Value Chain activities of Small and Medium Food Manufacturers in Wales, United Kingdom: The KITE Project

The Knowledge Innovation Technology Exchange (KITE) Feasibility Project (2008-2015) was implemented in Wales, to improve food science/technology knowledge and sustainable innovation in food manufacturing small to medium enterprises (SMEs). From this model, the study aimed to identify the salient features of such a paradigm to contribute to ‘value-added gains’ for competitive advantage. Cumulatively, >90 KITE interventions in 43 Welsh SME partners, were evaluated according to mappable value chain ‘primary activities’ and ‘support activities’. Findings from case study purposive samples conducted in 13 out of 43 KITE partner SMEs, identified added value activity across manufacturing and processing activities that positively impacted the food sector

Stakeholder Growth Platforms for the Development of Food Sector Small to Medium Enterprises (SMEs): A case study experience from Wales, United Kingdom

Project HELIX 2016-2020 was developed and implemented in Wales, to improve technical/ safety/science knowledge; and sustainable innovation in food manufacturing small to medium enterprises (SMEs). The paper aims to place Project HELIX within the wider context of regional and food sector development and then examine the project's rationale and delivery methods in relation to this. It reflects on the effectiveness of the project (or otherwise) in constructing regional advantage from knowledge transfer and knowledge spillovers. Finally, the paper identifies areas of further research both in terms of the firm level and in relation to other food sector initiatives more generally

On the Complexity of Determining Defeat Relations Consistent with Abstract Argumentation Semantics

Typically in abstract argumentation, one starts with arguments and a defeat relation, and applies some semantics in order to determine the acceptability status of the arguments. We consider the converse case where we have knowledge of the acceptability status of arguments and want to identify a defeat relation that is consistent with the known acceptability data – the σ-consistency problem. Focusing on complete semantics as underpinning the majority of the major semantic types, we show that the complexity of determining a defeat relation that is consistent with some set of acceptability data is highly dependent on how the data is labelled. The extension-based 2-valued σ-consistency problem for complete semantics is revealed as NP-complete, whereas the labelling-based 3-valued σ-consistency problem is solvable within polynomial time. We then present an informal discussion on application to grounded, stable, and preferred semantics.</jats:p

Cathepsin B abundance, activity and microglial localisation in Alzheimer's disease-Down syndrome and early onset Alzheimer's disease; the role of elevated cystatin B

Cathepsin B is a cysteine protease that is implicated in multiple aspects of Alzheimer's disease pathogenesis. The endogenous inhibitor of this enzyme, cystatin B (CSTB) is encoded on chromosome 21. Thus, individuals who have Down syndrome, a genetic condition caused by having an additional copy of chromosome 21, have an extra copy of an endogenous inhibitor of the enzyme. Individuals who have Down syndrome are also at significantly increased risk of developing early-onset Alzheimer's disease (EOAD). The impact of the additional copy of CSTB on Alzheimer's disease development in people who have Down syndrome is not well understood. Here we compared the biology of cathepsin B and CSTB in individuals who had Down syndrome and Alzheimer's disease, with disomic individuals who had Alzheimer's disease or were ageing healthily. We find that the activity of cathepsin B enzyme is decreased in the brain of people who had Down syndrome and Alzheimer's disease compared with disomic individuals who had Alzheimer's disease. This change occurs independently of an alteration in the abundance of the mature enzyme or the number of cathepsin B+ cells. We find that the abundance of CSTB is significantly increased in the brains of individuals who have Down syndrome and Alzheimer's disease compared to disomic individuals both with and without Alzheimer's disease. In mouse and human cellular preclinical models of Down syndrome, three-copies of CSTB increases CSTB protein abundance but this is not sufficient to modulate cathepsin B activity. EOAD and Alzheimer's disease-Down syndrome share many overlapping mechanisms but differences in disease occur in individuals who have trisomy 21. Understanding this biology will ensure that people who have Down syndrome access the most appropriate Alzheimer's disease therapeutics and moreover will provide unique insight into disease pathogenesis more broadly

Global avian influenza surveillance in wild birds: A strategy to capture viral diversity

Wild birds play a major role in the evolution, maintenance, and spread of avian influenza viruses. However, surveillance for these viruses in wild birds is sporadic, geographically biased, and often limited to the last outbreak virus. To identify opportunities to optimize wild bird surveillance for understanding viral diversity, we reviewed responses to a World Organisation for Animal Health-administered survey, government reports to this organization, articles on Web of Knowledge, and the Influenza Research Database. At least 119 countries conducted avian influenza virus surveillance in wild birds during 2008-2013, but coordination and standardization was lacking among surveillance efforts, and most focused on limited subsets of influenza viruses. Given high financial and public health burdens of recent avian influenza outbreaks, we call for sustained, cost-effective investments in locations with high avian influenza diversity in wild birds and efforts to promote standardized sampling, testing, and reporting methods, including full-genome sequencing. (Résumé d'auteur

