Globalization, new ecologies, new zoologies and the purported death of the eclectic paradigm

This paper provides a commentary to John Mathews' article in issue 23(1) of the Asia Pacific Journal of Management. I discuss how globalisation is fundamentally altering the milieu within which international business is conducted, and this new ‘ecology’ may indeed require scholars to consider a new ‘zoology’ of firms in the future. However, his specific suggestions are based on sparse evidence, and his alternative to the eclectic paradigm is founded on a misunderstanding of some fundamental concepts.

Punk, Politics and British (fan)zines, 1974-84:'While the world was dying, did you wonder why?

This article recovers and contextualizes the politics of British punk fanzines produced in the late 1970s and early 1980s. It argues that fanzines – and youth cultures more generally – provide a contested cultural space for young people to express their ideas, opinions and anxieties. Simultaneously, it maintains that punk fanzines offer the historian a portal into a period of significant socio-economic, political and cultural change. As well as presenting alternative cultural narratives to the formulaic accounts of punk and popular music now common in the mainstream media, fanzines allow us a glimpse of the often radical ideas held by a youthful milieu rarely given expression in the political arena.

Living to die and dying to live: the survival strategy behind leaf senescence

Senescence represents the final developmental act of the leaf, during which the leaf cell is dismantled in a coordinated manner to remobilize nutrients and to secure reproductive success. The process of senescence provides the plant with phenotypic plasticity to help it adapt to adverse environmental conditions. Here, we provide a comprehensive overview of the factors and mechanisms that control the onset of senescence. We explain how the competence to senesce is established during leaf development, as depicted by the senescence window model. We also discuss the mechanisms by which phytohormones and environmental stresses control senescence, as well as the impact of source-sink relationships on plant yield and stress tolerance. In addition, we discuss the role of senescence as a strategy for stress adaptation and how crop production and food quality could benefit from engineering or breeding crops with altered onset of senescence.

Dying young: a palaeopathological analysis of child health in Roman Britain

Children represent the most vulnerable members of society, and as such provide valuable insight into past lifeways. Adverse environmental conditions translate more readily into the osteological record of children, making them primary evidence for the investigation of ill-health in the past. To date, most information on growing up in Roman Britain has been based on the Classical literature, or discussed in palaeopathological studies with a regional focus, e.g. Dorset or Durnovaria. Thus, the lifestyles and everyday realities of children throughout Britannia remained largely unknown. This study sets out to fill this gap by providing the first large scale analysis of Romano-British children from town and country. The palaeopathological analysis of 1643 non-adult (0-17 years) skeletons, compiled from the literature (N=690) and primary osteological analysis (N=953), from 27 urban and rural settlements has highlighted diverse patterns in non-adult mortality and morbidity. The distribution of ages-at-death suggest that older children and adolescents migrated from country to town, possibly for commencing their working lives. True prevalence rates suggest that caries (1.8%) and enamel hypoplasia (11.4%) were more common in children from major urban towns, whereas children in the countryside displayed higher frequencies of scurvy (6.9%), cribra orbitalia (27.7%), porotic hyperostosis (6.2%) and endocranial lesions (10.9%). Social inequality in late Roman Britain may have been the driving force behind these urban-rural dichotomies. The results may point to exploitation of the peasantry on the one hand, and higher status of the urban population as a more ‘Romanised’ group on the other. Comparison with Iron Age and post-medieval non-adults also demonstrated a decline in health in the Roman period, with some levels of ill-health, particularly in the rural children, similar to those from post-medieval London. This research provides the most comprehensive study of non-adult morbidity and mortality in Roman Britain to date. It has provided new insights into Romano-British lifeways and presents suggestions for further work.

Effects of 15-deoxy-Delta(12, 14) prostaglandin J(2) and ciglitazone on human cancer cell cycle progression and death: The role of PPAR gamma

The role of PPAR-gamma in ciglitazone and 15-d PGJ(2)-induced apoptosis and cell cycle arrest of Jurkat (before and after PPAR gamma gene silencing), U937 (express high levels of PPAR gamma) and HeLa (that express very low levels of PPAR gamma) cells was investigated. PPAR gamma gene silencing, per se, induced a G2/M cell arrest, loss of membrane integrity and DNA fragmentation of Jurkat cells, indicating that PPAR gamma is important for this cell survival and proliferation. Ciglitazone-induced apoptosis was abolished after knockdown of PPAR gamma suggesting a PPAR gamma-dependent pro-apoptotic effect. However, ciglitazone treatment was toxic for U937 and HeLa cells regardless of the presence of PPAR gamma. This treatment did not change the cell cycle distribution corroborating with a PPAR gamma-independent mechanism. On the other hand, 15-d PGJ(2) induced apoptosis of the three cancer cell lines regardless of the expression of PPAR gamma. These results suggest that PPAR gamma plays an important role for death of malignant T lymphocytes (Jurkat cells) and PPAR gamma agonists exert their effects through PPAR gamma-dependent and -independent mechanisms depending on the drug and the cell type. (C) 2007 Elsevier B.V. All rights reserved.

