Bridging Science with Society: Defining Pathways for Engagement

Science communication training organizations, are uniquely positioned at the nexus of science and society. Through research and training, they empower scientists to engage with the public to ultimately improve how science informs decision-making processes at the individual, organizational, and community levels. This paper argues that science communication training organizations must unite to provide a comprehensive and exhaustive set of offerings that empower scientists to master foundational communication skills while recognizing the complete social and cultural systems in which their science communication occurs. We present three separate possible pathways training programs could take, depending on the contexts and audiences for engagement. We differentiate between the goals, sites, and audiences for engagement, and the forms of knowledge or preparation needed for productive engagement

Plaque size is decreased but M1 macrophage polarization and rupture related metalloproteinase expression are maintained after deleting T-bet in ApoE null mice

BACKGROUND:Thelper1 (Th1) lymphocytes have been previously implicated in atherosclerotic plaque growth but their role in plaque vulnerability to rupture is less clear. We investigated whether T-bet knockout that prevents Th1 lymphocyte differentiation modulates classical (M1) macrophage activation or production of matrix degrading metalloproteinases (MMPs) and their tissue inhibitors, TIMPs. METHODS & RESULTS:We studied the effect of T-bet deletion in apolipoproteinE (ApoE) knockout mice fed a high fat diet (HFD) or normal chow diet (ND). Transcript levels of M1/M2 macrophage polarization markers, selected MMPs and TIMPs were measured by RT-qPCR in macrophages isolated from subcutaneous granulomas or in whole aortae. Immunohistochemistry of aortic sinus (AS) and brachiocephalic artery (BCA) plaques was conducted to quantify protein expression of the same factors. Deletion of T-bet decreased mRNA for the M1 marker NOS-2 in granuloma macrophages but levels of M2 markers (CD206, arginase-1 and Ym-1), MMPs-2, -9, -12, -13, -14 and -19 or TIMPs-1 to -3 were unchanged. No mRNA differences were observed in aortic extracts from mice fed a HFD for 12 weeks. Moreover, AS and BCA plaques were similarly sized between genotypes, and had similar areas stained for NOS-2, COX-2, MMP-12 and MMP-14 proteins. T-bet deletion increased MMP-13, MMP-14 and arginase-1 in AS plaques. After 35 weeks of ND, T-bet deletion reduced the size of AS and BCA plaques but there were no differences in the percentage areas stained for M1 or M2 markers, MMPs-12, -13, -14, or TIMP-3. CONCLUSIONS:Absence of Th1 lymphocytes is associated with reduced plaque size in ApoE knockout mice fed a normal but not high fat diet. In either case, M1 macrophage polarization and expression of several MMPs related to plaque instability are either maintained or increased

Ecological role of an offshore industry artificial structure

Decommissioning of oil and gas infrastructure globally has focused attention on its importance as hard substratum on continental shelf and slope habitats. Observational studies are needed to improve understanding of faunal assemblages supported by offshore infrastructure and better predict the effect of removal. Here, we present results from visual inspection and physical sampling of a small oil and gas industry structure decommissioned from an oil field in the North East Atlantic. This is supported by observations of similar structures nearby and by photographs of the surrounding seabed from environmental baseline surveys. The structure supported a reasonably high biomass and diversity of invertebrates (>10 kg and >39 macrofaunal and 17 megafaunal species) and fishes (>20 kg biomass and >4 species). The invertebrate megafaunal species present on the structure were a sub-set of the hard substratum fauna observed on surrounding seabed. Porifera were absent from the structure. Biological succession in the first 2 years occurred as follows. Sparse colonies of the hydroid Obelia sp. stet were early colonisers then subsequent development of thick hydroid turf (Obelia sp. stet. and Halecium sp. stet.) supported an invertebrate assemblage (2654 individuals kg wet mass–1) dominated by saddle oysters [Pododesmus squama (Gmelin, 1791) and Heteranomia sp. stet.)] and scale worms (Harmothoe spp.). Percentage cover of hydroid turf varied significantly over the structure, with most growth on sections exposed to strongest currents. Commercially important fish species present around the structure included Gadus morhua (Atlantic cod), Pollachius virens (saithe) and Lophius piscatorius (monkfish). Studies of artificial structures such as this provide much needed data to understand their role in the ecology of seafloor habitats and inform environmental decision making on all stages of industry from exploration to decommissioning. We show that the ecological role of the decommissioned three-dimensional structures was to enhance the biomass of a sub-set of epifaunal invertebrates found in the area. This supported diverse associated macrofaunal organisms, providing a food source for motile invertebrates and fishes in an area where background hard substratum can be lost through the impacts of drilling

Draft Genome Sequence Of Burkholderia Andropogonis Type Strain Icmp2807, Isolated From Sorghum Bicolor.

