40 research outputs found

    Risky Decisions and Decision Support - Does Stress Make a Difference?

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    Studies of human decision making have demonstrated that stress exacerbates risk taking. Since all decisions involve some element of risk, stress has critical impact on decision quality. Decisions are found to improve with stress up to an optimal threshold beyond which deterioration is observed. However, few studies have examined the psychological experiences underlying risk-taking behavior in conjunction with stress creators. In this paper we propose a research framework that integrates pre-conditions of stress (perceptions of high gain/loss, risk, complexity, and organizational pressure) with observed psychological experiences (time pressure, uncertainty, information overload, and dynamism) that potentially result in risky decision making. This framework suggests that decision support systems have the potential of mitigating or enhancing the psychological perceptions of stress and, hence, impacting decision quality. Empirical testing of a component of this framework provided interesting preliminary results. Subjects experiencing high stress indicated the same levels of perceived uncertainty and dynamism as subjects exposed to low stress, suggesting that use of a decision support system mitigated the perceptions of dynamism and uncertainty for the high stress group. Contrary to hypotheses, the use of a decision support system did not mitigate perceptions of information overload

    A Critical Review of Decision Support Systems Foundational Articles

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    Abstract Decision Support Systems (DSS) is a mature field of study with an extensive conceptual and empirical literature. This research study provides a starting point for learning and reviewing the foundation literature of the field. Decision support and analytics researchers can benefit from revisiting the methodologies, identifying under-explored ideas, and hopefully identifying visionary concepts from thought leaders who established the DSS research stream. This article reports a systematic examination of the DSS foundational literature published in MIS Quarterly during its first fifteen years of publication -- 1977-1991. In addition to examining the relevance of these articles to current and future research, the findings of the study provide a reference point of DSS research categories. Articles were categorized in terms of theory, methods, concepts and perspectives about computerized decision support that enrich research and encourage future exploration

    Business Analytics in the Context of Big Data: A Roadmap for Research

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    This paper builds on academic and industry discussions from the 2012 and 2013 pre-ICIS events: BI Congress III and the Special Interest Group on Decision Support Systems (SIGDSS) workshop, respectively. Recognizing the potential of “big data” to offer new insights for decision making and innovation, panelists at the two events discussed how organizations can use and manage big data for competitive advantage. In addition, expert panelists helped to identify research gaps. While emerging research in the academic community identifies some of the issues in acquiring, analyzing, and using big data, many of the new developments are occurring in the practitioner community. We bridge the gap between academic and practitioner research by presenting a big data analytics framework that depicts a process view of the components needed for big data analytics in organizations. Using practitioner interviews and literature from both academia and practice, we identify the current state of big data research guided by the framework and propose potential areas for future research to increase the relevance of academic research to practice

    The Current State of Business Intelligence in Academia

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    Current trends suggest that academia may be behind the curve in delivering effective Business Intelligence programs and course offerings to students. In December 2009 and 2010, the AIS Special Interest Group on Decision Support, Knowledge and Data Management Systems (SIGDSS) and the Teradata University Network (TUN) cosponsored the Business Intelligence Congresses and conducted surveys to improve the understanding of the state of BI in academia. This panel report describes the key findings and best practices that were identified. The article also serves as a “call to action” for universities regarding the need to close a widening gap between the BI skills of university graduates in Information Systems and other fields and BI market needs. The IS field is well positioned to be the leader in creating the next generation BI workforce. To do so, it is important for IS to begin moving on this opportunity now. We believe the necessary first step is for BI and IS leaders to advance the BI curriculum

    The Current State of Business Intelligence in Academia: The Arrival of Big Data

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    In December 2012, the AIS Special Interest Group on Decision Support, Knowledge and Data Management Systems (SIGDSS) and the Teradata University Network (TUN) cosponsored the Business Intelligence Congress 3 and conducted surveys to assess academia’s response to the growing market need for students with Business Intelligence (BI) and Business Analytics (BA) skill sets. This panel report describes the key findings and best practices that were identified, with an emphasis on what has changed since the BI Congress efforts in 2009 and 2010. The article also serves as a “call to action” for universities regarding the need to respond to emerging market needs in BI/BA, including “Big Data.” The IS field continues to be well positioned to be the leader in creating the next generation BI/BA workforce. To do so, we believe that IS leaders need to continuously refine BI/BA curriculum to keep pace with the turbulent BI/BA marketplace

    Women in Health Data Science and Statistics

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    Opportunities are expanding for women interested in health data science. This panel of leading professionals from academia and industry will highlight the accomplishments, perspectives and varied roles available for data professionals in the healthcare sector. Learn how to leverage your skills and talents into this expanding and dynamic field. Presentation: 58:4

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

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    IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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