24 research outputs found

    Would the Real Loneliness Please Stand Up? The Validity of Loneliness Scores and the Reliability of Single-Item Scores

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    Several measures that assess loneliness have been developed for adults. Across three studies, we investigated psychometric features of scores of different versions of the Rasch-Type Loneliness Scale, the University of California Los Angeles Loneliness Scale, and three single-item measures. In Study 1 (N = 697 self-ratings, N = 282 informant-ratings of 160 targets) and Study 2 (N = 1,216 individuals from 608 couples), we investigated convergent validity, self-informant agreement, and nomological nets of the item scores using correlates related to demographic aspects, personality, satisfaction, and network characteristics. In Study 3 (N = 411), we estimated a reliability of rxx > .70 for scores of three single-item measures of loneliness. Overall, scores of all measures and their nomological nets were highly correlated within and across studies, indicating that the scores of the included measures are all reliable and valid. Recommendations for choosing a loneliness measure are discussed

    Drosophila selenophosphate synthetase 1 regulates vitamin B6 metabolism: prediction and confirmation

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    <p>Abstract</p> <p>Background</p> <p>There are two selenophosphate synthetases (SPSs) in higher eukaryotes, SPS1 and SPS2. Of these two isotypes, only SPS2 catalyzes selenophosphate synthesis. Although SPS1 does not contain selenophosphate synthesis activity, it was found to be essential for cell growth and embryogenesis in <it>Drosophila</it>. The function of SPS1, however, has not been elucidated.</p> <p>Results</p> <p>Differentially expressed genes in <it>Drosophila </it>SL2 cells were identified using two-way analysis of variance methods and clustered according to their temporal expression pattern. Gene ontology analysis was performed against differentially expressed genes and gene ontology terms related to vitamin B6 biosynthesis were found to be significantly affected at the early stage at which megamitochondria were not formed (day 3) after <it>SPS1 </it>knockdown. Interestingly, genes related to defense and amino acid metabolism were affected at a later stage (day 5) following knockdown. Levels of pyridoxal phosphate, an active form of vitamin B6, were decreased by <it>SPS1 </it>knockdown. Treatment of SL2 cells with an inhibitor of pyridoxal phosphate synthesis resulted in both a similar pattern of expression as that found by <it>SPS1 </it>knockdown and the formation of megamitochondria, the major phenotypic change observed by <it>SPS1 </it>knockdown.</p> <p>Conclusions</p> <p>These results indicate that SPS1 regulates vitamin B6 synthesis, which in turn impacts various cellular systems such as amino acid metabolism, defense and other important metabolic activities.</p

    Does Smile Intensity in Photographs Really Predict Longevity? A Replication and Extension of Abel and Kruger (2010)

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    Abel and Kruger (2010) found that the smile intensity of professional baseball players who were active in 1952, as coded from photographs, predicted these players' longevity. In the current investigation, we sought to replicate this result and to extend the initial analyses. We analyzed (a) a sample that was almost identical to the one from Abel and Kruger's study using the same database and inclusion criteria (N = 224), (b) a considerably larger nonoverlapping sample consisting of other players from the same cohort (N = 527), and (c) all players in the database (N = 13,530 valid cases). Like Abel and Kruger, we relied on categorical smile codings as indicators of positive affectivity, yet we supplemented these codings with subjective ratings of joy intensity and automatic codings of positive affectivity made by computer programs. In both samples and for all three indicators, we found that positive affectivity did not predict mortality once birth year was controlled as a covariate

    Adaptive evolution of Saccharomyces cerevisiae to generate strains with enhanced glycerol production

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    The development of new wine yeast strains with improved characteristics is critical in the highly competitive wine market, which faces the demand of ever-changing consumer preferences. Although new strains can be constructed using recombinant DNA technologies, consumer concerns about genetically modified (GM) organisms strongly limit their use in food and beverage production. We have applied a non-GM approach, adaptive evolution with sulfite at alkaline pH as a selective agent, to create a stable yeast strain with enhanced glycerol production; a desirable characteristic for wine palate. A mutant isolated using this approach produced 41% more glycerol than the parental strain it was derived from, and had enhanced sulfite tolerance. Backcrossing to produce heterozygous diploids revealed that the high-glycerol phenotype is recessive, while tolerance to sulfite was partially dominant, and these traits, at least in part, segregated from each other. This work demonstrates the potential of adaptive evolution for development of novel non-GM yeast strains, and highlights the complexity of adaptive responses to sulfite selection.D. R. Kutyna, C. Varela, G. A. Stanley, A. R. Borneman, P. A. Henschke, P. J. Chamber

    Repression of ADH1 and ADH3 during zinc deficiency by Zap1-induced intergenic RNA transcripts

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    The transcriptional activator Zap1 induces target gene expression in response to zinc deficiency. We demonstrate that during zinc starvation, Zap1 is required for the repression of ADH1 expression. ADH1 encodes the major zinc-dependent alcohol dehydrogenase that is utilized during fermentation. During zinc starvation, Zap1 binds upstream of the activator Rap1 and induces an intergenic RNA transcript, ZRR1. ZRR1 expression leads to the transient displacement of Rap1 from the ADH1 promoter resulting in ADH1 repression. Using a microarray-based approach, we screened for additional genes repressed by Zap1 intergenic transcripts. We found that ADH3, the major mitochondrial alcohol dehydrogenase, is regulated in a manner similar to ADH1. Thus, during zinc deficiency, Zap1 mediates the repression of two of the most abundant zinc-requiring enzymes
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