Cutaneus myxosporidiasis in the Australian green tree frog (Litoria caerulea)

This case is reported with the intention of highlighting the presentation of cutaneous myxosporidiasis in Australian tree frog (Litoria caerulea) caused by genus Myxobolus. The morphology and morphometric characteristic of the spores were determined using light microscopy and differential interference contrast microscopy. Spores were pyriform in shape in frontal view and oval in lateral view, and the average size was respectively 11.4 × 6.0 × 4.5 μm (12.1 − 9.5 × 6.3 − 5.4 × 5.0 − 4.1 μm). To the best of our knowledge, this is the second case of skin invasion caused by myxosporeans in amphibians

Elabela/Toddler is an Endogenous Agonist of the Apelin APJ Receptor in the Adult Cardiovascular System, and Exogenous Administration of the Peptide Compensates for the Downregulation of its Expression in Pulmonary Arterial Hypertension

BACKGROUND: -Elabela/Toddler (ELA) is a critical cardiac developmental peptide that acts through the G protein-coupled apelin receptor, despite lack of sequence similarity to the established ligand apelin. Our aim was to investigate the receptor pharmacology, expression pattern and in vivo function of ELA peptides in the adult cardiovascular system, to seek evidence for alteration in pulmonary arterial hypertension (PAH) in which apelin signaling is down-regulated, and to demonstrate attenuation of PAH severity with exogenous administration of ELA in a rat model. METHODS: -In silico docking analysis, competition binding experiments and down-stream assays were used to characterize ELA receptor binding in human heart and signaling in cells expressing the apelin receptor. ELA expression in human cardiovascular tissues and plasma was determined using RT-qPCR, dual-labelling immunofluorescent staining and immunoassays. Acute cardiac effects of ELA-32 and [Pyr(1)]apelin-13 were assessed by magnet resonance imaging and cardiac catheterization in anesthetized rats. Cardiopulmonary human and rat tissues from PAH patients and monocrotaline (MCT) and Sugen/hypoxia exposed rats were used to show changes in ELA expression in PAH. The effect of ELA treatment on cardiopulmonary remodeling in PAH was investigated in the MCT rat model. RESULTS: -ELA competed for binding of apelin in human heart with overlap for the two peptides indicated by in silico modeling. ELA activated G protein- and Β-arrestin-dependent pathways. We detected ELA expression in human vascular endothelium and plasma. Comparable to apelin, ELA increased cardiac contractility, ejection fraction, cardiac output and elicited vasodilatation in rat in vivo ELA expression was reduced in cardiopulmonary tissues from PAH patients and PAH rat models, respectively. ELA treatment significantly attenuated elevation of right ventricular systolic pressure and right ventricular hypertrophy and pulmonary vascular remodeling in MCT exposed rats. CONCLUSIONS: -These results show ELA is an endogenous agonist of the human apelin receptor, exhibits a cardiovascular profile comparable to apelin, is down-regulated in human disease and rodent PAH models and exogenous peptide can reduce the severity of cardiopulmonary remodeling and function in PAH in rats. This study provides additional proof of principle that an apelin receptor agonist may be of therapeutic use in PAH in man.Supported by the Wellcome Trust 107715/Z/15/Z and Programme in Metabolic and Cardiovascular Disease 096822/Z/11/Z, Medical Research Council MC_PC_14116, British Heart Foundation PS/02/001, PG/05/127/19872, FS/14/59/31282 and in part by the National Institute for Health Research Cambridge Biomedical Research Centre and the Pulmonary Hypertension Association UK

Providing education on evidence-based practice improved knowledge but did not change behaviour: a before and after study

