KT Force - Knowledge as a Value: Regional Implementation Plan

EXECUTIVE SUMMARY The KTForce INTERREG IVC project involves, at its core. the benchmarking and investigation of best practices in knowledge transfer policies and practices at regional level. Its ultimate goal is to Improve Europe's innovation environment. The project focuses on three components within Knowledge Transfer (KT) and seeks to assess and benchmark these within an innovation and regional development context. KTForce looks at how university-industry relations can be enhanced, how technology licensing can be improved and the Identification of the optimum conditions for creating spin-outs and increasing entrepreneurial activity. Along with a brief contextualisation of the South East Region of Ireland this booklet gives a concise overview of the overall methodology set up and applied over the course of the KT project. Specifically. this booklet provides a characterisation of the South East Region, the focus (however. most data available is only for the Southern and Eastern region). through a regional SWOT analysis supported by detailed illustration of both scenario 0 and future scenarios. based on the analysis of key innovation performance indicators. In considering both practices and policies relevant to knowledge transfer, at national and regional levels. the process for practice selection and implementation and the analysis used for policy benchmarking are also illustrated. This booklet ends with the main conclusions and some policy recommendations resulting from the analysis and work performed over the course of the KT Force project

Outflows from Luminous YSOs: An Infrared Polarimetric Study

e present Near Infrared imaging polarimetry of three regions of massive star formation, G$192.16 - 3.82$, Cepheus A, and W42. In W42 we have discovered a new bipolar nebula located at the far side of the HII region behind the visible cluster of exciting stars. The axis of this new nebula is aligned with the magnetic field threading the entire cluster region. Polarization in the bipolar outflow nebulosity associated with G192.16 is consistent with a single illuminating source, too faint to be detected at 2 \micron. Polarization in the reflection nebulosity associated with Ceph A requires more than one illuminating source, although HW2 is clearly dominant. In all three objects, the magnetic field in the outflow at distances greater than $\sim 0.2$ pc is radial. In G192.16 the magnetic field geometry closer than $\sim 0.2$ pc to the embedded star appears chaotic. For G192.16 the outflow is not aligned with the surrounding magnetic field, which lies in the galactic plane. In Ceph A, the outflow axis could be interpreted as being aligned with the galactic plane, but the magnetic field threading the region is not. Only in the case of W42 is the magnetic field threading the HII region aligned with the mean field in the surrounding galactic plane.Comment: 1 LaTeX file, 10 figure

Family and neighborhood welfare dependency and sons' labor supply

This article tests four models of how parental and childhood welfare use affects sons' labor supply: the correlated disadvantages model, Wilson's structural-environmental model, Mead's welfare culture model, and Murray's incentives model. Past research is extended by including measures of all seven factors that these models predict will shape sons' labor supply: parental welfare use, neighborhood welfare use, parental income, family noneconomic resources, neighborhood resources, labor market conditions, and state welfare benefits. There are four main findings. First, welfare use in the childhood neighborhood has no effects on sons' work hours. Second, only one group of sons is affected by parental welfare use: black sons' whose parents average $7,500 or more in welfare income per year. Third, black sons' adult work hours are strongly predicted by parental poverty and by labor market conditions; together these account for half the estimated relationships between heavy parental welfare use and black sons' labor supply. Fourth, parents' and neighbors' work hours strongly predict nonblack sons' labor supply.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44655/1/10834_2006_Article_BF02353710.pd

A fibril-specific, conformation-dependent antibody recognizes a subset of Aβ plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain

