Explore the vast range of titles available.

Relationships necessarily include others, but equally they have boundaries that exclude. Frequently these boundaries are challenged or crossed. This book draws together research on individual motivation, small group processes, stigmatization and intergroup relations, to provide a comprehensive social psychological account of social inclusion and exclusion.

Arrhythmogenic cardiomyopathy is a genetic disorder characterized by the risk of life-threatening arrhythmias, myocardial dysfunction and fibrofatty replacement of myocardial tissue. Mutations in genes that encode components of desmosomes, the adhesive junctions that connect cardiomyocytes, are the predominant cause of arrhythmogenic cardiomyopathy and can be identified in about half of patients with the condition. However, the molecular mechanisms leading to myocardial destruction, remodelling and arrhythmic predisposition remain poorly understood. Through the development of animal, induced pluripotent stem cell and other models of disease, advances in our understanding of the pathogenic mechanisms of arrhythmogenic cardiomyopathy over the past decade have brought several signalling pathways into focus. These pathways include canonical and non-canonical WNT signalling, the Hippo–Yes-associated protein (YAP) pathway and transforming growth factor-β signalling. These studies have begun to identify potential therapeutic targets whose modulation has shown promise in preclinical models. In this Review, we summarize and discuss the reported molecular mechanisms underlying the pathogenesis of arrhythmogenic cardiomyopathy.Mutations in genes that encode components of desmosomes are the predominant cause of arrhythmogenic cardiomyopathy, a genetic disorder characterized by fibrofatty replacement of myocardial tissue and the risk of life-threatening arrhythmias. In this Review, the authors discuss the molecular mechanisms underlying the pathogenesis of this condition.

Background Timothy syndrome (OMIM #601005) is a rare disease caused by variants in the gene CACNA1C . Initially, Timothy syndrome was characterized by a cardiac presentation of long QT syndrome and syndactyly of the fingers and/or toes, all associated with the CACNA1C variant, Gly406Arg. However, subsequent identification of diverse variants in CACNA1C has expanded the clinical spectrum, revealing various cardiac and extra-cardiac manifestations. It remains underexplored whether individuals with the canonical Gly406Arg variants in mutually exclusive exon 8A (Timothy syndrome 1) or exon 8 (Timothy syndrome 2) exhibit overlapping symptoms. Moreover, case reports have indicated that some CACNA1C variants may produce a cardiac-selective form of Timothy syndrome often referred to as non-syndromic long QT type 8 or cardiac-only Timothy syndrome, however few reports follow up on these patients to confirm the cardiac selectivity of the phenotype over time. Methods A survey was administered to the parents of patients with Timothy syndrome, querying a broad range of symptoms and clinical features. Study participants were organized into 5 separate categories based on genotype and initial diagnosis, enabling comparison between groups of patients which have been described differentially in the literature. Results Our findings reveal that Timothy syndrome patients commonly exhibit both cardiac and extra-cardiac features, with long QT syndrome, neurodevelopmental impairments, hypoglycemia, and respiratory issues being frequently reported. Notably, the incidence of these features was similar across all patient categories, including those diagnosed with non-syndromic long QT type 8, suggesting that the ‘non-syndromic’ classification may be incomplete. Conclusions This study represents the first Natural History Study of Timothy syndrome, offering a comprehensive overview of the disease’s clinical manifestations. We demonstrate that both cardiac and extra-cardiac features are prevalent across all patient groups, underscoring the syndromic nature of CACNA1C variants. While the critical role of long QT syndrome and cardiac arrhythmias in Timothy syndrome has been well recognized, our findings indicate that hypoglycemia and respiratory dysfunction also pose significant life-threatening risks, emphasizing the need for comprehensive therapeutic management of affected individuals.

