Towards a cross-cultural assessment of binge-watching: Psychometric evaluation of the “watching TV series motives” and “binge-watching engagement and symptoms” questionnaires across nine languages

In view of the growing interest regarding binge-watching (i.e., watching multiple episodes of television (TV) series in a single sitting) research, two measures were developed and validated to assess binge-watching involvement (“Binge-Watching Engagement and Symptoms Questionnaire”, BWESQ) and related motivations (“Watching TV Series Motives Questionnaire”, WTSMQ). To promote international and cross-cultural binge-watching research, the present article reports on the validation of these questionnaires in nine languages (English, French, Spanish, Italian, German, Hungarian, Persian, Arabic, Chinese). Both questionnaires were disseminated, together with additional self-report measures of happiness, psychopathological symptoms, impulsivity and problematic internet use among TV series viewers from a college/university student population (N = 12,616) in 17 countries. Confirmatory factor, measurement invariance and correlational analyses were conducted to establish structural and construct validity. The two questionnaires had good psychometric properties and fit in each language. Equivalence across languages and gender was supported, while construct validity was evidenced by similar patterns of associations with complementary measures of happiness, psychopathological symptoms, impulsivity and problematic internet use. The results support the psychometric validity and utility of the BWESQ and WTSMQ for conducting cross-cultural research on binge-watching

Reduced end-systolic pressure-volume ratio response to exercise: A marker of subclinical myocardial disease in type 2 diabetes

Background-Limitations in the predictive value of negative exercise echocardiography in type 2 diabetes mellitus has been linked to a reduced end-systolic pressure-volume response (ESPVR). We sought whether abnormal ESPVR reflected subclinical diabetic heart disease by examining the association between the ESPVR and markers of myocardial dysfunction and to establish if the change (Delta) or peak systolic blood pressure/end-systolic left ventricular volume ratio (SP/ESV) is a better marker of contractile reserve in type 2 diabetes mellitus

Various mutations compensate for a deleterious lacZα insert in the replication enhancer of M13 bacteriophage

<div><p>M13 and other members of the Ff class of filamentous bacteriophages have been extensively employed in myriad applications. The Ph.D. series of phage-displayed peptide libraries were constructed from the M13-based vector M13KE. As a direct descendent of M13mp19, M13KE contains the lacZα insert in the intergenic region between genes IV and II, where it interrupts the replication enhancer of the (+) strand origin. Phage carrying this 816-nucleotide insert are viable, but propagate in <i>E</i>. <i>coli</i> at a reduced rate compared to wild-type M13 phage, presumably due to a replication defect caused by the insert. We have previously reported thirteen compensatory mutations in the 5’-untranslated region of gene II, which encodes the replication initiator protein gIIp. Here we report several additional mutations in M13KE that restore a wild-type propagation rate. Several clones from constrained-loop variable peptide libraries were found to have ejected the majority of lacZα gene in order to reconstruct the replication enhancer, albeit with a small scar. In addition, new point mutations in the gene II 5’-untranslated region or the gene IV coding sequence have been spontaneously observed or synthetically engineered. Through phage propagation assays, we demonstrate that all these genetic modifications compensate for the replication defect in M13KE and restore the wild-type propagation rate. We discuss the mechanisms by which the insertion and ejection of the lacZα gene, as well as the mutations in the regulatory region of gene II, influence the efficiency of replication initiation at the (+) strand origin. We also examine the presence and relevance of fast-propagating mutants in phage-displayed peptide libraries.</p></div

Schematics of the M13KE genome.

<p>(A) The map of M13KE is shown. The (+) strand origin is divided into Domains A and B [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0176421#pone.0176421.ref020" target="_blank">20</a>]. Domain A (nucleotides 5769–5819 in both WT-M13 and M13KE) is the “core origin” and is required for both (+) strand initiation and termination. Domain A is extremely sensitive to deletions and insertions, which reduce biological activity to ≤ 0.01% [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0176421#pone.0176421.ref020" target="_blank">20</a>]. Domain B stretches from position 5820 to about 5910 in wild-type M13 (WT-M13), but it is interrupted in M13KE by the lacZα insert (the separated segments are indicated as B1 and B2). Dubbed the “replication enhancer,” Domain B is required for (+) strand initiation and is moderately sensitive to inserts and deletions, which reduce biological activity to ≥ 1% [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0176421#pone.0176421.ref020" target="_blank">20</a>,<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0176421#pone.0176421.ref031" target="_blank">31</a>]. The locations of spontaneous mutations and ejections in M13KE are labeled as gene II 5’-UTR, ΔlacZα, and T5091C. The T5091C mutation is a reversion back to the WT-M13 nucleotide at position 5092 (the number is lower by 1 nt due a missing 1565T in M13mp18,19 and M13KE). The map of WT-M13 would be identical to M13KE with the exception of the lacZα insert (all downstream numbering is 815 nt lower in WT-M13). The (-) strand origin (not labeled) is upstream of the (+) strand origin in the intergenic region. The map was constructed using SnapGene^®. (B) The exact locations of the lacZα insert and ejections are indicated. Nucleotide numbering corresponds to WT-M13. Domain A is not shown except for last downstream base, 5819C. In M13mp-based phage, an 816-nt insert containing the lacZα gene is placed in Domain B between nucleotides 5868 and 5869. Two different spontaneous ejections have arisen in M13KE, ΔlacZα-827 and ΔlacZα-838, both of which left behind eleven nucleotides of the lacZα insert. The vast majority of the lacZα insert was removed, in addition to a small section of Domain B: 22 nucleotides in the smaller (827-nt) ejection and 33 nt in the larger (838-nt) ejection.</p