Ruyi Jin

Emotion regulation plays a vital role in individuals’ well-being and successful functioning. In this study, we attempted to develop a computerized adaptive testing to efficiently evaluate ER, namely the CAT-ER. The initial CAT-ER item bank comprised 154 items from six commonly used ER scales, which were completed by 887 participants recruited in China. We conducted unidimensionality testing, item response theory model comparison and selection, and IRT item analysis including local independence, item fit, differential item functioning, and item discrimination. Sixty-three items with good psychometric properties were retained in the final CAT-ER. Then, two CAT simulation studies were implemented to assess the CAT-ER, which revealed that the CAT-ER developed in this study performed reasonably well, considering that it greatly lessened the test items and time without losing measurement accuracy.

© 2015 The Authors. Cellular Microbiology published by John Wiley & Sons Ltd. Botulinum neurotoxins are some of the most poisonous natural toxins. Botulinum neurotoxins associate with neurotoxin-associated proteins forming large complexes that are protected from the harsh environment of the gastrointestinal tract. However, it is still unclear how BoNT complexes as large as 900kDa traverse the epithelial barrier and what role NAPs play in toxin translocation. In this study, we examined the transit of BoNT serotype A holotoxin, complex and recombinantly purified NAP complex through cultured and polarized Caco-2 cells and, for the first time, in the small mouse intestine. Botulinum neurotoxin serotype A and NAPs in the toxin complex were detectable inside intestinal cells beginning at 2h post intoxication. Appearance of the BoNT/A holotoxin signal was slower, with detection starting at 4-6h. This indicated that the holotoxin alone was sufficient for entry but the presence of NAPs enhanced the rate of entry. Botulinum neurotoxin serotype A detection peaked at approximately 6 and 8h for complex and holotoxin, respectively, and thereafter began to disperse with some toxin remaining in the epithelia after 24h. Purified HA complexes alone were also internalized and followed a similar time course to that of BoNT/A complex internalization. However, recombinant HA complexes did not enhance BoNT/A holotoxin entry in the absence of a physical link with BoNT/A. We propose a model for BoNT/A toxin complex translocation whereby toxin complex entry is facilitated by NAPs in a receptor-mediated mechanism. Understanding the intestinal uptake of BoNT complexes will aid the development of new measures to prevent or treat oral intoxications.