The authors of Social Identifications set out to make accessible to students of social psychology the social identity approach developed by Henri Tajfel, John Turner, and their colleagues in Bristol during the 1970s and 1980s. Michael Hogg and Dominic Abrams give a comprehensive and readable account of social identity theory as well as setting it in the context of other approaches and perspectives in the psychology of intergroup relations. They look at the way people derive their identity from the social groups to which they belong, and the consequences for their feelings, thoughts, and behaviour of psychologically belonging to a group. They go on to examine the relationship between the individual and society in the context of a discussion of discrimination, stereotyping and intergroup relations, conformity and social influence, cohesiveness and intragoup solidariy, language and ethnic group relations, and collective behaviour. Social Identifications fills a gap in the literature available to students of social psychology. The authors' presentation of social identity theory in a complete and integrated form and the extensive references and suggestions for further reading they provide will make this an essential source book for social psychologists and other social scientists looking at group behaviour.

A mutation that abrogates the function of ADAM17, an enzyme that cleaves cell-surface proteins such as tumor necrosis factor α, was found to be associated with inflammatory skin and bowel disease in a pair of siblings. Inflammatory disorders of the skin and gut, including eczema, psoriasis, and celiac disease, have been linked to changes in barrier function and immune responses, by means of genetic and functional studies. Large case–control studies combined with genomewide association studies have identified common genetic risk factors, with low penetrance, for a plethora of human disorders. Such studies have also identified numerous single-nucleotide polymorphisms (SNPs) in genes linked to the regulation of immunity and inflammation affecting epithelial tissues. 1 , 2 High-throughput sequence technology can be used to identify rare but penetrant disease-associated mutations in affected members of families with mendelian conditions. 3 – 6 We . . .

In this paper, we document changes in political trust in the UK throughout 2020 so as to consider wider implications for the ongoing handling of the COVID-19 pandemic. We analysed data from 18 survey organisations with measures on political trust (general, leadership, and COVID-19-related) spanning the period December 2019–October 2020. We examined the percentage of trust and distrust across time, identifying where significant changes coincide with national events. Levels of political trust were low following the 2019 UK General Election. They rose at the onset of UK lockdown imposed in March 2020 but showed persistent gradual decline throughout the remainder of the year, falling to pre-COVID levels by October 2020. Inability to sustain the elevated political trust achieved at the onset of the pandemic is likely to have made the management of public confidence and behaviour increasingly challenging, pointing to the need for strategies to sustain trust levels when handling future crises.

The investigation of the aetiology of sudden cardiac arrest or death in a young person combines features of a traditional clinical medical examination with those of forensic medicine. Nuances of the immediate peri-event history, when available, can be paramount. New genetic tools have greatly improved the yield of such investigations, but they must be carefully interpreted by genetic specialists. The approach to surviving patients, their family members, and to family members of non-survivors is best achieved in a structured programme that includes all appropriate specialists and support personnel. As an example, this may include all appropriate paediatric and internal medicine specialists, a geneticist, a genetic counsellor, a clinical psychologist, nurse specialist(s), and a programme coordinator. This family-centred strategy affords the patient, if surviving, and all family members the necessary emotional and medical support while at the same time providing the necessary diagnostic and therapeutic approaches.

To the Editor: Stanley and colleagues (Sept. 17 issue) 1 report a secure molecular diagnosis in five stillbirths that was based on variants identified in cardiac disease–associated genes, thus implying a causal relationship between genotype and mechanism of fetal death. No associated phenotype was detected on ultrasonography in any fetus or on autopsy in the three fetuses who underwent the procedure. Parental genotypes and phenotypes were unknown. Owing to the low, age-related penetrance and varied expressivity of such variants, 2 postmortem identification does not equate to a clinical diagnosis but can be the basis for initiating a robust investigative pipeline to determine . . .

In Study 1, 167 English children aged 6-8 or 9-11 evaluated peer English or French soccer fans that were loyal or partially disloyal. In Study 2, 149 children aged 5-11 made judgments about generic inclusion norms between and within competitive groups. In both studies, children's understanding of intergroup inclusion/exclusion norms (group nous) was predicted by theory of social mind (a social perspective taking measure) but not multiple classification skill. In Study 2, the number of groups children belonged to (an index of peer group experience) also predicted group nous. Supporting the developmental subjective group dynamics model (D. Abrams, A. Rutland, & L. Cameron, 2003), children's experience and perspective taking help them make sense of inter- and intragroup inclusion and exclusion.

