Previous linkage analyses of families with multiple cases of schizophrenia by us and others have confirmed the involvement of the chromosome 11q22-24 region in the etiology of schizophrenia, with LOD scores of 3.4 and 3.1. We now report fine mapping of a susceptibility gene in the 11q22-24 region, determined on the basis of a University College London (UCL) sample of 496 cases and 488 supernormal controls. Confirmation was then performed by the study of an Aberdeen sample consisting of 858 cases and 591 controls (for a total of 2,433 individuals: 1,354 with schizophrenia and 1,079 controls). Seven microsatellite or single-nucleotide polymorphism (SNP) markers localized within or near the FXYD6 gene showed empirically significant allelic associations with schizophrenia in the UCL sample (for D11S1998, P=.021; for rs3168238, P=.009; for TTTC20.2, P=.048; for rs1815774, P=.049; for rs4938445, P=.010; for rs4938446, P=.025; for rs497768, P=.023). Several haplotypes were also found to be associated with schizophrenia; for example, haplotype Hap-F21 comprising markers rs10790212-rs4938445-rs497768 was found to be associated with schizophrenia, by a global permutation test (P=.002). Positive markers in the UCL sample were then genotyped in the Aberdeen sample. Two of these SNPs were found to be associated with schizophrenia in the Scottish sample (for rs4938445, P=.044; for rs497768, P=.037). The Hap-F21 haplotype also showed significant association with schizophrenia in the Aberdeen sample, with the same alleles being associated (P=.013). The FXYD6 gene encodes a protein called "phosphohippolin" that is highly expressed in regions of the brain thought to be involved in schizophrenia. The protein functions by modulating the kinetic properties of Na,K-ATPase to the specific physiological requirements of the tissue. Etiological base-pair changes in FXYD6 or in associated promoter/control regions are likely to cause abnormal function or expression of phosphohippolin and to increase genetic susceptibility to schizophrenia.
ObjectiveAlcohol-related admissions are increasing. A significant number of these admissions are attributable to a small number of complex patients with other comorbidities who do not engage well with mainstream services. Assertive outreach teams have been used in the field of psychiatry to engage patients who are poorly compliant. This study examines whether an alcohol assertive outreach team (AAOT) can engage with this group and reduce hospital admissions.DesignThe AAOT is a multidisciplinary team with medical, psychiatric, substance misuse, psychology, nursing and social work specialists. The team worked with patients with the highest number of alcohol-related admissions and case managed in a community setting for 6 months. The admission and emergency department attendances of the cohort were compared for the 3-month period before and after the intervention. Christo inventory for substance misuse services (CISS) scores were determined pre and post the intervention period.Results54 patients were case managed. The total number of admissions in 3 months fell from 151 prior to the intervention period to 50 following the intervention. Emergency department attendances also fell from 360 in 3 months to 146 following the intervention period. CISS scores fell from 11 preintervention to eight postintervention.ConclusionsAn AAOT model appears to reduce hospital admissions and emergency department attendances in a complex group of patients that display high alcohol-related admissions.
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