The Revenge of Coordinated Capitalism? Reflections from the Presidential Plenary in Montreal

The global financial crisis of 2008 initially seemed to mark the bankruptcy of neoliberal deregulation and a transition to a new era of renewed faith in government, yet the rising fortunes of parties on the right seem to belie this easy lesson. This essay considers the persistence of managed and relatively egalitarian capitalism after the crisis of finance capitalism. I reflection why some societies are more equitable and solidaristic than others, question whether our beliefs about cross-national variation continue to hold true, and ponder how the financial crisis might affect nations’ capacities to construct coalitions for social solidarity

The influence of pigmentation patterning on bumblebee foraging from flowers of <em>Antirrhinum majus</em>

Patterns of pigmentation overlying the petal vasculature are common in flowering plants and have been postulated to play a role in pollinator attraction. Previous studies report that such venation patterning is significantly more attractive to bee foragers in the field than ivory or white flowers without veins. To dissect the ways in which venation patterning of pigment can influence bumblebee behaviour, we investigated the response of flower-naïve individuals of Bombus terrestris to veined, ivory and red near-isogenic lines of Antirrhinum majus. We find that red venation shifts flower colour slightly, although the ivory background is the dominant colour. Bees were readily able to discriminate between ivory and veined flowers under differential conditioning but showed no innate preference when presented with a free choice of rewarding ivory and veined flowers. In contrast, both ivory and veined flowers were selected significantly more often than were red flowers. We conclude that advantages conferred by venation patterning might stem from bees learning of their use as nectar guides, rather than from any innate preference for striped flowers. © 2013 Springer-Verlag Berlin Heidelberg

Flavonoids from engineered tomatoes inhibit gut barrier pro-inflammatory cytokines and chemokines, via SAPK/JNK and p38 MAPK pathways

Flavonoids are a diverse group of plant secondary metabolites, known to reduce inflammatory bowel disease symptoms. How they achieve this is largely unknown. Our study focuses on the gut epithelium as it receives high topological doses of dietary constituents, maintains gut homeostasis, and orchestrates gut immunity. Dysregulation leads to chronic gut inflammation, via dendritic cell (DC)-driven immune responses. Tomatoes engineered for enriched sets of flavonoids (anthocyanins or flavonols) provided a unique and complex naturally consumed food matrix to study the effect of diet on chronic inflammation. Primary murine colonic epithelial cell-based inflammation assays consist of chemokine induction, apoptosis and proliferation, and effects on kinase pathways. Primary murine leukocytes and DCs were used to assay effects on transmigration. A murine intestinal cell line was used to assay wound healing. Engineered tomato extracts (enriched in anthocyanins or flavonols) showed strong and specific inhibitory effects on a set of key epithelial pro-inflammatory cytokines and chemokines. Chemotaxis assays showed a resulting reduction in the migration of primary leukocytes and DCs. Activation of epithelial cell SAPK/JNK and p38 MAPK signaling pathways were specifically inhibited. The epithelial wound healing-associated STAT3 pathway was unaffected. Cellular migration, proliferation, and apoptosis assays confirmed that wound healing processes were not affected by flavonoids. We show flavonoids target epithelial pro-inflammatory kinase pathways, inhibiting chemotactic signals resulting in reduced leukocyte and DC chemotaxis. Thus, both anthocyanins and flavonols modulate epithelial cells to become hyporesponsive to bacterial stimulation. Our results identify a viable mechanism to explain the in vivo anti-inflammatory effects of flavonoids

