bluuebunny/crossref_metadata_2025_split huggingface dataset:
Media Convergence as Exogenous Forces in a NCAA DI Athletic Department: Organizational Climate and Resource Allocation Decision Making
Authors: Lee Seungbum , Kim Yongjae , Tang Tang 
Published: June 2020

To successfully evolve, organizations should change at the same pace as the environment changes. It is particularly important when adapting and utilizing new media technology is a huge part of an organization’s success. Presently, media professionals in all industries including intercollegiate athletics are experiencing a significant change in their work environment due to the ever-changing nature of new media technology. In particular, media convergence, an integration of production by combining both old (e.g., television) and new media (e.g., the Internet), has been one of the most influential phenomena creating unexpected changes and complex dynamics in the current media industry. Nonetheless, what have been previously overlooked in sport communication literature are challenges generated by media convergence, which affects the nature of sport communication. This case study provides a scenario based on semi-fictitious information so that students can critically examine the dynamic nature as well as the effect of media convergence facing sport communication in intercollegiate sport. Further, the students are provided with an opportunity to practice decision-making skills to address the challenges stemming from media convergence. By doing so, discussion regarding media convergence in the context of intercollegiate sport could be better presented to relevant classroom discussion.
A Comparison of Cardiopulmonary Exercise Testing and Field Walking Tests in Community-Dwelling Older Adults With Mild-to-Moderate Alzheimer’s Dementia
Authors: Salisbury Dereck L. , Yu Fang 
Published: June 2020

The purpose of this study was to investigate the relationships among peak exercise parameters on 6-min walk test, shuttle walk test, and laboratory-based cardiopulmonary exercise testing in persons with Alzheimer’s dementia. This study is a cross-sectional analysis of the baseline data of 90 participants (age 77.1 [6.6] years, 43% female) from the FIT-AD trial. Cardiopulmonary exercise testing produced significantly higher peak heart rate (118.6 [17.5] vs. 106 [22.8] vs. 106 [18.8] beats/min), rating of perceived exertion (16 [2.1] vs. 12 [2.3] vs. 11 [2.1]), and systolic blood pressure (182 [23.7] vs. 156 [18.9] vs. 150 [16.9] mmHg) compared with the shuttle walk test and 6-min walk test, respectively. Peak walking distance on shuttle walk test (241.3 [127.3] m) and 6-min walk test (365.0 [107.9] m) significantly correlated with peak oxygen consumption (17.1 [4.3] ml·kg−1·min−1) on cardiopulmonary exercise testing (r = .449, p ≤ .001 and r = .435, p ≤ .001), respectively, which is considerably lower than what is seen in older adults and persons with cardiopulmonary diseases.
One Shot—No Hit? Evaluation of a Stress-Prevention Workshop for Adolescent Soccer Players in a Randomized Controlled Trial
Authors: Belz Johanna , Kleinert Jens , Anderten Moritz 
Published: June 2020

Adolescent soccer players experience many stressors and negative stress-related outcomes. Short-term stress-prevention programs are frequently implemented in youth sports, although there is limited evidence of their usefulness and effectiveness. Thus, the present study evaluated the usefulness and effectiveness of a stress-prevention workshop for adolescent soccer players. Ninety-two soccer players (age: M = 15.5 years, SD = 1.43; 31.5% female) were randomly allocated to either an intervention group or an intervention control group. To evaluate effectiveness, stress, coping, and depression were assessed at baseline (t1) and 4 weeks postworkshop (t2). To investigate usefulness, the perceived quality of results was assessed at t2. No intervention effects on stress, coping, and depression emerged, but both groups exhibited high values regarding perceived quality of results. Although one workshop might not be enough to modify stress-related parameters, it may be useful for adolescent soccer players and pave the way for long-term interventions.
Time-driven activity-based costing for patients with multiple chronic conditions: a mixed-method study to cost care in a multidisciplinary and integrated care delivery centre at a university-affiliated tertiary teaching hospital in Stockholm, Sweden
Authors: Keel George , Muhammad Rafiq , Savage Carl , Spaak Jonas , Gonzalez Ismael , Lindgren Peter , Guttmann Christian , Mazzocato Pamela 
Published: June 2020

