The Role of Evaluability Bias and the Fairness Effect in the Escalation of Commitment to Troubled Software Product Development Projects

New software product development entails considerable risks. One significant risk is that decision makers can become overly committed to troubled software product development projects (i.e., escalation of commitment). While prior research has identified factors that promote escalation in information technology projects, there has been little attempt to leverage the context of software product development, which can include evaluating attributes of a software product under development and weighing a personal financial reward tied to a successful product launch. In this study, we conducted two experiments to investigate how evaluability bias concerning software attributes and the fairness effect that arises from the relative amount of a personal financial reward influence the escalation of commitment to troubled software product development projects. Our findings suggest that the escalation of commitment to troubled software product development projects is influenced by both evaluability bias, which affects the perceived attractiveness of a software product under development, and the fairness effect, which influences the perceived attractiveness of a personal financial reward tied to a successful product launch. This study contributes to both the information systems literature and the escalation literature by providing novel theoretical explanations as to why escalation occurs in the context of new software product developmen

Absolutely 0 Evidence

Statistical analysis is often used to evaluate the strength of evidence for or against scientific hypotheses. Here we consider evidence measurement from the point of view of representational measurement theory, focusing in particular on the 0-points of measurement scales. We argue that a properly calibrated evidence measure will need to count up from absolute 0, in a sense to be defined, and that this 0-point is likely to be something other than what one might have expected. This suggests the need for a new theory of statistical evidence in the context of which calibrated evidence measurement becomes tractable

SNP@Ethnos: a database of ethnically variant single-nucleotide polymorphisms

Inherited genetic variation plays a critical but largely uncharacterized role in human differentiation. The completion of the International HapMap Project makes it possible to identify loci that may cause human differentiation. We have devised an approach to find such ethnically variant single-nucleotide polymorphisms (ESNPs) from the genotype profile of the populations included in the International HapMap database. We selected ESNPs using the nearest shrunken centroid method (NSCM), and performed multiple tests for genetic heterogeneity and frequency spectrum on genes having ESNPs. The function and disease association of the selected SNPs were also annotated. This resulted in the identification of 100 736 SNPs that appeared uniquely in each ethnic group. Of these SNPs, 1009 were within disease-associated genes, and 85 were predicted as damaging using the Sorting Intolerant From Tolerant system. This study resulted in the creation of the SNP@Ethnos database, which is designed to make this type of detailed genetic variation approach available to a wider range of researchers. SNP@Ethnos is a public database of ESNPs with annotation information that currently contains 100 736 ESNPs from 10 138 genes, and can be accessed at and or directly at

Investigation of grain-boundary effect on hydrogen behaviors in single- and poly- crystalline medium-entropy CrCoNi alloy

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Control of mammalian G protein signaling by N-terminal acetylation and the N-end rule pathway

Rgs2, a regulator of G proteins, lowers blood pressure by decreasing signaling through Gαq. Human patients expressing Met-Leu-Rgs2 (ML-Rgs2) or Met-Arg-Rgs2 (MR-Rgs2) are hypertensive relative to people expressing wild-type Met-Gln-Rgs2 (MQ-Rgs2). We found that wild-type MQ-Rgs2 and its mutant, MR-Rgs2, were destroyed by the Ac/N-end rule pathway, which recognizes Nα-terminally acetylated (Nt-acetylated) proteins. The shortest-lived mutant, ML-Rgs2, was targeted by both the Ac/N-end rule and Arg/N-end rule pathways. The latter pathway recognizes unacetylated N-terminal residues. Thus, the Nt-acetylated Ac-MX-Rgs2 (X = Arg, Gln, Leu) proteins are specific substrates of the mammalian Ac/N-end rule pathway. Furthermore, the Ac/N-degron of Ac-MQ-Rgs2 was conditional, and Teb4, an endoplasmic reticulum (ER) membrane-embedded ubiquitin ligase, was able to regulate G protein signaling by targeting Ac-MX-Rgs2 proteins for degradation through their N^α-terminal acetyl group