Galapagos evolution continues

Summary of symposium "Evolution in the Galapagos" held December 8, 1982 in London

Zinc transporters maintain longevity by influencing insulin/IGF-1 activity in Caenorhabditis elegans

Adequate dietary intake of essential metals such as zinc is important for maintaining homeostasis. Abnormal zinc intake in Caenorhabditis elegans has been shown to increase or decrease normal lifespan by influencing the insulin/IGF-1 pathway. Distribution of zinc is achieved by a family of highly conserved zinc transport proteins (ZIPT in C. elegans). This study investigated the role of the zipt family of genes and showed that depletion of individual zipt genes results in a decreased lifespan. Moreover, zipt-16 and zipt-17 mutants synthetically interact with the insulin/IGF cofactors daf-16 and skn-1, and cause abnormal localisation of DAF-16. This study suggests that the zipt family of genes are required for maintaining normal lifespan through influencing the insulin/IGF-1 pathway. © 2019 Federation of European Biochemical SocietiesThis study was supported by the resources at Federation University; no external funding was used to fund this study. We acknowledge the Caenorhabditis elegans Genetics Centre for the strains used in this study and Hannah Tatnell (Federation University) for technical assistance

Simulation-based training for increasing health service board members' effectiveness : protocol for a cluster-randomised controlled trial

Introduction Research indicates that health service boards can influence quality of care. However, government reviews have indicated that board members may not be as effective as possible in attaining this goal. Simulation-based training may help to increase board members' ability to effectively communicate and hold hospital staff to account during board meetings. Methods and analysis To test effectiveness and feasibility, a prospective, cluster-randomised controlled trial will be used to compare simulation-based training with no training. Primary outcome variables will include board members' perceived skill and confidence in communicating effectively during board meetings, and board members' perceptions of board meeting processes. These measures will be collected both immediately before training, and 3 months post-training, with boards randomly assigned to intervention or control arms. Primary analyses will comprise generalised estimating equations examining training effects on each of the primary outcomes. Secondary analyses will examine participants' feedback on the training. Ethics and dissemination Research ethics approval has been granted by Monash University (reference number: 2018-12076). We aim to disseminate results through peer-reviewed journal publication, conference presentation and social media. Trial registration number Open Science Framework: http://osf.io/jaxt6/; Pre-results. © 2019 Author(s). **Please note that there are multiple authors for this article therefore only the name of the first 5 including Federation University Australia affiliate “Jane Boag” is provided in this record*

Pathogen Interactions, Population Cycles, and Phase Shifts

Interspecific pathogen interactions can profoundly affect pathogen population dynamics and the efficacy of control strategies. However, many pathogens exhibit cyclic abundance patterns (e.g. seasonality) and temporal asynchrony between interacting pathogens has the potential to reduce the impact of those interactions. Here we use an extension of our previously published model to investigate the effects of cyclic abundance patterns on pathogen interaction. We demonstrate that for interactions mediated through host immunity, immune memory can maintain the impact of an interaction even when the effector pathogen abundance is low or the pathogen is absent. Paradoxically, immune memory can result in pathogens interacting more strongly when temporally out of phase. We find that interactions between species can not only alter pathogen abundance but can also result in changes to the temporal pattern of the affected species. We further demonstrate that this phenomenon may be observed in a natural host / pathogen data set. Given that there is both a continuing debate as to the relevance of pathogen interactions in natural systems and increasing concern regarding treatment of coinfections of veterinary and medical importance, both the discovery of this measurable shift in cycle in the empirical data and the mechanism by which we identified the shift are important. Finally, as the model structure used here is analogous to simple predator-prey system models we also consider the consequences of these findings in the context of that system

Autoantibodies against cytochrome P450 side-chain cleavage enzyme in dogs (Canis lupus familiaris) affected with hypoadrenocorticism (Addison’s Disease)

Canine hypoadrenocorticism likely arises from immune-mediated destruction of adrenocortical tissue, leading to glucocorticoid and mineralocorticoid deficiency. In humans with autoimmune Addison's disease (AAD) or autoimmune polyendocrine syndrome (APS), circulating autoantibodies have been demonstrated against enzymes associated with adrenal steroid synthesis. The current study investigates autoantibodies against steroid synthesis enzymes in dogs with spontaneous hypoadrenocorticism. Coding regions of canine CYP21A2 (21-hydroxylase; 21-OH), CYP17A1 (17-hydroxylase; 17-OH), CYP11A1 (P450 side-chain cleavage enzyme; P450scc) and HSD3B2 (3β hydroxysteroid dehydrogenase; 3βHSD) were amplified, cloned and expressed as 35S-methionine radiolabelled recombinant protein. In a pilot study, serum samples from 20 dogs with hypoadrenocorticism and four unaffected control dogs were screened by radio-immunoprecipitation assay. There was no evidence of reactivity against 21-OH, 17-OH or 3βHSD, but five dogs with hypoadrenocorticism showed immunoreactivity to P450scc compared with controls. Serum samples were subsequently obtained from 213 dogs diagnosed with hypoadrenocorticism and 110 dogs from a hospital control population. Thirty control dogs were randomly selected to establish a threshold for antibody positivity (mean + 3 × standard deviation). Dogs with hypoadrenocorticism were more likely to be P450scc autoantibody positive than hospital controls (24% vs. 1.2%, respectively; p = 0.0016). Sex was significantly associated with the presence of P450scc autoantibodies in the case population, with 30% of females testing positive compared with 17% of males (p = 0.037). Significant associations with breed (p = 0.015) and DLA-type (DQA1*006:01 allele; p = 0.017) were also found. This cross-sectional study indicates that P450scc autoantibodies are present in a proportion of dogs affected with hypoadrenocorticism