Evolution of IFN subgroups in bony fish - 2. analysis of subgroup appearance and expansion in teleost fish with a focus on salmonids

Acknowledgements FL was supported by a Newton International Fellowship funded by the Academy of Medical Sciences, UK (AMS, NIF004\1036). Thanks go to Mingli Liu (Shanghai Ocean University) for help with the bioinformatics analysis of the Icefish/Toothfish, and to Drs Dan Macqueen and Manu Gundappa (Roslin Institute, University of Edinburgh) for helpful discussions and advice on the analysis.Peer reviewedPostprin

Relief of branch pulmonary artery stenosis reduces pulmonary valve insufficiency in a swine model

ObjectiveWe sought to determine the impact of relieving branch pulmonary artery stenosis on pulmonary valve insufficiency and right ventricular function. Long-standing pulmonary insufficiency causes progressive right ventricular dilatation, leading to decreased right ventricular function. Adults with pulmonary insufficiency are at risk of decreased exercise tolerance, arrhythmias, and sudden cardiac death. Branch pulmonary artery stenosis frequently occurs in these patients, and the presence of branch stenosis may exacerbate valve insufficiency.MethodsNeonatal piglets (n = 7) underwent surgery to create pulmonary insufficiency and left pulmonary artery stenosis. At 3 months of age, the animals underwent baseline cardiac magnetic resonance imaging followed by stenting of the left pulmonary artery. A repeat magnetic resonance imaging scan was performed 1 week after intervention. Magnetic resonance imaging evaluation included (1) velocity mapping to assess the forward and reverse flow at the main, left and right pulmonary arteries, and aorta; and (2) volumetric assessment of the right ventricle.ResultsLeft pulmonary artery flow increased from 14.5% to 36.3% of total net flow after stenting (P < .01). Pulmonary regurgitation decreased from 38.7% to 27.4% (P < .02). Right ventricular ejection fraction improved from a median of 53.5% to 58.2% after stenting (P < .01). Cardiac index improved from a median of 2.7 to 3.5 L/min/m2 (P = .01).ConclusionRelief of branch pulmonary artery stenosis reduces insufficiency and improves right ventricular systolic function in this animal model. This supports the practice of aggressive intervention in patients with branch pulmonary artery stenosis and pulmonary insufficiency

Word Detection in Individual Subjects Is Difficult to Probe With Fast Periodic Visual Stimulation

Measuring cognition in single subjects presents unique challenges. On the other hand, individually sensitive measurements offer extraordinary opportunities, from informing theoretical models to enabling truly individualised clinical assessment. Here, we test the robustness of fast, periodic, and visual stimulation (FPVS), an emerging method proposed to elicit detectable responses to written words in the electroencephalogram (EEG) of individual subjects. The method is non-invasive, passive, and requires only a few minutes of testing, making it a potentially powerful tool to test comprehension in those who do not speak or who struggle with long testing procedures. In an initial study, Lochy et al. (2015) used FPVS to detect word processing in eight out of 10 fluent French readers. Here, we attempted to replicate their study in a new sample of 10 fluent English readers. Participants viewed rapid streams of pseudo-words with words embedded at regular intervals, while we recorded their EEG. Based on Lochy et al. (2015) we expected that words would elicit a steady-state response at the word-presentation frequency (2 Hz) over parieto-occipital electrode sites. However, across 40 datasets (10 participants, two conditions, and two regions of interest–ROIs), only four datasets met the criteria for a unique response to words. This corresponds to a 10% detection rate. We conclude that FPVS should be developed further before it can serve as an individually-sensitive measure of written word processing

Epidemiology of eating disorders part III: Social epidemiology and case definitions revisited.

Accepted manuscript version. Published version at <a href=http://doi.org/10.1080/21662630.2015.1022197>http://doi.org/10.1080/21662630.2015.1022197</a>.The previous papers in this series outlined a historical panorama and presented updated knowledge about putative risk factors and how eating disorders are distributed in various populations. In this final paper, we discuss in what way comorbidity findings and transdiagnostic issues may change our conceptions about ‘an epidemiological case’ from the current definition of eating disorders based on the recent version of the Diagnostic and Statistical Manual of Mental Disorders (i.e. the DSM-5), and to what extent an alternative definition may introduce new perspectives of prevention. The paper also provides an update on issues relevant for treatment dissemination

Comprehensive comparative outcomes in children with congenital heart disease: The rationale for the Congenital Catheterization Research Collaborative

Clinical research in the treatment of patients with congenital heart disease (CHD) is limited by the wide variety of CHD manifestations and therapeutic options as well as the generally low incidence of CHD. The availability of comprehensive, contemporary outcomes studies is therefore limited. This inadequacy may result in a lack of data‐driven medical decision making. In 2013, clinician scientists at two centers began a research collaboration, the Congenital Catheterization Research Collaborative (CCRC). Over time, the CCRC has grown to include nine cardiac centers from across the United States, with a common data coordinating center. The CCRC seeks to generate high‐quality, contemporary, statistically robust, and generalizable outcomes research which can help address important clinical questions in the treatment of CHD. To date, the CCRC has reported on multicenter outcomes in: neonates with congenital aortic stenosis, infants undergoing right ventricular decompression for pulmonary atresia and intact ventricular septum, and infants with ductal‐dependent pulmonary blood flow. The CCRC has been successful at leveraging large multicenter cohorts of patients in a contemporary period to perform comparative studies. In the future, the CCRC plans to continue to perform hypothesis‐driven retrospective and prospective observational studies of CHD populations where controversy exists or where novel interventions or therapies have emerged. Quality improvement efforts including lesion‐specific registry development may be an additional potential future target.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149494/1/chd12737.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149494/2/chd12737_am.pd

