Worry and the inhibition of emotionally valanced stimuli in a directed forgetting paradigm

There is considerable evidence in support of an attentional bias among clinically anxious individuals for threatening stimuli. However, a similar bias is not usually found in non-clinical anxious individuals and neither population has tended to show a response bias for mood-congruent information. We proposed that the measurement of anxiety in normals has previously been flawed due to questionnaires which do not accurately select pathological worry, the cognitive component of anxiety. First, we administered the Penn State Worry Questionnaire and selected only those with the most extreme high and low scores. At the time of testing, these subjects were given a state anxiety measure. From these scores, the high and low state anxiety within trait anxiety subjects were selected. With this selection procedure, we compared all high state anxious individuals to all low state anxious individuals. Our hypothesis was that, we would find significant differences between the high and low state within trait groups in a Directed Forgetting Paradigm. Directed forgetting was observed as a function of state within trait and the valence of the word on recall. Word fragment also showed a directed forgetting effect but no differences were seen for the worry groups. However, a secondary recognition procedure on the completed word fragments showed a bias as a function of worry group. The results are interpreted to suggest that worry has an effect on the availability episodic memory

Busier bees:increasing nest traffic in commercial bumblebee colonies

Commercially-reared bumblebee colonies contribute to the pollination of crops globally. If the efficiency of commercial colonies at providing pollination services could be increased, it would have implications for agricultural outputs. Commercial colonies are sold with an internal nectar reservoir on which bees can forage from within the nest. Nectar stores in naturally-produced nectar pots of colonies can affect forager recruitment and activity outside the nest. Thus, it is possible that artificial nectar reservoirs could impact the foraging activity of colonies. To investigate this, commercial Bombus terrestris audax colonies were placed in a university parkland campus. Colonies were split into three treatment groups: those with (1) access to an unaltered nectar reservoir; (2) access to a diluted reservoir; and (3) no reservoir access. Foraging observations were made for all colonies over a 19-day period. The mass of each colony was measured and demographic data were collected. Colonies with diluted reservoirs had 131% and 39% more bees entering and leaving than colonies with no reservoir access and unaltered reservoirs respectively. Both treatments with access to a nectar reservoir gained more mass, had a higher proportion of pollen foraging bees, and had more workers, males, larvae and pupae, than colonies with no access to a reservoir. These results demonstrate that manipulating the availability and concentration of internal nectar reservoirs of commercial B. terrestris colonies significantly affects the number of bees entering and leaving the colony. Dilution of the nectar reservoir could be a strategy for increasing the pollination services commercial colonies provide to crops. Further research in commercial crops is required before such a strategy could be implemented on farms

Persistence of Supplemented Bifidobacterium longum subsp. infantis EVC001 in Breastfed Infants.

Attempts to alter intestinal dysbiosis via administration of probiotics have consistently shown that colonization with the administered microbes is transient. This study sought to determine whether provision of an initial course of Bifidobacterium longum subsp. infantis (B. infantis) would lead to persistent colonization of the probiotic organism in breastfed infants. Mothers intending to breastfeed were recruited and provided with lactation support. One group of mothers fed B. infantis EVC001 to their infants from day 7 to day 28 of life (n = 34), and the second group did not administer any probiotic (n = 32). Fecal samples were collected during the first 60 postnatal days in both groups. Fecal samples were assessed by 16S rRNA gene sequencing, quantitative PCR, mass spectrometry, and endotoxin measurement. B. infantis-fed infants had significantly higher populations of fecal Bifidobacteriaceae, in particular B. infantis, while EVC001 was fed, and this difference persisted more than 30 days after EVC001 supplementation ceased. Fecal milk oligosaccharides were significantly lower in B. infantis EVC001-fed infants, demonstrating higher consumption of human milk oligosaccharides by B. infantis EVC001. Concentrations of acetate and lactate were significantly higher and fecal pH was significantly lower in infants fed EVC001, demonstrating alterations in intestinal fermentation. Infants colonized by Bifidobacteriaceae at high levels had 4-fold-lower fecal endotoxin levels, consistent with observed lower levels of Gram-negative Proteobacteria and Bacteroidetes. IMPORTANCE The gut microbiome in early life plays an important role for long-term health and is shaped in large part by diet. Probiotics may contribute to improvements in health, but they have not been shown to alter the community composition of the gut microbiome. Here, we found that breastfed infants could be stably colonized at high levels by provision of B. infantis EVC001, with significant changes to the overall microbiome composition persisting more than a month later, whether the infants were born vaginally or by caesarean section. This observation is consistent with previous studies demonstrating the capacity of this subspecies to utilize human milk glycans as a nutrient and underscores the importance of pairing a probiotic organism with a specific substrate. Colonization by B. infantis EVC001 resulted in significant changes to fecal microbiome composition and was associated with improvements in fecal biochemistry. The combination of human milk and an infant-associated Bifidobacterium sp. shows, for the first time, that durable changes to the human gut microbiome are possible and are associated with improved gut function

