Hotspot politics―or, when the EU state gets real

This paper was published in the journal Political Geography and the definitive published version is available at https://doi.org/10.1016/j.polgeo.2017.02.012

Mastiha has efficacy in immune-mediated inflammatory diseases through a microRNA-155 Th17 dependent action

Mastiha is a natural nutritional supplement with known anti-inflammatory properties. Non-alcoholic fatty liver disease (NAFLD) and Inflammatory bowel disease (IBD) are immune mediated inflammatory diseases that share common pathophysiological features. Mastiha has shown beneficial effects in both diseases. MicroRNAs have emerged as key regulators of inflammation and their modulation by phytochemicals have been extensively studied over the last years. Therefore, the aim of this study was to investigate whether a common route exists in the anti-inflammatory activity of Mastiha, specifically through the regulation of miRNA levels. Plasma miR-16, miR-21 and miR-155 were measured by Real-Time PCR before and after two double blinded and placebo-controlled randomized clinical trials with Mastiha. In IBD and particularly in ulcerative colitis patients in relapse, miR-155 increased in the placebo group (p = 0.054) whereas this increase was prevented by Mastiha. The mean changes were different in the two groups even after adjusting for age, sex and BMI (p = 0.024 for IBD and p = 0.042). Although the results were not so prominent in NAFLD, miR-155 displayed a downward trend in the placebo group (p = 0.054) whereas the levels did not changed significantly in the Mastiha group in patients with less advanced fibrosis. Our results propose a regulatory role for Mastiha in circulating levels of miR-155, a critical player in T helper-17 (Th17) differentiation and function

Dietary interventions for induction and maintenance of remission in inflammatory bowel disease

Background Inflammatory bowel disease (IBD), comprised of Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic mucosal inflammation, frequent hospitalizations, adverse health economics, and compromised quality of life. Diet has been hypothesised to influence IBD activity. Objectives To evaluate the efficacy and safety of dietary interventions on IBD outcomes. Search methods We searched the Cochrane IBD Group Specialized Register, CENTRAL, MEDLINE, Embase, Web of Science, Clinicaltrials.gov and the WHO ICTRP from inception to 31 January 2019. We also scanned reference lists of included studies, relevant reviews and guidelines. Selection criteria We included randomized controlled trials (RCTs) that compared the effects of dietary manipulations to other diets in participants with IBD. Studies that exclusively focused on enteral nutrition, oral nutrient supplementation, medical foods, probiotics, and parenteral nutrition were excluded. Data collection and analysis Two review authors independently performed study selection, extracted data and assessed bias using the risk of bias tool. We conducted meta‐analyses where possible using a random‐effects model and calculated the risk ratio (RR) and corresponding 95% confidence interval (CI) for dichotomous outcomes. We assessed the certainty of evidence using GRADE. Main results The review included 18 RCTs with 1878 participants. The studies assessed different dietary interventions for active CD (six studies), inactive CD (seven studies), active UC (one study) and inactive UC (four studies). Dietary interventions involved either the consumption of low amounts or complete exclusion of one or more food groups known to trigger IBD symptoms. There was limited scope for data pooling as the interventions and control diets were diverse. The studies were mostly inadequately powered. Fourteen studies were rated as high risk of bias. The other studies were rated as unclear risk of bias. The effect of high fiber, low refined carbohydrates, low microparticle diet, low calcium diet, symptoms‐guided diet and highly restricted organic diet on clinical remission in active CD is uncertain. At 4 weeks, remission was induced in: 100% (4/4) of participants in the low refined carbohydrates diet group compared to 0% (0/3) of participants in the control group (RR 7.20, 95% CI 0.53 to 97.83; 7 participants; 1 study; very low certainty evidence). At 16 weeks, 44% (23/52) of participants in the low microparticle diet achieved clinical remission compared to 25% (13/51) of control‐group participants (RR 3.13, 95% CI 0.22 to 43.84; 103 participants; 2 studies; I² = 73%; very low certainty evidence). Fifty per cent (16/32) of participants in the symptoms‐guided diet group achieved clinical remission compared to 0% (0/19) of control group participants (RR 20.00, 95% CI 1.27 to 315.40; 51 participants ; 1 study; very low certainty evidence) (follow‐up unclear). At 24 weeks, 50% (4/8) of participants in the highly restricted organic diet achieved clinical remission compared to 50% (5/10) of participants in the control group (RR 1.00, 95% CI 0.39 to 2.53; 18 participants; 1 study; very low certainty evidence). At 16 weeks, 37% (16/43) participants following a low calcium diet achieved clinical remission compared to 30% (12/40) in the control group (RR 1.24, 95% CI 0.67 to 2.29; 83 participants; 1 study; very low certainty evidence). The effect of low refined carbohydrate diets, symptoms‐guided diets and low red processed meat diets on relapse in inactive CD is uncertain. At 12 to 24 months, 67% (176/264) of participants in low refined carbohydrate diet relapsed compared to 64% (193/303) in the control group (RR 1.04, 95% CI 0.87 to 1.25; 567 participants; 3 studies; I² = 35%; low certainty evidence). At 6 to 24 months, 48% (24/50) of participants in the symptoms‐guided diet group relapsed compared to 83% (40/48) participants in the control diet (RR 0.53, 95% CI 0.28 to 1.01; 98 participants ; 2 studies; I² = 54%; low certainty evidence). At 48 weeks, 66% (63/96) of participants in the low red and processed meat diet group relapsed compared to 63% (75/118) of the control group (RR 1.03, 95% CI 0.85 to 1.26; 214 participants; 1 study; low certainty evidence). At 12 months, 0% (0/16) of participants on an exclusion diet comprised of low disaccharides / grains / saturated fats / red and processed meat experienced clinical relapse compared to 26% (10/38) of participants on a control group (RR 0.11, 95% CI 0.01 to 1.76; 54 participants; 1 study; very low certainty evidence). The effect of a symptoms‐guided diet on clinical remission in active UC is uncertain. At six weeks, 36% (4/11) of symptoms‐guided diet participants achieved remission compared to 0% (0/10) of usual diet participants (RR 8.25, 95% CI 0.50 to 136.33; 21 participants; 1 study; very low certainty evidence). The effect of the Alberta‐based anti‐inflammatory diet, the Carrageenan‐free diet or milk‐free diet on relapse rates in inactive UC is uncertain. At 6 months, 36% (5/14) of participants in the Alberta‐based anti‐inflammatory diet group relapsed compared to 29% (4/14) of participants in the control group (RR 1.25, 95% CI 0.42 to 3.70; 28 participants; 1 study; very low certainty evidence). Thirty per cent (3/10) of participants following the carrageenan‐free diet for 12 months relapsed compared to 60% (3/5) of the participants in the control group (RR 0.50, 95% CI 0.15 to 1.64; 15 participants; 1 study; very low certainty evidence). At 12 months, 59% (23/39) of milk free diet participants relapsed compared to 68% (26/38) of control diet participants (RR 0.83, 95% CI 0.60 to 1.15; 77 participants; 2 studies; I² = 0%; low certainty evidence). None of the included studies reported on diet‐related adverse events

