Representing Death in the News : Journalism, Media and Mortality

Recent years have seen a renewed interest in the relationship between the news, media and death. Driven by a perceived ubiquity of death and dying on television, in newspapers and on the internet, many scholars have attempted to more closely examine aspects of this coverage. The result is that there now exists a large body of scholarly work on death in the news, yet what has been lacking is a comprehensive synthesis of the field. This book seeks to close this gap by analyzing the scholarship on death in the news by way of a thematic approach. It provides a historical overview, looks at the conditions of production, content and reception, and also analyzes emerging trends in the representation of death online. This fascinating account provides a much needed overview of what we currently know about death in the news and provides food for thought for future studies in the field.

Whose business is dying? Death, the home and palliative care

The process of dying at home brings the nexus between the paternalism of conventional palliative care and a social understanding of end of life care into sharp focus. Away from institutional places of care, issues of ownership, compliance and communal responsibility are heightened. At this interface, palliative care services are confronted with the irony of relinquishing their 'ownership' of dying whilst leading communities to reclaim their principal role in the business of dying. This benign – but enduring – paternalism remains a barrier to a paradigmatic shift towards a more complete understanding of the business of dying. Whilst nascent attempts to promote community engagement in end of life issues are evident in the interface between palliative care and public health, dying remains, for the most part, the remit of health care services. In this article, I contend that the business of dying is incompletely attended. This lack of attention will be partially redressed here by considering the home as a fitting death scene.

The strange death and curious after-lives of the academic journal

Discussion at a session featuring a panel of editors of six leading media and communication journals. Annual conference of the Australian and New Zealand Communication Association, University of Melbourne, July 2007.

Synergism between Wnt3a and heparin enhances osteogenesis via a phosphoinositide 3-kinase/Akt/RUNX2 pathway

A new strategy has emerged to improve healing of bone defects using exogenous glycosaminoglycans by increasing the effectiveness of bone-anabolic growth factors. Wnt ligands play an important role in bone formation. However, their functional interactions with heparan sulfate/heparin have only been investigated in non-osseous tissues. Our study now shows that the osteogenic activity of Wnt3a is cooperatively stimulated through physical interactions with exogenous heparin. N-Sulfation and to a lesser extent O-sulfation of heparin contribute to the physical binding and optimal co-stimulation of Wnt3a. Wnt3a-heparin signaling synergistically increases osteoblast differentiation with minimal effects on cell proliferation. Thus, heparin selectively reduces the effective dose of Wnt3a needed to elicit osteogenic, but not mitogenic responses. Mechanistically, Wnt3a-heparin signaling strongly activates the phosphoinositide 3-kinase/Akt pathway and requires the bone-related transcription factor RUNX2 to stimulate alkaline phosphatase activity, which parallels canonical beta-catenin signaling. Collectively, our findings establish the osteo-inductive potential of a heparin-mediated Wnt3a-phosphoinositide 3-kinase/Akt-RUNX2 signaling network and suggest that heparan sulfate supplementation may selectively reduce the therapeutic doses of peptide factors required to promote bone formation.

Loss of chromosomal integrity in human mammary epithelial cells subsequent to escape from senescence

The genomic changes that foster cancer can be either genetic or epigenetic in nature. Early studies focused on genetic changes and how mutational events contribute to changes in gene expression. These point mutations, deletions and amplifications are known to activate oncogenes and inactivate tumor suppressor genes. More recently, multiple epigenetic changes that can have a profound effect on carcinogenesis have been identified. These epigenetic events, such as the methylation of promoter sequences in genes, are under active investigation. In this review we will describe a methylation event that occurs during the propagation of human mammary epithelial cells (HMEC) in culture and detail the accompanying genetic alterations that have been observed.

Colonizing while migrating : how do individual enteric neural crest cells behave?

