Agitating for a design and regeneration agenda in a postconflict city: the case of Belfast

Introduction

Belfast has been a focus of academic attention for the last forty years with most interest centred on various aspects of ‘the Troubles’. Where there has been interest in the built environment, it has largely been about how the ‘security situation’ impacted directly on architecture and on the design and layout of social housing. This paper seeks to go beyond this to explore how the political- administrative culture of ‘the Troubles’ interacted with ‘normal’ market forces to shape the central area of the city, and to consider the responses of a recently formed activist group, known as the Forum for Alternative Belfast (hereafter referred to as the Forum). The paper is written by three of the directors of the Forum.1 Moreover, the empirical research presented here was undertaken by the Forum as part of a campaign to address issues relating to the design, layout and quality of Belfast’s built environment. In the longstanding tradition of participant observation working within an action-research paradigm, the participants have attempted to offer an account that is evidentially and purposefully selfcritical and reflective. It is of course recognised that while this approach offers many positive attributes, such as phenomenological access through immersion in the project, it also has the potential to bring compromise on research detachment and objectivity.2 To address the latter, the authors have attempted
to avoid polemical argument, and to support claims with primary or secondary research evidence. The authors also acknowledge that action-research has a chequered history; however, they would argue
that their approach is faithful to a concept that sees ‘research’ defined as understanding and ‘action’ defined as seeking change. The Forum’s very purpose is to seek change, but to do this requires evidence, collaboration and demonstration. And in this sense, it is a learning process for all participants, including the research activists, government officials, community organisations and students. The authors also recognise the complexity of factors that affect urban management and change, particularly in a city such as Belfast, which has had to cope with political violence for over thirty years. And they appreciate that in the context of conflict, governance is skewed to cope with political realities. Hamdi reminds us, however, that in practice there is an ‘important dialectic between top-down planning, with its formal and designed laws and structures, and bottom-up selforganizing collectivism—those “quantum and emergent systems” which Jane Jacobs argued long ago give cities their life and order.’3

Contesting Territorial Fixity?: A Case Study of Regeneration in Belfast

This paper looks at urban regeneration in Belfast as a stage on which the interaction between different structural dynamics (political, economic and cultural) is manifested in the city. It discusses how contested ideas of ‘space’, ‘place’ and ‘territory’ frame the ways in which Belfast has changed over recent years and asks if regeneration itself has the potential to transform the dynamic of deep-rooted ethno-national divisions. The research question is explored through a case study of proposed urban regeneration in north Belfast. It is found that, while there is evidence of transition to less exclusivistic attitudes in leisure and work spaces, asymmetrical conflict over residential space persists in ways which reproduce deep-rooted political and cultural patterns of territorial fixity and division.

FMRFamide-like peptides (FLPs) enhance voltage-gated calcium currents to elicit muscle contraction in the human parasite Schistosoma mansoni.

Schistosomes are amongst the most important and neglected pathogens in the world, and schistosomiasis control relies almost exclusively on a single drug. The neuromuscular system of schistosomes is fertile ground for therapeutic intervention, yet the details of physiological events involved in neuromuscular function remain largely unknown. Short amidated neuropeptides, FMRFamide-like peptides (FLPs), are distributed abundantly throughout the nervous system of every flatworm examined and they produce potent myoexcitation. Our goal here was to determine the mechanism by which FLPs elicit contractions of schistosome muscle fibers. Contraction studies showed that the FLP Tyr-Ile-Arg-Phe-amide (YIRFamide) contracts the muscle fibers through a mechanism that requires Ca2+ influx through sarcolemmal voltage operated Ca2+ channels (VOCCs), as the contractions are inhibited by classical VOCC blockers nicardipine, verapamil and methoxyverapamil. Whole-cell patch-clamp experiments revealed that inward currents through VOCCs are significantly and reversibly enhanced by the application of 1 µM YIRFamide; the sustained inward currents were increased to 190% of controls and the peak currents were increased to 180%. In order to examine the biochemical link between the FLP receptor and the VOCCs, PKC inhibitors calphostin C, RO 31–8220 and chelerythrine were tested and all produced concentration dependent block of the contractions elicited by 1 µM YIRFamide. Taken together, the data show that FLPs elicit contractions by enhancing Ca2+ influx through VOCC currents using a PKC-dependent pathway.

Glucose lowers the threshold for human aortic vascular smooth muscle cell migration: inhibition by protein phosphatase-2A

AIMS/HYPOTHESIS: Atherosclerosis, which occurs prematurely in individuals with diabetes, incorporates vascular smooth muscle cell (VSMC) chemotaxis. Glucose, through protein kinase C-beta(II) signalling, increases chemotaxis to low concentrations of platelet-derived growth factor (PDGF)-BB. In VSMC, a biphasic response in PDGF-beta receptor (PDGF-betaR) level occurs as PDGF-BB concentrations increase. The purpose of this study was to determine whether increased concentrations of PDGF-BB and raised glucose level had a modulatory effect on the mitogen-activated protein kinase/extracellular-regulated protein kinase pathway, control of PDGF-betaR level and chemotaxis.

