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This article explores an emerging strategy by sections of the British radical right towards the LGBTQ+ (lesbian, gay, bisexual, transgender and queer) community, who the radical right claim are existentially threatened by the alleged violent homophobia of Islam and their ostensible betrayal by ‘the left’. Consequently, parts of the radical right present themselves as the ‘true’ protectors of LGBTQ+ individuals through what we term alter-progressivism. By analysing recorded speeches, discussions and interviews by and with key British radical right figures, we demonstrate three themes: (1) the broad radical right discourse of a ‘Great Replacement’ specifically tailored towards LGBTQ+ anxieties, (2) a narrative in which the radical right portray themselves as the defenders of (some) minorities and (3) an emerging distinction between the far-right and radical right concerning LGBTQ+ rights. We conclude that these themes represent a significant rhetorical shift and reveal the flexibility of radical right narratives in an attempt to appeal to diverse communities. This represents a serious challenge, which compels social scientists to adapt their understandings of radical right ideologies, objectives and strategies.

Foster provides an overview of the hormone melatonin, discussing its role in seasonal biology and its more controversial function in human sleep.

In his fifth-century BCE chronicle of the Graeco-Persian Wars, Herodotus describes a challenge that European scholars have faced for two and a half millennia (Drace-Francis, 2013: 1). Since Antiquity, discussions of just what ‘Europe’ is, descriptively and normatively, have not been resolved and consensus has been reached that multiple ‘Europes’ exist. Recent events in Europe, though, suggest that while the boundaries of Europe are, and will forever remain, quite unknown, the boundaries of EUrope are becoming identifiable.

Is the European Union (EU) in a state of crisis? Over recent years, a series of systemic and spontaneous challenges, including Brexit, the rise of Euroscepticism and the Eurozone and refugee crises, have manifested in landmark moments for European integration. First published as a special issue of the journal Global Discourse, this edited collection investigates whether these crises are isolated phenomena or symptoms of a deeper malaise across the EU. Experts from across disciplines analyse and rethink the forces which pull Europeans together, as well as those which push them apart.

Is the European Union (EU) in a state of crisis? Over recent years, a series of systemic and spontaneous challenges, including Brexit, the rise of Euroscepticism and the Eurozone and refugee crises, have manifested in landmark moments for European integration. First published as a special issue of the journal Global Discourse, this edited collection investigates whether these crises are isolated phenomena or symptoms of a deeper malaise across the EU. Experts from across disciplines analyse and rethink the forces which pull Europeans together, as well as those which push them apart.

Circadian rhythms are essential for the survival of all organisms, enabling them to predict daily changes in the environment and time their behaviour appropriately. The molecular basis of such rhythms is the circadian clock, a self-sustaining molecular oscillator comprising a transcriptional–translational feedback loop. This must be continually readjusted to remain in alignment with the external world through a process termed entrainment, in which the phase of the master circadian clock in the suprachiasmatic nuclei (SCN) is adjusted in response to external time cues. In mammals, the primary time cue, or “zeitgeber”, is light, which inputs directly to the SCN where it is integrated with additional non-photic zeitgebers. The molecular mechanisms underlying photic entrainment are complex, comprising a number of regulatory factors. This review will outline the photoreception pathways mediating photic entrainment, and our current understanding of the molecular pathways that drive it in the SCN.

Since the early 1990s a dominant modernist narrative has assumed that European integration and the progressive march of secularism, multiculturalism and increased material prosperity would lead to the fading-away of tribal, national, racial and other parochial identities; identities ostensibly incompatible with a meta-national ‘European’ identity founded not in ethnosymbolic myth, but in cosmopolitanism. This has informed not only academic theory but has also guided 60 years of EU policy making, with Ernst Haas’ doctrine of neofunctionalist spill-over dominating European assumptions that a pan-European identity would replace national affiliations. Brexit contradicts this in four ways. First, Brexit demonstrates the renewed appeal of ethnic nationalism on multiple levels: nationalist (British), sub-nationalist (English), and meta-nationalist (white nationalism). Second, Brexit demonstrates shifts in traditional nationalism in the form of gulfs in a neo-medieval society. Third, Brexit demonstrates the existence of multiple and incompatible ‘European’ identities. Finally, Brexit demonstrates how a specifically EUropean identity can be just as hostile and exclusionary as ethnic nationalism. This reappearance of social discord, ethnosymbolic identities, and the praxis of ethnic identity exemplified by the British, but seen across the EU, necessitates a fundamental reconsideration of the apparently irreversible trends of an unfalsifiable theory of modernist, neofunctionalist progressivism in the form of European integration. Using the British as a case study, this paper argues that the very processes of European integration have, by accelerating antagonistic national and EU identities, inadvertently constructed the apparatus for EUrope’s potential disintegration.