The effect of novel nitrogen-rich plasma polymer coatings on the phenotypic profile of notochordal cells

Background: The loss of the notochordal cells from the nucleus pulposus is associated with ageing and disc degeneration. However, understanding the mechanisms responsible for the loss of these cells has been hampered in part due to the difficulty of culturing and maintaining their phenotype. Furthermore, little is known about the influence of the substratum on the molecular markers of notochordal cells. Methods: Notochordal cells were isolated from lumbar spine of non-chondrodystrophoid dogs and cultured on N-rich plasma polymer layers, so-called "PPE:N" ( N-doped plasma-polymerised ethylene, containing up to 36% [N]) surfaces, for 3, 7 or 14 days. Gene expression of vimentin ( VIM), pleiotrophin ( PTN), matrix Gla protein ( MGP), cartilage oligomeric matrix protein ( COMP), keratin 18 ( KRT 18), aggrecan ( AGG), collagen type 1 ( COL1A2), collagen type 2 ( COL2A1) was analyzed through semi-quantitative reverse transcription-polymerase chain reaction ( RT-PCR).Results: Notochordal cells were maintained in culture on PPE:N for up to 14 days with no loss in cell viability. Except for VIM, gene expression varied depending on the culture periods and [ N] concentration of the substratum. Generally, PPE: N surfaces altered gene expression significantly when cells were cultured for 3 or 7 days.Conclusion: The present study has shown that notochordal cells from dogs can attach to and grow on PPE: N surfaces. Analysis of the expression of different genes in these cells cultured on different N-functionalized surfaces indicates that cellular behaviour is gene-specific and time-dependent. Further studies are required to better understand the roles of specific surface functionalities on receptor sites, and their effects on cellular phenotypes

Food abundance does not determine bird use of early-successional habitat.

Abstract. Few attempts have been made to experimentally address the extent to which temporal or spatial variation in food availability influences avian habitat use. We used an experimental approach to investigate whether bird use differed between treated (arthropods reduced through insecticide application) and control (untreated) forest canopy gaps within a bottomland hardwood forest in the Upper Coastal Plain of South Carolina, USA. Gaps were two- to three-year-old group selection timber harvest openings of three sizes (0.13, 0.26, and 0.50 ha). Our study was conducted during four bird use periods (spring migration, breeding, post-breeding, and fall migration) in 2002 and 2003. Arthropods were reduced in treated gaps by 68% in 2002 and 73% in 2003. We used mist-netting captures and foraging attack rates to assess the influence of arthropod abundance on avian habitat use. Evidence that birds responded to arthropod abundance was limited and inconsistent. In 2002, we generally captured more birds in treated gaps of the smallest size (0.13 ha) and fewer birds in treated gaps of the larger sizes. In 2003, we recorded few differences in the number of captures in treated and control gaps. Foraging attack rates generally were lower in treated than in control gaps, indicating that birds were able to adapt to the reduced food availability and remain in treated gaps. We conclude that arthropod abundance was not a proximate factor controlling whether forest birds used our gaps. The abundance of food resources may not be as important in determining avian habitat selection as previous research has indicated, at least for passerines in temperate subtropical regions

Modification of BRCA1-associated breast cancer risk by HMMR overexpression

Breast cancer risk for carriers of BRCA1 pathological variants is modified by genetic factors. Genetic variation in HMMR may contribute to this effect. However, the impact of risk modifiers on cancer biology remains undetermined and the biological basis of increased risk is poorly understood. Here, we depict an interplay of molecular, cellular, and tissue microenvironment alterations that increase BRCA1-associated breast cancer risk. Analysis of genome-wide association results suggests that diverse biological processes, including links to BRCA1-HMMR profiles, influence risk. HMMR overexpression in mouse mammary epithelium increases Brca1-mutant tumorigenesis by modulating the cancer cell phenotype and tumor microenvironment. Elevated HMMR activates AURKA and reduces ARPC2 localization in the mitotic cell cortex, which is correlated with micronucleation and activation of cGAS-STING and non-canonical NF-kappa B signaling. The initial tumorigenic events are genomic instability, epithelial-to-mesenchymal transition, and tissue infiltration of tumor-associated macrophages. The findings reveal a biological foundation for increased risk of BRCA1-associated breast cancer. The effect of hyaluronan-mediated motility receptor (HMMR) expression in BRCA1-associated breast cancer risk remains unknown. Here, HMMR overexpression induces the activation of cGAS-STING and non-canonical NF-kappa B signalling, instigating an immune permissive environment for breast cancer development