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Are hallucinations and delusions really symptoms of an illness called ‘schizophrenia’? Are mental health problems really caused by chemical imbalances and genetic predispositions? Are psychiatric drugs as effective and safe as the drug companies claim? Is madness preventable? This second edition of Models of Madness challenges those who hold to simplistic, pessimistic and often damaging theories and treatments of madness. In particular it challenges beliefs that madness can be explained without reference to social causes and challenges the excessive preoccupation with chemical imbalances and genetic predispositions as causes of human misery, including the conditions that are given the name 'schizophrenia'. This edition updates the now extensive body of research showing that hallucinations, delusions etc. are best understood as reactions to adverse life events and that psychological and social approaches to helping are more effective and far safer than psychiatric drugs and electroshock treatment. A new final chapter discusses why such a damaging ideology has come to dominate mental health and, most importantly, how to change that. Models of Madness is divided into three sections: Section One provides a history of madness, including examples of violence against the ‘mentally ill’, before critiquing the theories and treatments of contemporary biological psychiatry and documenting the corrupting influence of drug companies. Section Two summarises the research showing that hallucinations, delusions etc. are primarily caused by adverse life events (eg. parental loss, bullying, abuse and neglect in childhood, poverty, etc) and can be understood using psychological models ranging from cognitive to psychodynamic. Section Three presents the evidence for a range of effective psychological and social approaches to treatment, from cognitive and family therapy to primary prevention. This book brings together thirty-seven contributors from ten countries and a wide range of scientific disciplines. It provides an evidence-based, optimistic antidote to the pessimism of biological psychiatry. Models of Madness will be essential reading for all involved in mental health, including service users, family members, service managers, policy makers, nurses, clinical psychologists, psychiatrists, psychotherapists, counsellors, psychoanalysts, social workers, occupational therapists, art therapists. 　 John Read is a Professor of Clinical Psychology at the University of Liverpool and is Editor of the scientific journal Psychosis: Psychological, Social and Integrative Approaches . He is author of numerous books and over 100 research articles. In 2010 Professor Read was awarded the New Zealand Psychological Society’s Hunter Award, presented every three years, for excellence in scholarship and contribution to the profession. Jacqui Dillon is a campaigner, writer, international speaker and trainer specialising in hearing voices, psychosis, dissociation, trauma, abuse, healing and recovery. She is the national Chair of the Hearing Voices Network in England, a Board member of Intervoice – the International Network for Training, Education and Research into Hearing Voices. Jacqui is an Honorary Lecturer in Clinical Psychology at the University of East London. This is her third co-edited book about psychosis. 　 Preface to 1 st edition. Preface to 2 nd edition. Forewords. Part I: The Illness Model of Psychosis and ‘Schizophrenia’ . Read, Mosher, Bentall , ‘Schizophrenia’ is Not an Illness. Read , A History of Madness. Read , The Invention of ‘Schizophrenia’: Kraepelin and Bleuler. Read, Masson , Genetics, Eugenics and the Mass Murder of ‘Schizophrenics’. Read , Does ‘Schizophrenia’ Exist? Reliability and Validity. Read , Biological Psychiatry’s Lost Cause: The ‘Schizophrenic’ Brain. Joseph , Schizophrenia and Heredity: Why the Emperor has no Genes. Read, Bentall, Johnstone, Fosse, Bracken , Electroconvulsive therapy. Hutton, Weinmann, Bola, Read , Anti-psychotic drugs. Mosher, Gosden, Beder , Drug Companies and Schizophrenia: Unbridled Capitalism Meets Madness. Part II: Social and Psychological Approaches to Understanding Madness. Read, Magliano, Beavan , Public Beliefs about the Causes of ‘Schizophrenia’: Bad Things Happen and can Drive you Crazy. Read, Haslam, Magliano , Prejudice, Stigma and ‘Schizophrenia’: The Role of Bio-Genetic Ideology. Geekie , Listening to the Voices we Hear: Clients’ Understandings of Psychotic Experiences. Read, Johnstone, Taitimu , Psychosis, Poverty and Ethnicity. Read, Beavan , Gender and Psychosis. Bentall , Understanding Psychotic Symptoms: Cognitive and Integrative Models. Koehler, Silver, Karon , Psychodynamic Approaches to Psychosis: Defences against Terror. Read , Childhood Adversity and Psychosis: From Heresy to Certainty. Read, Seymour , Psychosis and Families: Intergenerational Parenting Problems. PART III: Social and Psychological Approaches to Responding to Madness. Clements, Davies , Prevention of Psychosis:　Creating Societies Where More People Flourish. Dillon, Bullimore, Lampshire, Chamberlain , The Work of Experience Based Experts. Morrison , Cognitive Therapy for People with Psychosis. Summers, Rosenbaum, Psychodynamic Psychotherapy for Psychosis: Empirical Evidence. Johannessen, Joa, Klarsen, Langeveld , The Development of Early Intervention Services. Mosher, Bola , Non-Hospital, Non-Medication Interventions in First Episode Psychosis. Aderhold, Gottwalz , Family Therapy and Psychosis: Replacing Ideology with Openness. Read, Dillon , Creating Evidence-Based, Effective and Humane Mental Health Services: Overcoming Barriers to a Paradigm Shift. \"This book is a major development on from the (2004) 1st edition, edited by John Read, Loren Mosher & Richard Bentall; all well-known authors in this growing field of ‘re-explaining’ madness and psychosis...This book ... promotes a much more humane and effective response to treating severely distressed people; it should prove essential reading for psychotherapists, clinical psychologists, psychiatrists and other mental health workers; and of great interest to all those who work in – or who are treated by – current mental health services.\" - Courtenay Young, Edinburgh, Scotland, Theodor Itten, St Gallen, Switzerland, IJP \"Truly, a revolution is occurring in our understanding of severe mental illness. ... This volume will serve as an inspiration, not only to established clinicians and researchers, but to the young people who will develop better services for people with psychosis in the future.\" - Richard Bentall, from the Foreword