Effect of olive oil-based emulsion on human lymphocyte and neutrophil death

Background The incorporation of lipid emulsions in parenteral diets is a requirement for energy and essential fatty acid supply to critically ill patients. The most frequently used IV lipid emulsions (LE) are composed with long-chain triacylglycerols rich in omega-6 polyunsaturated fatty acids (PUFA) from soybean oil, but these LE promote lymphocyte and neutrophil death. A new emulsion containing 20% soybean oil and 80% olive oil rich in (omega-9 monounsaturated fatty acids (MUFA) has been hypothesized not to cause impairment of immune function. In this study, the toxicity of an olive oil-based emulsion (OOE) on lymphocytes and neutrophils from healthy volunteers was investigated. Methods: Twenty volunteers were recruited and blood was. collected before a 6-hour infusion of an OOE, immediately after infusion, and again 18 hours postinfusion. Lymphocytes and neutrophils were isolated by gradient density. The cells were studied immediately after isolation and after 24 hours or 48 hours in culture. The following determinations were carried out: triacylglycerol levels and fatty acid composition and levels in plasma, lymphocyte proliferation, production of reactive oxygen species, and parameters of lymphocyte and neutrophil death (viability, DNA fragmentation, phosphatidylserine externalization, mitochondrial depolarization, and neutral lipid accumulation). Results: OOE decreased lymphocyte proliferation, provoked lymphocyte necrosis, and had no effect on the proportion of viable neutrophils. The mechanism of cell death induced by OOE involved neutral lipid accumulation but had no effect on mitochondrial membrane depolarization. Conclusions: The OOE given as a single dose of 500 mL induced low toxicity to lymphocytes from healthy volunteers, probably by necrosis.

Hyperglycaemia protects the heart after myocardial infarction: aspects of programmed cell survival and cell death

Exposure to a high glucose medium or diabetes has been found to protect the heart against ischaemia. The activation of antiapoptotic and proliferative factors seems to be involved in this cardioprotection. This study was designed to evaluate the role of hyperglycaemia in cardiac function, programmed cell survival, and cell death in diabetic rats after myocardial infarction (MI). Male Wistar rats were divided into four groups (n = 8): control (C), diabetic (D), myocardial infarcted (MI), and diabetic myocardial infarcted (DI). The following measures were assessed in the left ventricle: size of MI, systolic and diastolic function by echocardiography, cytokines by ELISA (TNF-alpha, IL-1 beta, IL-6, and IL-10), gene expression by real-time PCR (Bax, Fas, p53, Bcl-2, HIF1-alpha, VEGF, and IL8r), caspase-3 activity by spectrofluorometric assay, glucose transporter type 1 and 4 (GLUT-1 and GLUT-4) protein expression by western blotting, and capillary density and fibrosis by histological analysis. Systolic function was improved by hyperglycaemia in the DI group, and this was accompanied by no improvement in diastolic dysfunction, a reduction of 36% in MI size, reduced proinflammatory cytokines, apoptosis activation, and an increase in cell survival factors (HIF1-alpha, VEGFa and IL8r) assessed 15 days post-MI. Moreover, hyperglycaemia resulted in angiogenesis (increased capillary density) before and after MI, accompanied by a reduction in fibrosis. Together, these results suggest that greater plasticity and cellular resistance to ischaemic injury result from chronic diabetic hyperglycaemia in rat hearts.

The effect of an adventure race on lymphocyte and neutrophil death

The effect of an adventure race (Ecomotion Pr), which lasted for 4-5 days, on neutrophil and lymphocyte death from elite athletes was investigated. Blood was collected from 11 athletes at rest and after the adventure race. The following parameters of cell death were measured in neutrophils and lymphocytes: cell membrane integrity, DNA fragmentation, mitochondrial transmembrane depolarization and reactive oxygen species (ROS) production. Phagocytosis capacity was also evaluated in neutrophils. The adventure race raised the proportion of cells with the loss of membrane integrity; lymphocytes by 14% and neutrophils by 16.4%. The proportion of lymphocytes with DNA fragmentation (2.9-fold) and mitochondrial transmembrane depolarization (1.5-fold) increased. However, these parameters did not change in neutrophils. ROS production remained unchanged in lymphocytes, whereas an increase by 2.2-fold was found in neutrophils due to the race. Despite these changes, the phagocytosis capacity did not change in neutrophils after the race. In conclusion, the Ecomotion Pr race-induced neutrophil death by necrosis (as indicated by the loss of membrane integrity) and led to lymphocyte death by apoptosis (as indicated by increase DNA fragmentation and depolarization of mitochondrial membrane).