Clinical simulation in Australia and New Zealand: Through the lens of an advisory group

Across Australia, innovations in simulation to enhance learning in nursing have been occurring for three decades and nursing is, and needs to be, a leading player in simulation knowledge diffusion. However, expertise is unevenly distributed across health services and education providers. Rather than build on the expertise and achievements of others, there is a tendency for resource duplication and for trial and error problem solving, in part related to a failure to communicate achievements for the benefits of the professional collective. For nursing to become a leader in the use of simulation and drive ongoing development, as well as conducting high quality research and evaluation, academics need to collaborate, aggregate best practice in simulation learning, and disseminate that knowledge to educators working in health services and higher education sectors across the whole of Australia and New Zealand. To achieve this strategic intent, capacity development principles and committed action are necessary. In mid 2010 the opportunity to bring together nurse educators with simulation learning expertise within Australia and New Zealand became a reality. The Council of Deans of Nursing and Midwifery (CDNM) Australia and New Zealand decided to establish an expert reference group to reflect on the state of Australian nursing simulation, to pool expertise and to plan ways to share best practice knowledge on simulation more widely. This paper reflects on the achievements of the first 18 months since the group's establishment and considers future directions for the enhancement of simulation learning practice, research and development in Australian nursing

Chemostat culture systems support diverse bacteriophage communities from human feces

BACKGROUND: Most human microbiota studies focus on bacteria inhabiting body surfaces, but these surfaces also are home to large populations of viruses. Many are bacteriophages, and their role in driving bacterial diversity is difficult to decipher without the use of in vitro ecosystems that can reproduce human microbial communities. RESULTS: We used chemostat culture systems known to harbor diverse fecal bacteria to decipher whether these cultures also are home to phage communities. We found that there are vast viral communities inhabiting these ecosystems, with estimated concentrations similar to those found in human feces. The viral communities are composed entirely of bacteriophages and likely contain both temperate and lytic phages based on their similarities to other known phages. We examined the cultured phage communities at five separate time points over 24 days and found that they were highly individual-specific, suggesting that much of the subject-specificity found in human viromes also is captured by this culture-based system. A high proportion of the community membership is conserved over time, but the cultured communities maintain more similarity with other intra-subject cultures than they do to human feces. In four of the five subjects, estimated viral diversity between fecal and cultured communities was highly similar. CONCLUSIONS: Because the diversity of phages in these cultured fecal communities have similarities to those found in humans, we believe these communities can serve as valuable ecosystems to help uncover the role of phages in human microbial communities

Use of human splenocytes in an innovative humanised mouse model for prediction of immunotherapy-induced cytokine release syndrome.

OBJECTIVES: Humanised mice have emerged as valuable models for pre-clinical testing of the safety and efficacy of immunotherapies. Given the variety of models available, selection of the most appropriate humanised mouse model is critical in study design. Here, we aimed to develop a model for predicting cytokine release syndrome (CRS) while minimising graft-versus-host disease (GvHD). METHODS: To overcome donor-induced variation, we directly compared the in vitro and in vivo immune phenotype of immunodeficient NSG mice reconstituted with human bone marrow (BM) CD34+ haematopoietic stem cells (HSCs), peripheral blood mononuclear cells (PBMCs) or spleen mononuclear cells (SPMCs) from the same human donors. SPMC engraftment in NSG-dKO mice, which lack MHC class I and II, was also evaluated as a strategy to limit GvHD. Another group of mice was engrafted with umbilical cord blood (UCB) CD34+ HSCs. Induction of CRS in vivo was investigated upon administration of the anti-CD3 monoclonal antibody OKT3. RESULTS: PBMC- and SPMC-reconstituted NSG mice showed short-term survival, with engrafted human T cells exhibiting mostly an effector memory phenotype. Survival in SPMC-reconstituted NSG-dKO mice was significantly longer. Conversely, both BM and UCB-HSC models showed longer survival, without demonstrable GvHD and a more naïve T-cell phenotype. PBMC- and SPMC-reconstituted mice, but not BM-HSC or UCB-HSC mice, experienced severe clinical signs of CRS upon administration of OKT3. CONCLUSION: PBMC- and SPMC-reconstituted NSG mice better predict OKT3-mediated CRS. The SPMC model allows generation of large experimental groups, and the use of NSG-dKO mice mitigates the limitation of early GvHD

