20 research outputs found

    Linking Higher Education and Social Change

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    More than four thousand stories could be told about the remarkable individuals who received fellowships under the Ford Foundation International Fellowships Program (IFP) between 2001 and 2010. Over the decade, the program enabled 4,314 emerging social justice leaders from Asia, Russia, Africa, the Middle East, and Latin America to pursue advanced degrees at more than 600 universities in almost 50 countries. By April 2013, nearly 4,000 Fellows had completed their fellowships, receiving degrees in development-related fields ranging from social and environmental science to the arts. A survey done in early 2012 showed that 82 percent of more than 3,300 former Fellows were working in their home countries to improve the lives and livelihoods of those around them, while many of the rest were studying for additional advanced degrees or working in international organizations. The final group of Fellows enrolled in universities around the world will complete their fellowships by the end of 2013.In 2001, the Ford Foundation funded IFP with a 280milliongrant,thelargestsingledonationintheFoundationshistory.TheprogramwasintendedtoprovidegraduatefellowshipstoindividualsincountriesoutsidetheUnitedStateswheretheFoundationhadgrantmakingprograms.In2006,theFoundationpledgedupto280 million grant, the largest single donation in the Foundation's history. The program was intended to provide graduate fellowships to individuals in countries outside the United States where the Foundation had grant-making programs. In 2006, the Foundation pledged up to 75 million in additional funds, allowing IFP to award more than 800 fellowships beyond its original projections. As extraordinary as the level and duration of funding, though, was IFP's singular premise: that extending higher education opportunities to leaders from marginalized communities would help further social justice in some of the world's poorest and most unequal countries. If successful, IFP would advance the Ford Foundation's mission to strengthen democratic values, reduce poverty and injustice, promote international cooperation and advance human achievement. It would decisively demonstrate that an international scholarship program could help build leadership for social justice and thus contribute to broader social change.In striving toward its ambitious goals, the program would transform a traditional mechanism -- an individual fellowship program for graduate degree study -- into a powerful tool for reversing discrimination and reducing long-standing inequalities in higher education and in societies at large. This report is the story of that transformation

    Incidental Mycobacterium-induced granulomatous inflammation of the follicular pharyngeal tonsils in a South African farmed ostrich (Struthio camelus)

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    Avian mycobacteriosis (AM) is a zoonotic disease caused by Mycobacterium avium complex (MAC), which can spread from avians to other farmed animals such as cattle and pigs as well as to humans. This study is the first report of granulomatous inflammation, as a result of avian mycobacteriosis, in the follicular pharyngeal tonsils of a farmed ostrich. The head of an apparently healthy farmed adult ostrich was obtained after slaughter. Each pharyngeal fold displayed a large tissue mass. This tissue was routinely prepared for light microscopy and stained with haematoxylin and eosin, periodic acid Schiff, Grocott methenamine silver, Gram and Ziehl-Neelsen. Immunohistochemistry (IHC) and polymerase chain reaction (PCR) were performed to identify Mycobacterium spp. and Mycobacterium tuberculosis complex, respectively. Histologically, the tissue masses consisted of confluent mature micro-granulomata that were characterised by central caseous necrosis surrounded by multinucleated giant cells, macrophages and lymphoid cells and an outer mature fibrous connective tissue capsule. Within some foci of caseous necrosis were variably sized colonies of small, Gram-negative, acid-fast bacilli, which showed positive IHC labelling for Mycobacterium spp., leading to a presumptive diagnosis of AM. PCR thus proved useful in excluding the presence of notifiable Mycobacterium spp. The significance and role of the pharyngeal tonsils of ratites in diseases such as AM warrant specific attention. Moreover, as ratites are known to present with AM infections with apparently no visible loss in body condition, as presumably occurred in the present case, it is imperative that unusual masses in apparently healthy ratites be thoroughly investigated.The Faculty of Veterinary Science, University of Pretoriahttp://www.jsava.co.zaam2014ab201

    The PP2A inhibitor I2PP2A is essential for sister chromatid segregation in oocyte meiosis II.

