51 research outputs found
Forever is a Long Time: Reconsidering Universities' Perpetual Endowment Policies in the Twenty - First Century
College and university officials in the United States have long invoked a combination of Anglo-Saxon legal precedents, plus the obligations of responsible philanthropic stewardship, to justify policies of perpetual endowments. Closely related to this general principle has been the practice of not spending more than the annual earnings (in other words, interest and dividends) from an endowment. Our historical analysis provides a counter to this contemporary conventional wisdom that has been accepted with little critical consideration in American higher education. Rediscovery of philosophical arguments, and actual cases of foundations and philanthropists who placed limits on the life span of gifts, demonstrates how historical research can provide an informed base for reconsideration of government and institutional policies and practices that shape giving and spending at colleges and universities in the twenty-first century.The grounding in economics for our study is Howard Bowen's 1980 "revenue theory" of college costs. The historical precedent for our policy analysis comes from eighteenth-century France, as advanced by A.J. Turgot, to shape national economic development. Its implications for higher education in the United States is illustrated by philanthropist John D. Rockefeller's reservations about a perpetual endowment for an educational project: "Forever is a long time . . ." Our historical research addresses the consequences -- pro and con -- of government policies requiring colleges to spend endowments at more than a marginal annual rate and in a fixed period of time; and, secondly, are there good reasons for donors to colleges to voluntarily opt to increase spending and place time limits on gifts
Time Is Of The Essence: Foundations And The Policies Of Limited Life And Endowment Spend-Down
In contrast to congressional hearings and proposed punitive legislation, we consider the present and past proposition that institutions, especially nonprofit foundations, opt voluntarily and by decision to spend down endowments. And, by extension, for many cases, it includes consideration that boards and donors may wish to plan for deliberate dissolution of funds or foundations to coincide with a fixed, finite target date for addressing solutions to specific foundation programs and agenda items
[Review of] \u3cem\u3ePedagogues and Protesters: The Harvard College Student Diary of Stephen Peabody, 1767-1768\u3c/em\u3e. Edited by Conrad Edick Wright.
The Cystic Fibrosis Transmembrane Conductance Regulator Is Regulated by a Direct Interaction with the Protein Phosphatase 2A
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated chloride channel expressed at the apical surface of epithelia. Although the regulation of CFTR by protein kinases is well documented, channel deactivation by phosphatases is not well understood. We find that the serine/threonine phosphatase PP2A can physically associate with the CFTR COOH terminus. PP2A is a heterotrimeric phosphatase composed of a catalytic subunit and two divergent regulatory subunits (A and B). The cellular localization and substrate specificity of PP2A is determined by the unique combination of A and B regulatory subunits, which can give rise to at least 75 different enzymes. By mass spectrometry, we identified the exact PP2A regulatory subunits associated with CFTR as Aalpha and B'epsilon and find that the B'epsilon subunit binds CFTR directly. PP2A subunits localize to the apical surface of airway epithelia and PP2A phosphatase activity co-purifies with CFTR in Calu-3 cells. In functional assays, inhibitors of PP2A block rundown of basal CFTR currents and increase channel activity in excised patches of airway epithelia and in intact mouse jejunum. Moreover, PP2A inhibition in well differentiated human bronchial epithelial cells results in a CFTR-dependent increase in the airway surface liquid. Our data demonstrate that PP2A is a relevant CFTR phosphatase in epithelial tissues. Our results may help reconcile differences in phosphatase-mediated channel regulation observed for different tissues and cells. Furthermore, PP2A may be a clinically relevant drug target for CF, which should be considered in future studies
Modified Cav1.4 Expression in the Cacna1fnob2 Mouse Due to Alternative Splicing of an ETn Inserted in Exon 2
The Cacna1fnob2 mouse is reported to be a naturally occurring null mutation for the Cav1.4 calcium channel gene and the phenotype of this mouse is not identical to that of the targeted gene knockout model. We found two mRNA species in the Cacna1fnob2 mouse: approximately 90% of the mRNA represents a transcript with an in-frame stop codon within exon 2 of CACNA1F, while approximately 10% of the mRNA represents a transcript in which alternative splicing within the ETn element has removed the stop codon. This latter mRNA codes for full length Cav1.4 protein, detectable by Western blot analysis that is predicted to differ from wild type Cav1.4 protein in a region of approximately 22 amino acids in the N-terminal portion of the protein. Electrophysiological analysis with either mouse Cav1.4wt or Cav1.4nob2 cDNA revealed that the alternatively spliced protein does not differ from wild type with respect to activation and inactivation characteristics; however, while the wild type N-terminus interacted with filamin proteins in a biochemical pull-down experiment, the alternatively spliced N-terminus did not. The Cacna1fnob2 mouse electroretinogram displayed reduced b-wave and oscillatory potential amplitudes, and the retina was morphologically disorganized, with substantial reduction in thickness of the outer plexiform layer and sprouting of bipolar cell dendrites ectopically into the outer nuclear layer. Nevertheless, the spatial contrast sensitivity (optokinetic response) of Cacna1fnob2 mice was generally similar to that of wild type mice. These results suggest the Cacna1fnob2 mouse is not a CACNA1F knockout model. Rather, alternative splicing within the ETn element can lead to full-length Cav1.4 protein, albeit at reduced levels, and the functional Cav1.4 mutant may be incapable of interacting with cytoskeletal filamin proteins. These changes, do not alter the ability of the Cacna1fnob2 mouse to detect and follow moving sine-wave gratings compared to their wild type counterparts
Higher Education and Athletics: Probing an American Ethos
In 1874 student teams from McGill and Harvard met in a series of games which were credited with shaping the modern style of intercollegiate football. In the century since that series, American colleges and universities have accommodated large competitive sports programs; these, in turn, have been celebrated and justified in terms of distinctive American beliefs in connections between sports, education, and social mobility. This essay attempts to break the conspiracy of silence which characterizes the response of American faculty and educators toward intercollegiate athletic policy. And, this is an invitation for scholars and educators in Canada to critically study the not-so-obvious connections between schools and sports
Thelin, John R., The Anatomy of Institutions: Historians and the Search for the Unwritten Constitution, pp. 66-70 in Craig Kridel, ed., Curriculum History . Lanham, MD: University Press of America, 1989.
Discusses problems of writing histories of particular institutions of higher education
John B. Boles. University Builder: Edgar Odell Lovett and the Founding of the Rice Institute. Baton Rouge: Louisiana State University Press, 2007. 328 pp. Cloth $35.00.
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