BACKGROUND: Many health professionals lack the skills to find and appraise published research. This lack of skills and associated knowledge needs to be addressed, and practice habits need to change, for evidence-based practice to occur. The aim of this before and after study was to evaluate the effect of a multifaceted intervention on the knowledge, skills, attitudes and behaviour of allied health professionals. METHODS: 114 self-selected occupational therapists were recruited. The intervention included a 2-day workshop combined with outreach support for eight months. Support involved email and telephone contact and a workplace visit. Measures were collected at baseline, post-workshop, and eight months later. The primary outcome was knowledge, measured using the Adapted Fresno Test of Evidence-Based Practice (total score 0 to 156). Secondary outcomes were attitude to evidence-based practice (% reporting improved skills and confidence; % reporting barriers), and behaviour measured using an activity diary (% engaging/not engaging in search and appraisal activities), and assignment completion. RESULTS: Post-workshop, there were significant gains in knowledge which were maintained at follow-up. The mean difference in the Adapted Fresno Test total score was 20.6 points (95% CI, 15.6 to 25.5). The change from post-workshop to follow-up was small and non-significant (mean difference 1.2 points, 95% CI, -6.0 to 8.5). Fewer participants reported lack of searching and appraisal skills as barriers to evidence-based practice over time (searching = 61%, 53%, 24%; appraisal 60%, 65%, 41%). These differences were statistically significant (p = 0.0001 and 0.010 respectively). Behaviour changed little. Pre-workshop, 6% engaged in critical appraisal increasing to 18% post-workshop and 18% at follow-up. Nearly two thirds (60%) were not reading any research literature at follow-up. Twenty-three participants (20.2%) completed their assignment. CONCLUSION: Evidence-based practice skills and knowledge improved markedly with a targetted education intervention and outreach support. However, changes in behaviour were small, based on the frequency of searching and appraisal activities. Allied health educators should focus more on post-workshop skill development, particularly appraisal, and help learners to establish new routines and priorities around evidence-based practice. Learners also need to know that behaviour change of this nature may take months, even years

What evidence is there to support skill mix changes between GPs, pharmacists and practice nurses in the care of elderly people living in the community?

Background: Workforce shortages in Australia are occurring across a range of health disciplines but are most acute in general practice. Skill mix change such as task substitution is one solution to workforce shortages. The aim of this systematic review was to explore the evidence for the effectiveness of task substitution between GPs and pharmacists and GPs and nurses for the care of older people with chronic disease. Published, peer reviewed (black) and non-peer reviewed (grey) literature were included in the review if they met the inclusion criteria. Results: Forty-six articles were included in the review. Task substitution between pharmacists and GPs and nurses and GPs resulted in an improved process of care and patient outcomes, such as improved disease control. The interventions were either health promotion or disease management according to guidelines or use of protocols, or a mixture of both. The results of this review indicate that pharmacists and nurses can effectively provide disease management and/or health promotion for older people with chronic disease in primary care. While there were improvements in patient outcomes no reduction in health service use was evident. Conclusion: When implementing skill mix changes such as task substitution it is important that the health professionals' roles are complementary otherwise they may simply duplicate the task performed by other health professionals. This has implications for the way in which multidisciplinary teams are organised in initiatives such as the GP Super Clinics

Variation at the Calpain 3 gene is associated with meat tenderness in zebu and composite breeds of cattle

<p>Abstract</p> <p>Background</p> <p>Quantitative Trait Loci (QTL) affecting meat tenderness have been reported on Bovine chromosome 10. Here we examine variation at the Calpain 3 (<it>CAPN3</it>) gene in cattle, a gene located within the confidence interval of the QTL, and which is a positional candidate gene based on the biochemical activity of the protein.</p> <p>Results</p> <p>We identified single nucleotide polymorphisms (SNP) in the genomic sequence of the <it>CAPN3 </it>gene and tested three of these in a sample of 2189 cattle. Of the three SNP genotyped, the <it>CAPN3:c.1538+225G>T </it>had the largest significant additive effect, with an allele substitution effect in the Brahman of <it>α </it>= -0.144 kg, SE = 0.060, <it>P </it>= 0.016, and the polymorphism explained 1.7% of the residual phenotypic variance in that sample of the breed. Significant haplotype substitution effects were found for all three breeds, the Brahman, the Belmont Red, and the Santa Gertrudis. For the common haplotype, the haplotype substitution effect in the Brahman was <it>α </it>= 0.169 kg, SE = 0.056, <it>P </it>= 0.003. The effect of this gene was compared to Calpastatin in the same sample. The SNP show negligible frequencies in taurine breeds and low to moderate minor allele frequencies in zebu or composite animals.</p> <p>Conclusion</p> <p>These associations confirm the location of a QTL for meat tenderness in this region of bovine chromosome 10. SNP in or near this gene may be responsible for part of the overall difference between taurine and zebu breeds in meat tenderness, and the greater variability in meat tenderness found in zebu and composite breeds. The evidence provided so far suggests that none of these tested SNP are causative mutations.</p

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death