New East Manchester: urban renaissance or urban opportunism?

In this paper we ask how a shrinking city responds when faced with a perforated urban fabric. Drawing on Manchester’s response to its perforated eastern flank - and informed by a parallel study of Leipzig - we use the city’s current approach to critique urban regeneration policy in England. Urban renaissance holds out the promise of delivering more sustainable - that is more compact, more inclusive and more equitable - cities. However, the Manchester study demonstrated that the attempt to stem population loss from the city is at best fragile, despite a raft of policies now in place to support urban renaissance in England. It is argued here that Manchester like Leipzig is likely to face an ongoing battle to attract residents back from their suburban hinterlands. This is especially true of the family market that we identify as being an important element for long-term sustainable population growth in both cities. We use the case of New East Manchester to consider how discourses linked to urban renaissance – particularly those that link urbanism with greater densities - rule out some of the options available to Leipzig, namely, managing the long-term perforation of the city. We demonstrate that while Manchester is inevitably committed to the urban renaissance agenda, in practice New East Manchester demonstrates a far more pragmatic – but equally unavoidable – approach. This we attribute to the gap between renaissance and regeneration described by Amin et al (2000) who define the former as urbanism for the middle class and the latter as urbanism for the working class. While this opportunistic approach may ultimately succeed in producing development on the ground, it will not address the fundamental, and chronic, problem; the combination of push and pull that sees families relocating to suburban areas. Thus, if existing communities in East Manchester are to have their area buoyed up – or sustained - by incomers, and especially families, with greater levels of social capital and higher incomes urban policy in England will have to be challenged

Molecular and Clinical Analyses of Greig Cephalopolysyndactyly and Pallister-Hall Syndromes: Robust Phenotype Prediction from the Type and Position of GLI3 Mutations

Mutations in the GLI3 zinc-finger transcription factor gene cause Greig cephalopolysyndactyly syndrome (GCPS) and Pallister-Hall syndrome (PHS), which are variable but distinct clinical entities. We hypothesized that GLI3 mutations that predict a truncated functional repressor protein cause PHS and that functional haploinsufficiency of GLI3 causes GCPS. To test these hypotheses, we screened patients with PHS and GCPS for GLI3 mutations. The patient group consisted of 135 individuals: 89 patients with GCPS and 46 patients with PHS. We detected 47 pathological mutations (among 60 probands); when these were combined with previously published mutations, two genotype-phenotype correlations were evident. First, GCPS was caused by many types of alterations, including translocations, large deletions, exonic deletions and duplications, small in-frame deletions, and missense, frameshift/nonsense, and splicing mutations. In contrast, PHS was caused only by frameshift/nonsense and splicing mutations. Second, among the frameshift/nonsense mutations, there was a clear genotype-phenotype correlation. Mutations in the first third of the gene (from open reading frame [ORF] nucleotides [nt] 1–1997) caused GCPS, and mutations in the second third of the gene (from ORF nt 1998–3481) caused primarily PHS. Surprisingly, there were 12 mutations in patients with GCPS in the 3′ third of the gene (after ORF nt 3481), and no patients with PHS had mutations in this region. These results demonstrate a robust correlation of genotype and phenotype for GLI3 mutations and strongly support the hypothesis that these two allelic disorders have distinct modes of pathogenesis

sj-docx-2-eso-10.1177_23969873221136927 – Supplemental material for Molecular biomarkers predicting newly detected atrial fibrillation after ischaemic stroke or TIA: A systematic review

Supplemental material, sj-docx-2-eso-10.1177_23969873221136927 for Molecular biomarkers predicting newly detected atrial fibrillation after ischaemic stroke or TIA: A systematic review by Kirsty Ward, Andy Vail, Alan Cameron, Mira Katan, Gregory YH Lip, Jesse Dawson, Craig J Smith and Amit K Kishore in European Stroke Journa

sj-docx-2-eso-10.1177_23969873221136927 – Supplemental material for Molecular biomarkers predicting newly detected atrial fibrillation after ischaemic stroke or TIA: A systematic review

Supplemental material, sj-docx-2-eso-10.1177_23969873221136927 for Molecular biomarkers predicting newly detected atrial fibrillation after ischaemic stroke or TIA: A systematic review by Kirsty Ward, Andy Vail, Alan Cameron, Mira Katan, Gregory YH Lip, Jesse Dawson, Craig J Smith and Amit K Kishore in European Stroke Journa