Panel 1: The Use of Qualitative Methods in MIS Research

The objective of this panel is to discuss how qualitative research methods, such as case studies, ethnography, and action research, can be effectively used in the study of M IS. While there has been a call for greater reliance on qualitative methods in both the social sciences and in management (see, for example, the 1979 issue of Administrative Science Quarterly devoted to qualitative methods), there has simultaneously been a shift away from these methods in MIS. Laboratory studies and surveys are seen with increasing frequency in journals such as MIS Quarterly. Qualitative methods, however, when properly applied, can provide a great deal of information for MIS researchers who are posing research questions in which organizational context and depth of knowledge are important. This panel will explore both areas of information systems research in which qualitative methods have been successfully used and areas in which they could be applied in the future. The moderator will first present a framework for analyzing the role of qualitative methods in MIS research. The framework will be based on a paper entitled The Case Research Strategy in IS Research currently being written by Benbasat, Goldstein, and Mead. The three panelists will each discuss some research in which qualitative techniques were recently employed or will be employed in the near future. Each researcher will present a different technique - case, research, ethnography, and action research. They will focus on why these methods were appropriate for the specific problem they studied. In addition, the researchers will discuss the strengths and weaknesses of the method they used and any difficulties they had in applying the method to an lS research problem. Following this, the discussant will integrate the presentations and critique the methods used by the researchers

The galactose elimination capacity and mortality in 781 Danish patients with newly-diagnosed liver cirrhosis: a cohort study

<p>Abstract</p> <p>Background</p> <p>Despite its biologic plausibility, the association between liver function and mortality of patients with chronic liver disease is not well supported by data. Therefore, we examined whether the galactose elimination capacity (GEC), a physiological measure of the total metabolic capacity of the liver, was associated with mortality in a large cohort of patients with newly-diagnosed cirrhosis.</p> <p>Methods</p> <p>By combining data from a GEC database with data from healthcare registries we identified cirrhosis patients with a GEC test at the time of cirrhosis diagnosis in 1992–2005. We divided the patients into 10 equal-sized groups according to GEC and calculated all-cause mortality as well as cirrhosis-related and not cirrhosis-related mortality for each group. Cox regression was used to adjust the association between GEC and all-cause mortality for confounding by age, gender and comorbidity, measured by the Charlson comorbidity index.</p> <p>Results</p> <p>We included 781 patients, and 454 (58%) of them died during 2,617 years of follow-up. Among the 75% of patients with a decreased GEC (<1.75 mmol/min), GEC was a strong predictor of 30-day, 1-year, and 5-year mortality, and this could not be explained by confounding (crude hazard ratio for a 0.5 mmol/min GEC increase = 0.74, 95% CI 0.59–0.92; adjusted hazard ratio = 0.64, 95% CI 0.51–0.81). Further analyses showed that the association between GEC and mortality was identical for patients with alcoholic or non-alcoholic cirrhosis etiology, that it also existed among patients with comorbidity, and that GEC was only a predictor of cirrhosis-related mortality. Among the 25% of patients with a GEC in the normal range (≥ 1.75 mmol/min), GEC was only weakly associated with mortality (crude hazard ratio = 0.79, 95% CI 0.59–1.05; adjusted hazard ratio = 0.80, 95% CI 0.60–1.08).</p> <p>Conclusion</p> <p>Among patients with newly-diagnosed cirrhosis and a decreased GEC, the GEC was a strong predictor of short- and long-term all-cause and cirrhosis-related mortality. These findings support the expectation that loss of liver function increases mortality.</p

The tmRDB and SRPDB resources

Maintained at the University of Texas Health Science Center at Tyler, Texas, the tmRNA database (tmRDB) is accessible at the URL with mirror sites located at Auburn University, Auburn, Alabama () and the Royal Veterinary and Agricultural University, Denmark (). The signal recognition particle database (SRPDB) at is mirrored at and the University of Goteborg (). The databases assist in investigations of the tmRNP (a ribonucleoprotein complex which liberates stalled bacterial ribosomes) and the SRP (a particle which recognizes signal sequences and directs secretory proteins to cell membranes). The curated tmRNA and SRP RNA alignments consider base pairs supported by comparative sequence analysis. Also shown are alignments of the tmRNA-associated proteins SmpB, ribosomal protein S1, alanyl-tRNA synthetase and Elongation Factor Tu, as well as the SRP proteins SRP9, SRP14, SRP19, SRP21, SRP54 (Ffh), SRP68, SRP72, cpSRP43, Flhf, SRP receptor (alpha) and SRP receptor (beta). All alignments can be easily examined using a new exploratory browser. The databases provide links to high-resolution structures and serve as depositories for structures obtained by molecular modeling

Gill transcriptomic responses to toxin-producing alga Prymnesium parvum in rainbow trout

This work was supported by the BBSRC EastBio PhD studentship awarded to MC, the Danish Strategic Research Council grant No 060300449B HABFISH, and the European Maritime and Fisheries Fund and the Danish Fisheries Agency joint grant “Sundt Dambrug”. Molecular work at University of Aberdeen was funded by Scottish Aquaculture Innovation grant SL 2017 08. EK was supported by BBSRC grant BB/R018812/1.The gill of teleost fish is a multifunctional organ involved in many physiological processes, including protection of the mucosal gill surface against pathogens and other environmental antigens by the gill-associated lymphoid tissue (GIALT). Climate change associated phenomena, such as increasing frequency and magnitude of harmful algal blooms (HABs) put extra strain on gill function, contributing to enhanced fish mortality and fish kills. However, the molecular basis of the HAB-induced gill injury remains largely unknown due to the lack of high-throughput transcriptomic studies performed on teleost fish in laboratory conditions. We used juvenile rainbow trout (Oncorhynchus mykiss) to investigate the transcriptomic responses of the gill tissue to two (high and low) sublethal densities of the toxin-producing alga Prymnesium parvum, in relation to non-exposed control fish. The exposure time to P. parvum (4–5 h) was sufficient to identify three different phenotypic responses among the exposed fish, enabling us to focus on the common gill transcriptomic responses to P. parvum that were independent of dose and phenotype. The inspection of common differentially expressed genes (DEGs), canonical pathways, upstream regulators and downstream effects pointed towards P. parvum-induced inflammatory response and gill inflammation driven by alterations of Acute Phase Response Signalling, IL-6 Signalling, IL-10 Signalling, Role of PKR in Interferon Induction and Antiviral Response, IL-8 Signalling and IL-17 Signalling pathways. While we could not determine if the inferred gill inflammation was progressing or resolving, our study clearly suggests that P. parvum blooms may contribute to the serious gill disorders in fish. By providing insights into the gill transcriptomic responses to toxin-producing P. parvum in teleost fish, our research opens new avenues for investigating how to monitor and mitigate toxicity of HABs before they become lethal.Publisher PDFPeer reviewe