Purposive Pattern Recognition: The Nature of Visual Choice in Graphic Design

Every pamphlet, brochure, booklet, advert, package, poster, etc that has ever been produced involved a visual choice made by a human being - even if the choice were restricted to ‘doing it like the last time’ or ‘copy this one’. Whether graphic designer, information designer, advertising executive, programmer, printer or the Managing Director’s wife, someone decided this picture, this type face, this layout etc rather than some available alternative. How are visual choices made? And, in particular, how do professional graphic designers make choices between visual alternatives. It was decided to probe this question by interviewing professional designers and looking at their work. The initial plan involved some sophisticated analysis of variables but it soon became apparent that such an approach was not possible. Specific interview questions such as, “You decided to use a picture of an elephant. Why an elephant and why this particular one?” met with responses along the lines of, “It just felt right” or “It’s intuitive”. It became clear that although some designers can tell a story about their choices, most designers make use of their experience and the experience of others to arrive at a decision that is not the result of some carefully thought out decision tree or a calculus of competing requirements. It was felt by both of us that there ought to be a better way to describe this process of ‘just knowing its right’ than intuition. Eventually we came up with Purposive Pattern Recognition, abbreviated to PPR. One of us (M A-R) gathered the evidence from interviews, case studies and existing studies of Masters in Design (a title awarded by a US magazine, following a poll of its readership) The other one (J Z L) placed the notion of PPR in a conceptual framework using current thinking in neuroscience and in evolutionary memetics. Keywords: Graphic Design, Intuition, Neuroscience, Memetics.</p

From vocational training to education: the development of a no-frontiers education policy for Europe?

This article focuses on developments towards an EU educational policy. Education was not included as one of the Community competencies in the Treaty of Rome. The first half of the article analyses the way that the European Court of Justice and the Commission of the European Communities between them managed to develop a series of substantial Community programmes out of Article 128 on vocational training. The second half of the article discusses educational developments in the community following the Treaty on European Union and the Treaty of Amsterdam. Whilst the legal competence of the community now includes education, the author's argument is that the inclusion of an educational competence will not result in further developments to mirror those in the years before the Treaty on Europe</p

The parasitic helminth product ES-62 suppresses pathogenesis in collagen-induced arthritis by targeting the interleukin-17–producing cellular network at multiple sites

Among many survival strategies, parasitic worms secrete molecules to modulate host immune responses. One such product, ES-62, is protective in the collagen-induced arthritis (CIA) model of rheumatoid arthritis. As IL-17 has been reported to play a pathological role in the development of rheumatoid arthritis, we investigated whether targeting of IL-17 may explain the protection afforded by ES-62 in the CIA model. DBA/1 mice progressively display arthritis following immunization with type-II collagen. The protective effects of ES-62 were assessed by determination of cytokine levels, flow cytometric analysis of relevant cellular populations and in situ analysis of joint inflammation. ES-62 was found to downregulate IL-17 responses in the CIA model. Firstly, it acts to inhibit priming and polarisation of IL-17 responses by targeting a complex IL-17-producing network, involving signalling between dendritic cells and γδ or CD4+ T cells. In addition, ES-62 directly targets Th17 cells by downregulating MyD88 expression to suppress responses mediated by IL-1 and TLR ligands. Moreover, ES-62 modulates migration of γδ T cells and this is reflected by direct suppression of CD44 upregulation and, as evidenced by in situ analysis, dramatically reduced levels of IL-17-producing cells, including lymphocytes, infiltrating the joint. Finally, there is strong suppression of IL-17 production by cells resident in the joint, such as osteoclasts within the bone areas. Such unique multi-site manipulation of the initiation and effector phases of the IL-17 inflammatory network could be exploited in the development of novel therapeutics for rheumatoid arthritis

T-cell subpopulations αβ and γδ in cord blood of very preterm infants : The influence of intrauterine infection

Open Access: This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are creditedPreterm infants are very susceptible to infections. Immune response mechanisms in this group of patients and factors that influence cord blood mononuclear cell populations remain poorly understood and are considered insufficient. However, competent immune functions of the cord blood mononuclear cells are also described. The aim of this work was to evaluate the T-cell population (CD3+) with its subpopulations bearing T-cell receptor (TCR) αβ or TCR γδ in the cord blood of preterm infants born before 32 weeks of gestation by mothers with or without an intrauterine infection. Being a pilot study, it also aimed at feasibility check and assessment of an expected effect size. The cord blood samples of 46 infants age were subjected to direct immunofluorescent staining with monoclonal antibodies and then analyzed by flow cytometry. The percentage of CD3+ cells in neonates born by mothers with diagnosis of intrauterine infection was significantly lower than in neonates born by mothers without infection (p = 0.005; Mann-Whitney U test). The number of cells did not differ between groups. Infection present in the mother did not have an influence on the TCR αβ or TCR γδ subpopulations. Our study contributes to a better understanding of preterm infants' immune mechanisms, and sets the stage for further investigations.Peer reviewedFinal Published versio

High-sensitivity troponin I concentrations are a marker of an advanced hypertrophic response and adverse outcomes in patients with aortic stenosis