This revised and updated tenth edition of the bestselling textbook Politics UK is an indispensable introduction to British politics. It provides a thorough and accessible overview of the institutions and processes of British government, an excellent grounding in British political history and an incisive introduction to the issues and challenges facing Britain today. This edition welcomes three brand new chapters - 'Elites in the United Kingdom', 'Gender and British politics' and 'UK Immigration policy in hostile environment' - alongside rigorously updated revised chapters. It delivers excellent coverage of contemporary events, with significant new material covering: the Johnson premiership and the national challenge of Covid-19, the end of the May premiership and the implementation of Brexit, the Labour Party's transition from Corbyn to Starmer, infrastructure and innovation, 'fake news', populism and nationalism, the UK's place in a post-Brexit world, climate change, social mobility and elite recruitment, devolution and regionalism, constitutional strain, the role of political advisers, abuse and incivility in politics and much more. Other features of the new edition include: A wide range of illustrative material, boxes and case studies providing illuminating examples alongside the analysis. A comprehensive 'who's who' of politics in the form of Profile boxes featuring key political figures. And another thing . . . pieces containing short articles on salient and pressing topics, written by distinguished commentators including Sir John Curtice, Sir Simon Jenkins, Andrew Rawnsley, Baroness Julie Smith of Newnham, and Philip Collins. Online interviews on the book's website see notable figures from British political life discussing the pressing issues of today. With chapters written by highly respected scholars in the field and contemporary articles on real-world politics from well-known political commentators, this textbook is an essential guide for all students of British politics. © 2022 selection and editorial matter, Bill Jones, Philip Norton and Isabelle Hertner;. All rights reserved.

This article introduces the special issue on populism and technocracy in the integration and governance of the European Union (EU), framing these opposing approaches in the context of polarised debate on the (il)legitimacy of the EU. The special issue was conceived as an interdisciplinary approach to questions of the EU’s legitimacy in the aftermath of structural crises (the eurozone, sovereign debt and the election and appointment of governing agents) and spontaneous crises (migration, external state and non-state security challenges, Brexit and Euroscepticism). Since the special issue’s conception the unanticipated Covid-19 pandemic, and responses from the EU and its member states (current and former) starkly illuminated debates on how the EU should operate, the limits of its power and the limits of its popular legitimacy. The era of passive consensus has been replaced by claims of legitimacy based on active expert-informed intervention, alongside populist claims of the EU’s inherent illegitimacy as an undemocratic technocracy. As such the special issue’s objective is to critically analyse manifold ways in which the populist-technocratic divide is narrated and performed in different regions, disciplines, and social and political systems in an era of growing internal and external challenges to the Union. We observe that the EU’s institutions remain highly adaptable in responding to challenges, but that member-states have continued and accelerated a tendency to nationalise success and Europeanise failure, with the EU acting as a perennial scapegoat largely due to the ease with which it can be narrated as a site of projection for mistrust, resentment, and social grievances. We argue that the relationship between populism and technocracy is rapidly evolving from an imagined binary into a much more fluid, overlapping, and reversible set of political narratives. We conclude that despite the changing nature of populist-technocratic debates and the resilience and adaptability of the EU, it faces accelerating challenges to its legitimacy in the new era of ‘politics of necessity’.

Political geography has an established tradition of engaging with religiously-driven geopolitik. However, despite the remarkable growth in professed atheist beliefs in recent decades and the popular expression of an imagined geopolitical binary between secular/atheist and religious societies, the geopolitics of irreligion have received almost no attention among academic practitioners. This paper outlines the core tenets of ‘New Atheist’ philosophy, before addressing how its key representatives have taken positions on the ‘Global War on Terror.’ In particular, we critically interrogate the works of Richard Dawkins, Sam Harris, and the late Christopher Hitchens and identify a belligerent geopolitical imagination which posits a civilizational clash between an existentially-threatened secular, liberal West with responsibility to use extraordinary violence to protect itself and the world from a backwards oriental Islam. The paper concludes with four possible explanations for the paradox that the New Atheist critique of religion for being violent acts itself as a geopolitical incitement to violence. In so doing, we seek to navigate debates about the nature and purpose of critical geopolitical research given that the historical, intellectual and political contexts in which it was formed have changed.