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    Haploid gametes are generated through two consecutive meiotic divisions, with the segregation of chromosome pairs in meiosis I and sister chromatids in meiosis II. Separase-mediated stepwise removal of cohesion, first from chromosome arms and later from the centromere region, is a prerequisite for maintaining sister chromatids together until their separation in meiosis II [1]. In all model organisms, centromeric cohesin is protected from separase-dependent removal in meiosis I through the activity of PP2A-B56 phosphatase, which is recruited to centromeres by shugoshin/MEI-S332 (Sgo) [2-5]. How this protection of centromeric cohesin is removed in meiosis II is not entirely clear; we find that all the PP2A subunits remain colocalized with the cohesin subunit Rec8 at the centromere of metaphase II chromosomes. Here, we show that sister chromatid separation in oocytes depends on a PP2A inhibitor, namely I2PP2A. I2PP2A colocalizes with the PP2A enzyme at centromeres at metaphase II, independently of bipolar attachment. When I2PP2A is depleted, sister chromatids fail to segregate during meiosis II. Our findings demonstrate that in oocytes I2PP2A is essential for faithful sister chromatid segregation by mediating deprotection of centromeric cohesin in meiosis II

    COVID-19 in congenital heart disease (COaCHeD) study

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    Background: COVID-19 has caused significant worldwide morbidity and mortality. Congenital heart disease (CHD) is likely to increase vulnerability and understanding the predictors of adverse outcomes is key to optimising care.// Objective: Ascertain the impact of COVID-19 on people with CHD and define risk factors for adverse outcomes.// Methods: Multicentre UK study undertaken 1 March 2020–30 June 2021 during the COVID-19 pandemic. Data were collected on CHD diagnoses, clinical presentation and outcomes. Multivariable logistic regression with multiple imputation was performed to explore predictors of death and hospitalisation.// Results: There were 405 reported cases (127 paediatric/278 adult). In children (age <16 years), there were 5 (3.9%) deaths. Adjusted ORs (AORs) for hospitalisation in children were significantly lower with each ascending year of age (OR 0.85, 95% CI 0.75 to 0.96 (p<0.01)). In adults, there were 24 (8.6%) deaths (19 with comorbidities) and 74 (26.6%) hospital admissions. AORs for death in adults were significantly increased with each year of age (OR 1.05, 95% CI 1.01 to 1.10 (p<0.01)) and with pulmonary arterial hypertension (PAH; OR 5.99, 95% CI 1.34 to 26.91 (p=0.02)). AORs for hospitalisation in adults were significantly higher with each additional year of age (OR 1.03, 95% CI 1.00 to 1.05 (p=0.04)), additional comorbidities (OR 3.23, 95% CI 1.31 to 7.97 (p=0.01)) and genetic disease (OR 2.87, 95% CI 1.04 to 7.94 (p=0.04)).// Conclusions: Children were at low risk of death and hospitalisation secondary to COVID-19 even with severe CHD, but hospital admission rates were higher in younger children, independent of comorbidity. In adults, higher likelihood of death was associated with increasing age and PAH, and of hospitalisation with age, comorbidities and genetic disease. An individualised approach, based on age and comorbidities, should be taken to COVID-19 management in patients with CHD

    The role of manufacturing in affecting the social dimension of sustainability

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    Consumers and self assembly products: problems and solutions

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    Children sometimes have accidents when using large items of play equipment, and whilst many are due to poor design or lack of supervision, some are due to inadequate or incorrect assembly. OBJECTIVES To examine the possibility of incorrect assembly and identify the consequences of errors and the resultant increase in hazards. METHODS The study collected accident statistics, surveyed the market and reviewed the literature. A variety of equipment was purchased and the instructions evaluated. Finally, trials with users were completed where the assembly procedure, time taken, errors made and subjective ratings were recorded. RESULTS Little literature was found but accident data from the UK, US and Australia showed minor injuries possibly attributable to assembling the product. Expert appraisals were conducted on 40 products to assess the instructions, assembly process and design, as well as the hazards presented during assembly and in use. Trials involving 100 representative subjects allowed observation of the assembly of products. The results showed a number of minor problems and hazards with the products. CONCLUSIONS The following improvements were recommended: • Standards applying to products requiring self-assembly should address the self-assembly process; • Accurate and meaningful information should be provided on the packaging;• Attention should be paid to the presentation and content of the product instructions • Products should be designed so that the assembly process is possible, relatively easy and safe to complete; Product components should be well designed, well machined and strong enough for the intended purpose. Furthermore, consumers must recognise their duty to make sensible purchases and to be responsible during assembly and use

