The 3M National Teaching Fellowship: A high impact community of practice in higher education

The 3M National Teaching Fellowship is a national teaching award program that has recognized over 300 teachers at more than 80 Canadian universities for their teaching excellence and outstanding educational leadership. Despite its rich, 30 plus-year history, its impact has remained largely anecdotal. In this study, we build on Hannah and Lester’s (2009) original, multilevel approach that looks at interactions between the individual, network, and systems levels to explore the impact of the 3M National Teaching Fellowship program on furthering and enriching teaching and learning in higher education. Through the analysis of a large collection of program artefacts corroborated with in-depth interviews with 11 fellows (key informants), we were able to gain a deeper understanding of the ways in which the program has had impact at the individual (micro), departmental (meso), institutional (macro), and national/international (mega) levels. In this article, we outline our scholarly exploration of the program’s influence and explore its role as a high-impact community of practice in higher education

The 3M National Teaching Fellowship: A High Impact Community of Practice in Higher Education

The 3M National Teaching Fellowship is a national teaching award program that has recognized over 300 teachers at more than 80 Canadian universities for their teaching excellence and outstanding educational leadership. Despite its rich, 30 plus-year history, its impact has remained largely anecdotal. In this study, we build on Hannah and Lester’s (2009) original, multilevel approach that looks at interactions between the individual, network, and systems levels to explore the impact of the 3M National Teaching Fellowship program on furthering and enriching teaching and learning in higher education. Through the analysis of a large collection of program artefacts corroborated with in-depth interviews with 11 fellows (key informants), we were able to gain a deeper understanding of the ways in which the program has had impact at the individual (micro), departmental (meso), institutional (macro), and national/international (mega) levels. In this article, we outline our scholarly exploration of the program’s influence and explore its role as a high-impact community of practice in higher education

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

John Clare and place

This chapter tackles issues of place in the self-presentation and critical reception of John Clare, and pursues it across a number of axes. The argument centres on the placing of Clare both socio-economically and ‘naturally’, and limitations exerted upon perceptions of his work. Interrogating criticism this chapter finds a pervasive awkwardness especially in relation to issues of class and labour. It assesses the contemporary ‘placing’ of Clare, and seemingly unavoidable insensitivities to labour and poverty in the history industry, place-naming, and polemical ecocriticism. It assesses the ways Clare represents place – in poverty, in buildings, in nature – and, drawing on Michel de Certeau, considers the tactics Clare uses to negotiate his place. It pursues trajectories to ‘un-place’ Clare: the flight of fame in Clare’s response to Byron; and the flight of an early poem in songbooks and beyond, across the nineteenth century

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

BACKGROUND: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. METHODS: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). FINDINGS: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29-146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0- 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25-1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39-1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65-1·60]; p=0·92). INTERPRETATION: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention. FUNDING: British Heart Foundation

Release of Evaluated 239Pu(n,f) Prompt Fission Neutron Spectra Including the CEA and Chi-Nu High-precision Experimental Data

This report documents an evaluation of 239Pu prompt fission neutron spectra (PFNS) that isa release candidate for the upcoming U.S. nuclear data library, ENDF/B-VIII.1. This evaluationdiffers from its predecessor, ENDF/B-VIII.0, mainly by the inclusion of two 239Pu PFNS high-precision experiments: one measured by the Chi-Nu team of LANL and LLNL, and the secondone by the CEA team using the liquid-scintillator Chi-Nu array. These two data sets are the firstones that cover the 239Pu PFNS for continuous incident-neutron energies of 1–20 MeV and broadoutgoing-neutron energies with high precision. Chi-Nu covers outgoing-neutron energies from 10keV–10 MeV, while CEA data are given for 0.25–11.3175 MeV. Previous data sets were eithermeasured in a limited energy range or with less precision. Hence, these new CEA and Chi-Nudata provide decisive information for the evaluation. The resulting evaluated data correspond wellto the new experimental PFNS, but are distinctly different than ENDF/B-VIII.0 values at allincident-neutron energies. These large differences compared to ENDF/B-VIII.0 can also be seen inthe average mean energies computed from the new evaluated PFNS. However, the evaluated meanenergies agree well with experimental data from Chi-Nu and CEA data, again, indicating that whilethe changes are large compared to ENDF/B-VIII.0, they are supported by experimental data. Dueto those differences, large drops (e.g., -128 pcm for Jezebel or -114 for Flattop-Plutonium) in thepredicted effective neutron multiplication factor, keff , of selected ICSBEP critical assemblies can beobserved when these new PFNS are used compared to using ENDF/B-VIII.0. These large changescan be counter-balanced by considering, in addition to the new 239Pu PFNS, new evaluated data forthe neutron-induced 239Pu fission cross section from the Neutron Data Standards project and the average prompt fission neutron multiplicity from an NCSP project. A further indication that theevaluated data describe high-precision experimental data well is that the the evaluated PFNS alsoproduce 239Pu/235U PFNS in agreement with associated Chi-Nu data. Changes in the simulationof 239Pu LLNL pulsed-sphere neutron-leakage spectra are modest compared to ENDF/B-VIIII.0PFN

Anorectal stenosis after treatment with tumor necrosis factor α antibodies: a case series

<p>Abstract</p> <p>Introduction</p> <p>We identified three patients who developed anorectal stenosis after successful treatment with anti-tumor necrosis factor α (anti-TNF-α) agents.</p> <p>Case presentation</p> <p>Two patients, a 24-year-old Irish Caucasian man and a 64-year-old Irish Caucasian woman, developed symptoms attributable to anorectal stenosis four to six weeks after treatment. A further patient, a 25-year-old Irish Caucasian male, presented three years after treatment with anorectal stenosis, having been asymptomatic with his stenosis for the preceding three years. No patients had evidence of active inflammation at time of representation or had previous anal canal surgery.</p> <p>Conclusion</p> <p>Anorectal stenosis in these patients appears to be independent of active inflammation. No other cause of new stenosis could be identified. We postulate that rapid clinical response to anti-TNF-α agents led to aberrant mucosal healing. This in turn led to anorectal stenosis. This is the first report of this complication in association with the use of biologic agents.</p