ObjectiveThis study can be applied to cost the complex non-standardised processes used to treat patients with multiple chronic conditions.DesignA mixed-method approach to cost analysis, following a modified healthcare-specific version of the seven-step Time-Driven Activity-Based Costing (TDABC) approach.SettingA multidisciplinary integrated and person-centred care delivery centre at a university-affiliated tertiary teaching hospital in Stockholm, Sweden, designed to improve care coordination for patients with multiple chronic conditions, specifically diabetes, cardiovascular disease and kidney disease.Participants314 patients (248 men and 66 women) fit inclusion criteria. Average age was 80 years.ResultsThis modified TDABC analysis costed outpatient care for patients with multiple chronic conditions. The approach accounted for the difficulty of conceptualising care cycles. The estimated total cost, stratified by resources, can be reviewed together with existing managerial accounting statements to inform management decisions regarding the multidisciplinary centre.ConclusionsThis article demonstrates that the healthcare-specific seven-step approach to TDABC can be applied to cost care for patients with multiple chronic conditions, where pathways are not yet discernable. It became clear that there was a need for slight methodological adaptations for this particular patient group to make it possible to cost these pathways, stratified by activity and resource. The value of this approach can be discerned from the way management incorporated the results of this analysis into the development of their hospital strategy. In the absence of integrated data infrastructures that can link patients and resources across financial, clinical and process data sets, the scalability of this method will be difficult.
Fair measures for countable-to-one maps
Authors: Rodrigues Ana , Roth Samuel , Roth Zuzana 
Published: June 2020

In this paper, we generalize the recently introduced concept of fair measure [M. Misiurewicz and A. Rodrigues, Counting preimages, Ergod. Theor. Dyn. Syst. 38 (2018) 1837–1856]. We study fair measures for Markov and mixing interval maps with countably many branches. We investigate them in terms of the recurrence properties of some underlying countable Markov shifts, both from the stochastic viewpoint and from the viewpoint of thermodynamical formalism. Finally, we move beyond the interval and look for fair measures for graph maps.
Abstract A05: Nomograms based on the SEER database for predicting the prognosis of pulmonary large-cell neuroendocrine carcinoma: A population-based STROBE cohort study
Authors: Wu Hong-fen 
Published: June 2020

Abstract
Background: This work aimed at the development and validation of nomograms for predicting patient survival cancer-specific survival (CSS) and overall survival (OS) in the context of pulmonary large-cell neuroendocrine carcinoma (LCNEC).
Material and Methods: Based on the SEER database, patients were selected who received diagnosis between the period 2004 and 2014, through the Surveillance, Epidemiology, and End Results (SEER) database. Variables were subjected to univariate and multivariate studies, performed through Cox’s Proportional Hazards Regression model. The 3- and 5-year CSS and OS were predicted based on a nomogram constructed from prognostic factors that were independent. The accuracy of the nomogram was evaluated using discrimination and calibration plots.
Results: From 1,837 eligible patients based on the SEER database, assignment of 1,276 patients was done to the training set, while that of 561 patients was done to the validation set. Multivariate analyses revealed that age, laterality, tumor size, N stage, M stage, surgery, and chemotherapy were significant prognostic factors for CSS, while those of OS were age, laterality, tumor size, surgery, N and M stages, chemotherapy, and radiation. The concordance index (C-index) for CSS was 0.781 (95% CI: 0.766-0.796) and 0.754 (95% CI: 0.730-0.778) for the internal and external validations, respectively. The values for OS were 0.791 (95%CI: 0.776-0.806) and 0.775 (95% CI: 0.751-0.799), respectively. For the training and the validation sets, discrimination in terms of prediction of OS and CSS was better in the nomograms against the SEER summary stage as well as AJCC TNM staging systems (6th edition) (P&lt;0.001). The CSS and OS predicted by the nomograms closely corresponded to actual observation as shown by calibration plots.
Conclusion: Prediction of the 3- and 5-year CSS and OS of patients with pulmonary LCNEC by nomograms with higher accuracy than existing staging models was demonstrated.
Note: This abstract was not presented at the conference.
Citation Format: Hong-fen Wu. Nomograms based on the SEER database for predicting the prognosis of pulmonary large-cell neuroendocrine carcinoma: A population-based STROBE cohort study [abstract]. In: Proceedings of the AACR Special Conference on the Evolving Landscape of Cancer Modeling; 2020 Mar 2-5; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2020;80(11 Suppl):Abstract nr A05.
Abstract A09: Pregnancy reprograms the epigenome of mammary epithelial cells and blocks the development of premalignant mammary lesions in response to cMYC-overexpression
Authors: Feigman Mary J. , Moss Matthew A. , Chen Chen , Cyrill Samantha L. , Ciccone Michael , Trousdell Marygrace , Yang Shih Ting , Frey Wesley D. , Wilkinson John E. , dos Santos Camila O. 
Published: June 2020

