Graph Data-Models and Semantic Web Technologies in Scholarly Digital Editing

This volume is based on the selected papers presented at the Workshop on Scholarly Digital Editions, Graph Data-Models and Semantic Web Technologies, held at the Uni- versity of Lausanne in June 2019. The Workshop was organized by Elena Spadini (University of Lausanne) and Francesca Tomasi (University of Bologna), and spon- sored by the Swiss National Science Foundation through a Scientific Exchange grant, and by the Centre de recherche sur les lettres romandes of the University of Lausanne. The Workshop comprised two full days of vibrant discussions among the invited speakers, the authors of the selected papers, and other participants.1 The acceptance rate following the open call for papers was around 60%. All authors – both selected and invited speakers – were asked to provide a short paper two months before the Workshop. The authors were then paired up, and each pair exchanged papers. Paired authors prepared questions for one another, which were to be addressed during the talks at the Workshop; in this way, conversations started well before the Workshop itself. After the Workshop, the papers underwent a second round of peer-review before inclusion in this volume. This time, the relevance of the papers was not under discus- sion, but reviewers were asked to appraise specific aspects of each contribution, such as its originality or level of innovation, its methodological accuracy and knowledge of the literature, as well as more formal parameters such as completeness, clarity, and coherence. The bibliography of all of the papers is collected in the public Zotero group library GraphSDE20192, which has been used to generate the reference list for each contribution in this volume. The invited speakers came from a wide range of backgrounds (academic, commer- cial, and research institutions) and represented the different actors involved in the remediation of our cultural heritage in the form of graphs and/or in a semantic web en- vironment. Georg Vogeler (University of Graz) and Ronald Haentjens Dekker (Royal Dutch Academy of Sciences, Humanities Cluster) brought the Digital Humanities research perspective; the work of Hans Cools and Roberta Laura Padlina (University of Basel, National Infrastructure for Editions), as well as of Tobias Schweizer and Sepi- deh Alassi (University of Basel, Digital Humanities Lab), focused on infrastructural challenges and the development of conceptual and software frameworks to support re- searchers’ needs; Michele Pasin’s contribution (Digital Science, Springer Nature) was informed by his experiences in both academic research, and in commercial technology companies that provide services for the scientific community. The Workshop featured not only the papers of the selected authors and of the invited speakers, but also moments of discussion between interested participants. In addition to the common Q&A time, during the second day one entire session was allocated to working groups delving into topics that had emerged during the Workshop. Four working groups were created, with four to seven participants each, and each group presented a short report at the end of the session. Four themes were discussed: enhancing TEI from documents to data; ontologies for the Humanities; tools and infrastructures; and textual criticism. All of these themes are represented in this volume. The Workshop would not have been of such high quality without the support of the members of its scientific committee: Gioele Barabucci, Fabio Ciotti, Claire Clivaz, Marion Rivoal, Greta Franzini, Simon Gabay, Daniel Maggetti, Frederike Neuber, Elena Pierazzo, Davide Picca, Michael Piotrowski, Matteo Romanello, Maïeul Rouquette, Elena Spadini, Francesca Tomasi, Aris Xanthos – and, of course, the support of all the colleagues and administrative staff in Lausanne, who helped the Workshop to become a reality. The final versions of these papers underwent a single-blind peer review process. We want to thank the reviewers: Helena Bermudez Sabel, Arianna Ciula, Marilena Daquino, Richard Hadden, Daniel Jeller, Tiziana Mancinelli, Davide Picca, Michael Piotrowski, Patrick Sahle, Raffaele Viglianti, Joris van Zundert, and others who preferred not to be named personally. Your input enhanced the quality of the volume significantly! It is sad news that Hans Cools passed away during the production of the volume. We are proud to document a recent state of his work and will miss him and his ability to implement the vision of a digital scholarly edition based on graph data-models and semantic web technologies. The production of the volume would not have been possible without the thorough copy-editing and proof reading by Lucy Emmerson and the support of the IDE team, in particular Bernhard Assmann, the TeX-master himself. This volume is sponsored by the University of Bologna and by the University of Lausanne. Bologna, Lausanne, Graz, July 2021 Francesca Tomasi, Elena Spadini, Georg Vogele