Beta-amyloid (Aβ) is thought to be a key contributor to the pathogenesis of Alzheimer disease (AD) in the general population and in adults with Down syndrome (DS). Different assembly states of Aβ have been identified that may be neurotoxic. Aβ oligomers can assemble into soluble prefibrillar oligomers, soluble fibrillar oligomers and insoluble fibrils. Using a novel antibody, OC, recognizing fibrils and soluble fibrillar oligomers, we characterized fibrillar Aβ deposits in AD and DS cases. We further compared human specimens to those obtained from the Tg2576 mouse model of AD. Our results show that accumulation of fibrillar immunoreactivity is significantly increased in AD relative to nondemented aged subjects and those with select cognitive impairments (p < 0.0001). Further, there was a significant correlation between the extent of frontal cortex fibrillar deposit accumulation and dementia severity (MMSE r = −0.72). In DS, we observe an early age of onset and age-dependent accumulation of fibrillar OC immunoreactivity with little pathology in similarly aged non-DS individuals. Tg2576 mice show fibrillar accumulation that can be detected as young as 6 months. Interestingly, fibril-specific immunoreactivity was observed in diffuse, thioflavine S-negative Aβ deposits in addition to more mature neuritic plaques. These results suggest that fibrillar deposits are associated with disease in both AD and in adults with DS and their distribution within early Aβ pathology associated with diffuse plaques and correlation with MMSE suggest that these deposits may not be as benign as previously thought

Non-Steroidal Anti-Inflammatory Drugs and Cognitive Function: Are Prostaglandins at the Heart of Cognitive Impairment in Dementia and Delirium ?

Studies of non-steroidal anti-inflammatory drugs (NSAIDs) in rheumatoid arthritis imply that inflammation is important in the development of Alzheimer’s disease (AD). However, these drugs have not alleviated the symptoms of AD in those who have already developed dementia. This suggests that the primary mediator targeted by these drugs, PGE2, is not actively suppressing memory function in AD. Amyloid-β oligomers appear to be important for the mild cognitive changes seen in AD transgenic mice, yet amyloid immunotherapy has also proven unsuccessful in clinical trials. Collectively, these findings indicate that NSAIDs may target a prodromal process in mice that has already passed in those diagnosed with AD, and that synaptic and neuronal loss are key determinants of cognitive dysfunction in AD. While the role of inflammation has not yet become clear, inflammatory processes definitely have a negative impact on cognitive function during episodes of delirium during dementia. Delirium is an acute and profound impairment of cognitive function frequently occurring in aged and demented patients exposed to systemic inflammatory insults, which is now recognised to contribute to long-term cognitive decline. Recent work in animal models is beginning to shed light on the interactions between systemic inflammation and CNS pathology in these acute exacerbations of dementia. This review will assess the role of prostaglandin synthesis in the memory impairments observed in dementia and delirium and will examine the relative contribution of amyloid, synaptic and neuronal loss. We will also discuss how understanding the role of inflammatory mediators in delirious episodes will have major implications for ameliorating the rate of decline in the demented population

Alzheimer disease models and human neuropathology: similarities and differences

Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease. Numerous mouse transgenic lines have now succeeded in partially reproducing its lesions: the extracellular deposits of Aβ peptide and the intracellular accumulation of tau protein. Mutated human APP transgenes result in the deposition of Aβ peptide, similar but not identical to the Aβ peptide of human senile plaque. Amyloid angiopathy is common. Besides the deposition of Aβ, axon dystrophy and alteration of dendrites have been observed. All of the mutations cause an increase in Aβ 42 levels, except for the Arctic mutation, which alters the Aβ sequence itself. Overexpressing wild-type APP alone (as in the murine models of human trisomy 21) causes no Aβ deposition in most mouse lines. Doubly (APP × mutated PS1) transgenic mice develop the lesions earlier. Transgenic mice in which BACE1 has been knocked out or overexpressed have been produced, as well as lines with altered expression of neprilysin, the main degrading enzyme of Aβ. The APP transgenic mice have raised new questions concerning the mechanisms of neuronal loss, the accumulation of Aβ in the cell body of the neurons, inflammation and gliosis, and the dendritic alterations. They have allowed some insight to be gained into the kinetics of the changes. The connection between the symptoms, the lesions and the increase in Aβ oligomers has been found to be difficult to unravel. Neurofibrillary tangles are only found in mouse lines that overexpress mutated tau or human tau on a murine tau −/− background. A triply transgenic model (mutated APP, PS1 and tau) recapitulates the alterations seen in AD but its physiological relevance may be discussed. A number of modulators of Aβ or of tau accumulation have been tested. A transgenic model may be analyzed at three levels at least (symptoms, lesions, cause of the disease), and a reading key is proposed to summarize this analysis