Concurrent validity of self-rating scale of self-directed learning and self-directed learning instrument among Italian nursing students

BACKGROUND: Self-Directed Learning develops when students take the initiative for their learning, recognising needs, formulating goals, identifying resources, implementing appropriate strategies and evaluating learning outcomes. This should be seen as a collaborative process between the nurse educator and the learner. At the international level, various instruments have been used to measure Self-Directed Learning abilities (SDL), both in original and in culturally-adapted versions. However, few instruments have been subjected to full validation, and no gold standard reference has been established to date. In addition, few researchers have adopted the established tools to assess the concurrent validity of the emerging new tools. Therefore, the aim of this study was to measure the concurrent validity between the Self-Rating Scale of Self-Directed Learning (SRSSDL_Ita) - Italian version and the Self-Directed Learning Instruments (SDLI) in undergraduate nursing students. METHODS: A concurrent validity study design was conducted in a Bachelor level nursing degree programme located in Italy. All nursing students attending the first, second or third year (n=428) were the target sample. The SRSSDL_Ita, and the SDLI were used. The Pearson correlation was used to determine the concurrent validity between the instruments; the confidence of intervals (CI 95%) bias-corrected and accelerated bootstrap (BCa), were also calculated. RESULTS: The majority of participants were students attending their first year (47.9%), and were predominately female (78.5%). Their average age was 22.5\ub14.1. The SDL abilities scores, as measured with the SRSSDL_Ita (min 40, max 200), were, on average, 160.79 (95% CI 159.10-162.57; median 160); while with the SDLI (min 20, max 100), they were on average 82.57 (95% CI 81.79-83.38; median 83). The Pearson correlation between the SRSSDL_Ita and SDLI instruments was 0.815 (CI BCa 95% 0.774-0.848), (p=0.000). CONCLUSIONS: The findings confirm the concurrent validity of the SRSSDL_Ita with the SDLI. The SRSSDL_Ita instrument can be useful in the process of identifying Self-Directed Learning abilities, which are essential for students to achieve the expected learning goals and become lifelong learners

Sialyl Residues Modulate LPS-Mediated Signaling through the Toll-Like Receptor 4 Complex

We previously reported that neuraminidase (NA) pretreatment of human PBMCs markedly increased their cytokine response to lipopolysaccharide (LPS). To study the mechanisms by which this occurs, we transfected HEK293T cells with plasmids encoding TLR4, CD14, and MD2 (three components of the LPS receptor complex), as well as a NFκB luciferase reporting system. Both TLR4 and MD2 encoded by the plasmids are α-2,6 sialylated. HEK293T cells transfected with TLR4/MD2/CD14 responded robustly to the addition of LPS; however, omission of the MD2 plasmid abrogated this response. Addition of culture supernatants from MD2 (sMD2)-transfected HEK293T cells, but not recombinant, non-glycosylated MD2 reconstituted this response. NA treatment of sMD2 enhanced the LPS response as did NA treatment of the TLR4/CD14-transfected cell supplemented with untreated sMD2, but optimal LPS-initiated responses were observed with NA-treated TLR4/CD14-transfected cells supplemented with NA-treated sMD2. We hypothesized that removal of negatively charged sialyl residues from glycans on the TLR4 complex would hasten the dimerization of TLR4 monomers required for signaling. Co-transfection of HEK293T cells with separate plasmids encoding either YFP- or FLAG-tagged TLR4, followed by treatment with NA and stimulation with LPS, led to an earlier and more robust time-dependent dimerization of TLR4 monomers on co-immunoprecipitation, compared to untreated cells. These findings were confirmed by fluorescence resonance energy transfer (FRET) analysis. Overexpression of human Neu1 increased LPS-initiated TLR4-mediated NFκB activation and a NA inhibitor suppressed its activation. We conclude that (1) sialyl residues on TLR4 modulate LPS responsiveness, perhaps by facilitating clustering of the homodimers, and that (2) sialic acid, and perhaps other glycosyl species, regulate MD2 activity required for LPS-mediated signaling. We speculate that endogenous sialidase activity mobilized during cell activation may play a role in this regulation

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