Aims: High-sensitivity cardiac troponin I (cTnI) assays hold promise in detecting the transition from hypertrophy to heart failure in aortic stenosis. We sought to investigate the mechanism for troponin release in patients with aortic stenosis and whether plasma cTnI concentrations are associated with long-term outcome. Methods and results: Plasma cTnI concentrations were measured in two patient cohorts using a high-sensitivity assay. First, in the Mechanism Cohort, 122 patients with aortic stenosis (median age 71, 67% male, aortic valve area 1.0 ± 0.4 cm2) underwent cardiovascular magnetic resonance and echocardiography to assess left ventricular (LV) myocardial mass, function, and fibrosis. The indexed LV mass and measures of replacement fibrosis (late gadolinium enhancement) were associated with cTnI concentrations independent of age, sex, coronary artery disease, aortic stenosis severity, and diastolic function. In the separate Outcome Cohort, 131 patients originally recruited into the Scottish Aortic Stenosis and Lipid Lowering Trial, Impact of REgression (SALTIRE) study, had long-term follow-up for the occurrence of aortic valve replacement (AVR) and cardiovascular deaths. Over a median follow-up of 10.6 years (1178 patient-years), 24 patients died from a cardiovascular cause and 60 patients had an AVR. Plasma cTnI concentrations were associated with AVR or cardiovascular death HR 1.77 (95% CI, 1.22 to 2.55) independent of age, sex, systolic ejection fraction, and aortic stenosis severity. Conclusions: In patients with aortic stenosis, plasma cTnI concentration is associated with advanced hypertrophy and replacement myocardial fibrosis as well as AVR or cardiovascular death

Alternatively activated dendritic cells regulate CD4+ T-cell polarization in vitro and in vivo

Interleukin-4 is a cytokine widely known for its role in CD4(+) T cell polarization and its ability to alternatively activate macrophage populations. In contrast, the impact of IL-4 on the activation and function of dendritic cells (DCs) is poorly understood. We report here that DCs respond to IL-4 both in vitro and in vivo by expression of multiple alternative activation markers with a different expression pattern to that of macrophages. We further demonstrate a central role for DC IL-4Rα expression in the optimal induction of IFNγ responses in vivo in both Th1 and Th2 settings, through a feedback loop in which IL-4 promotes DC secretion of IL-12. Finally, we reveal a central role for RELMα during T-cell priming, establishing that its expression by DCs is critical for optimal IL-10 and IL-13 promotion in vitro and in vivo. Together, these data highlight the significant impact that IL-4 and RELMα can have on DC activation and function in the context of either bacterial or helminth pathogens

The role of wall deposition and re‐entrainment in swirl spray dryers

A new experimental method is outlined to study fouling in spray dryers and similar devices. In essence, it makes the deposits traceable so that one can quantify the material that comes off the walls, how long it remains there and how the deposits agglomerate with particles in the air. This paper investigates a countercurrent swirl spray dryer of detergent and provides sound evidence that fouling is a dynamic process: clusters form and break at the walls renewing an active layer of deposits. Remarkably, the wall generates >20% of the product and most of the large granules, and increases drastically the residence time of the powder. The assumptions of current numerical models are clearly invalid (i.e. particles rebound at the wall or deposit indefinitely). Several re-entrainment mechanisms and their times scales are identified in this work, and accordingly, a new general framework to describe fouling in spray dryers is proposed

Severe respiratory illness caused by a novel coronavirus, in a patient transferred to the United Kingdom from the Middle East, September 2012

Coronaviruses have the potential to cause severe transmissible human disease, as demonstrated by the severe acute respiratory syndrome (SARS) outbreak of 2003. We describe here the clinical and virological features of a novel coronavirus infection causing severe respiratory illness in a patient transferred to London, United Kingdom, from the Gulf region of the Middle East

Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

OBJECTIVE: Subclinical gut inflammation is common in spondylarthritis, but the immunologic abnormalities underlying this process are undefined. Perturbation of the interleukin-23 (IL-23)/Th17 axis has emerged as a fundamental trigger of chronic inflammation. This study was undertaken to investigate the expression and tissue distribution of IL-23/Th17-related molecules in Crohn's disease (CD) and in subclinical gut inflammation in ankylosing spondylitis (AS). METHODS: Quantitative gene expression analysis of Th1/Th2 and IL-23/Th17 responses was performed in intestinal biopsy samples obtained from 12 patients with CD, 15 patients with AS, and 13 controls. IL-23 tissue distribution and identification of IL-23-producing cells were evaluated by immunohistochemistry. RESULTS: We demonstrated a strong and significant up-regulation of IL-23p19 transcripts in the terminal ileum in patients with AS and patients with CD. IL-23 was abundantly produced by infiltrating monocyte-like cells in inflamed mucosa from AS and CD patients. Notably, we also identified Paneth cells as a major source of IL-23 in patients with AS, patients with CD, and normal controls. Unlike CD, in AS patients, IL-23 was not associated with up-regulation of IL-17 and the IL-17-inducing cytokines IL-6 and IL-1beta. Finally, while the Th1-related cytokines interferon-gamma, IL-12p35, and IL-27p28 were overexpressed only in CD patients, IL-4, IL-5, and STAT-6 were also significantly increased in AS patients. CONCLUSION: Our findings indicate that overexpression of IL-23, but not IL-17, is a pivotal feature of subclinical gut inflammation in AS. Identification of resident Paneth cells as a pivotal source of IL-23 in physiologic and pathologic conditions strongly suggests that IL-23 is a master regulator of gut mucosal immunity, providing a pathophysiologic significance to the reported association between IL-23 receptor polymorphisms and intestinal inflammation

A Sermon preached by the Rt Revd Michael Langrish, Bishop Of Exeter at a Eucharist to mark the Golden Jubilee of the Mary Harris Memorial Chapel in the University of Exeter,on Sunday 22nd June 2008

Readings: Proverbs 1/2-7; 1 Corinthians 2/6- 13; John 14/1-1