Manipulation and Misconduct in the Handling of Image Data

No abstract available

Can compassion be taught? A medical students' compassion discourse

Background: Universities of Brighton, Surrey and the Brighton and Sussex Medical School responded to a regional bid to provide compassion awareness training to the local health care workforce. An appreciative inquiry methodology was used to develop a toolkit which included a number of different activities focused on the following pillars. Appreciate (best of what has been), imagine (what might be), determine (what should be) and finally create (what will be). One of the toolkit resources focused on seeking and celebrating acts of compassion. Methods: Following a cultivating compassion workshop, a group of medical students in their third year decided to use this activity from the Compassion toolkit to observe acts of compassion occurring within their clinical setting and reflected on the impact this activity had on them. Results: Themes deduced from the 34 acts of compassion witnessed included; team compassion, patient-centred compassion, peer to peer compassion and patient to patient compassion. Students’ reflections about undertaking this activity were thematically analysed and emerging themes included self compassion, confidence about talking about compassion, changes in behaviour and finally how could compassion be taught at medical school. Conclusion: This study generated discussions on what was the difference between acts of compassion and normal human behaviour and the “hidden curriculum” of health professionals’ behaviour. Students realised the importance of compassion and yet the absence of that word within their own curriculum. This small pilot study made it possible to consider how compassion can be taught within the undergraduate curriculum, simply by empowering students to open their eyes and witness compassionate acts. The medical students were able to see compassionate behaviour that they wished to model and that would support them once qualified

Improving medication adherence in stroke survivors: Mediators and moderators of treatment effects

OBJECTIVE: The purpose of the current study was to test theory-based predictions of mediators and moderators of treatment effects of a pilot randomized controlled trial, which aimed to increase adherence to preventive medication in stroke survivors via addressing both automatic (i.e., habitual responses) and reflective (i.e., beliefs and value systems) aspects of medication-taking behavior. METHOD: Sixty-two stroke survivors were randomly allocated to either an intervention or control group. Intervention participants received a brief 2-session intervention aimed at increasing adherence via (a) helping patients establish better medication-taking routines using implementation intentions plans (automatic), and (b) eliciting and modifying any mistaken patient beliefs regarding medication and/or stroke (reflective). The control group received similar levels of non-medication-related contact. Primary outcome was adherence to antihypertensive medicine measured objectively over 3 months using an electronic pill bottle. Secondary outcome measures included self-reported adherence (including forgetting) and beliefs about medication. RESULTS Intervention participants had 10% greater adherence on doses taken on schedule (intervention, 97%; control, 87%; 95% CI [0.2, 16.2], p = .048), as well as significantly greater increases in self-reported adherence and reductions in concerns about medication. Treatment effects were mediated by reductions in both forgetting and concerns about medication, and moderated by the presence of preexisting medication-taking routines. CONCLUSIONS: Addressing both automatic and reflective aspects of behavior via helping stroke survivors develop planned regular routines for medication-taking, and addressing any concerns or misconceptions about their medication, can improve adherence and thus potentially patient outcomes

Differential gene expression in multiple neurological, inflammatory and connective tissue pathways in a spontaneous model of human small vessel stroke

Aims: Cerebral small vessel disease (SVD) causes a fifth of all strokes plus diffuse brain damage leading to cognitive decline, physical disabilities and dementia. The aetiology and pathogenesis of SVD are unknown, but largely attributed to hypertension or microatheroma. Methods: We used the spontaneously hypertensive stroke-prone rat (SHRSP), the closest spontaneous experimental model of human SVD, and age-matched control rats kept under identical, non-salt-loaded conditions, to perform a blinded analysis of mRNA microarray, qRT-PCRand pathway analysis in two brain regions (frontal and midcoronal) commonly affected by SVD in the SHRSP at age five, 16 and 21 weeks. Results: We found gene expression abnormalities, with fold changes ranging from 2.5 to 59 for the 10 most differentially expressed genes, related to endothelial tight junctions (reduced), nitric oxide bioavailability (reduced), myelination (impaired), glial and microglial activity (increased), matrix proteins (impaired), vascular reactivity (impaired) and albumin (reduced), consistent with protein expression defects in the same rats. All were present at age 5 weeks thus pre-dating blood pressure elevation. ‘Neurological’ and ‘inflammatory’ pathways were more affected than ‘vascular’ functional pathways. Conclusions: This set of defects, although individually modest, when acting in combination could explain the SHRSP's susceptibility to microvascular and brain injury, compared with control rats. Similar combined, individually modest, but multiple neurovascular unit defects, could explain susceptibility to spontaneous human SVD