Here, we report the draft genome sequence of Burkholderia andropogonis ICMP2807, a phytopathogenic bacterium isolated from Sorghum bicolor plants in the United States.

Prevalence of CADASIL and Fabry Disease in a Cohort of MRI Defined Younger Onset Lacunar Stroke.

BACKGROUND AND PURPOSE: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), caused by mutations in the NOTCH3 gene, is the most common monogenic disorder causing lacunar stroke and cerebral small vessel disease (SVD). Fabry disease (FD) due to mutations in the GLA gene has been suggested as an underdiagnosed cause of stroke, and one feature is SVD. Previous studies reported varying prevalence of CADASIL and FD in stroke, likely due to varying subtypes studied; no studies have looked at a large cohort of younger onset SVD. We determined the prevalence in a well-defined, MRI-verified cohort of apparently sporadic patients with lacunar infarct. METHODS: Caucasian patients with lacunar infarction, aged ≤70 years (mean age 56.7 (SD8.6)), were recruited from 72 specialist stroke centres throughout the UK as part of the Young Lacunar Stroke DNA Resource. Patients with a previously confirmed monogenic cause of stroke were excluded. All MRI's and clinical histories were reviewed centrally. Screening was performed for NOTCH3 and GLA mutations. RESULTS: Of 994 subjects five had pathogenic NOTCH3 mutations (R169C, R207C, R587C, C1222G and C323S) all resulting in loss or gain of a cysteine in the NOTCH3 protein. All five patients had confluent leukoaraiosis (Fazekas grade ≥2). CADASIL prevalence overall was 0.5% (95% CI 0.2%-1.1%) and among cases with confluent leukoaraiosis 1.5% (95% CI 0.6%-3.3%). No classic pathogenic FD mutations were found; one patient had a missense mutation (R118C), associated with late-onset FD. CONCLUSION: CADASIL cases are rare and only detected in SVD patients with confluent leukoaraiosis. No definite FD cases were detected.The UK Young Lacunar Stroke DNA Study was funded by a grants from the Wellcome Trust (WT072952, www.wellcome.ac.uk) and the Stroke Association (TSA 2010/01& TSA 2013/02, www.stroke.org.uk). Fabry disease screening was supported by an unrestricted scientific grant from Shire Human Genetic Therapies (www.shire.com). The sponsors of the study had no role in the study design, data collection, data analysis, interpretation, writing of the manuscript, or the decision to submit the manuscript for publication. L R-J’s salary is funded by a Stroke Association/ British Heart Foundation grant. (TSA/BHF 2010/01). HM is supported by an National Institute for Health Research Senior Investigator award (www.nihr.ac.uk). HM and SB are supported by the Cambridge University Trust National Institute for Health Research Comprehensive Research Centre (www.cambridge-brc.org.uk).This is the final version of the article. It first appeared from PLoS via http://dx.doi.org/10.1371/journal.pone.013635

GABA-ergic Dynamics in Human Frontotemporal Networks Confirmed by Pharmaco-Magnetoencephalography.

To bridge the gap between preclinical cellular models of disease and in vivo imaging of human cognitive network dynamics, there is a pressing need for informative biophysical models. Here we assess dynamic causal models (DCM) of cortical network responses, as generative models of magnetoencephalographic observations during an auditory oddball roving paradigm in healthy adults. This paradigm induces robust perturbations that permeate frontotemporal networks, including an evoked 'mismatch negativity' response and transiently induced oscillations. Here, we probe GABAergic influences in the networks using double-blind placebo-controlled randomized-crossover administration of the GABA reuptake inhibitor, tiagabine (oral, 10 mg) in healthy older adults. We demonstrate the facility of conductance-based neural mass mean-field models, incorporating local synaptic connectivity, to investigate laminar-specific and GABAergic mechanisms of the auditory response. The neuronal model accurately recapitulated the observed magnetoencephalographic data. Using parametric empirical Bayes for optimal model inversion across both drug sessions, we identify the effect of tiagabine on GABAergic modulation of deep pyramidal and interneuronal cell populations. We found a transition of the main GABAergic drug effects from auditory cortex in standard trials to prefrontal cortex in deviant trials. The successful integration of pharmaco- magnetoencephalography with dynamic causal models of frontotemporal networks provides a potential platform on which to evaluate the effects of disease and pharmacological interventions.SIGNIFICANCE STATEMENT Understanding human brain function and developing new treatments require good models of brain function. We tested a detailed generative model of cortical microcircuits that accurately reproduced human magnetoencephalography, to quantify network dynamics and connectivity in frontotemporal cortex. This approach identified the effect of a test drug (GABA-reuptake inhibitor, tiagabine) on neuronal function (GABA-ergic dynamics), opening the way for psychopharmacological studies in health and disease with the mechanistic precision afforded by generative models of the brain