Karen refuses to wear a face mask for her 5 minute trip to the supermarket during a pandemic. She harasses the workers, asks to see the manager and threatens to sue.
Karen sues the local city council after they installed a new STOP sign that hides the sun from her window for two minutes a day. The sign was installed after a school boy on his bicycle was hit by a speeding driver and died.
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These example sentences are selected automatically from various online news sources to reflect current usage of the word ‘publication.’ Views expressed in the examples do not represent the opinion of Merriam-Webster or its editors. Send us feedback.
Open access (OA) refers to free, unrestricted online access to research outputs such as journal articles and books. OA content is open to all, with no access fees.
There are two main routes to making research outputs openly accessible. One involves publishing articles or books via the OA route on a publisher’s platform (often referred to as gold open access). The other involves archiving a version of the manuscript in an OA repository (often described as green open access). Content published via the gold OA route is accessible immediately on publication, while manuscripts deposited via the green OA route may, in many cases, be made accessible only once a self-archiving embargo period has elapsed. The terms for onward sharing and re-use of OA content will depend on the licence under which it has been made available.
If entering a book chapter, list the name of the book in this field. Publication Source should be capitalized using Headline Style Capitalization (see Title for more information). Special characters will need to be formatted using HTML tags.
Publication Source is a single line text field used to display the official title of the journal, book, or other medium in which the document was published.
Shwachman-Diamond syndrome (SDS) is an inherited bone marrow failure syndrome with predisposition to developing leukemia. We found that multiple independent somatic hematopoietic clones arise early in life, most commonly harboring heterozygous mutations in EIF6 or TP53. EIF6 mutations cause functional compensation for the germline deficiency by alleviating the SDS ribosome joining defect, improving translation, and reducing p53 activation. TP53 mutations decrease checkpoint activation without affecting ribosome assembly. We link development of leukemia with acquisition of biallelic TP53 alterations. Our results define distinct pathways of clonal selection driven by germline fitness constraint and provide a mechanistic framework for clinical surveillance.
Kennedy, A. L., Myers, K. C., Bowman, J., Gibson, C. J., Camarda, N. D., Furutani, E. M., Muscato, G. M., Klein, R. H., Ballotti, K., Liu, S., Harris, C. E., Galvin, A., Malsch, M., Dale, D., Gansner, J. M., Nakano, T. A., Bertuch, A., Vlachos, A., Lipton, J. M., Castillo, P., Connelly, J., Churpek, J., Edwards, J. R., Hijiya, N., Ho, R. H., Hofmann, I., Huang, J. N., Keel, S., Lamble, A., Lau, B. W., Norkin, M., Stieglitz, E., Stock, W., Walkovich, K., Boettcher, S., Brendel, C., Fleming, M. D., Davies, S. M., Weller, E. A., Bahl, C., Carter, S. L., Shimamura, A., Lindsley, R. C.