Abstract
Pregnancy instates a series of cellular and molecular modifications in the mammary epithelial cells (MECs) of the adult female mammary gland. Pregnancy is also known for decreasing the predisposition of rodent and human MECs to oncogenesis. In order to understand the molecular basis for this protective effect, we analyzed the epigenetic changes in the enhancer landscape of murine, post-pregnancy MECs, and their effect on gene regulation, tissue development, and oncogenesis. Using in vivo and in vitro models of normal and malignant mammary development, we found that completion of a pregnancy cycle changed the dynamics of cellular proliferation and gene expression in response to a second wave of pregnancy hormones. Our results also demonstrated that post-pregnancy MECs are resistant to the molecular programs driven by cMYC overexpression, a response that blocked the development of premalignant lesions but did not perturb the pregnancy-induced epigenomic landscape.
Citation Format: Mary J. Feigman, Matthew A. Moss, Chen Chen, Samantha L. Cyrill, Michael Ciccone, Marygrace Trousdell, Shih Ting Yang, Wesley D. Frey, John E. Wilkinson, Camila O. dos Santos. Pregnancy reprograms the epigenome of mammary epithelial cells and blocks the development of premalignant mammary lesions in response to cMYC-overexpression [abstract]. In: Proceedings of the AACR Special Conference on the Evolving Landscape of Cancer Modeling; 2020 Mar 2-5; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2020;80(11 Suppl):Abstract nr A09.
Abstract A13: ASCL1 confers tolerance to tyrosine kinase inhibitors in EGFR mutant lung cancer
Authors: Hu Bomiao , de Miguel Fernando J. , Liu Zongzhi , Chan Lok-Hei , Melnick Mary Ann , Yan Qin , Nguyen Don , Fan Rong , Politi Katerina 
Published: June 2020

Abstract
The majority of EGFR mutant lung adenocarcinomas respond well to EGFR tyrosine kinase inhibitors (TKIs). However, the majority of these responses are partial, with drug-tolerant residual disease remaining even at the time of maximal response. This residual disease serves as a reservoir for the emergence of acquired resistance and tumor relapse, which inevitably occurs in patients treated with TKIs. It is thus critical to understand the biology of residual tumor cells and find out the mechanisms that underlie drug tolerance. Knowledge of such mechanisms could lead to the identification of potential strategies to forestall the emergence of drug resistance. Studies of residual disease have been hampered by the difficulty of studying these persister cells in patient specimens, and most studies to date have relied on analysis of established cell lines in culture. To investigate the cellular and molecular properties of residual tumor cells in vivo, we leveraged patient-derived models of EGFR mutant lung cancer. Three EGFR mutant PDXs were treated with the 3rd-generation TKI osimertinib. Tumors regressed in all cases, but measurable residual tumor remained in 2 out of the 3 PDXs even after 6 weeks of osimertinib treatment. Whole-exome sequencing (WES) of the untreated PDXs compared to the residual tumors revealed an unchanged mutational landscape between the samples, indicating that genetic mechanisms did not account for drug tolerance. Bulk RNA-sequencing, however, revealed extensive transcriptional changes between the untreated PDX and residual disease. In one of the PDXs, we identified upregulation of neuroendocrine lineage transcription factor ASCL1 in residual disease compared to untreated tumors. Using single-cell RNA-sequencing, we found a pre-existing ASCL1hi tumor cell population in untreated tumors, suggesting that these cells, which possessed drug-tolerant properties, were selected for during drug treatment. Depending on the cell line examined, expression of ASCL1 in human mutant EGFR lung cancer cell lines increased the number of persister clones following osimertinib treatment, indicating that the cellular context contributed to ASCL1’s role in conferring drug tolerance. Our studies provide insights into the role of neuroendocrine factor ASCL1 as a potential driver of drug tolerance in mutant EGFR lung cancer, and ongoing work is focused on identifying the mechanistic underpinnings of these findings.
Citation Format: Bomiao Hu, Fernando J. de Miguel, Zongzhi Liu, Lok-Hei Chan, Mary Ann Melnick, Qin Yan, Don Nguyen, Rong Fan, Katerina Politi. ASCL1 confers tolerance to tyrosine kinase inhibitors in EGFR mutant lung cancer [abstract]. In: Proceedings of the AACR Special Conference on the Evolving Landscape of Cancer Modeling; 2020 Mar 2-5; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2020;80(11 Suppl):Abstract nr A13.
Abstract A16: Patient-derived organoid-based models for endometrial cancer
Authors: Berg Hege F. , Fonnes Tina , Strand Elin , Espedal Heidi , Stefansson Ingunn M. , McCormack Emmet , Bjørge Line , Trovik Jone , Haldorsen Ingfrid S. , Hoyvik Erling A. , Krakstad Camilla 
Published: June 2020

