Montana DEQ’s Approach to a Standardized Sediment Assessment Protocol: A Biological Consideration in the 303(D) Listing Process

The Montana Department of Environmental Quality (DEQ) has been delegated by the Environmental Protection Agency (EPA) to implement provisions of the Clean Water Act. This includes submitting a 305(b) report every two years to the EPA describing the condition of all waters within the state’s jurisdiction and creating a 303(d) list of impaired waters. This reporting process involves assessing water quality for various parameters including sediment, metals, and nutrients. DEQ is currently reforming the assessment process by addressing inconsistencies in the way assessments were performed in the past and writing standardized protocols that will lead to more consistent decisions regarding impairment determinations. Here we focus on the assessment protocol being developed for sediment; a pollutant that can cause harm to aquatic life and fisheries. DEQ has applied the “Sufficient Credible Data/Beneficial Use Determination” since 2000. This process is well suited for an initial (screening) assessment, but has been challenged on the grounds of rigor and reproducibility by stakeholders when a specific pollutant is identified as harming a beneficial use. Our approach to this reforming process has been to study the literature, what other states have developed for assessment protocol, and methods that have already been developed by DEQ. Current considerations for what may be included in the assessment protocol will be discussed. We would like this process to be in the open for the public to comment and contribute. DEQ welcomes input in the process via a wiki page found at http://montanastag.pbworks.com and/or contacting any of the contributing authors

A systematic review and meta-analysis of predictive and prognostic models for outcome prediction using positron emission tomography radiomics in head and neck squamous cell carcinoma patients

FUNDING INFORMATIONMMP was funded by the University of Aberdeen under the Elphinstone Scholarship. The University of Aberdeen Open Access Fund supported the open access publication.Peer reviewedPublisher PD

Neuronal human BACE1 knock-in induces systemic diabetes in mice

Acknowledgements The authors thank S. Tammireddy (Diabetes and Cardiovascular Science, University of the Highlands and Islands, Inverness, UK) for technical support with the lipidomics component. Funding We would like to thank R. Simcox, Romex Oilfield Chemicals, for financial support for KP, and acknowledge additional contributions from the Scottish Alzheimer’s Research UK network for the lipidomics work. The College of Life Science and Medicine, University of Aberdeen, sponsored the imaging study. MD was funded by British Heart Foundation and Diabetes UK; NM was funded by a British Heart Foundation Intermediate Fellowship; KS was funded by a European Foundation for the Study of Diabetes/Lilly programme grant; and RD was funded by an Institute of Medical Sciences PhD studentship.Peer reviewedPublisher PDFPublisher PD

VAMPS : a website for visualization and analysis of microbial population structures

© The Author(s), 2014. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in BMC Bioinformatics 15 (2014): 41, doi:10.1186/1471-2105-15-41.The advent of next-generation DNA sequencing platforms has revolutionized molecular microbial ecology by making the detailed analysis of complex communities over time and space a tractable research pursuit for small research groups. However, the ability to generate 105–108 reads with relative ease brings with it many downstream complications. Beyond the computational resources and skills needed to process and analyze data, it is difficult to compare datasets in an intuitive and interactive manner that leads to hypothesis generation and testing. We developed the free web service VAMPS (Visualization and Analysis of Microbial Population Structures, http://vamps.mbl.edu webcite) to address these challenges and to facilitate research by individuals or collaborating groups working on projects with large-scale sequencing data. Users can upload marker gene sequences and associated metadata; reads are quality filtered and assigned to both taxonomic structures and to taxonomy-independent clusters. A simple point-and-click interface allows users to select for analysis any combination of their own or their collaborators’ private data and data from public projects, filter these by their choice of taxonomic and/or abundance criteria, and then explore these data using a wide range of analytic methods and visualizations. Each result is extensively hyperlinked to other analysis and visualization options, promoting data exploration and leading to a greater understanding of data relationships. VAMPS allows researchers using marker gene sequence data to analyze the diversity of microbial communities and the relationships between communities, to explore these analyses in an intuitive visual context, and to download data, results, and images for publication. VAMPS obviates the need for individual research groups to make the considerable investment in computational infrastructure and bioinformatic support otherwise necessary to process, analyze, and interpret massive amounts of next-generation sequence data. Any web-capable device can be used to upload, process, explore, and extract data and results from VAMPS. VAMPS encourages researchers to share sequence and metadata, and fosters collaboration between researchers of disparate biomes who recognize common patterns in shared data.Funding provided by the National Science Foundation [grant NSF/BDI 0960626 to SMH] and the Sloan Foundation through a collaborative project with the Microbiology of the Built Environment program

