The Influence of Clinical Placements on the Emotional Intelligence of Therapy Students

This research investigated changes in emotional intelligence (EI) in undergraduate speech, occupational and physical therapy students as they completed their final year of fieldwork. Undergraduate business students were a control group. The study used a longitudinal, mixed methods design measuring EI at three-points, with follow up interviews to explore reasons for changes in emotional intelligence. The study highlights the important role of clinical placements, reflective practice, and supervisor quality on the development of emotional intelligence

GRACE: An Innovative Program of Clinical Education in Allied Health

This paper describes the Gribble Rosenwax Advanced Clinical Education (GRACE) program that has resolved the 15 year-old issue for one occupational therapy (OT) program of an undersupply of practice placements for OT students who, without completing 1,000 hours of placement, cannot graduate. Based on relationship marketing, Gribble and Rosenwax's approach to reforming clinical education was innovative by regarding potential host sites as offering the School a service by hosting students to one of regarding each host site as a partner in the clinical education process. Relative to the previous clinical education program, GRACE enhances student learning experiences primarily through the cultivation and enrichment of key relationships with host placement sites; by the appointment of a Clinical Education Coordinator at each host site to oversee student placements; and the provision of clinical education as 42 consecutive weeks of the year, rather than intermittently, and thus ensuring continuity for consumers and closer supervision of students, particular those students with performance issues. Now in its second year, one indication of GRACE's success is that all placements for 2009 (n = 490) were allocated to students earlier than in previous years. GRACE offers shared responsibility for clinical education between host sites and the School which has cultivated mutually beneficial relationships, resulting in improved outcomes for student learning and enhanced services for consumers

An intervention to enhance the supervision of health science students who struggle during work placements

Supervisors are often reluctant to make an adverse assessment of the student's performance during work placements, which leads to a phenomenon known as "failure to fail". This Australian study evaluated resources designed to enhance the management of students who fail to meet the required standard of performance during work placements. Staff from a range of health disciplines evaluated the training program comprised of a half-day workshop and written guide using a questionnaire and semi-structured interviews. Staff reported renewed confidence in working with underperforming students,increased comfort with failing students who did not reach the required standards. The Staff Guide was seens as useful with all students undertaking work placements, not just underperforming students. The Student Guide was perceived as relevant to the student experience. The findings of this research are important to university educators engaged with work placements, work placement supervisors, and students who undertake work placements

Positive Effects of NPY1 Receptor Activation on Islet Structure Are Driven by Pancreatic Alpha- and Beta-Cell Transdifferentiation in Diabetic Mice

Enzymatically stable and specific neuropeptide Y1 receptor (NPYR1) agonists, such as sea lamprey PYY(1-36) (SL-PYY(1-36)), are believed to improve glucose regulation in diabetes by targeting pancreatic islets. In this study, streptozotocin (STZ) diabetic transgenic GluCreERT2 ; ROSA26-eYFP and Ins1 Cre/+; Rosa26-eYFP mouse models have been used to study effects of sustained NPYR1 activation on islet cell composition and alpha- and beta-cell lineage transitioning. STZ induced a particularly severe form of diabetes in Ins1 Cre/+; Rosa26-eYFP mice, but twice-daily administration (25 nmol/kg) of SL-PYY(1-36) for 11 days consistently improved metabolic status. Blood glucose was decreased (p < 0.05 - p < 0.001) and both fasted plasma and pancreatic insulin significantly increased by SL-PYY(1-36). In both GluCreERT2 ; ROSA26-eYFP and Ins1 Cre/+; Rosa26-eYFP mice, STZ provoked characteristic losses (p < 0.05 - p < 0.001) of islet numbers, beta-cell and pancreatic islet areas together with increases in area and central islet location of alpha-cells. With exception of alpha-cell area, these morphological changes were fully, or partially, returned to non-diabetic control levels by SL-PYY(1-36). Interestingly, STZ apparently triggered decreased (p < 0.001) alpha- to beta-cell transition in GluCreERT2 ; ROSA26-eYFP mice, together with increased loss of beta-cell identity in Ins1 Cre/+; Rosa26-eYFP mice, but both effects were significantly (p < 0.001) reversed by SL-PYY(1-36). SL-PYY(1-36) also apparently reduced (p < 0.05) beta- to alpha-cell conversion in Ins1 Cre/+; Rosa26-eYFP mice and glucagon expressing alpha-cells in GluCreERT2 ; ROSA26-eYFP mice. These data indicate that islet benefits of prolonged NPY1R activation, and especially restoration of beta-cell mass, are observed irrespective of diabetes status, being linked to cell lineage alterations including transdifferentiation of alpha- to beta-cells

Positive Effects of NPY1 Receptor Activation on Islet Structure Are Driven by Pancreatic Alpha- and Beta-Cell Transdifferentiation in Diabetic Mice

