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Institution

University of Rochester

EducationRochester, New York, United States
About: University of Rochester is a education organization based out in Rochester, New York, United States. It is known for research contribution in the topics: Population & Laser. The organization has 63915 authors who have published 112762 publications receiving 5484122 citations. The organization is also known as: Rochester University.


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Journal ArticleDOI
TL;DR: In this paper, a model of earnings, cash flows and accruals is developed assuming a random walk sales process, variable and fixed costs, and that the only accrual are accounts receivable and payable, and inventory.

1,481 citations

Journal ArticleDOI
TL;DR: Cicchetti et al. as mentioned in this paper used equifinality to explain why in any open system (i.e., one come have been conceived as among the hall where there is maintenance in change, dymarks of the developmental psychopathology namic order of processes, organization, selfperspective) the same end state may be mezy & Streitman, 1974; Kohlberg, Lareached from a variety of different initial conCrosse, & Riclcs, 1972; Sameroff, 1989; ditions and through different processes.
Abstract: Since its inception as an emergent interdisciepigenesis, may lead to the same outcome, plinary science, diversity in process and outStated differently, in an open system (i.e., one come have been conceived as among the hallwhere there is maintenance in change, dymarks of the developmental psychopathology namic order of processes, organization, selfperspective (Cicchetti, 1984, 1990; Garregulation, etc.) the same end state may be mezy & Streitman, 1974; Kohlberg, Lareached from a variety of different initial conCrosse, & Riclcs, 1972; Sameroff, 1989; ditions and through different processes. This Sroufe, 1986, 1989; Sroufe & Rutter, 1984). is referred to as equifinality, an organismic Thus, developmental psychopathologists have process that possesses significant implications articulated the expectations that there are mulfor psychological and biological regulatory tiple contributors to adaptive or maladaptive systems (Cicchetti, 1996) and for behavioral outcomes in any individual, that these factors and biological plasticity (Cicchetti & Tucker, and their relative contributions vary among 1994b). In contrast, in a closed system the end individuals, and that there are myriad pathstate is inextricably linked to and determined ways to any particular manifestation of adapby the initial conditions: if either the conditive or disordered behavior (Cicchetti, 1993; tions change or the processes are modified, Richters & Cicchetti, 1993; Robins, 1966; then the end state will also be modified (von Robins & Rutter, 1990; Rutter, 1989, 1995; Bertalanffy, 1968). Sroufe & Jacobvitz, 1989). Additionally, it is Initial descriptions of equifinality emabelieved that there is heterogeneity among innated from work in embryology. For example, dividuals who develop a specific disorder the development of a normal organism was with respect to the features of their disturbshown to occur from a whole ovum, a divided ance, as well as among individuals who eviovum, or two fused ova. Further, it was demdence maladaptation but who do not develop onstrated that different initial sizes and differa disorder. In accord with this view, the prinent courses of growth can eventuate in the ciples of equifinality and multifinality derived same ultimate size of an organism (von Bertafrom general systems theory (von Bertalanffy, lanffy, 1968; Waddington, 1957). Within the 1968) are germane. discipline of developmental psychopathology, Equifinality refers to the observation that equifinality has been invoked to explain why in any open system (cf. Mayr, 1964, 1988) a a variety of developmental pathways may diversity of pathways, including chance eventuate in a given outcome, rather than exevents or what biologists refer to as nonlinear pecting a singular primary pathway to the adaptive or maladaptive outcome. Address correspondence to: Dr. Dante Cicchetti or Dr. T h e Principle of multifinality (Wilden, Fred A. Rogosch, Mt. Hope Family Center, Univ. of 1980) suggests that any one component may Rochester, 187 Edinburgh St., Rochester, NY 14608. function differently depending on the organi-

1,476 citations

Proceedings ArticleDOI
04 Mar 2014
TL;DR: The largest-scale study of video engagement to date is presented, using data from 6.9 million video watching sessions across four courses on the edX MOOC platform, finding that shorter videos are much more engaging, that informal talking-head videos are more engage, and that Khan-style tablet drawings are more engaging.
Abstract: Videos are a widely-used kind of resource for online learning. This paper presents an empirical study of how video production decisions affect student engagement in online educational videos. To our knowledge, ours is the largest-scale study of video engagement to date, using data from 6.9 million video watching sessions across four courses on the edX MOOC platform. We measure engagement by how long students are watching each video, and whether they attempt to answer post-video assessment problems.Our main findings are that shorter videos are much more engaging, that informal talking-head videos are more engaging, that Khan-style tablet drawings are more engaging, that even high-quality pre-recorded classroom lectures might not make for engaging online videos, and that students engage differently with lecture and tutorial videos.Based upon these quantitative findings and qualitative insights from interviews with edX staff, we developed a set of recommendations to help instructors and video producers take better advantage of the online video format. Finally, to enable researchers to reproduce and build upon our findings, we have made our anonymized video watching data set and analysis scripts public. To our knowledge, ours is one of the first public data sets on MOOC resource usage.

