Delivering race equality in mental health in England: the importance of pathways.

The programme on Delivering Race Equality in mental health care has been working to address inequalities in care. These inequalities cannot take a reductionist approach to understanding these inequalities. Individual identities are complex comprising many overlapping aspects of lived experience. A better, systems-wide understanding of care services is also needed to address any inequalities, rather than focusing on one aspect, such as admission rates. To achieve equality of access, experience and outcome we need to review and improve whole pathways of care. The Enhancing Pathways into Care project has been helpful in furthering this understanding of quality improvement and exploring practical approaches to delivering the desired equality. The equalities programme for mental health is building on this understanding for better quality services.

A genomic rearrangement resulting in a tandem duplication is associated with split hand-split foot malformation 3 (SHFM3) at 10q24.

Split hand-split foot malformation (SHFM) is characterized by hypoplasia/aplasia of the central digits with fusion of the remaining digits. SHFM is usually an autosomal dominant condition and at least five loci have been identified in humans. Mutation analysis of the DACTYLIN gene, suspected to be responsible for SHFM3 in chromosome 10q24, was conducted in seven SHFM patients. We screened the coding region of DACTYLIN by single-strand conformation polymorphism and sequencing, and found no point mutations. However, Southern, pulsed field gel electrophoresis and dosage analyses demonstrated a complex rearrangement associated with a approximately 0.5 Mb tandem duplication in all the patients. The distal and proximal breakpoints were within an 80 and 130 kb region, respectively. This duplicated region contained a disrupted extra copy of the DACTYLIN gene and the entire LBX1 and beta-TRCP genes, known to be involved in limb development. The possible role of these genes in the SHFM3 phenotype is discussed.