From brown envelopes to community benefits: the co-option of planning gain agreements under deepening neoliberalism

The provision of physical and social infrastructure in the form of roads, green spaces and community facilities has traditionally been provided for by the state through the general taxation system. However, as the state has been transformed along more neoliberal lines, the private sector is increasingly relied upon to deliver public goods and services. Planning gain agreements have flourished within this context by offering another vehicle through which local facilities are privately funded. Whilst these agreements reflect the broader dynamics of neoliberalism, they are commonly viewed as a tool which can be employed to challenge these very dynamics by empowering local communities to secure more just planning outcomes. This paper counters such claims. Based on evidence gathered from 80 interviews with planners, councillors, developers and community groups in Ireland, the paper demonstrates how planning gain agreements have been strategically redeployed by the holders of political and economic power to serve their own ends. In seeking to understand why and how this has occurred, specific consideration is given to the changing power dynamics between the state and private capital under neoliberalism. The paper highlights how institutional arrangements have enabled developers to infiltrate the political sphere in more subtle and implicit ways than ever before. We conclude by arguing that planning gain must be understood as a mechanism which has been manipulated in ways which essentially work to preserve and enhance, rather than redress, existing power imbalances in the planning system by facilitating large scale transfers of wealth upwards in society.

Self-perceptions of the role of the planner

The role of the planning practitioner has received considerable attention in a diverse range of theoretical and empirical debates within the broad spectrum of planning scholarship from normative debates surrounding the planner's role in society, to more empirical investigations into the skills, attributes, and evolving nature of planning practitioners. Fundamental questions surrounding the role and purpose of planners have also entered into more mainstream discussions as the democratic nature of the planning system has been consistently undermined by allegations of misconduct, corruption, and incompetence. Despite the broad range of literature and debate which centres on the role of the planner, relatively few studies have explored the views of planning practitioners themselves, making it difficult to judge whether the ideas of planning academics are actually shared by those in the field. In this paper we seek to address this particular gap and argue that such insights are critical in determining the extent to which planning practitioners serve to challenge, maintain, or reinforce existing power imbalances in the planning system. The methodology consists of a series of qualitative interviews with twenty local authority planners working throughout the Greater Dublin Area, Ireland. The results suggest that planners' self-perceptions of their role tend to reflect traditional pluralist and managerialist perspectives. More broadly, the results suggest that the role orientations of contemporary planners are being shaped by dominant discourses in current planning ideology — namely, collaborative and participatory approaches

Specific JAK2 mutation (JAK2R683) and multiple gene deletions in Down syndrome acute lymphoblastic leukemia

Children with Down syndrome (DS) have a greatly increased risk of acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic leukemia (ALL). Both DS-AMKL and the related transient myeloproliferative disorder (TMD) have GATA1 mutations as obligatory, early events. To identify mutations contributing to leukemogenesis in DS-ALL, we undertook sequencing of candidate genes, including FLT3, RAS, PTPN11, BRAF, and JAK2. Sequencing of the JAK2 pseudokinase domain identified a specific, acquired mutation, JAK2R683, in 12 (28%) of 42 DS-ALL cases. Functional studies of the common JAK2R683G mutation in murine Ba/F3 cells showed growth factor independence and constitutive activation of the JAK/STAT signaling pathway. High-resolution SNP array analysis of 9 DS-ALL cases identified additional submicroscopic deletions in key genes, including ETV6, CDKN2A, and PAX5. These results infer a complex molecular pathogenesis for DS-ALL leukemogenesis, with trisomy 21 as an initiating or first hit and with chromosome aneuploidy, gene deletions, and activating JAK2 mutations as complementary genetic events. (Blood. 2009; 113: 646-648)

Deletions of CDKN2C in Multiple Myeloma: Biological and Clinical Implications

Purpose: Deletions of chromosome 1 have been described in 7% to 40% of cases of myeloma with inconsistent clinical consequences. CDKN2C at 1p32.3 has been identified in myeloma cell lines as the potential target of the deletion. We tested the clinical impact of 1p deletion and used high-resolution techniques to define the role of CDKN2C in primary patient material.Experimental Design: We analyzed 515 cases of monoclonal gammopathy of undetermined significance (MGUS), smoldering multiple myeloma (SMM), and newly diagnosed multiple myeloma using fluorescence in situ hybridization (FISH) for deletions of CDKN2C. In 78 myeloma cases, we carried out Affymetrix single nucleotide polymorphism mapping and U133 Plus 2.0 expression arrays. In addition, we did mutation, methylation, and Western blotting analysis.Results: By FISH we identified deletion of 1p32.3 (CDKN2C) in 3 of 66 MGUS (4.5%), 4 of 39 SMM (10.3%), and 55 of 369 multiple myeloma cases (15%). We examined the impact of copy number change at CDKN2C on overall survival (OS), and found that the cases with either hemizygous or homozygous deletion of CDKN2C had a worse OS compared with cases that were intact at this region (22 months versus 38 months; P = 0.003). Using gene mapping we identified three homozygous deletions at 1p32.3, containing CDKN2C, all of which lacked expression of CDKN2C. Cases with homozygous deletions of CDKN2C were the most proliferative myelomas, defined by an expression-based proliferation index, consistent with its biological function as a cyclin-dependent kinase inhibitor.Conclusions: Our results suggest that deletions of CDKN2C are important in the progression and clinical outcome of myeloma.

Abnormalities on 1q and 7q are associated with poor outcome in sporadic Burkitt's lymphoma. A cytogenetic and comparative genomic hybridization study.

Comparative genomic hybridization (CGH) studies have demonstrated a high incidence of chromosomal imbalances in non-Hodgkin's lymphoma. However, the information on the genomic imbalances in Burkitt's Lymphoma (BL) is scanty. Conventional cytogenetics was performed in 34 cases, and long-distance PCR for t(8;14) was performed in 18 cases. A total of 170 changes were present with a median of four changes per case (range 1-22). Gains of chromosomal material (143) were more frequent than amplifications (5) or losses (22). The most frequent aberrations were gains on chromosomes 12q (26%), Xq (22%), 22q (20%), 20q (17%) and 9q (15%). Losses predominantly involved chromosomes 13q (17%) and 4q (9%). High-level amplifications were present in the regions 1q23-31 (three cases), 6p12-p25 and 8p22-p23. Upon comparing BL vs Burkitt's cell leukemia (BCL), the latter had more changes (mean 4.3 +/- 2.2) than BL (mean 2.7 +/- 3.2). In addition, BCL cases showed more frequently gains on 8q, 9q, 14q, 20q, and 20q, 9q, 8q and 14q, as well as losses on 13q and 4q. Concerning outcome, the presence of abnormalities on 1q (ascertained either by cytogenetics or by CGH), and imbalances on 7q (P=0.01) were associated with a short survival.