for all intents and purposes, this chapter attends to two complex cases in the genre of author fictions: Coetzee’s Foe and Campbell’s Defoe
Author Talk: Daniel Herman Discusses His Novel, The Feudist
No full textPoster for an event where CWU History professor Daniel Herman discusses his historical novel The Feudisthttps://digitalcommons.cwu.edu/libraryevents/1223/thumbnail.jp
The Alström syndrome protein, ALMS1, interacts with α-actinin and components of the endosome recycling pathway.
No full textAlström syndrome (ALMS) is a progressive multi-systemic disorder characterized by cone-rod dystrophy, sensorineural hearing loss, childhood obesity, insulin resistance and cardiac, renal, and hepatic dysfunction. The gene responsible for Alström syndrome, ALMS1, is ubiquitously expressed and has multiple splice variants. The protein encoded by this gene has been implicated in ciliary function, cell cycle control, and intracellular transport. To gain better insight into the pathways through which ALMS1 functions, we carried out a yeast two hybrid (Y2H) screen in several mouse tissue libraries to identify ALMS1 interacting partners. The majority of proteins found to interact with the murine carboxy-terminal end (19/32) of ALMS1 were α-actinin isoforms. Interestingly, several of the identified ALMS1 interacting partners (α-actinin 1, α-actinin 4, myosin Vb, rad50 interacting 1 and huntingtin associated protein1A) have been previously associated with endosome recycling and/or centrosome function. We examined dermal fibroblasts from human subjects bearing a disruption in ALMS1 for defects in the endocytic pathway. Fibroblasts from these patients had a lower uptake of transferrin and reduced clearance of transferrin compared to controls. Antibodies directed against ALMS1 N- and C-terminal epitopes label centrosomes and endosomal structures at the cleavage furrow of dividing MDCK cells, respectively, suggesting isoform-specific cellular functions. Our results suggest a role for ALMS1 variants in the recycling endosome pathway and give us new insights into the pathogenesis of a subset of clinical phenotypes associated with ALMS
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