This book is about the social psychological dynamics and phenomenology of social inclusion and exclusion. The editors take as their starting point the assumption that social life is conducted in a framework of relationships in which individuals seek inclusion and belongingness. Relationships necessarily include others, but equally they have boundaries that exclude. Frequently these boundaries are challenged or crossed. The book will draw together research on individual motivation, small group processes, stigmatization and intergroup relations, to provide a comprehensive social psychological account of social inclusion and exclusion. Acknowledgements Contributors Chapter 1. A Social Psychological Framework for Understanding Social Inclusion and Exclusion Dominic Abrams, Michael A. Hogg and José M. Marques SECTION A: INDIVIDUAL INCLUSION AND EXCLUSION Chapter 2. Social Exclusion Increases Aggression and Self-defeating Behavior while Reducing Intelligent Thought and Prosocial Behavior Jean M. Twenge and Roy F. Baumeister Chapter 3. Reacting to Ostracism: Retaliation or Reconciliation? Kipling D. Williams and Cassandra L. Govan Chapter 4. Stigma and Social Exclusion Brenda Major and Collette P. Eccleston Chapter 5. The Role of Exclusion in Maintaining Ingroup Inclusion Cynthia L. Pickett and Marilynn B. Brewer Chapter 6. Exclusion of the Self by Close Others and by Groups: Implications of the Self-Expansion Model Tracy McGlaughlin-Volpe, Art Aron, Stephen C. Wright and Gary W. Lewandowski Jr. SECTION B: GROUP DYNAMICS OF INCLUSION AND EXCLUSION Chapter 7. Managing Group Composition: Inclusive and Exclusive Role Transitions John M. Levine, Richard L. Moreland, and Leslie R. M. Hausmann Chapter 8. When Bad Becomes Good (and Vice Versa): Why Social Exclusion Is Not Based on Difference Dominic Abrams, Georgina Randsley de Moura, Paul Hutchison and G.Tendayi Viki Chapter 9. Fringe Dwellers: Processes of Deviance and Marginalization in Groups Michael A. Hogg and Kelly S. Fielding and John Darley Chapter 10. Delinquency: Cause or consequence of social exclusion? Nicholas Emler and Stephen Reicher SECTION C: INTERGROUP INCLUSION AND EXCLUSION Chapter 11. Social Inclusion and Exclusion: Recategorization and the Perception of Intergroup Boundaries John F. Dovidio, Samuel L. Gaertner, Gordon Hodson, Melissa A. Houlette and Kelly M. Johnson Chapter 12. Intergroup Contact in a Divided Society: Challenging Segregation in Northern Ireland Miles Hewstone, Ed Cairns, Alberto Voci, Stefania Paolini, Frances McLernon, Richard J. Crisp, Ulrike, Niens and Jean Craig Chapter 13. Cognitive Representations and Exclusion of Immigrants: Why Red-Nosed Reindeer Don't Play Games Diana R. Rice and Brian Mullen Chapter 14. Attitudes toward Immigrants and Immigration: The Role of National and International Identity Victoria M. Esses, John F. Dovidio, Antoinette Semenya and Lynne M. Jackson Author Index Subject Index \"This volume spans the full range from global to personal analysis of people in the process of including and excluding each other. The editors have assembled an impressive array of experts who shed light on people in (and out) of groups. Policy implications leap out from every chapter. A crucial book for all of us concerned with the current, unprecedented intergroup challenges to the human social condition.\" - Susan T. Fiske, Princeton University \"The Social Psychology of Inclusion and Exclusion is an important and timely publication. With 14 pointed chapters written by leading social psychologists, this edited volume provides a summary of where the intergroup field stands at present. I especially like the focus on social inclusion and exclusion at all three levels of analysis – micro-individual, meso-group, and macro-societal. Thus, this volume covers the effects of exclusion from laboratory studies on individuals to survey studies of Northern Ireland. In short, this volume can be highly recommended for all who are concerned with intergroup phenomena.\" - Thomas F. Pettigrew, University of California at Santa Cruz