METHODS: Cultured aortic VSMC, exposed to normal glucose (NG) (5 mmol/l) or high glucose (HG) (25 mmol/l) in the presence of PDGF-BB, were assessed for migration (chemotaxis chamber) or else extracted and immunoblotted.

RESULTS: At concentrations of PDGF-BB <540 pmol/l, HG caused an increase in the level of PDGF-betaR in VSMC (immunoblotting) versus NG, an effect that was abrogated by inhibition of aldose reductase or protein kinase C-beta(II). At higher concentrations of PDGF-BB (>540 pmol/l) in HG, receptor level was reduced but in the presence of aldose reductase or protein kinase C-beta(II) inhibitors the receptor levels increased. It is known that phosphatases may be activated at high concentrations of growth factors. At high concentrations of PDGF-BB, the protein phosphatase (PP)2A inhibitor, endothall, caused an increase in PDGF-betaR levels and a loss of biphasicity in receptor levels in HG. At higher concentrations of PDGF-BB in HG, the chemoattractant effect of PDGF-BB was lost (chemotaxis chamber). Under these conditions inhibition of PP2A was associated with a restoration of chemotaxis to high concentrations of PDGF-BB.

CONCLUSION/INTERPRETATION: The biphasic response in PDGF-betaR level and in chemotaxis to PDGF-BB in HG is due to PP2A activation.

Changes in muscle sympathetic nerve activity and vascular responses evoked in the spinotrapezius muscle of the rat by systemic hypoxia.

Responses evoked in muscle sympathetic nerve activity (MSNA) by systemic hypoxia have received relatively little attention. Moreover, MSNA is generally identified from firing characteristics in fibres supplying whole limbs: their actual destination is not determined. We aimed to address these limitations by using a novel preparation of spinotrapezius muscle in anaesthetised rats. By using focal recording electrodes, multi-unit and discriminated single unit activity were recorded from the surface of arterial vessels. This had cardiac- and respiratory-related activities expected of MSNA, and was increased by baroreceptor unloading, decreased by baroreceptor stimulation and abolished by autonomic ganglion blockade. Progressive, graded hypoxia (breathing sequentially 12, 10, 8% O2 for 2 min each) evoked graded increases in MSNA. In single units, mean firing frequency increased from 0.2 ± 0.04 in 21% O2 to 0.62 ± 0.14 Hz in 8% O2, while instantaneous frequencies ranged from 0.04–6 Hz in 21% O2 to 0.09–20 Hz in 8% O2. Concomitantly, arterial pressure (ABP), fell and heart rate (HR) and respiratory frequency (RF) increased progressively, while spinotrapezius vascular resistance (SVR) decreased (Spinotrapezius blood flow/ABP), indicating muscle vasodilatation. During 8% O2 for 10 min, the falls in ABP and SVR were maintained, but RF, HR and MSNA waned towards baselines from the second to the tenth minute. Thus, we directly show that MSNA increases during systemic hypoxia to an extent that is mainly determined by the increases in peripheral chemoreceptor stimulation and respiratory drive, but its vasoconstrictor effects on muscle vasculature are largely blunted by local dilator influences, despite high instantaneous frequencies in single fibres.

Peptide IC-20, encoded by skin kininogen-1 of the European yellow-bellied toad, Bombina variegata, antagonizes bradykinin-induced arterial smooth muscle relaxation

The objectives were to determine if the skin secretion of the European yellow-bellied toad (Bombina variegata), in common with other related species, contains a bradykinin inhibitor peptide and to isolate and structurally characterize this peptide. Materials and Methods: Lyophilized skin secretion obtained from this toad was subjected to reverse phase HPLC fractionation with subsequent bioassay of fractions for antagonism of the bradykinin activity using an isolated rat tail artery smooth muscle preparation. Subsequently, the primary structure of the peptide was established by a combination of microsequencing, mass spectroscopy, and molecular cloning, following which a synthetic replicate was chemically synthesised for bioassay. Results: A single peptide of molecular mass 2300.92 Da was resolved in HPLC fractions of skin secretion and its primary structure determined as IYNAIWP-KH-NK-KPGLL-. Database interrogation with this sequence indicated that this peptide was encoded by skin kininogen-1 previously cloned from B. variegata. The blank cycles were occupied by cysteinyl (C) residues and the peptide was located toward the C-terminus of the skin kininogen, and flanked N-terminally by a classical -KR- propeptide convertase processing site. The peptide was named IC-20 in accordance (I = N-terminal isoleucine, C = C-terminal cysteine, 20 = number of residues). Like the natural peptide, its synthetic replicate displayed an antagonism of bradykinin-induced arterial smooth muscle relaxation. Conclusion: IC-20 represents a novel bradykinin antagonizing peptide from amphibian skin secretions and is the third such peptide found to be co-encoded with bradykinins within skin kininogens.