Abstract
Introduction: Comprehensive profiling of tumors using omics technologies has improved our understanding of the molecular landscape of endometrial cancer (EC), building the foundation for precision medicine. However, targeted therapies that show promise in preclinical research are failing clinical trials, which is partly explained by the lack of models that mimic the physiopathology of patients. We aimed at establishing organoids and organoid-based patient-derived xenograft (O-PDX) models as part of a new preclinical platform for endometrial cancer.
Methods: Aggregates of tumor cells were isolated from fresh tumor samples, followed by long-term culturing as organoids in a chemically defined medium. Established organoids were implanted into the left uterine horn of NSG mice, and tumor growth was monitored using near-infrared fluorescence imaging (NIRF). Patient tissue, organoids, and corresponding O-PDXs were characterized by histology and whole-exome sequencing and by immunohistochemical staining of important endometrial cancer biomarkers. For proof of concept, selected models were treated with conventional therapeutic agents, including in vivo treatment with carboplatin.
Results: Organoids and orthotopic O-PDXs representing different subtypes of endometrial cancer were successfully established. Histologic and molecular profiles of organoids are similar to patient tissue, also after long-term culturing, and characteristics of O-PDXs were sustained after rederivation in vivo. Proof-of-concept drug testing shows heterogenous sensitivity to clinically administered chemotherapeutics.
Conclusion: We have extended the collection of EC organoids and established O-PDX models for in vivo studies. This state-of-the-art preclinical platform enables more clinically relevant drug testing that will facilitate translation into relevant clinical trials.
Citation Format: Hege F. Berg, Tina Fonnes, Elin Strand, Heidi Espedal, Ingunn M. Stefansson, Emmet McCormack, Line Bjørge, Jone Trovik, Ingfrid S. Haldorsen, Erling A. Hoyvik, Camilla Krakstad. Patient-derived organoid-based models for endometrial cancer [abstract]. In: Proceedings of the AACR Special Conference on the Evolving Landscape of Cancer Modeling; 2020 Mar 2-5; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2020;80(11 Suppl):Abstract nr A16.
Abstract A17: Polyploid giant cancer cells lead to evolution of drug resistance in high-grade ovarian cancer
Authors: Niu Na , Li Xiaoran , Yao Jun , Sood Anil , Liu Jinsong 
Published: June 2020

