What is a cinema? Death, closure and the database

This chapter explores the possible ontological questions and epistemological propositions that arise from detailed empirical research into cinema closures. Repeated pronouncements of the ‘Death of Cinema’ in the wake of technological, social and industrial change serve to reinforce the coincidence of ‘death’ with a type of ‘closure’. The evocation of a ‘crisis’ in the cinema is ordinarily articulated within the terms of specific cultural concerns around transience and transformation in the social experience of the cinema. However, rather than adding another chapter to the apocalyptic historiography of the cinema this paper proposes instead the constitutive importance of ‘closure’ as a critical tool for rethinking our defining assumptions about cinema(s). Specifically, the chapter will demonstrate how the conceptual granularity entailed in the development of a detailed database of venue openings and closings (the Cinema and Audiences in Australia Project database) can in turn lead to a fundamental reconsideration of the ontology of the cinema itself.

Effects of early-life environment and epigenetics on cardiovascular disease risk in children: highlighting the role of twin studies

Cardiovascular disease (CVD) is the leading cause of death worldwide and originates in early life. The exact mechanisms of this early-life origin are unclear, but a likely mediator at the molecular level is epigenetic dysregulation of gene expression. Epigenetic factors have thus been posited as the likely drivers of early-life programming of adult-onset diseases. This review summarizes recent advances in epidemiology and epigenetic research of CVD risk in children, with a particular focus on twin studies. Classic twin studies enable partitioning of phenotypic variance within a population into additive genetic, shared, and nonshared environmental variances, and are invaluable in research in this area. Longitudinal cohort twin studies, in particular, may provide important insights into the role of epigenetics in the pathogenesis of CVD. We describe candidate gene and epigenome-wide association studies (EWASs) and transgenerational epigenetic inheritance of CVD, and discuss the potential for evidence-based interventions. Identifying epigenetic changes associated with CVD-risk biomarkers in children will provide new opportunities to unravel the underlying biological mechanism of the origins of CVD and enable identification of those at risk for early-life interventions to alter the risk trajectory and potentially reduce CVD incidence later in life.

A truncated fragment of Src protein kinase generated by calpain-mediated cleavage is a mediator of neuronal death in excitotoxicity

Excitotoxicity resulting from overstimulation of glutamate receptors is a major cause of neuronal death in cerebral ischemic stroke. The overstimulated ionotropic glutamate receptors exert their neurotoxic effects in part by overactivation of calpains, which induce neuronal death by catalyzing limited proteolysis of specific cellular proteins. Here, we report that in cultured cortical neurons and in vivo in a rat model of focal ischemic stroke, the tyrosine kinase Src is cleaved by calpains at a site in the N-terminal unique domain. This generates a truncated Src fragment of ?52 kDa, which we localized predominantly to the cytosol. A cell membrane-permeable fusion peptide derived from the unique domain of Src prevents calpain from cleaving Src in neurons and protects against excitotoxic neuronal death. To explore the role of the truncated Src fragment in neuronal death, we expressed a recombinant truncated Src fragment in cultured neurons and examined how it affects neuronal survival. Expression of this fragment, which lacks the myristoylation motif and unique domain, was sufficient to induce neuronal death. Furthermore, inactivation of the prosurvival kinase Akt is a key step in its neurotoxic signaling pathway. Because Src maintains neuronal survival, our results implicate calpain cleavage as a molecular switch converting Src from a promoter of cell survival to a mediator of neuronal death in excitotoxicity. Besides unveiling a new pathological action of Src, our discovery of the neurotoxic action of the truncated Src fragment suggests new therapeutic strategies with the potential to minimize brain damage in ischemic stroke.

Sex and death: CHD1Z associated with high mortality in moorhens

Sex ratios in clutches of moorhens (Gallinula chloropus) in Britain were measured on 83 chicks using the sex-linked CHD1 gene (Chromo-helicase/ATPase-DNA binding protein 1). Among birds, the female is the hetero-gametic sex (Z and W chromosomes), and the male is homogametic (two copies of the Z chromosome). We report variation among the PCR-amplified fragments of the CHD1Z, and the death of nearly all heterozygous male chicks (92%). In contrast, survivorship among females and homozygote males was 54–60%. Mortality in male heterozygotes was significantly higher than that of male homozygotes (P < 0.001). Chick and egg biometrics were not significantly different between these males. The CHD1Z was unlikely to be directly responsible but may have been hitchhiked by the causal gene(s). The observations appear to follow a classic underdominance (heterozygote inferiority) pattern, but raise the paradoxical question of why one form of the Z chromosome has not been fixed, as is expected from evolutionary theory. We discuss possible explanations and include a survey of British populations based on skin specimens.

Review of Pat Jalland's 'Changing way of death in twentieth century Australia: war, medicine and the funeral business'

Tanja Luckins of La Trobe University reviews Changing Ways of Death in Twentieth Century Australia: War, Medicine and the Funeral Business, by Pat Jalland. (Sydney: University of New South Wales Press; 2006)

A book about death : group exhibition : Tweed Regional Gallery, Murwillumbah, NSW

Group exhibition curated by Heather Matthew and Julie Barratt and held at The Boyd Gallery, Tweed Regional Gallery, Murwillumbah, NSW.

Death or survival from invasive pneumococcal disease in Scotland: associations with serogroups and multilocus sequence types

We describe associations between death from invasive pneumococcal disease (IPD) and particular serogroups and sequence types (STs) determined by multilocus sequence typing (MLST) using data from Scotland. All IPD episodes where blood or cerebrospinal fluid (CSF) culture isolates were referred to the Scottish Haemophilus, Legionella, Meningococcal and Pneumococcal Reference Laboratory (SHLMPRL) from January 1992 to February 2007 were matched to death certification records by the General Register Office for Scotland. This represented 5959 patients. The median number of IPD cases in Scotland each year was 292. Deaths, from any cause, within 30 days of pneumococcal culture from blood or CSF were considered to have IPD as a contributing factor. Eight hundred and thirty-three patients died within 30 days of culture of Streptococcus pneumoniae from blood or CSF [13.95 %; 95 % confidence interval (13.10, 14.80)]. The highest death rates were in patients over the age of 75. Serotyping data exist for all years but MLST data were only available from 2001 onward. The risk ratio of dying from infection due to particular serogroups or STs compared to dying from IPD due to all other serogroups or STs was calculated. Fisher’s exact test with Bonferroni adjustment for multiple testing was used. Age adjustment was accomplished using the Cochran–Mantel–Haenszel test and 95 % confidence intervals were reported. Serogroups 3, 11 and 16 have increased probability of causing fatal IPD in Scotland while serogroup 1 IPD has a reduced probability of causing death. None of the 20 most common STs were significantly associated with death within 30 days of pneumococcal culture, after age adjustment. We conclude that there is a stronger association between a fatal outcome and pneumococcal capsular serogroup than there is between a fatal outcome and ST.