The Earth’s daily rotation affects almost every living creature. From dawn through to dusk, there are changes in light, temperature, humidity, and rainfall. However, these changes are regular, rhythmic, and therefore predictable. Thus, the near 24-hour circadian rhythm is innate: a genetically programmed clock. Circadian Rhythms: A Very Short Introduction explains how organisms can ‘know’ the time and reveals what we now understand of the nature and operation of chronobiological processes. Covering variables such as light, the metabolism, human health, and the seasons, it illustrates how jet lag and shift work can impact on human well-being, and considers circadian rhythms alongside a wide range of disorders, from schizophrenia to obesity.

Geopolitics remains a cornerstone of contemporary human geography, with new introductions on the topic frequently appearing. Among these, Colin Flint's second edition of Introduction to geopolitics...

Drugs that are clinically effective against generalized anxiety disorder preferentially alter rodent risk assessment behavior, whereas drugs that are clinically effective against panic disorder preferentially alter rodent flight behavior. The theoretical principle of “defensive direction” explains the pattern of associations between emotion and defensive behavior in terms of the differing functional demands arising from cautious approach to threat (anxiety) versus departure from threat (fear), offering the prospect that clinically important emotions may be explained using a single rubric of defense. We used a within-subjects, placebo-controlled, design to test this theory, measuring the effects of citalopram and lorazepam on the defensive behavior of 30 healthy adult male humans. We indexed human defensive behavior with a translation of an active avoidance task used to measure rodent defense and found that lorazepam significantly reduced the intensity of defensive behavior during approach to threat (hypothetically anxiety-related) but not departure from threat (hypothetically fear-related). Contrary to prediction, citalopram did not affect either form of defensive reaction. Since lorazepam is a drug with well established anxiety reducing properties, these data support the hypothesis that anxiety is an emotion elicited by threat stimuli that require approach. These data also contribute to the validation of a novel human analog of an established experimental model of rodent fear and anxiety.

The Mental Capacity Act 2007 affects doctors in all areas of practice. The act recognises that capacity is a 'balance of probability rather than certainty', and based on this it attempts to 'maximise capacity' in an individual, so to facilitate a decision-making process. The act comprises five key principles as well as a test to determine lack of capacity. It also alludes to areas such as consent by proxy, restraint and capacity, and regulations regarding clinical research. This paper provides a brief background into the fundamental tenets of the act as well as a simple scheme for assessing capacity in hospital inpatients. It also looks at what physicians should be aware of and what will be required of them, particularly from a medico-legal perspective.

Schizophrenia is associated with a number of pathological changes, including alterations in levels of specific proteins. Calprotectin is a novel 36 kDa calcium-binding protein of the S100 family and appears to be a nonspecific marker of inflammation. Calprotectin has not previously been investigated in brain tissue. Samples of post-mortem brain tissue from Brodmann area 9 were obtained from prefrontal cortex from subjects with schizophrenia, bipolar affective disorder, major depression, and from controls. Calprotectin levels were determined by ELISA. To determine cellular localization, immunocytochemical and fluorescent double-labelling analyses were performed. Exogenous calprotectin was added to retinoic acid-differentiated human SH-SY5Y neuroblastoma cell cultures in order to investigate mechanisms of action of calprotectin. Calprotectin was detectable in all samples, and mean levels were noted to be highest in schizophrenic brains (P < 0.05) and lowest in controls. Levels were intermediate in bipolar affective disorder and major depression. Exogenous calprotectin appeared to induce dendritic extension in SH-SY5Y cell culture in a dose-dependent manner. Calprotectin was found to be localized to microglia. These findings suggest that increased levels of calprotecitn in the brain may reflect inflammatory processes, which play a role in the pathogenesis of major psychiatric disorders. Furthermore, calprotectin may influence dendritic plasticity.