Cardiovascular disease and arsenic exposure in Inner Mongolia, China: a case control study

BackgroundMillions of people are at risk from the adverse effects of arsenic exposure through drinking water. Increasingly, non-cancer effects such as cardiovascular disease have been associated with drinking water arsenic exposures. However, most studies have been conducted in highly exposed populations and lacked individual measurements.ObjectiveTo evaluate the association between cardiovascular disease and well-water arsenic exposure.MethodsWe conducted a hospital based case control study in Inner Mongolia, China. Cases and controls were prospectively identified and enrolled from a large hospital in the Hangjin Hou area. Cases were patients diagnosed with cardiovascular disease and controls were patients free from cardiovascular disease, admitted for conditions unrelated to arsenic exposure. Water from the primary water source and toenail samples were collected from each subject and tested for inorganic arsenic.ResultsArsenic exposures were moderate with mean and median arsenic exposures of 8.9μg/L and 13.1μg/L, respectively. A total of 298 cases and 275 controls were enrolled. The adjusted odds ratio (AOR) and corresponding 95% confidence interval (95% CI) for a 10μg/L increase in water arsenic were 1.19 (95% CI: 1.03, 1.38). Compared to exposures less than 10μg/L, the AOR for water arsenic exposures above 40μg/L was 4.05 (95% CI: 1.1-14.99, p = 0.04). Nail arsenic above 1.38μg/g was also associated with an increased risk of cardiovascular disease.ConclusionsBy using standardized case definitions and collecting individual measurements of arsenic, this study addressed several limitations of previous studies. The results provide further evidence of the association between cardiovascular disease and arsenic at moderate exposures.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-015-0022-y) contains supplementary material, which is available to authorized users

Zoonotic tuberculosis in human beings caused by Mycobacterium bovis—a call for action

Mycobacterium tuberculosis is recognised as the primary cause of human tuberculosis worldwide. However, substantial evidence suggests that the burden of Mycobacterium bovis, the cause of bovine tuberculosis, might be underestimated in human beings as the cause of zoonotic tuberculosis. In 2013, results from a systematic review and meta-analysis of global zoonotic tuberculosis showed that the same challenges and concerns expressed 15 years ago remain valid. These challenges faced by people with zoonotic tuberculosis might not be proportional to the scientific attention and resources allocated in recent years to other diseases. The burden of zoonotic tuberculosis in people needs important reassessment, especially in areas where bovine tuberculosis is endemic and where people live in conditions that favour direct contact with infected animals or animal products. As countries move towards detecting the 3 million tuberculosis cases estimated to be missed annually, and in view of WHO's end TB strategy endorsed by the health authorities of WHO Member States in 2014 to achieve a world free of tuberculosis by 2035, we call on all tuberculosis stakeholders to act to accurately diagnose and treat tuberculosis caused by M bovis in human beings

Genetic mapping of APP and amyloid-β biology modulation by trisomy 21

Individuals who have Down syndrome (DS) frequently develop early onset Alzheimer's disease (AD), a neurodegenerative condition caused by the build-up of aggregated amyloid-β and tau proteins in the brain. Amyloid-β is produced by amyloid precursor protein (APP), a gene located on chromosome 21. People who have Down syndrome have three copies of chromosome 21 and thus also an additional copy of APP; this genetic change drives the early development of Alzheimer's disease in these individuals. Here we use a combination of next-generation mouse models of Down syndrome (Tc1, Dp3Tyb, Dp(10)2Yey and Dp(17)3Yey) and a knockin mouse model of amyloid-β accumulation (AppNL-F ) to determine how chromosome 21 genes, other than APP, modulate APP/amyloid-β in the brain when in three copies. Using both male and female mice, we demonstrate that three copies of other chromosome 21 genes are sufficient to partially ameliorate amyloid-β accumulation in the brain. We go on to identify a subregion of chromosome 21 that contains the gene/genes causing this decrease in amyloid-β accumulation and investigate the role of two lead candidate genes Dyrk1a and Bace2 Thus an additional copy of chromosome 21 genes, other than APP, can modulate APP/amyloid-β in the brain under physiological conditions. This work provides critical mechanistic insight into the development of disease and an explanation for the typically later age of onset of dementia in people who have AD-DS, compared to those who have familial AD caused by triplication of APP Significance Statement:Trisomy of chromosome 21 is a commonly occurring genetic risk factor for early-onset Alzheimer's disease, which has been previously attributed to people with Down syndrome having three copies of the APP gene, which is encoded on chromosome 21. However, we have shown that an extra copy of other chromosome 21 genes modifies AD-like phenotypes independently of APP copy number (Wiseman et al. 2018, Brain; Tosh et al. 2021 Scientific Reports). Here, we use a mapping approach to narrow-down the genetic cause of the modulation of pathology; demonstrating that gene(s) on chromosome 21 decrease amyloid-β accumulation in the brain, independently of alterations to full-length APP or C-terminal fragment abundance and that just 38 genes are sufficient to cause this