Background Directed cell migration is essential for normal development. In most of the migratory cell populations that have been analysed in detail to date, all of the cells migrate as a collective from one location to another. However, there are also migratory cell populations that must populate the areas through which they migrate, and thus some cells get left behind while others advance. Very little is known about how individual cells behave to achieve concomitant directional migration and population of the migratory route. We examined the behavior of enteric neural crest-derived cells (ENCCs), which must both advance caudally to reach the anal end and populate each gut region. Results The behaviour of individual ENCCs was examined using live imaging and mice in which ENCCs express a photoconvertible protein. We show that individual ENCCs exhibit very variable directionalities and speed; as the migratory wavefront of ENCCs advances caudally, each gut region is populated primarily by some ENCCs migrating non-directionally. After populating each region, ENCCs remain migratory for at least 24 hours. Endothelin receptor type B (EDNRB) signaling is known to be essential for the normal advance of the ENCC population. We now show that perturbation of EDNRB principally affects individual ENCC speed rather than directionality. The trajectories of solitary ENCCs, which occur transiently at the wavefront, were consistent with an unbiased random walk and so cell-cell contact is essential for directional migration. ENCCs migrate in close association with neurites. We showed that although ENCCs often use neurites as substrates, ENCCs lead the way, neurites are not required for chain formation and neurite growth is more directional than the migration of ENCCs as a whole. Conclusions Each gut region is initially populated by sub-populations of ENCCs migrating non-directionally, rather than stopping. This might provide a mechanism for ensuring a uniform density of ENCCs along the growing gut.

The body in grief : death investigations, objections to autopsy, and the religious and cultural 'other'

Sudden, violent and otherwise unexplained deaths are investigated in most western jurisdictions through a Coronial or medico-legal process. A crucial element of such an investigation is the legislative requirement to remove the body for autopsy and other medical interventions, processes which can disrupt traditional religious and cultural grieving practices. While recent legislative changes in an increasing number of jurisdictions allow families to raise objections based on religious and cultural grounds, such concerns can be over-ruled, often exacerbating the trauma and grief of families. Based on funded research which interviews a range of Coronial staff in one Australian jurisdiction, this paper explores the disjuncture between medico-legal discourses, which position the body as corpse, and the rise of more ‘therapeutic’ discourses which recognise the family’s wishes to reposition the body as beloved and lamented.

Does withdrawing life-sustaining treatment cause death or allow the patient to die?

The paper discusses the view of Franklin Miller and Robert Truog that withdrawing life-sustaining treatment causes death and so is a form of killing. I reject that view. I argue that even if we think there is no morally relevant difference between allowing a patient to die and killing her (itself a controversial view), it does not follow that allowing to die is a form of killing. I then argue that withdrawing life-sustaining treatment is properly classified as allowing the patient to die rather than as killing her. Once this is accepted, the law cannot be criticised for inconsistency by holding, as it does, that it is lawful to withdraw life-sustaining treatment but unlawful to give patients a lethal injection.

Classification of cancer-related death certificates using machine learning

Background Cancer monitoring and prevention relies on the critical aspect of timely notification of cancer cases. However, the abstraction and classification of cancer from the free-text of pathology reports and other relevant documents, such as death certificates, exist as complex and time-consuming activities. Aims In this paper, approaches for the automatic detection of notifiable cancer cases as the cause of death from free-text death certificates supplied to Cancer Registries are investigated. Method A number of machine learning classifiers were studied. Features were extracted using natural language techniques and the Medtex toolkit. The numerous features encompassed stemmed words, bi-grams, and concepts from the SNOMED CT medical terminology. The baseline consisted of a keyword spotter using keywords extracted from the long description of ICD-10 cancer related codes. Results Death certificates with notifiable cancer listed as the cause of death can be effectively identified with the methods studied in this paper. A Support Vector Machine (SVM) classifier achieved best performance with an overall F-measure of 0.9866 when evaluated on a set of 5,000 free-text death certificates using the token stem feature set. The SNOMED CT concept plus token stem feature set reached the lowest variance (0.0032) and false negative rate (0.0297) while achieving an F-measure of 0.9864. The SVM classifier accounts for the first 18 of the top 40 evaluated runs, and entails the most robust classifier with a variance of 0.001141, half the variance of the other classifiers. Conclusion The selection of features significantly produced the most influences on the performance of the classifiers, although the type of classifier employed also affects performance. In contrast, the feature weighting schema created a negligible effect on performance. Specifically, it is found that stemmed tokens with or without SNOMED CT concepts create the most effective feature when combined with an SVM classifier.

Physiological basis of salt stress tolerance in rice expressing the antiapoptotic gene SfIAP

Programmed cell death-associated genes, especially antiapoptosis-related genes have been reported to confer tolerance to a wide range of biotic and abiotic stresses in dicotyledonous plants such as tobacco (Nicotiana tabacum L.) and tomato (Solanum lycopersicum L.). This is the first time the antiapoptotic gene SfIAP was transformed into a monocotyledonous representative: rice (Oryza sativa L.). Transgenic rice strains expressing SfIAP were generated by the Agrobacterium-mediated transformation method and rice embryogenic calli, and assessed for their ability to confer tolerance to salt stress at both the seedling and reproductive stages using a combination of molecular, agronomical, physiological and biochemical techniques. The results show that plants expressing SfIAP have higher salt tolerance levels in comparison to the wild-type and vector controls. By preventing cell death at the onset of salt stress and maintaining the cell membrane’s integrity, SfIAP transgenic rice plants can retain plant water status, ion homeostasis, photosynthetic efficiency and growth to combat salinity successfully.

The biology of breast tumor progression : acquisition of hormone independence and resistance to cytotoxic drugs

Many breast tumors appear to follow a predictable clinical pattern, being initially responsive to endocrine therapy and to cytotoxic chemotherapy but ultimately exhibiting a phenotype resistant to both modalities. Using the MCF-7 human breast cancer cell line as an example of an 'early' phenotype (estrogen and progesterone receptor positive, steroid responsive, low metastatic potential), we have isolated and characterized a series of hormone-independent but hormone-responsive variants (MIII and MCF7/LCC1). However, these variants remain responsive to both antiestrogens and cytotoxic drugs (methotrexate and colchicine). MIII and MCF7/LCCl cells appear to mimic some of the critical aspects of the early progression to a more aggressive phenotype. An examination of the phenotype of these cells suggests that some hormone-independent breast cancer cells are derived from hormone-dependent parental cells. The development of a hormone-independent phenotype can arise independently of acquisition of a cytotoxic drug resistant phenotype.

Engineering salinity tolerance in rice by exogenous expression of cell death regulators

Rice, an important crop that feeds more than half of the world's population is very sensitive to salinity stress – a growing problem affecting crop production globally. This PhD study addressed this problem by manipulating the programmed cell death pathways in rice resulting in significant enhancement of salinity stress tolerance. The impact of this work is that farmers would be in a position to grow rice containing such a trait in environments where salinisation of the soil exists, thereby addressing food security needs.

Anti-proliferative and cytotoxic activity of pentadactylin isolated from Leptodactylus labyrinthicus on melanoma cells

Nowadays, the emergence of resistance to the current available chemotherapeutic drugs by cancer cells makes the development of new agents imperative. The skin secretion of amphibians is a natural rich source of antimicrobial peptides (AMP), and researchers have shown that some of these wide spectrum molecules are also toxic to cancer cells. The aim of this study was to verify a putative anticancer activity of the AMP pentadactylin isolated for the first time from the skin secretion of the frog Leptodactylus labyrinthicus and also to study its cytotoxic mechanism to the murine melanoma cell line B16F10. The results have shown that pentadactylin reduces the cell viability of B16F10 cells in a dose-dependent manner. It was also cytotoxic to normal human fibroblast cells; nevertheless, pentadactylin was more potent in the first case. The studies of action mechanism revealed that pentadactylin causes cell morphology alterations (e.g., round shape and shrinkage morphology), membrane disruption, DNA fragmentation, cell cycle arrest at the S phase, and alteration of mitochondrial membrane potential, suggesting that B16F10 cells die by apoptosis. The exact mechanism that causes reduction of cell viability and cytotoxicity after treatment with pentadactylin is still unknown. In conclusion, as cancer cells become resilient to death, it is worthwhile the discovery of new drugs such as pentadactylin that induces apoptosis.