Meningococcal conjugate vaccines protect individuals directly, but can also confer herd protection by interrupting carriage transmission. We assessed the effects of meningococcal quadrivalent glycoconjugate (MenACWY-CRM) or serogroup B (4CMenB) vaccination on meningococcal carriage rates in 18–24-year-olds. In this phase 3, observer-blind, randomised controlled trial, university students aged 18–24 years from ten sites in England were randomly assigned (1:1:1, block size of three) to receive two doses 1 month apart of Japanese Encephalitis vaccine (controls), 4CMenB, or one dose of MenACWY-CRM then placebo. Participants were randomised with a validated computer-generated random allocation list. Participants and outcome-assessors were masked to the treatment group. Meningococci were isolated from oropharyngeal swabs collected before vaccination and at five scheduled intervals over 1 year. Primary outcomes were cross-sectional carriage 1 month after each vaccine course. Secondary outcomes included comparisons of carriage at any timepoint after primary analysis until study termination. Reactogenicity and adverse events were monitored throughout the study. Analysis was done on the modified intention-to-treat population, which included all enrolled participants who received a study vaccination and provided at least one assessable swab after baseline. This trial is registered with ClinicalTrials.gov, registration number NCT01214850. Between Sept 21 and Dec 21, 2010, 2954 participants were randomly assigned (987 assigned to control [984 analysed], 979 assigned to 4CMenB [974 analysed], 988 assigned to MenACWY-CRM [983 analysed]); 33% of the 4CMenB group, 34% of the MenACWY-CRM group, and 31% of the control group were positive for meningococcal carriage at study entry. By 1 month, there was no significant difference in carriage between controls and 4CMenB (odds ratio 1·2, 95% CI 0·8–1·7) or MenACWY-CRM (0·9, [0·6–1·3]) groups. From 3 months after dose two, 4CMenB vaccination resulted in significantly lower carriage of any meningococcal strain (18·2% [95% CI 3·4–30·8] carriage reduction), capsular groups BCWY (26·6% [10·5–39·9] carriage reduction), capsular groups CWY (29·6% [8·1–46·0] carriage reduction), and serogroups CWY (28·5% [2·8–47·5] carriage reduction) compared with control vaccination. Significantly lower carriage rates were also noted in the MenACWY-CRM group compared with controls: 39·0% (95% CI 17·3–55·0) carriage reduction for serogroup Y and 36·2% (15·6–51·7) carriage reduction for serogroup CWY. Study vaccines were generally well tolerated, with increased rates of transient local injection pain and myalgia in the 4CMenB group. No safety concerns were identified. Although we detected no significant difference between groups at 1 month after vaccine course, MenACWY-CRM and 4CMenB vaccines reduced meningococcal carriage rates during 12 months after vaccination and therefore might affect transmission when widely implemented. Novartis Vaccines.

Bacillus anthracis is the etiologic agent of anthrax, an acute fatal disease among mammals. It was thought to differ from Bacillus cereus, an opportunistic pathogen and cause of food poisoning, by the presence of plasmids pXO1 and pXO2, which encode the lethal toxin complex and the poly-γ-D-glutamic acid capsule, respectively. This work describes a non-B. anthracis isolate that possesses the anthrax toxin genes and is capable of causing a severe inhalation anthrax-like illness. Although initial phenotypic and 16S rRNA analysis identified this isolate as B. cereus, the rapid generation and analysis of a high-coverage draft genome sequence revealed the presence of a circular plasmid, named pBCXO1, with 99.6% similarity with the B. anthracis toxin-encoding plasmid, pXO1. Although homologues of the pXO2 encoded capsule genes were not found, a polysaccharide capsule cluster is encoded on a second, previously unidentified plasmid, pBC218. A/J mice challenged with B. cereus G9241 confirmed the virulence of this strain. These findings represent an example of how genomics could rapidly assist public health experts responding not only to clearly identified select agents but also to novel agents with similar pathogenic potentials. In this study, we combined a public health approach with genome analysis to provide insight into the correlation of phenotypic characteristics and their genetic basis.

This timely book provides a framework for practice for professionals developing and running psychologically-informed services to meet the needs of socially excluded people with complex needs. It covers theory and practice from a psychodynamic perspective and provides practical interventions and case studies.