Nurse educators’ views on implementation and use of high-fidelity simulation in nursing programmes

Background. Clinical skills development of student nurses is a concern in nursing education owing to limited clinical exposure and learning opportunities. High-fidelity simulation as a teaching-learning strategy creates an environment where student nurses develop clinical skills through interactive participation.Objectives. The aim of this research study was to explore nurse educators’ views of high-fidelity simulation as an educational approach in nursing programmes.Methods. A qualitative descriptive design was used. Data were collected through individual semi-structured interviews. Data saturation occurred within 19 interviews. The population consisted out of 33 (N=33; n=19) nurse educators. Direct content analysis was done using Hsieh and Shannon’s approach. The study was conducted at a South African private higher education institution.Results. Five main themes were identified. The nurse educators had not been exposed to or had limited experience with high-fidelity simulation. Limited resources and/or the lack of nurse educators trained in high-fidelity simulation were identified. The nurse educators agreed that high-fidelity simulation would contribute to the enhancement of clinical skills development and theory and practice integration.Conclusion. High-fidelity simulation is not implemented owing to limited equipment or experience in using the equipment optimally. The nurse educators see high-fidelity simulation as a solution and valuable training method where clinical skills are developed before the student nurse is exposed to the private clinical environment

Influence of vitamin D supplementation on bone mineral content, bone turnover markers and fracture risk in South African schoolchildren: Multicentre double-blind randomised placebo-controlled trial (ViDiKids)

Randomised controlled trials (RCT) to determine the influence of vitamin D on bone mineral content (BMC) and fracture risk in children of Black African ancestry are lacking. We conducted a sub-study (n=450) nested within a Phase 3 RCT of weekly oral supplementation with 10,000 IU vitamin D3 vs. placebo for 3 years in HIV- uninfected Cape Town schoolchildren aged 6-11 years. Outcomes were BMC at the whole body less head (WBLH) and lumbar spine (LS) and serum 25-hydroxyvitamin D3 (25[OH]D3), parathyroid hormone (PTH), alkaline phosphatase, C-terminal telopeptide and procollagen type 1 N propeptide. Incidence of fractures was a secondary outcome of the main trial (n=1682). At baseline, mean serum 25(OH)D3 concentration was 70.0 nmol/L (s.d. 13.5), and 5.8% of participants had serum 25(OH)D3 concentrations <50 nmol/L. Among sub-study participants, end-trial serum 25(OH)D3 concentrations were higher for participants allocated to vitamin D vs. placebo (adjusted mean difference [aMD] 39.9 nmol/L, 95% CI 36.1 to 43.6) and serum PTH concentrations were lower (aMD -0.55 pmol/L, 95% CI -0.94 to -0.17). However, no interarm differences were seen for WBLH BMC (aMD -8.0 g, 95% CI - 30.7 to 14.7) or LS BMC (aMD -0.3 g, 95% CI -1.3 to 0.8) or serum concentrations of bone turnover markers. Fractures were rare among participants in the main trial randomised to vitamin D vs. placebo (7/755 vs. 10/758 attending at least one follow- up; adjusted odds ratio 0.70, 95% CI 0.27 to 1.85). In conclusion, a 3-year course of weekly oral vitamin D supplementation elevated serum 25(OH)D3 concentrations and suppressed serum PTH concentrations in HIV-uninfected South African schoolchildren of Black African ancestry but did not influence BMC or serum concentrations of bone turnover markers. Fracture incidence was low, limiting power to detect an effect of vitamin D on this outcome