1,473 citations

Journal ArticleDOI
TL;DR: This purified system of five purified proteins should facilitate understanding of how eukaryotlc hsp70 and hsp90 work together as essential components of a process that alters the conformations of substrate proteins to states that respond in signal transduction.
Abstract: Nearly 100 proteins are known to be regulated by hsp90. Most of these substrates or "client proteins" are involved in signal transduction, and they are brought into complex with hsp90 by a multiprotein hsp90/hsp70-based chaperone machinery. In addition to binding substrate proteins at the chaperone site(s), hsp90 binds cofactors at other sites that are part of the heterocomplex assembly machinery as well as immunophilins that connect assembled substrate*hsp90 complexes to protein-trafficking systems. In the 5 years since we last reviewed this subject, much has been learned about hsp90 structure, nucleotide-binding, and cochaperone interactions; the most important concept is that ATP hydrolysis by an intrinsic ATPase activity results in a conformational change in hsp90 that is required to induce conformational change in a substrate protein. The conformational change induced in steroid receptors is an opening of the steroid-binding cleft so that it can be accessed by steroid. We have now developed a minimal system of five purified proteins-hsp90, hsp70, Hop, hsp40, and p23- that assembles stable receptor*hsp90 heterocomplexes. An hsp90*Hop*hsp70*hsp40 complex opens the cleft in an ATP-dependent process to produce a receptor*hsp90 heterocomplex with hsp90 in its ATP-bound conformation, and p23 then interacts with the hsp90 to stabilize the complex. Stepwise assembly experiments have shown that hsp70 and hsp40 first interact with the receptor in an ATP-dependent reaction to produce a receptor*hsp70*hsp40 complex that is "primed" to be activated to the steroid-binding state in a second ATP-dependent step with hsp90, Hop, and p23. Successful use of the five-protein system with other substrates indicates that it can assemble signal protein*hsp90 heterocomplexes whether the substrate is a receptor, a protein kinase, or a transcription factor. This purified system should facilitate understanding of how eukaryotic hsp70 and hsp90 work together as essential components of a process that alters the conformations of substrate proteins to states that respond in signal transduction.

1,463 citations

Journal ArticleDOI
07 Jan 2010-Nature
TL;DR: Findings establish chronic active BCR signalling as a new pathogenetic mechanism in ABC DLBCL, suggesting several therapeutic strategies.
Abstract: A role for B-cell-receptor (BCR) signalling in lymphomagenesis has been inferred by studying immunoglobulin genes in human lymphomas and by engineering mouse models, but genetic and functional evidence for its oncogenic role in human lymphomas is needed. Here we describe a form of 'chronic active' BCR signalling that is required for cell survival in the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). The signalling adaptor CARD11 is required for constitutive NF-kappaB pathway activity and survival in ABC DLBCL. Roughly 10% of ABC DLBCLs have mutant CARD11 isoforms that activate NF-kappaB, but the mechanism that engages wild-type CARD11 in other ABC DLBCLs was unknown. An RNA interference genetic screen revealed that a BCR signalling component, Bruton's tyrosine kinase, is essential for the survival of ABC DLBCLs with wild-type CARD11. In addition, knockdown of proximal BCR subunits (IgM, Ig-kappa, CD79A and CD79B) killed ABC DLBCLs with wild-type CARD11 but not other lymphomas. The BCRs in these ABC DLBCLs formed prominent clusters in the plasma membrane with low diffusion, similarly to BCRs in antigen-stimulated normal B cells. Somatic mutations affecting the immunoreceptor tyrosine-based activation motif (ITAM) signalling modules of CD79B and CD79A were detected frequently in ABC DLBCL biopsy samples but rarely in other DLBCLs and never in Burkitt's lymphoma or mucosa-associated lymphoid tissue lymphoma. In 18% of ABC DLBCLs, one functionally critical residue of CD79B, the first ITAM tyrosine, was mutated. These mutations increased surface BCR expression and attenuated Lyn kinase, a feedback inhibitor of BCR signalling. These findings establish chronic active BCR signalling as a new pathogenetic mechanism in ABC DLBCL, suggesting several therapeutic strategies.

1,463 citations


Authors

Showing all 64186 results

NameH-indexPapersCitations
Eugene Braunwald2301711264576
Cyrus Cooper2041869206782
Eric J. Topol1931373151025
Dennis W. Dickson1911243148488
Scott M. Grundy187841231821
John C. Morris1831441168413
Ronald C. Petersen1781091153067
David R. Williams1782034138789
John Hardy1771178171694
Russel J. Reiter1691646121010
Michael Snyder169840130225
Jiawei Han1681233143427
Gang Chen1673372149819
Marc A. Pfeffer166765133043
Salvador Moncada164495138030
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023101
2022383
20213,841
20203,895
20193,699
20183,541