Enzymatically stable and specific neuropeptide Y1 receptor (NPYR1) agonists, such as sea lamprey PYY(1-36) (SL-PYY(1-36)), are believed to improve glucose regulation in diabetes by targeting pancreatic islets. In this study, streptozotocin (STZ) diabetic transgenic GluCreERT2 ; ROSA26-eYFP and Ins1 Cre/+; Rosa26-eYFP mouse models have been used to study effects of sustained NPYR1 activation on islet cell composition and alpha- and beta-cell lineage transitioning. STZ induced a particularly severe form of diabetes in Ins1 Cre/+; Rosa26-eYFP mice, but twice-daily administration (25 nmol/kg) of SL-PYY(1-36) for 11 days consistently improved metabolic status. Blood glucose was decreased (p < 0.05 - p < 0.001) and both fasted plasma and pancreatic insulin significantly increased by SL-PYY(1-36). In both GluCreERT2 ; ROSA26-eYFP and Ins1 Cre/+; Rosa26-eYFP mice, STZ provoked characteristic losses (p < 0.05 - p < 0.001) of islet numbers, beta-cell and pancreatic islet areas together with increases in area and central islet location of alpha-cells. With exception of alpha-cell area, these morphological changes were fully, or partially, returned to non-diabetic control levels by SL-PYY(1-36). Interestingly, STZ apparently triggered decreased (p < 0.001) alpha- to beta-cell transition in GluCreERT2 ; ROSA26-eYFP mice, together with increased loss of beta-cell identity in Ins1 Cre/+; Rosa26-eYFP mice, but both effects were significantly (p < 0.001) reversed by SL-PYY(1-36). SL-PYY(1-36) also apparently reduced (p < 0.05) beta- to alpha-cell conversion in Ins1 Cre/+; Rosa26-eYFP mice and glucagon expressing alpha-cells in GluCreERT2 ; ROSA26-eYFP mice. These data indicate that islet benefits of prolonged NPY1R activation, and especially restoration of beta-cell mass, are observed irrespective of diabetes status, being linked to cell lineage alterations including transdifferentiation of alpha- to beta-cells

The impact of clinical placements on the emotional intelligence of occupational therapy, physiotherapy, speech pathology, and business students: a longitudinal study

Background: Emotional intelligence (EI) is a critical skill for healthcare practitioners. Minimal longitudinal research has tracked the changes in EI of therapy students over their final full-time clinical placements. Methods: The Emotional Quotient Inventory (EQ-i2.0) measured the EI of 283 therapy students and 93 business students (control group who do no clinical placements) at three time points over a 16-month period, the same period that the therapy students participated in clinical placements. Results: Analysis of the therapy students showed significant increases over the 16 months of the study in Total EI score, as well as nine other EI skills. However, large percentages of students reported declining scores in emotional expression, assertiveness, self-expression, and stress tolerance, with some students reporting low EI scores before commencing full-time extended clinical placements. Conclusions: The study contributes to new knowledge about the changing EI skills of therapy students as they complete their full-time, extended placements. Emotional intelligence in student therapists should be actively fostered during coursework, clinical placements and when first entering the workforce. University educators are encouraged to include EI content through the therapy curricula. Employers are encouraged to provide peer coaching, mentoring and workshops focused on EI skills to recent graduates

Genomic and Genic Deletions of the FOX Gene Cluster on 16q24.1 and Inactivating Mutations of FOXF1 Cause Alveolar Capillary Dysplasia and Other Malformations

Alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV) is a rare, neonatally lethal developmental disorder of the lung with defining histologic abnormalities typically associated with multiple congenital anomalies (MCA). Using array CGH analysis, we have identified six overlapping microdeletions encompassing the FOX transcription factor gene cluster in chromosome 16q24.1q24.2 in patients with ACD/MPV and MCA. Subsequently, we have identified four different heterozygous mutations (frameshift, nonsense, and no-stop) in the candidate FOXF1 gene in unrelated patients with sporadic ACD/MPV and MCA. Custom-designed, high-resolution microarray analysis of additional ACD/MPV samples revealed one microdeletion harboring FOXF1 and two distinct microdeletions upstream of FOXF1, implicating a position effect. DNA sequence analysis revealed that in six of nine deletions, both breakpoints occurred in the portions of Alu elements showing eight to 43 base pairs of perfect microhomology, suggesting replication error Microhomology-Mediated Break-Induced Replication (MMBIR)/Fork Stalling and Template Switching (FoSTeS) as a mechanism of their formation. In contrast to the association of point mutations in FOXF1 with bowel malrotation, microdeletions of FOXF1 were associated with hypoplastic left heart syndrome and gastrointestinal atresias, probably due to haploinsufficiency for the neighboring FOXC2 and FOXL1 genes. These differences reveal the phenotypic consequences of gene alterations in cis

Accelerating cryoprotectant diffusion kinetics improves cryopreservation of pancreatic islets

Funder: W. D. Armstrong Fund (School of Technology, University of Cambridge)Abstract: Cryopreservation offers the potential to increase the availability of pancreatic islets for treatment of diabetic patients. However, current protocols, which use dimethyl sulfoxide (DMSO), lead to poor cryosurvival of islets. We demonstrate that equilibration of mouse islets with small molecules in aqueous solutions can be accelerated from > 24 to 6 h by increasing incubation temperature to 37 °C. We utilize this finding to demonstrate that current viability staining protocols are inaccurate and to develop a novel cryopreservation method combining DMSO with trehalose pre-incubation to achieve improved cryosurvival. This protocol resulted in improved ATP/ADP ratios and peptide secretion from β-cells, preserved cAMP response, and a gene expression profile consistent with improved cryoprotection. Our findings have potential to increase the availability of islets for transplantation and to inform the design of cryopreservation protocols for other multicellular aggregates, including organoids and bioengineered tissues

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead