Special issue of PDS - Based on PDDG meeting, Aston University, September 2007, in honour of Professor Norman Billingham

This edition of Polymer Degradation and Stability comprises selected papers presented at the 27th Polymer Degradation Discussion Group (PDDG) Conference, affiliated to the Macromolecular Group of the Royal Society of Chemistry, held at Aston University, Birmingham (UK), September 2007, in honour of Professor Norman Billingham for lifelong career in Polymer Science. Norman Billingham was one of the main founders of the PDDG meetings which have been held annually at different venues in the UK since 1976, and biennially since 1998. The PDDG meetings are forums for scientific developments and open discussion of all aspects of polymer degradation and stabilisation and have always provided younger researchers a platform for presenting and discussing their work in the field. This 27th PDDG meeting, chaired by Sahar Al-Malaika (Aston University), was dedicated to Norman Billingham, the Guest of Honour, in recognition for his distinguished contributions to Polymer Science particularly in the area of polymer degradation and stabilisation. The meeting was attended by 65 delegates from 15 countries in Europe, USA and Australia, many of whom have worked and collaborated with Norman at some points of their career. The guest editors of this issue wish to add their Congratulations to Norman Billingham for his outstanding contributions and achievements in the field of polymer degradation and stabilisation and to wish him very happy years ahead. We wish also to express our gratitude to Elsevier for sponsoring the 27th PDDG event and our appreciation to Professor Norman Billingham in his capacity as the Editor-in-Chief of Polymer Degradation and Stability, for the support and help received during the preparation of this special issue.

Importance of tissue transglutaminase in repair of extracellular matrices and cell death of dermal fibroblasts after exposure to a solarium ultraviolet A source

Investigations were undertaken to study the role of the protein cross-linking enzyme tissue transglutaminase in changes associated with the extracellular matrix and in the cell death of human dermal fibroblasts following exposure to a solarium ultraviolet A source consisting of 98.8% ultraviolet A and 1.2% ultraviolet B. Exposure to nonlethal ultraviolet doses of 60 to 120 kJ per m2 resulted in increased tissue transglutaminase activity when measured either in cell homogenates, "in situ" by incorporation of fluorescein-cadaverine into the extracellular matrix or by changes in the epsilon(gamma-glutamyl) lysine cross-link. This increase in enzyme activity did not require de novo protein synthesis. Incorporation of fluorescein-cadaverine into matrix proteins was accompanied by the cross-linking of fibronectin and tissue transglutaminase into nonreducible high molecular weight polymers. Addition of exogenous tissue transglutaminase to cultured cells mimicking extensive cell leakage of the enzyme resulted in increased extracellular matrix deposition and a decreased rate of matrix turnover. Exposure of cells to 180 kJ per m2 resulted in 40% to 50% cell death with dying cells showing extensive tissue transglutaminase cross-linking of intracellular proteins and increased cross-linking of the surrounding extracellular matrix, the latter probably occurring as a result of cell leakage of tissue transglutaminase. These cells demonstrated negligible caspase activation and DNA fragmentation but maintained their cell morphology. In contrast, exposure of cells to 240 kJ per m2 resulted in increased cell death with caspase activation and some DNA fragmentation. These cells could be partially rescued from death by addition of caspase inhibitors. These data suggest that changes in cross-linking both in the intracellular and extracellular compartments elicited by tissue transglutaminase following exposure to ultraviolet provides a rapid tissue stabilization process following damage, but as such may be a contributory factor to the scarring process that results.

Increased TG2 expression can result in induction of transforming growth factor β1, causing increased synthesis and deposition of matrix proteins, which can be regulated by nitric oxide

In fibrotic conditions increases in TG2 activity has been linked to an increase in the deposition of extracellular matrix proteins. Using TG2 transfected Swiss 3T3 fibroblasts expressing TG2 under the control of the tetracycline-regulated inducible promoter, we demonstrate that induction of TG2 not only stimulates an increase in collagen and fibronectin deposition but also an increase in the expression of these proteins. Increased TG2 expression in these fibroblasts led to NF-kappaB activation, resulting in the increased expression of transforming growth factor (TGF) beta(1). In addition, cells overexpressing TG2 demonstrated an increase in biologically active TGFbeta(1) in the extracellular environment. A specific site-directed inhibitor of TG abolished the NF-kappaB and TGFbeta1 activation and the subsequent elevation in the synthesis and deposition of extracellular matrix proteins, confirming that this process depends on the induction of transglutaminase activity. Treatment of TG2-induced fibroblasts with nontoxic doses of nitric oxide donor S-nitroso-N-acetylpenicillamine resulted in decreased TG2 activity and apprehension of the inactive enzyme on the cell surface. This was paralleled by a reduction in activation of NF-kappaB and TGFbeta(1) production with a subsequent decrease in collagen expression and deposition. These findings support a role for NO in the regulation of TG2 function in the extracellular environment.

Reinsurance trading in Lloyd’s of London:balancing conflicting-yet-complementary logics in practice

Drawing on a year-long ethnographic study of reinsurance trading in Lloyd’s of London, this paper makes three contributions to current discussions of institutional complexity. First, we shift focus from purposeful organizational responses to institutional complexity to the everyday practices by which individuals collectively address competing demands on their work. Based on our findings, we develop a model of how individuals can balance conflicting institutional demands through a set of four interrelated practices, labeled segmenting, switching, bridging, and demarcating. Second, moving beyond the dominant focus on contradiction between logics, we show how these practices comprise a system of conflicting-yet-complementary logics, through which actors are able to both work within contradictions, whilst also exploiting the benefits of interdependent logics. Third, in contrast to most studies of newly formed hybrids and/or novel complexity, our focus on a long-standing context of institutional complexity, shows how balancing logics can become a matter of settled complexity, enacted routinely within everyday practice.

Words and intelligence II:essays in honor of Yorick Wilks

Yorick Wilks is a central figure in the fields of Natural Language Processing and Artificial Intelligence. His influence has extends to many areas of these fields and includes contributions to Machine Translation, word sense disambiguation, dialogue modeling and Information Extraction.This book celebrates the work of Yorick Wilks from the perspective of his peers. It consists of original chapters each of which analyses an aspect of his work and links it to current thinking in that area. His work has spanned over four decades but is shown to be pertinent to recent developments in language processing such as the Semantic Web.This volume forms a two-part set together with Words and Intelligence I, Selected Works by Yorick Wilks, by the same editors.

Role of transglutaminase 1 in stabilisation of intercellular junctions of the vascular endothelium

Microvascular endothelial monolayers from mouse myocardium (MyEnd) cultured for up to 5 days postconfluency became increasingly resistant to various barrier-compromising stimuli such as low extracellular Ca2+ and treatment with the Ca2+ ionophore A23187 and with the actin depolymerising compound cytochalasin D. In contrast, microvascular endothelial monolayers from mouse lung microvessels (PulmEnd) remained sensitive to these conditions during the entire culture period which corresponds to the well-known in vivo sensitivity of the lung microvasculature to Ca2+depletion and cytochalasin D treatment. One molecular difference between pulmonary and myocardial endothelial cells was found to be transglutaminase 1 (TGase1) which is strongly expressed in myocardial endothelial cells but is absent from pulmonary endothelial cells. Resistance of MyEnd cells to barrier-breaking conditions correlated strongly with translocation of TGase1 to intercellular junctions. Simultaneous inhibition of intracellular and extracellular TGase activity by monodansylcadaverine (MDC) strongly weakened barrier properties of MyEnd monolayers, whereas inhibition of extracellular TGases by the membrane-impermeable active site-directed TGase inhibitor R281 did not reduce barrier properties. Weakening of barrier properties could be also induced in MyEnd cells by downregulation of TGase1 expression using RNAi-based gene silencing. These findings suggest that crosslinking activity of intracellular TGase1 at intercellular junctions may play a role in controlling barrier properties of endothelial monolayers.