Motivation to learn in university science students studying anatomy: A mixed-methods analysis of what drives learning.

Exploring student motivation to learn is a research area that has rapidly expanded over the past decade, especially as the COVID-19 pandemic continues to influence education. In the field of anatomy, most research about motivation to learn targets medical and other health professional students, but little is known about factors that drive students enrolled in science degrees. The aims of this mixed-methods study were to determine: (1) what motivates undergraduate university science students to learn anatomy, and whether motivation differs between cohorts (second- and third-year) and gender; and (2) the impact of COVID-19 on motivation to learn. Students (n = 171) completed a survey (the Science Motivation Questionnaire II [SMQII] and questions about learning experiences during the pandemic) and a subset (n = 12) participated in focus groups/interviews. Quantitative data were analyzed using a combination of parametric and non-parametric statistics, and a general inductive approach was applied to qualitative data. Grade, intrinsic, and career factors were consistently identified as the key components of motivation. No statistically significant differences were found for motivation components between level of study or gender. Students reported that the COVID-19 pandemic negatively impacted motivational components, but it had also fast-tracked the development of online learning, with both positive and negative connotations. Students value traditional in-person lectures but support a blended approach of traditional and online teaching methods for learning anatomy. Educators should utilize these findings when considering how to teach and support science students in ways that embrace motivational components to foster success in those studying anatomy.

Sexual and reproductive health knowledges: a study with Pacific young people enrolled in an Aotearoa New Zealand tertiary institution.

Pacific young people living in Aotearoa New Zealand experience disparities in their sexual and reproductive health outcomes, thought to stem from cultural differences and educational inequities. Although these barriers have been characterised in literature, their influence on Pacific youth's understandings of sexual and reproductive health have been relatively unexplored. This study investigated the sexual and reproductive health knowledge of Pacific students enrolled at a university in Aotearoa New Zealand in 2020 and where they gained this knowledge. The study used the theoretical framework of the (revitalised) Fonofale health model and was guided by the Kakala research methodology. Data were collected by means of an online survey comprised of open-ended questions and Likert scales, completed by eighty-one eligible students. Open-ended questions were analysed for general themes and responses to Likert scale items are reported using descriptive statistical analysis. The study found that Pacific youth have strong foundations of health knowledge that is heavily influenced by Polynesian cultural beliefs. Both formal and non-formal learning environments were important in developing participants' health knowledge of these topics and for encouraging independent help-seeking behaviours. This is the first reported study to investigate the sexual and reproductive health knowledges of a pan-Pacific tertiary cohort of young people.

The cyclic AMP phosphodiesterase 4D5 (PDE4D5)/receptor for activated C-kinase 1 (RACK1) signalling complex as a sensor of the extracellular nano-environment.

The cyclic AMP and protein kinase C (PKC) signalling pathways regulate a wide range of cellular processes that require tight control, including cell proliferation and differentiation, metabolism and inflammation. The identification of a protein complex formed by receptor for activated C kinase 1 (RACK1), a scaffold protein for protein kinase C (PKC), and the cyclic AMP-specific phosphodiesterase, PDE4D5, demonstrates a potential mechanism for crosstalk between these two signalling routes. Indeed, RACK1-bound PDE4D5 is activated by PKCα, providing a route through which the PKC pathway can control cellular cyclic AMP levels. Although RACK1 does not appear to affect the intracellular localisation of PDE4D5, it does afford structural stability, providing protection against denaturation, and increases the susceptibility of PDE4D5 to inhibition by cyclic AMP-elevating pharmaceuticals, such as rolipram. In addition, RACK1 can recruit PDE4D5 and PKC to intracellular protein complexes that control diverse cellular functions, including activated G protein-coupled receptors (GPCRs) and integrins clustered at focal adhesions. Through its ability to regulate local cyclic AMP levels in the vicinity of these multimeric receptor complexes, the RACK1/PDE4D5 signalling unit therefore has the potential to modify the quality of incoming signals from diverse extracellular cues, ranging from neurotransmitters and hormones to nanometric topology. Indeed, PDE4D5 and RACK1 have been found to form a tertiary complex with integrin-activated focal adhesion kinase (FAK), which localises to cellular focal adhesion sites. This supports PDE4D5 and RACK1 as potential regulators of cell adhesion, spreading and migration through the non-classical exchange protein activated by cyclic AMP (EPAC1)/Rap1 signalling route.