The EC hotspot approach in Greece: creating liminal EU territory

This article makes a theoretical argument stemming from our study of the European Commission’s hotspot approach to the management of migrant populations. It draws on empirical research findings from field research which took place on the island of Lesbos and in the city of Athens over the course of 20 months and links these to emerging critical studies of the new EU border regime. No clear definition exists of what comprises a hotspot: instead, the European Commission describes this as an integrated ‘approach’ for the enhancement of the capacity of member states to deal with crises resulting from pressures at the Union’s external borders. Effective in its ambiguity, the ‘hotspot approach’ therefore constitutes, as we argue, an integral part of the Europeanisation and institutionalisation of border management: a powerfully ambiguous dispositif in the EU’s emerging border regime. The article unpacks the notion of the hotspot from a historical perspective and explores the ways in which the hotspot contributes toward the culmination of European integration, paving the way for the flexible governance of mobility and asylum. We situate the hotspot within the historical shift of migration and mobility control from the border to the territory as a whole and conclude by arguing that the hotspot plays the role of a territorial incubator for the liminal EU territory: a paradigmatic space for a new form of governance that further disentangles territory from rights

Flags Flying up a Trial Mast:Reflections on the Hotspot Mechanism in Mytilene

In one sense the hotspot is, then, already here: it lies in the reception centres, the detention centres, the temporary camps, the mechanisms of registration, filtering, hosting and relocating the people arriving in the EU. But in another sense, the hotspot is a future excess of the sum of all those parts: a glimpse into the all-encompassing population filtering apparatus yet to come

Flags Flying up a Trial Mast:Reflections on the Hotspot Mechanism in Mytilene

In one sense the hotspot is, then, already here: it lies in the reception centres, the detention centres, the temporary camps, the mechanisms of registration, filtering, hosting and relocating the people arriving in the EU. But in another sense, the hotspot is a future excess of the sum of all those parts: a glimpse into the all-encompassing population filtering apparatus yet to come