The mechanisms by which the lifestyle risk factors obesity, physical inactivity, and low fiber intake predispose to colorectal cancer (CRC) are unclear. Chronic bowel inflammation predisposes to malignancy in cases of inflammatory bowel disease. Many lifestyle risk factors for CRC are associated with evidence of systemic inflammation as indicated by circulating levels of C-reactive protein (CRP), but it is unknown how this relates to inflammation at tissue level. Little is known about the degree of bowel inflammation in general population and the factors that affect it. Therefore, we aimed to assess the relation of levels of bowel inflammation in the general population and lifestyle risk factors for CRC, and to additionally assess whether these associations, if present, were attenuated by controlling for evidence of systemic inflammation. Average CRC risk subjects (320) of either sex aged 50–70 were recruited in South London. A stool sample was provided for calprotectin measurement (a marker of bowel inflammation), serum for CRP, and a detailed dietary and lifestyle questionnaire completed. There was a significant positive relationship between fecal calprotectin and increasing age (P = 0.002), obesity (P = 0.04), physical inactivity (P = 0.01), and an inverse relationship with fiber intake (P = 0.02) and vegetable consumption (P = 0.04). The relationship with obesity was attenuated by controlling for serum CRP. Fecal calprotectin levels are associated with lifestyle risk factors for colorectal cancer. Low-level asymptomatic bowel inflammation may be the link between lifestyle and the pathogenesis of CRC, and circulating proinflammatory cytokines may be part of the mechanism for this link.

Calprotectin is a calcium and zinc binding protein of the S100 family derived predominantly from neutrophils and monocytes. It is detectable in body fluids and tissue samples and is emerging as a valuable marker in the diagnosis, and the monitoring and determining of the prognosis of commonly encountered gastroenterological conditions. Fecal calprotectin, in particular, has for a long time been regarded as a promising marker of gastrointestinal pathology and has now been established as a routine test in Norway and at several centers in the UK.

Objective We present a case of psychosis in an individual with known HIV infection whose symptoms developed approximately 1 month following the commencement of combination antiretroviral therapy consisting of abacavir (ABC), nevirapine and combivir. She presented with severe persecutory delusions, accompanied by mutism, posturing and catatonia. Following cessation of therapy and the introduction of a low-dose antipsychotic, her mental state resolved to a stable premorbid level, and no further disturbances of behaviour were noted. Furthermore, when re-challenged with the above combination minus ABC, there were no further episodes of psychosis. It is proposed that the aetiology of the psychosis was related to her antiretroviral therapy. Methods Cessation of antiretroviral medication and initiation of antipsychotic medication with appropriate monitoring and assessment. Results Subjective and objective improvements in psychotic symptoms and presentation. Conclusion The current case suggests that sudden onset psychotic disturbances in HIV-infected individuals in the absence of other known organic or other causal factors could be related to treatment with antiretroviral therapy, and that cessation of this can markedly improve psychiatric morbidity. Furthermore, treatment with antipsychotic medication can lead to alleviation of psychotic symptoms and enable the re-introduction of antiretroviral medication.

The fundamental pathological process behind ulcerative colitis and Crohn's disease is intestinal inflammation. As the precise cause of this is not yet completely understood, current treatment strategies are aimed at reducing or eliminating the inflammation. Endoscopic examination and histological analysis of biopsy specimens remain the 'gold standard' methods for detecting and quantifying bowel inflammation; however, these techniques are costly, invasive, and repeated examinations are unpopular with patients. Disease activity questionnaires and laboratory 'inflammatory markers', although widely used, show an unreliable correlation with endoscopy and histology. New markers need to be developed to detect and quantify bowel inflammation. These would be of use diagnostically and also an aid to pharmacological treatment.

BACKGROUND AND AIMS—Assessing the presence and degree of intestinal inflammation objectively, simply, and reliably is a significant problem in gastroenterology. We assessed faecal excretion of calprotectin, a stable neutrophil specific marker, as an index of intestinal inflammation and its potential use as a screening test to discriminate between patients with Crohn's disease and those with irritable bowel syndrome. METHODS—The validity of faecal calprotectin as a marker of intestinal inflammation was assessed in 22 patients with Crohn's disease (35 studies) by comparing faecal excretions and concentrations using four day faecal excretion of 111indium white cells. A cross sectional study assessed the sensitivity of faecal calprotectin concentration for the detection of established Crohn's disease (n=116). A prospective study assessed the value of faecal calprotectin in discriminating between patients with Crohn's disease and irritable bowel syndrome in 220 patients referred to a gastroenterology clinic. RESULTS—Four day faecal excretion of 111indium (median 8.7%; 95% confidence interval (CI) 7-17%; normal

