287 research outputs found
Governing researchers through public involvement
This paper focuses on recent developments in UK health research policy, which place new pressures on researchers to address issues of accountability and impact through the implementation of patient and public involvement (PPI). We draw on an in-depth interview study with 20 professional researchers, and we analyse their experiences of competing for research funding, focusing on PPI as a process of professional research governance. We unearth dominant professional narratives of scepticism and alternative identifications in their enactment of PPI policy. We argue that such narratives and identifications evidence a resistance to ways in which patient involvement has been institutionalised and to the resulting subject-positions researchers are summoned to take up. We show that the new subjectivities emerging in this landscape of research governance as increasingly disempowered, contradictory and fraught with unresolved tensions over the ethical dimensions of the researchers' own professional identities
Genetic background modulates behavioral impairments in R6/2 mice and suggests a role for dominant genetic modifiers in Huntington’s disease pathogenesis
Variability and modification of the symptoms of Huntington’s disease (HD) are commonly observed in both patient populations and animal models of the disease. Utilizing a stable line of the R6/2 HD mouse model, the present study investigated the role of genetic background in the onset and severity of HD symptoms in a transgenic mouse. R6/2 congenic C57BL/6J and C57BL/6J × DBA/2J F1 (B6D2F1) mice were evaluated for survival and a number of behavioral phenotypes. This study reports that the presence of the DBA/2J allele results in amelioration or exacerbation of several HD-like phenotypes characteristic of the R6/2 mouse model and indicates the presence of dominant genetic modifiers of HD symptoms. This study is the first step in identifying genes that confer natural genetic variation and modify the HD symptoms. This identification may lead to novel targets for treatment and help elucidate the molecular mechanisms of HD pathogenesis
Mapped Karst Groundwater Basins in the Lexington 30 x 60 Minute Quadrangle
This map shows karst groundwater basins in the Lexington quadrangle, determined primarily by groundwater tracer studies. It can be used to quickly identify the groundwater basins and springs to which a site may drain. Major springs and the relative size of their catchment areas can be evaluated for potential as water supplies. The map also serves as a geographic index to literature on karst groundwater in the area
Mapped Karst Groundwater Basins in the Harrodsburg 30 x 60 Minute Quadrangle
This map shows karst groundwater basins in the Harrodsburg quadrangle, determined primarily by groundwater tracer studies. It can be used to quickly identify the groundwater basins and springs to which a site may drain. Major springs and the relative size of their basin or catchment areas can be evaluated for potential as water supplies. The map also serves as a geographic index to literature on karst groundwater in the area
Performance evaluation and geologic utility of LANDSAT-4 thematic mapper data
The overall objective of the project was to evaluate LANDSAT-4 Thematic Mapper (TM) data in the context of geologic applications. This involved a quantitative assessment of the data quality including the spatial and spectral characteristics realized by the instrument. Three test sites were selected for the study: (1) Silver Bell, Arizona; (2) Death Valley, California; and (3) Wind River/Bighorn Basin area, Wyoming. Conclusions include: (1) Artificial and natural targets can be used to atmospherically calibrate TM data and investigate scanner radiometry, atmospheric parameters, and construction of atmospheric Modulation Transfer Functions (MTF's), (2) No significant radiometric degradation occurs in TM data as a result of SCROUNGE processing; however, the data exhibit narrow digital number (DN) distributiosn suggesting that the configuration of the instrument is not optimal for each science applications, (30 Increased spatial resolution, 1:24,000 enlargement capability, and good geometric fidelity of TM data allow accurate photogeologic/geomorphic mapping, including relative age dating of alluvial fans, measurement of structural and bedding attitudes, and construction of such things as structural cross sections and stratigraphic columns. (4) TM bands 5 and 7 are particularly useful for geologic applications because they span a region of the spectrum not previously sampled by multispectral scanner data and are important for characterizing clay and carbonate materials
Induced chromosome deletions cause hypersociability and other features of Williams-Beuren syndrome in mice
The neurodevelopmental disorder Williams-Beuren syndrome is caused by spontaneous similar to 1.5 Mb deletions comprising 25 genes on human chromosome 7q11.23. To functionally dissect the deletion and identify dosage-sensitive genes, we created two half-deletions of the conserved syntenic region on mouse chromosome 5G2. Proximal deletion (PD) mice lack Gtf2i to Limk1, distal deletion (DD) mice lack Limk1 to Fkbp6, and the double heterozygotes (D/P) model the complete human deletion. Gene transcript levels in brain are generally consistent with gene dosage. Increased sociability and acoustic startle response are associated with PD, and cognitive defects with DD. Both PD and D/P males are growth-retarded, while skulls are shortened and brains are smaller in DD and D/P. Lateral ventricle (LV) volumes are reduced, and neuronal cell density in the somatosensory cortex is increased, in PD and D/P. Motor skills are most impaired in D/P. Together, these partial deletion mice replicate crucial aspects of the human disorder and serve to identify genes and gene networks contributing to the neural substrates of complex behaviours and behavioural disorders
Pathogenic Potential of Hic1-Expressing Cardiac Stromal Progenitors
The cardiac stroma contains multipotent mesenchymal progenitors. However, lineage relationships within cardiac stromal cells are poorly defined. Here, we identified heart-resident PDGFRa(+) SCA-1(+) cells as cardiac fibro/adipogenic progenitors (cFAPs) and show that they respond to ischemic damage by generating fibrogenic cells. Pharmacological blockade of this differentiation step with an anti-fibrotic tyrosine kinase inhibitor decreases post-myocardial infarction (post-MI) remodeling and leads to improvement in cardiac function. In the undamaged heart, activation of cFAPs through lineage-specific deletion of the gene encoding the quiescence-associated factor HIC1 reveals additional pathogenic potential, causing fibrofatty infiltration within the myocardium and driving major pathological features pathognomonic in arrhythmogenic cardiomyopathy (AC). In this regard, cFAPs contribute to multiple pathogenic cell types within cardiac tissue and therapeutic strategies aimed at modifying their activity are expected to have tremendous benefit for the treatment of diverse cardiac diseases
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