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Paper won Best Student Paper Award from the International Transport Economics Association (ITEA 2022)

Ancient and medieval rhetorical theorists gave much attention to discovering an author’s intent (voluntas) from the letter of a document (scriptum). By contrast, resolving ambiguity (ambiguitas) was supposedly easy. But in fact, ambiguity proves the more slippery problem because it functions somewhere between argumentation (a controversy to be disputed) and stylistic embellishment. Legal discourse often tried to impose limits on ambiguity, but at the same time ambiguitas could be quietly weaponized — in both law and poetry — to transform legal and even theological meaning. Where rhetorical theorists such as Cicero, Quintilian, Augustine, William of Champeaux (c. 1100), Geoffrey of Vinsauf (c. 1210), and Boncompagno da Signa (c. 1235), as well as legal theorists such as Henry de Bracton, try to pin down how ambiguity works, poets such as William Langland seem to revel in the slippages that it affords.

January 2024: Rita Copeland is Sheli Z. and Burton X. Rosenberg Chair in the Humanities and Professor of Classics, English, and Comparative Literature at the University of Pennsylvnia.  Her publications include  Rhetoric, Hermeneutics, and Translation in the Middle Ages (Cambridge, 1991); Criticism and Dissent in the Middle Ages (Cambridge, 1996); Pedagogy, Intellectuals and Dissent in the Later Middle Ages (Cambridge 2001); Medieval Grammar and Rhetoric:  Language Arts and Literary Theory, AD 300-1475 (with I. Sluiter; Oxford, 2009); The Cambridge Companion to Allegory (with P. Struck; 2010), The Oxford History of Classical Reception in English Literature, 800-1558 (2016), and most recently, Emotion and the History of Rhetoric in the Middle Ages (Oxford, 2021).  She was a co-founder of the journal New Medieval Literatures.  She is General Editor (with the late Peter Mack) of the forthcoming Cambridge History of Rhetoric in five volumes.  She has been the recipient of NEH, ACLS, American Philosophical Society, and Guggenheim fellowships.  She is a Fellow of the Medieval Academy of America.  She has been a visiting professor at Hebrew University, University of Iceland, and University of Oxford, and a visiting fellow at the Warburg Institute, London.

POGZ (Pogo transposable element derived with ZNF domain) is known to function as a regulator of gene expression. While variations in the gene have been associated with intellectual disabilities and developmental delays in humans, the exact pathophysiological mechanisms remain unclear. To shed light on this, we created two lines of conditional knockout mice for , one specific to excitatory neurons (Emx1-Pogz mice) and the other to inhibitory neurons (Gad2-Pogz mice) in the brain. Emx1-Pogz mice showed a decrease in body weight, similar to total knockout mice. Although the two lines did not display significant morphological abnormalities in the telencephalon, impaired POGZ function affected the electrophysiological properties of both excitatory and inhibitory neurons differently. These findings suggest that these mouse lines could be useful tools for clarifying the precise pathophysiological mechanisms of neurodevelopmental disorders associated with gene abnormalities.

‘Outdegree’ from directed graph theory is used to measure the salience of individual locations in the transmission of Covid-19 morbidity through the spatiotemporal network of contagion and their salience in the spatiotemporal diffusion of vaccination rollout. A spatial econometric model in which morbidity varies inversely with vaccination rollout, and vaccination rollout varies directly with morbidity is used to calculate dynamic auto-outdegrees for morbidity, and dynamic cross-outdegrees for the effect of vaccination on morbidity. The former identifies hot spots of contagion, and the latter identifies locations in which vaccination rollout is particularly effective in reducing national morbidity. These outdegrees are calculated analytically rather than simulated numerically.   

Thioxanthone (TX) molecules and their derivatives are well-known photoactive compounds. Yet, there exist only a handful of luminescent systems combining TX with transition metals. Recently, we reported a TX-based PSP pincer ligand (L1) that appears as a promising platform for filling this niche. Herein, we demonstrate that with Cu(I) this ligand exclusively assembles into dimeric structures with either di- or polynuclear Cu(I) cores. With cationic Cu(I) precursors, complexes featuring solvent-bridged bis-cationic cores were obtained. These coordinatively unsaturated bimetallic systems showed surprisingly facile activation of the chloroform C–Cl bonds, suggesting a possible metal–metal cooperation. The reaction of L1 with binary Cu(I) halides afforded dimeric complexes with polynuclear [CuX]_n (n = 3 or 4) cores. With X = Br or I, emissive complexes containing stairstep [CuX]₄ clusters were obtained. Emission lifetimes in the microsecond range measured for these complexes were indicative of a triplet emission (phosphorescence), which according to our time-dependent density functional theory study originates from a halide-metal-to-ligand charge transfer between the [CuX]₄ cluster and the TX backbone of L1. Finally, the distinctive polynucleating behavior of L1 toward Cu(I) was also showcased by a comparison to another PSP ligand with a diaryl thioether backbone (L2), which formed only mononuclear pincer-type complexes, lacking any unusual reactivity or photoluminescence.

The MAPK p38α was proposed to be a prominent promoter of skeletal muscle aging. The skeletal muscle tissue is composed of various muscle types, and it is not known if p38α is associated with aging in all of them. It is also not known if p38α is associated with aging of other tissues. JNK and ERK were also proposed to be associated with aging of several tissues. Nevertheless, the pattern of p38α, JNK, and ERK activity during aging was not documented. Here, we documented the levels of phosphorylated/active p38α, Erk1/2, and JNKs in several organs as well as the soleus, tibialis anterior, quadriceps, gastrocnemius, and EDL muscles of 1-, 3-, 6-, 13-, 18-, and 24-month-old mice. We report that in most tissues and skeletal muscles, the MAPKs' activity does not change in the course of aging. In most tissues and muscles, p38α is in fact active at younger ages. The quadriceps and the lungs are exceptions, where p38α is significantly active only in mice 13 months old or older. Curiously, levels of active JNK and ERKs are also elevated in aged lungs and quadriceps. RNA-seq analysis of the quadriceps during aging revealed downregulation of proteins related to the extra-cellular matrix (ECM) and ERK signaling. A panel of mRNAs encoding cell cycle inhibitors and senescence-associated proteins, considered to be aging markers, was not found to be elevated. It seems that the pattern of MAPKs' activation in aging, as well as expression of known 'aging' components, are tissue- and muscle type-specific, supporting a notion that the process of aging is tissue- and even cell-specific.