Neuronal human BACE1 knockin induces systemic diabetes in mice

Aims: β-Secretase 1 (BACE1) is a key enzyme in Alzheimer’s disease pathogenesis that catalyses the amyloidogenic cleavage of amyloid precursor protein (APP). Recently, global Bace1 deletion was shown to protect against diet-induced obesity and diabetes, suggesting that BACE1 is a potential regulator of glucose homeostasis. Here, we investigated whether increased neuronal BACE1 is sufficient to alter systemic glucose metabolism, using a neuron-specific human BACE1 knockin mouse model (PLB4).Methods: Glucose homeostasis and adiposity were determined by glucose tolerance tests and EchoMRI, lipid species were measured by quantitative lipidomics, and biochemical and molecular alterations were assessed by western blotting, quantitative PCR and ELISAs. Glucose uptake in the brain and upper body was measured via 18FDG-PET imaging.Results: Physiological and molecular analyses demonstrated that centrally expressed human BACE1 induced systemic glucose intolerance in mice from 4 months of age onward, alongside a fatty liver phenotype and impaired hepatic glycogen storage. This diabetic phenotype was associated with hypothalamic pathology, i.e. deregulation of the melanocortin system, and advanced endoplasmic reticulum (ER) stress indicated by elevated central C/EBP homologous protein (CHOP) signalling and hyperphosphorylation of its regulator eukaryotic translation initiation factor 2α (eIF2α). In vivo 18FDG-PET imaging further confirmed brain glucose hypometabolism in these mice; this corresponded with altered neuronal insulin-related signalling, enhanced protein tyrosine phosphatase 1B (PTP1B) and retinol-binding protein 4 (RBP4) levels, along with upregulation of the ribosomal protein and lipid translation machinery. Increased forebrain and plasma lipid accumulation (i.e. ceramides, triacylglycerols, phospholipids) was identified via lipidomics analysis.Conclusions/interpretation: Our data reveal that neuronal BACE1 is a key regulator of metabolic homeostasis and provide a potential mechanism for the high prevalence of metabolic disturbance in Alzheimer’s disease.</p

FDG-PET imaging, EEG and sleep phenotypes as translational biomarkers for research in Alzheimer's disease

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Abnormal cognition, sleep, eeg and brain metabolism in a novel knock-in alzheimer mouse, plb1

Late-stage neuropathological hallmarks of Alzheimer's disease (AD) are β-amyloid (βA) and hyperphosphorylated tau peptides, aggregated into plaques and tangles, respectively. Corresponding phenotypes have been mimicked in existing transgenic mice, however, the translational value of aggressive over-expression has recently been questioned. As controlled gene expression may offer animal models with better predictive validity, we set out to design a transgenic mouse model that circumvents complications arising from pronuclear injection and massive over-expression, by targeted insertion of human mutated amyloid and tau transgenes, under the forebrain- and neurone-specific CaMKIIα promoter, termed PLB1 Double. Crossing with an existing presenilin 1 line resulted in PLB1 Triple mice. PLB1 Triple mice presented with stable gene expression and age-related pathology of intra-neuronal amyloid and hyperphosphorylated tau in hippocampus and cortex from 6 months onwards. At this early stage, pre-clinical 18FDG PET/CT imaging revealed cortical hypometabolism with increased metabolic activity in basal forebrain and ventral midbrain. Quantitative EEG analyses yielded heightened delta power during wakefulness and REM sleep, and time in wakefulness was already reliably enhanced at 6 months of age. These anomalies were paralleled by impairments in long-term and short-term hippocampal plasticity and preceded cognitive deficits in recognition memory, spatial learning, and sleep fragmentation all emerging at ~12 months. These data suggest that prodromal AD phenotypes can be successfully modelled in transgenic mice devoid of fibrillary plaque or tangle development. PLB1 Triple mice progress from a mild (MCI-like) state to a more comprehensive AD-relevant phenotype, which are accessible using translational tools such as wireless EEG and microPET/CT.</p

Food and drink consumption at school lunchtime:the impact of lunch type and contribution to overall intake in British 9-10-year-old children

To examine the differences in dietary intakes of children consuming school meals and packed lunches, the contribution of lunchtime intake to overall dietary intake, and how lunchtime intake relates to current food-based recommendations for school meals

Adipocyte-specific protein tyrosine phosphatase 1B deletion increases lipogenesis, adipocyte cell size and is a minor regulator of glucose homeostasis

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Deception has no acute or residual effect on cycling time trial performance but negatively effects perceptual responses.

Feedback deception is used to explore the importance of expectations on pacing strategy and performance in self-paced exercise. The deception of feedback from a previous performance explores the importance of experience knowledge on exercise behaviour. This study aimed to explore the acute and residual effects of the deception of previous performance speed on perceptual responses and performance in cycling time trials.A parallel-group design.Twenty cyclists were assigned to a control or deception group and performed 16.1km time trials. Following a ride-alone baseline time trial (FBL), participants performed against a virtual avatar representing their FBL performance (PACER), then completed a subsequent ride-alone time trial (SUB). The avatar in the deception group, however, was unknowingly set 2% faster than their FBL.Both groups performed faster in PACER than FBL and SUB (p<0.05), but SUB was not significantly different to FBL. Affect was more negative and Ratings of Perceived Exertion (RPE) were higher in PACER than FBL in the deception group (p<0.05).The presence of a visual pacer acutely facilitated time trial performance, but deceptive feedback had no additional effect on performance. The deception group, however, experienced more negative affect and higher RPE in PACER, whereas these responses were absent in the control group. The performance improvement was not sustained in SUB, suggesting no residual performance effects occurred