Macrophage phenotype in response to ECM bioscaffolds

Macrophage presence and phenotype are critical determinants of the healing response following injury. Downregulation of the pro-inflammatory macrophage phenotype has been associated with the therapeutic use of bioscaffolds composed of extracellular matrix (ECM), but phenotypic characterization of macrophages has typically been limited to small number of non-specific cell surface markers or expressed proteins. The present study determined the response of both primary murine bone marrow derived macrophages (BMDM) and a transformed human mononuclear cell line (THP-1 cells) to degradation products of two different, commonly used ECM bioscaffolds; urinary bladder matrix (UBM-ECM) and small intestinal submucosa (SIS-ECM). Quantified cell responses included gene expression, protein expression, commonly used cell surface markers, and functional assays. Results showed that the phenotype elicited by ECM exposure (MECM) is distinct from both the classically activated IFNγ + LPS phenotype and the alternatively activated IL-4 phenotype. Furthermore, the BMDM and THP-1 macrophages responded differently to identical stimuli, and UBM-ECM and SIS-ECM bioscaffolds induced similar, yet distinct phenotypic profiles. The results of this study not only characterized an MECM phenotype that has anti-inflammatory traits but also showed the risks and challenges of making conclusions about the role of macrophage mediated events without consideration of the source of macrophages and the limitations of individual cell markers

Hsf1 and Hsp90 orchestrate temperature-dependent global transcriptional remodelling and chromatin architecture in Candida albicans

We thank Karim Gharbi and Urmi Trivedi for their assistance with RNA sequencing, carried out in the GenePool genomics facility (University of Edinburgh). We also thank Susan Fairley and Eduardo De Paiva Alves (Centre for Genome Enabled Biology and Medicine, University of Aberdeen) for help with the initial bioinformatics analysis. We thank Aaron Mitchell for kindly providing the ALS3 mutant, Julian Naglik for the gift of TR146 cells, and Jon Richardson for technical assistance. We thank the Genomics and Bioinformatics core of the Faculty of Health Sciences for Next Generation Sequencing and Bioinformatics support, the Information and Communication Technology Office at the University of Macau for providing access to a High Performance Computer and Jacky Chan and William Pang for their expert support on the High Performance Computer. Finally, we thank Amanda Veri for generating CaLC2928. M.D.L. is supported by a Sir Henry Wellcome Postdoctoral Fellowship (Wellcome Trust 096072), R.A.F. by a Wellcome Trust-Massachusetts Institute of Technology (MIT) Postdoctoral Fellowship, L.E.C. by a Canada Research Chair in Microbial Genomics and Infectious Disease and by Canadian Institutes of Health Research Grants MOP-119520 and MOP-86452, A.J. P.B. was supported by the UK Biotechnology and Biological Sciences Research Council (BB/F00513X/1) and by the European Research Council (ERC-2009-AdG-249793-STRIFE), KHW is supported by the Science and Technology Development Fund of Macau S.A.R (FDCT) (085/2014/A2) and the Research and Development Administrative Office of the University of Macau (SRG2014-00003-FHS) and R.T.W. by the Burroughs Wellcome fund and NIH R15AO094406. Data availability RNA-sequencing data sets are available at ArrayExpress (www.ebi.ac.uk) under accession code E-MTAB-4075. ChIP-seq data sets are available at the NCBI SRA database (http://www.ncbi.nlm.nih.gov) under accession code SRP071687. The authors declare that all other data supporting the findings of this study are available within the article and its supplementary information files, or from the corresponding author upon request.Peer reviewedPublisher PD