    The sedimentary and tectonic evolution of the Amur River and North Sakhalin Basin: new evidence from seismic stratigraphy and Neogene–Recent sediment budgets

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    The North Sakhalin Basin in the western Sea of Okhotsk has been the main site of sedimentation from the Amur River since the Early Miocene. In this article, we present regional seismic reflection data and a Neogene–Recent sediment budget to constrain the evolution of the basin and its sedimentary fill, and consider the implications for sediment flux from the Amur River, in particular testing models of continental‐scale Neogene drainage capture. The Amur‐derived basin‐fill history can be divided into five distinct stages: the first Amur‐derived sediments (>21–16.5 Ma) were deposited during a period of transtension along the Sakhalin‐Hokkaido Shear Zone, with moderately high sediment flux to the basin (71 Mt year−1). The second stage sequence (16.5–10.4 Ma) was deposited following the cessation of transtension, and was characterised by a significant reduction in sediment flux (24 Mt year−1) and widespread retrogradation of deltaic sediments. The third (10.4–5.3 Ma) and fourth (5.3–2.5 Ma) stages were characterised by progradation of deltaic sediments and an associated increase in sediment flux (48–60 Mt year−1) to the basin. Significant uplift associated with regional transpression started during this time in southeastern Sakhalin, but the north‐eastward propagating strain did not reach the NE shelf of Sakhalin until the Pleistocene (<2.5 Ma). This uplift event, still ongoing today, resulted in recycling of older deltaic sediments from the island of Sakhalin, and contributed to a substantially increased total sediment flux to the adjacent basinal areas (165 Mt year−1). Adjusted rates to discount these local erosional products (117 Mt year−1) imply an Amur catchment‐wide increase in denudation rates during the Late Pliocene–Pleistocene; however, this was likely a result of global climatic and eustatic effects, combined with tectonic processes within the Amur catchment and possibly a smaller drainage capture event by the Sungari tributary, rather than continental‐scale drainage capture involving the entire upper Amur catchment

    Blood Flow-restricted Exercise Does Not Induce a Cross-Transfer of Effect: A Randomized Controlled Trial

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    © 2019 by the American College of Sports Medicine. Purpose The goal of this trial was to determine whether low-load blood flow-restricted (BFR) exercise of appendicular muscles induces a cross-transfer of effect to the trunk extensor (TE) muscles, such that low-load TE exercise would enhance TE size and function to a greater extent than standard low-load exercise in people with recurrent low back pain (LBP). We also investigated the direct effects of BFR exercise in the appendicular muscles. Methods Thirty-two adults with recurrent, nonspecific LBP were randomized into two groups: Appendicular BFR exercise (BFR exercise) or control exercise (CON exercise). All participants trained (two times per week) for 10 wk, with a 12-wk follow-up. Participants performed three sets of leg extension (LE), plantar flexion (PF), and elbow flexion (EF) exercises followed by low-load TE exercise without BFR. Outcome measures included magnetic resonance imaging-derived muscle size (quadriceps and TE), strength (LE, PF, EF, and TE), and endurance (LE and TE). Results There was no evidence for a cross-transfer of effect to the TE. There was also no statistically significant enhancement of limb skeletal muscle size or function of BFR relative to CON exercise at any time point; though, moderate effect sizes for BFR exercise were observed for enhanced muscle size and strength in the leg extensors. Conclusions Low-load BFR exercise of the appendicular muscles did not result in a cross-transfer of effect to the TE musculature. There was also no significant benefit of low-load BFR exercise on the appendicular muscle size and function, suggesting no benefit from low-load BFR exercise in adults with recurrent, nonspecific LBP
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