Anatomical and clinical aspects of Klinefelter's syndrome.

Klinefelter's syndrome, the most common sex disorder associated with chromosomal aberrations, is characterized by a plethora of clinical features. Parameters for diagnosis of the syndrome are constantly expanding as new anatomical and hormonal abnormalities are noted, yet Klinefelter's remains underdiagnosed and underreported. This review outlines the key anatomical characteristics associated with the syndrome, which are currently used for clinical diagnosis, or may provide means for improving diagnosis in the future. Clin. Anat. 29:606-619, 2016. © 2016 Wiley Periodicals, Inc.

Interaction with receptor for activated C-kinase 1 (RACK1) sensitizes the phosphodiesterase PDE4D5 towards hydrolysis of cAMP and activation by protein kinase C.

We have previously identified the PKC (protein kinase C)-anchoring protein RACK1 (receptor for activated C-kinase 1), as a specific binding partner for the cAMP-specific phosphodiesterase PDE4D5, suggesting a potential site for cross-talk between the PKC and cAMP signalling pathways. In the present study we found that elevation of intracellular cAMP, with the ß2-adrenoceptor agonist isoproterenol (isoprenaline), led to activation of PDE4 enzymes in the particulate and soluble fractions of HEK (human embryonic kidney)-293 cells. In contrast activation of PDE4D5, with isoproterenol and the PKC activator PMA, was restricted to the particulate fraction, where it interacts with RACK1; however, RACK1 is dispensable for anchoring PDE4D5 to the particulate fraction. Kinetic studies demonstrated that RACK1 alters the conformation of particulate-associated PDE4D5 so that it more readily interacts with its substrate cAMP and with rolipram, a PDE4 inhibitor that specifically targets the active site of the enzyme. Interaction with RACK1 was also essential for PKC-dependent and ERK (extracellular-signal-regulated kinase)-independent phosphorylation (on Ser¹²6), and activation of PDE4D5 in response to PMA and isoproterenol, both of which trigger the recruitment of PKCα to RACK1. Together these results reveal novel signalling cross-talk, whereby RACK1 mediates PKC-dependent activation of PDE4D5 in the particulate fraction of HEK-293 cells in response to elevations in intracellular cAMP.

Activation of protein kinase Calpha by EPAC1 is required for the ERK- and CCAAT/enhancer-binding protein beta-dependent induction of the SOCS-3 gene by cyclic AMP in COS1 cells.

We recently found that induction of the anti-inflammatory SOCS-3 gene by cyclic AMP occurs through novel cyclic AMP-dependent protein kinase-independent mechanisms involving activation of CCAAT/enhancer-binding protein (C/EBP) transcription factors, notably C/EBPbeta, by the cyclic AMP GEF EPAC1 and the Rap1 GTPase. In this study we show that down-regulation of phospholipase (PL) Cepsilon with small interfering RNA or blockade of PLC activity with chemical inhibitors ablates exchange protein directly activated by cyclic AMP (EPAC)-dependent induction of SOCS-3 in COS1 cells. Consistent with this, stimulation of cells with 1-oleoyl-2-acetyl-sn-glycerol and phorbol 12-myristate 13-acetate, both cell-permeable analogues of the PLC product diacylglycerol, are sufficient to induce SOCS-3 expression in a Ca2+-dependent manner. Moreover, the diacylglycerol- and Ca2+-dependent protein kinase C (PKC) isoform PKCalpha becomes activated following cyclic AMP elevation or EPAC stimulation. Conversely, down-regulation of PKC activity with chemical inhibitors or small interfering RNA-mediated depletion of PKCalpha or -delta blocks EPAC-dependent SOCS-3 induction. Using the MEK inhibitor U0126, we found that activation of ERK MAPKs is essential for SOCS-3 induction by either cyclic AMP or PKC. C/EBPbeta is known to be phosphorylated and activated by ERK. Accordingly, we found ERK activation to be essential for cyclic AMP-dependent C/EBP activation and C/EBPbeta-dependent SOCS-3 induction by cyclic AMP and PKC. Moreover, overexpression of a mutant form of C/EBPbeta (T235A), which lacks the ERK phosphorylation site, blocks SOCS-3 induction by cyclic AMP and PKC in a dominant-negative manner. Together, these results indicate that EPAC mediates novel regulatory cross-talk between the cyclic AMP and PKC signaling pathways leading to ERK- and C/EBPbeta-dependent induction of the SOCS-3 gene.