CRESCAT

A poster describing the CRESCAT project at the University of Chicago

University of Chicago CRESCAT Project

The CRESCAT project is an interdisciplinary collaboration between computer scientists, paleobiologists, archaeologists, economic historians, and other social scientists. The goal is to demonstrate the value of an integrative software ecosystem that spans the social and natural sciences and can facilitate any research characterized by overlapping models of temporal and spatial relations or by conflicting terminologies and taxonomies. CRESCAT’s representation of scientific knowledge eschews forced standardization, which is impractical in many cases due to lack of an enforcement mechanism and is also questionable in principle since divergent ontologies often legitimately reflect different theoretical assumptions and research agendas. Central to the CRESCAT suite of tools is an innovative data-integration system that represents explicitly both research data and the ontologies inherent in the data. CRESCAT’s data-integration system operates at a level of abstraction sufficient to provide a predictable and efficiently queryable database structure based on an abstract global schema, which in turn is based on an “upper ontology” specified in terms of fundamental concepts and relationships applicable to all scientific and scholarly disciplines. The data-integration system is implemented in an enterprise-class XQuery DBMS that serves as a data warehouse (using a non-relational graph data model) to store diverse data from a wide range of research projects representing many disciplines. The terminology and conceptual distinctions of each research project are fully preserved. The approach to research data taken in the CRESCAT project is (1) coherent, tightly integrating software tools and data formats within a single analytical framework; (2) open-ended, interconnecting existing tools while allowing the addition of new tools in the future; (3) non-exclusive, in no way preventing its component tools from participating in other software ecosystems; (4) scalable, designed to handle large-scale data management, analysis, and visualization; and (5) sustainable, maintaining shared resources to meet common needs for software and technical support and thus enabling substantial economies of scale

Chemogenetic activation of intracardiac cholinergic neurons improves cardiac function in pressure overload-induced heart failure

© 2020 the American Physiological Society. Chemogenetic activation of intracardiac cholinergic neurons improves cardiac function in pressure overload-induced heart failure. Am J Physiol Heart Circ Physiol 319: H3-H12, 2020. First published May 15, 2020; doi:10.1152/ajpheart.00150.2020.-Heart failure (HF) is characterized by autonomic imbalance with sympathetic hyperactivity and loss of parasympathetic tone. Intracardiac ganglia (ICG) neurons represent the final common pathway for vagal innervation of the heart and strongly regulate cardiac functions. This study tests whether ICG cholinergic neuron activation mitigates the progression of cardiac dysfunction and reduces mortality that occurs in HF. HF was induced by transaortic constriction (TAC) in male transgenic Long-Evans rats expressing Cre recombinase within choline acetyltransferase (ChAT) neurons. ChAT neurons were selectively activated by expression and activation of excitatory designer receptors exclusively activated by designer receptors (DREADDs) by clozapine-N-oxide (TAC + treatment and sham-treated groups). Control animals expressed DREADDs but received saline (sham and TAC groups). A separate set of animals were telemetry instrumented to record blood pressure (BP) and heart rate (HR). Acute activation of ICG neurons resulted in robust reductions in BP (∼20 mmHg) and HR (∼100 beats/min). All groups of animals were subjected to weekly echocardiography and treadmill stress tests from 3 to 6 wk post-TAC/sham surgery. Activation of ICG cholinergic neurons reduced the left ventricular systolic dysfunction (reductions in ejection fraction, fractional shortening, stroke volume, and cardiac output) and cardiac autonomic dysfunction [reduced HR recovery (HRR) post peak effort] observed in TAC animals. Additionally, activation of ICG ChAT neurons reduced mortality by 30% compared with untreated TAC animals. These data suggest that ICG cholinergic neuron activation reduces cardiac dysfunction and improves survival in HF, indicating that ICG neuron activation could be a novel target for treating HF

Chemogenetic activation of intracardiac cholinergic neurons improves cardiac function in pressure overload induced heart failure.

