Variants of Callous-unemotional traits in childhood: investigation of attachment profile and hostile attribution bias.

There is increasing evidence of interest in describing two variants of CallousUnemotional (CU) traits based on high (secondary variant) or low (primary variant) levels of anxiety. However, studies are limited in childhood. The present study aimed to further the understanding of the variants, specifically in association with hostile attribution bias (HAB) and attachment. In a community sample of children aged 4 to 9 (N = 70), the study examined whether anxiety moderated the association of CU traits with HAB, secure and disorganized attachment representations. Hierarchical regression analyses revealed that CU traits were positively associated with disorganized attachment, regardless of the anxiety level. In contrast, CU traits were not associated with secure attachment. A significant interaction revealed that CU traits were positively associated with HAB only at high levels of anxiety. Implications for understanding the variants of CU traits and hypotheses regarding their developmental trajectories are discussed.

Development and validation of a short version of the Sarcopenia Quality of Life questionnaire: the SF-SarQoL.

PURPOSE: To facilitate the measurement of quality of life in sarcopenia, we set out to reduce the number of items in the previously validated Sarcopenia Quality of Life (SarQoL®) questionnaire, and to evaluate the clinimetric properties of this new short form. METHODS: The item reduction process was carried out in two phases. First, information was gathered through item-impact scores from older people (n = 1950), a Delphi method with sarcopenia experts, and previously published clinimetric data. In the second phase, this information was presented to an expert panel that decided which of the items to include in the short form. The newly created SFSarQoL was then administered to older, community-dwelling participants who previously participated in the SarcoPhAge study. We examined discriminative power, internal consistency, construct validity, test-retest reliability, structural validity and examined item parameters with a graded response model (IRT). RESULTS: The questionnaire was reduced from 55 to 14 items, a 75% reduction. A total of 214 older, community-dwelling people were recruited for the validation study. The clinimetric evaluation showed that the SF-SarQoL® can discriminate on sarcopenia status [EWGSOP2 criteria; 34.52 (18.59-43.45) vs. 42.86 (26.56-63.69); p = 0.043], is internally consistent (α = 0.915, ω = 0.917) and reliable [ICC = 0.912 (0.847-0.942)]. A unidimensional model was fitted (CFI = 0.978; TLI = 0.975; RMSEA = 0.108, 90% CI 0.094-0.123; SRMR = 0.055) with no misfitting items and good response category separation. CONCLUSIONS: A new, 14-item, short form version of the Sarcopenia Quality of Life questionnaire has been developed and shows good clinimetric properties.

Spontaneous atopic dermatitis due to immune dysregulation in mice lacking Adamts2 and 14.

Since its first description, ADAMTS14 has been considered as an aminoprocollagen peptidase based on its high similarity with ADAMTS3 and ADAMTS2. As its importance for procollagen processing was never experimentally demonstrated in vivo, we generated Adamts14-deficient mice. They are healthy, fertile and display normal aminoprocollagen processing. They were further crossed with Adamts2-deficient mice to evaluate potential functional redundancies between these two highly related enzymes. Initial characterizations made on young Adamts2-Adamts14-deficient animals showed the same phenotype as that of Adamts2-deficient mice, with no further reduction of procollagen processing and no significant aggravation of the structural alterations of collagen fibrils. However, when evaluated at older age, Adamts2-Adamts14-deficient mice surprisingly displayed epidermal lesions, appearing in 2 month-old males and later in some females, and then worsening rapidly. Immunohistological evaluations of skin sections around the lesions revealed thickening of the epidermis, hypercellularity in the dermis and extensive infiltration by immune cells. Additional investigations, performed on young mice before the formation of the initial lesions, revealed that the primary cause of the phenotype was not related to alterations of the epidermal barrier but was rather the result of an abnormal activation and differentiation of T lymphocytes towards a Th1 profile. However, the primary molecular defect probably does not reside in the immune system itself since irradiated Adamts2-Adamts14-deficient mice grafted with WT immune cells still developed lesions. While originally created to better characterize the common and specific functions of ADAMTS2 and ADAMTS14 in extracellular matrix and connective tissues homeostasis, the Adamts2-Adamts14-deficient mice revealed an unexpected but significant role of ADAMTS in the regulation of immune system, possibly through a cross-talk involving mesenchymal cells and the TGFß pathways.