Identification of Srp9 as a febrile seizure susceptibility gene

Objective: Febrile seizures (FS) are the most common seizure type in young children. Complex FS are a risk factor for mesial temporal lobe epilepsy (mTLE). To identify new FS susceptibility genes we used a forward genetic strategy in mice and subsequently analyzed candidate genes in humans. Methods: We mapped a quantitative trait locus (QTL1) for hyperthermia-induced FS on mouse chromosome 1, containing the signal recognition particle 9 (Srp9) gene. Effects of differential Srp9 expression were assessed in vivo and in vitro. Hippocampal SRP9 expression and genetic association were analyzed in FS and mTLE patients. Results: Srp9 was differentially expressed between parental strains C57BL/6J and A/J. Chromosome substitution strain 1 (CSS1) mice exhibited lower FS susceptibility and Srp9 expression than C57BL/6J mice. In vivo knockdown of brain Srp9 reduced FS susceptibility. Mice with reduced Srp9 expression and FS susceptibility, exhibited reduced hippocampal AMPA and NMDA currents. Downregulation of neuronal Srp9 reduced surface expression of AMPA receptor subunit GluA1. mTLE patients with antecedent FS had higher SRP9 expression than patients without. SRP9 promoter SNP rs12403575(G/A) was genetically associated with FS and mTLE. Interpretation: Our findings identify SRP9 as a novel FS susceptibility gene and indicate that SRP9 conveys its effects through endoplasmic reticulum (ER)-dependent synthesis and trafficking of membrane proteins, such as glutamate receptors. Discovery of this new FS gene and mechanism may provide new leads for early diagnosis and treatment of children with complex FS at risk for mTLE

Mapping of a FEB3 homologous febrile seizure locus on mouse chromosome 2 containing candidate genes Scn1a and Scn3a

Febrile seizures (FS) are the most common seizure type in children. Recurrent FS are a risk factor for developing temporal lobe epilepsy later in life and are known to have a strong genetic component. Experimental FS (eFS) can be elicited in mice by warm-air induced hyperthermia. We used this model to screen the chromosome substitution strain (CSS) panel derived from C57BL/6J and A/J for FS susceptibility and identified C57BL/6J-Chr2(A)/NaJ (CSS2), as the strain with the strongest FS susceptibility phenotype. The aim of this study was to map FS susceptibility loci and select candidate genes on mouse chromosome 2. We generated an F-2 population by intercrossing the hybrids (F-1) that were derived from CSS2 and C57BL/6J mice. All CSS2-F-2 individuals were genotyped and phenotyped for eFS susceptibility, and QTL analysis was performed. Candidate gene selection was based on bioinformatics analyses and differential brain expression between CSS2 and C57BL/6J strains determined by microarray analysis. Genetic mapping of the eFS susceptibility trait identified two significant loci: FS-QTL2a (LOD-score 3.6) and FS-QTL2b (LOD-score 6.2). FS-QTL2a contained 44 genes expressed in the brain at post natal day 14. Four of these (Arl6ip6, Cytip, Fmnl2 Ifih1) contained a non-synonymous SNP comparing CSS2 and C57BL/6J, six genes (March7, Nr4a2, Gpd2, Grb14, Scn1a, Scn3a) were differentially expressed between these strains. A region within FS-QTL2a is homologous to the human FEB3 locus. The fact that we identify mouse FS-QTL2a with high FEB3 homology is strong support for the validity of the eFS mouse model to study genetics of human FS

Alternative splicing of glutamate transporter EAAT2 RNA in neocortex and hippocampus of temporal lobe epilepsy patients

Rationale: Altered expression of glutamate transporter EAAT2 protein has been reported in the hippocampus of patients with temporal lobe epilepsy (TLE). Two alternative EAAT2 mRNA splice forms, one resulting from a partial retention of intron 7 (I7R), the other from a deletion of exon 9 (E9S), were previously implicated in the loss of EAAT2 protein in patients with amyotrophic lateral sclerosis. Methods: By RT-PCR we studied the occurrence of 17R and E9S in neocortical and hippocampal specimens from TLE patients and non-neurological controls. Results: Both splice forms were found in all neocortical specimens from TLE patients (100% I7R, 100% E9S). This was significantly more than in controls (67% I7R, 60% E9S; P <0.05). We also detected I7R and E9S in all seven motor cortex post-mortem samples from patients with amyotrophic lateral sclerosis. Within the TLE patient group, both splice variants appeared significantly more in non-sclerotic (100%), than in sclerotic hippocampi (69%, P <0.05). Conclusion: These data indicate that the epileptic brain, especially that of TLE patients without hippocampal sclerosis, is highly prone to alternative EAAT2 mRNA splicing. Our data confirm that the presence of alternative EAAT2 splice forms is not disease specific. (C) 2004 Elsevier B.V. All rights reserve