Defining hope as a cognitive set that is composed of a reciprocally derived sense of successful (a) agency (goal-directed determination) and (b) pathways (planning of ways to meet goals), an individual-differences measure is developed. Studies demonstrate acceptable internal consistency and test-retest reliability, and the factor structure identifies the agency and pathways components of the Hope Scale. Convergent and discriminant validity are documented, along with evidence suggesting that Hope Scale scores augmented the prediction of goal-related activities and coping strategies beyond other self-report measures. Construct validational support is provided in regard to predicted goal-setting behaviors; moreover, the hypothesized goal appraisal processes that accompany the various levels of hope are corroborated. The importance of hope has long been recognized. In Western culture, the concept of hope was first elaborated in the myth of Pandora. As the story goes, Zeus was angry at Prometheus for stealing fire from the gods. With revenge in mind, Zeus sent Pandora to earth with a box full of evil creatures. Zeus told Pandora not to open the box, yet he knew that her curiosity would soon overwhelm her. As predicted, Pandora eventually opened the lid to look inside. When she did, a swarm of creatures flew out to forever plague humankind: gout, rheumatism, and colic for the body; envy, spite, and revenge for the mind. Only one creature remained in the box when Pandora finally managed to close the lid. That creature was hope, which supposedly makes human cares and troubles seem bearable as we journey toward the myriad of goals in a lifetime (Smith, 1983). Although the Pandora myth extols hope, other writings have characterized it as both a blessing and a curse. Tillich (1965) summarized this view by asserting that "hope is easy for the foolish, but hard for the wise. Everybody can lose himself into The present article is based, in part, on dissertations by Cheri Harris and John R. Anderson, as well as on master's theses by Lauren Yoshinobu, Charyle Langelle, and Pat Harney, all under the supervision of C. R. Snyder at the University of Kansas, and on a master's thesis in progress by June Gibb at the University of Illinois at Urbana-Champaign under the supervision of C. R. Snyder.

SUMMARYA comparison between solutions from simulations of a non-linear density current test problem was made in order to study the behaviour of a variety of numerical methods. The test problem was diffusion-limited so that a grid-converged reference solution could be generated using high spatial resolution. Solutions of the test problem using several different resolutions were computed by the participants of the 'Workshop on Numerical Methods for Solving Nonlinear Flow Problems', which was held on 11-13 September 1990 at the National Center for Supercomputing Applications (NCSA). In general, it was found that when the flow was adequately resolved, all of the numerical schemes produced solutions that contained the basic physics as well as most of the flow detail of the reference solution. However, when the flow was marginally resolved, there were significant differences between the solutions produced by the various models. Finally, when the flow was poorly resolved, none of the models performed very well. While higher-order and spectral-type schemes performed best for adequately and marginally resolved flow, solutions made with these schemes were virtually unusable for poorly resolved flow. In contrast, the monotonic schemes provided the most coherent and smooth solutions for poorly resolved flow, however with noticeable amplitude and phase speed errors, even at finer resolutions.

All arthropod-borne flaviviruses generate a short noncoding RNA (sfRNA) from the viral 39 untranslated region during infection due to stalling of the cellular 59-to-39 exonuclease XRN1. We show here that formation of sfRNA also inhibits XRN1 activity. Cells infected with Dengue or Kunjin viruses accumulate uncapped mRNAs, decay intermediates normally targeted by XRN1. XRN1 repression also resulted in the increased overall stability of cellular mRNAs in flavivirus-infected cells. Importantly, a mutant Kunjin virus that cannot form sfRNA but replicates to normal levels failed to affect host mRNA stability or XRN1 activity. Expression of sfRNA in the absence of viral infection demonstrated that sfRNA formation was directly responsible for the stabilization of cellular mRNAs. Finally, numerous cellular mRNAs were differentially expressed in an sfRNA-dependent fashion in a Kunjin virus infection. We conclude that flaviviruses incapacitate XRN1 during infection and dysregulate host mRNA stability as a result of sfRNA formation.

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