Abstract
Whole genomic duplications (WGD) have been reported in 37% to 56% of high-grade cancers. WGD leads to formation of polyploid giant cancer cells (PGCCs) with salient and atypical nuclear morphology noted by light microscopy. However, PGCCs are generally considered nonviable due to their inability to execute mitosis. We have recently reported that PGCCs are capable of generating mitosis-competent progeny cells via primitive amitotic division including budding, splitting, and burst. We have further demonstrated that PGCCs are part of the process of somatic reprogramming named the giant cell life cycle composed of four distinct but overlapping phases including initiation, self-renewal, termination, and stability. The giant cell life cycle resets the somatic cell from the mitotic cycle to stress-induced endoreplication cell cycle via WGD to form PGCCs. The PGCCs activate endogenous embryonic factors for the reprogramming, which leads to the birth of drug-resistant cells by clonal selection from newly generated heterogeneous cancer stem cells. However, the underlying genetic and epigenetic mechanisms during WGD remain unclear. By mapping DNA methylation and whole-genome sequencing, monitoring the telomere dynamics, and tracking the cellular and nuclear morphology using microscopic time-lapse imaging observations during the time course of giant cell life cycle, we hereby provide new evidence that the daughters cells derived from PGCCs have massive alterations at the whole-genome and epigenome levels. The reprogrammed resistant daughter cells are achieved, at least in part, by genomic instability via shortened telomeres. Targeting PGCCs and promoting their differentiation during the course of giant cell life cycle may represent a novel approach to intercept drug resistance.
Citation Format: Na Niu, Xiaoran Li, Jun Yao, Anil Sood, Jinsong Liu. Polyploid giant cancer cells lead to evolution of drug resistance in high-grade ovarian cancer [abstract]. In: Proceedings of the AACR Special Conference on the Evolving Landscape of Cancer Modeling; 2020 Mar 2-5; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2020;80(11 Suppl):Abstract nr A17.
Abstract A27: Heterotypic 3D bioprinted tissues to interrogate tumor-microenvironment crosstalk in cancer
Authors: Langer Ellen M. , English Isabel A. , Turnidge Megan A. , Doha Zinab O. , Sears Rosalie C. 
Published: June 2020

Abstract
The tumor microenvironment is composed of multiple cell types (e.g., fibroblast, vascular, and immune cells), extracellular matrix (ECM) proteins, and signaling molecules that critically influence tumor cell phenotypes. The study of isolated tumor cells in culture has contributed to the discovery of oncogenes and tumor suppressors that regulate oncogenic phenotypes. As tumors develop, however, cancer cells secrete factors that functionally reprogram the genetically “normal” stromal cells in their environment. These tumor-associated stromal cells then further alter the microenvironment, providing tumor-stromal cell and tumor-ECM interactions that critically regulate tumor behaviors such as early tumor initiation, metastatic progression, and response to therapies. We recently developed heterotypic, scaffold-free tissue models of advanced cancer using an extrusion-based bioprinter system. Multiple cell types including cancer cells, fibroblasts, bone marrow-derived mesenchymal stem cells, and endothelial cells can be incorporated into bioprinted tissues with defined architecture. We found that cells within these structures exhibit a tissue-like cellular density, proliferate, deposit ECM, migrate, and respond to extrinsic signals. Cells within these tissues self-organize to form complex structures, as indicated by nascent endothelial networks, and respond to extrinsic signals. We assessed intrinsic, extrinsic, and spatial tumorigenic phenotypes including cell survival, cell proliferation, differentiation state, ECM deposition, and cellular migration within these tissues in response to extrinsic signals or therapies. Together, this work demonstrates that bioprinted tumor tissue models recapitulate many aspects of in vivo neoplastic tissues. We are continuing to use 3D bioprinted tumor tissues, leveraging the manipulable nature of these models to interrogate the role of distinct tumor microenvironments on tumor cell phenotypes including proliferation, migration, and response to therapies. In pancreatic cancer models, we have printed tissues containing pancreatic stellate cells with and without knockdown of the prolyl isomerase PIN1, which we show inhibits stellate cell activation. We show that loss of PIN1 in the stellate cells surrounding the tumor has effects not only on activation markers of fibroblasts, but also on tumor, endothelial, and immune phenotypes within the tissues. Further work is focused on characterizing the signals that drive these changes.
Citation Format: Ellen M. Langer, Isabel A. English, Megan A. Turnidge, Zinab O. Doha, Rosalie C. Sears. Heterotypic 3D bioprinted tissues to interrogate tumor-microenvironment crosstalk in cancer [abstract]. In: Proceedings of the AACR Special Conference on the Evolving Landscape of Cancer Modeling; 2020 Mar 2-5; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2020;80(11 Suppl):Abstract nr A27.