Background The pathogenesis of NSAID-induced gastrointestinal damage is believed to involve a nonprostaglandin dependent effect as well as prostaglandin dependent effects. One suggestion is that the nonprostaglandin mechanism involves uncoupling of mitochondrial oxidative phosphorylation. Aims To assess the role of uncoupling of mitochondrial oxidative phosphorylation in the pathogenesis of small intestinal damage in the rat. Methods We compared key pathophysiologic events in the small bowel following (i) dinitrophenol, an uncoupling agent (ii) parenteral aspirin, to inhibit cyclooxygenase without causing a 'topical' effect and (iii) the two together, using (iv) indomethacin as a positive control. Results Dinitrophenol altered intestinal mitochondrial morphology, increased intestinal permeability and caused inflammation without affecting gastric permeability or intestinal prostanoid levels. Parenteral aspirin decreased mucosal prostanoids without affecting intestinal mitochondria in vivo, gastric or intestinal permeability. Aspirin caused no inflammation or ulcers. When dinitrophenol and aspirin were given together the changes in intestinal mitochondrial morphology, permeability, inflammation and prostanoid levels and the macro- and microscopic appearances of intestinal ulcers were similar to indomethacin. Conclusions These studies allow dissociation of the contribution and consequences of uncoupling of mitochondrial oxidative phosphorylation and cyclooxygenase inhibition in the pathophysiology of NSAID enteropathy. While uncoupling of enterocyte mitochondrial oxidative phosphorylation leads to increased intestinal permeability and low grade inflammation, concurrent decreases in mucosal prostanoids appear to be important in the development of ulcers.

It is suggested that the gastrointestinal toxicity of conventional non-steroid anti-inflammatory drugs (NSAIDs) is due to a 'topical' effect in addition to inhibition of the mucosal constitutive cyclo-oxygenase-1 (COX-1) enzyme. COX-2 selective inhibitors have been shown to have excellent gastrointestinal tolerability, but it is not known whether this is due to their selectivity and/or a lack of a 'topical' effect. We assessed the effects of celecoxib (a highly selective COX-2 inhibitor) on key pathophysiologic events in NSAID enteropathy.The 'topical' effects of indomethacin and celecoxib were assessed in vitro (coupled mitochondrial respiration) and in vivo (mitochondrial electron microscopy) and the consequences by study of intestinal permeability (51-Cr-labelled ethylenediamine-tetraacetic acid urinary excretion) and inflammation. We also assessed intestinal prostanoid levels (prostaglandin E, PGE) and the propensity of the drugs to induce intestinal ulcers.Indomethacin uncoupled mitochondrial oxidative phosphorylation in vitro and in vivo, caused a significant (P0.0001) increase in intestinal permeability, caused mucosal inflammation and a 90% decline in intestinal PGE levels, and was associated with multiple small intestinal ulcers. Celecoxib caused no significant increase in any of these parameters, did not decrease intestinal PGE levels, and caused no intestinal ulcers.The intestinal tolerability of celecoxib appears to be due to a combination of the absence of a 'topical' damaging effect and selective COX inhibition.

BACKGROUNDThe diagnosis of non-steroidal anti-inflammatory drug (NSAID) induced enteropathy is difficult, requiring enteroscopy or the use of four day faecal excretion of 111In labelled white cells.AIMSTo assess faecal calprotectin (a non-degraded neutrophil cytosolic protein) as a method for diagnosing NSAID enteropathy.METHODSSingle stool faecal calprotectin concentrations were compared with the four day faecal excretion of 111In labelled white cells in 47 patients taking NSAIDs. The prevalence and severity of NSAID enteropathy was assessed using this method in 312 patients (192 with rheumatoid arthritis, 65 with osteoarthritis, 55 with other conditions) taking 18 different NSAIDs.RESULTSThe four day faecal excretion of 111In white cells correlated significantly with faecal calprotectin concentrations. In the group of 312 patients on NSAIDs faecal calprotectin concentrations were significantly higher than in controls, the prevalence of NSAID enteropathy being 44%. The prevalence and severity of NSAID enteropathy was independent of the particular type or dose of NSAID being taken or other patient variables.CONCLUSIONSAssay of faecal calprotectin provides a simple practical method for diagnosing NSAID enteropathy in man. Forty four per cent of patients receiving these drugs had NSAID induced enteropathy when assessed by this technique; 20% of these had comparable levels of inflammation to that previously reported in patients with inflammatory bowel disease.