Heart failure (HF) is characterized by autonomic imbalance with sympathetic hyperactivity and loss of parasympathetic tone. Intracardiac ganglia (ICG) neurons represent the final common pathway for vagal innervation of the heart and strongly regulate cardiac functions. This study tests whether ICG cholinergic neuron activation mitigates the progression of cardiac dysfunction and reduces mortality that occurs in HF. HF was induced by transaortic constriction (TAC) in male transgenic Long-Evans rats expressing Cre recombinase within choline acetyltransferase (ChAT) neurons. ChAT neurons were selectively activated by expression and activation of excitatory designer receptors exclusively activated by designer receptors (DREADDs) by clozapine-N-oxide (TAC + treatment and sham-treated groups). Control animals expressed DREADDs but received saline (sham and TAC groups). A separate set of animals were telemetry instrumented to record blood pressure (BP) and heart rate (HR). Acute activation of ICG neurons resulted in robust reductions in BP (∼20 mmHg) and HR (∼100 beats/min). All groups of animals were subjected to weekly echocardiography and treadmill stress tests from 3 to 6 wk post-TAC/sham surgery. Activation of ICG cholinergic neurons reduced the left ventricular systolic dysfunction (reductions in ejection fraction, fractional shortening, stroke volume, and cardiac output) and cardiac autonomic dysfunction [reduced HR recovery (HRR) post peak effort] observed in TAC animals. Additionally, activation of ICG ChAT neurons reduced mortality by 30% compared with untreated TAC animals. These data suggest that ICG cholinergic neuron activation reduces cardiac dysfunction and improves survival in HF, indicating that ICG neuron activation could be a novel target for treating HF. NEW & NOTEWORTHY Intracardiac ganglia form the final common pathway for the parasympathetic innervation of the heart. This study has used a novel chemogenetic approach within transgenic ChAT-Cre rats [expressing only Cre-recombinase in choline acetyl transferase (ChAT) neurons] to selectively increase intracardiac cholinergic parasympathetic activity to the heart in a pressure overload-induced heart failure model. The findings from this study confirm that selective activation of intracardiac cholinergic neurons lessens cardiac dysfunction and mortality seen in heart failure, identifying a novel downstream cardiac-selective target for increasing cardioprotective parasympathetic activity in heart failure

Activation of Oxytocin Neurons Improves Cardiac Function in a Pressure-Overload Model of Heart Failure

© 2020 The Authors This work shows long-term restoration of the hypothalamic oxytocin (OXT) network preserves OXT release, reduces mortality, cardiac inflammation, fibrosis, and improves autonomic tone and cardiac function in a model of heart failure. Intranasal administration of OXT in patients mimics the short-term changes seen in animals by increasing parasympathetic—and decreasing sympathetic—cardiac activity. This work provides the essential translational foundation to determine if approaches that mimic paraventricular nucleus (PVN) OXT neuron activation, such as safe, noninvasive, and well-tolerated intranasal administration of OXT, can be beneficial in patients with heart failure

Activation of Oxytocin Neurons Improves Cardiac Function in a Pressure-Overload Model of Heart Failure.

© 2020 The Authors This work shows long-term restoration of the hypothalamic oxytocin (OXT) network preserves OXT release, reduces mortality, cardiac inflammation, fibrosis, and improves autonomic tone and cardiac function in a model of heart failure. Intranasal administration of OXT in patients mimics the short-term changes seen in animals by increasing parasympathetic—and decreasing sympathetic—cardiac activity. This work provides the essential translational foundation to determine if approaches that mimic paraventricular nucleus (PVN) OXT neuron activation, such as safe, noninvasive, and well-tolerated intranasal administration of OXT, can be beneficial in patients with heart failure