Urban vulnerability in Sydney: Policy and institutional ambiguities in bushfire protection

Despite the inevitability of the bushfires hazard across the Sydney region, a mismatch exists between reactive technological fixes and proactive social programs which have far-reaching vulnerability and governance consequences. This paper questions the adequacy of current policy and action, revealing contradictions and tensions that expose Sydney's vulnerability and have implications for other Australian cities.

Social Vulnerability Scale for older adults: Validation study

The Social Vulnerability Scale (SVS), an informant-report of social vulnerability for older adults, was piloted in a sample of 167 undergraduate students (63 male, 104 female) from the University of Queensland. Participants aged 18 - 53 (M = 25.53 years, SD = 7.83 years) completed the SVS by rating a relative or friend aged ≥50 years (M = 71.65 years, SD = 12.49 years): either someone with memory problems, stroke, dementia, or other neurological condition (n = 85); or a healthy older adult (n = 82). Excellent internal consistency and test - retest reliability were demonstrated, and the SVS effectively differentiated healthy older adults from those with a neurological condition based on proxy ratings of social vulnerability. The SVS is a potentially useful adjunct measure of older adults' capacity to reside independently. 1 *For information on using the Social Vulnerability Scale, email d.pinsker@psy.uq.edu.au or stone@psy.uq.edu.au

Modelling Apoptotic cell clearance within the atherosclerotic plaque

The aged population have an increased susceptibility to infection, therefore function of the innate immune system may be impaired as we age. Macrophages, and their precursors monocytes, play an important role in host defence in the form of phagocytosis, and also link the innate and adaptive immune system via antigen presentation. Classically-activated 'M1' macrophages are pro-inflammatory, which can be induced by encountering pathogenic material or pro-inflammatory mediators. Alternatively activated 'M2' macrophages have a largely reparative role, including clearance of apoptotic bodies and debris from tissues. Despite some innate immune receptors being implicated in the clearance of apoptotic cells, the process has been observed to have a dominant anti-inflammatory phenotype with cytokines such as IL-10 and TGF-ß being implicated. The atherosclerotic plaque contains recruited monocytes and macrophages, and is a highly inflammatory environment despite high levels of apoptosis. At these sites, monocytes differentiate into macrophages and gorge on lipoproteins, resulting in formation of 'foam cells' which then undergo apoptosis, recruiting further monocytes. This project seeks to understand why, given high levels of apoptosis, the plaque is a pro-inflammatory environment. This phenomenon may be the result of the aged environment or an inability of foam cells to elicit an anti-inflammatory effect in response to dying cells. Here we demonstrate that lipoprotein treatment of macrophages in culture results in reduced capacity to clear apoptotic cells. The effect of lipoprotein treatment on apoptotic cell-mediated immune modulation of macrophage function is currently under study.

Reduced transferrin binding in Down syndrome:a route to senile plaque formation and dementia

Plasma transferrin binding in Down syndrome and Alzheimer's disease is significantly reduced compared with age matched controls and it was thought this may help elucidate a pathological time sequence for the onset of dementia in Down syndrome. In Down syndrome, there was a reduction in gallium and aluminium transferrin binding both with age and the onset of dementia. Non-transferrin bound gallium species were identified as non-transportable phosphate or silicate. Thus, the route of entry of metals into the brain must be via a transferrin mediated complex only. A clear sequence of pathological events has been demonstrated in Down syndrome which shows the pathway to development of plaques and dementia and this is believed to have an immunological origin.

Between safety and vulnerability:the exiled other of international relations

Inspired by the idea of safe citizenship this article queries the possibilities of safety in an age of securitization. It challenges the cosmopolitan worldview and its iteration of a global cosmopolitan citizen. It champions an account of affective citizenship, narration and attends to the trauma of exile. It offers an account of exile before suggesting an institutional design premised on politicization. This design, it is argued, facilitates moments of storytelling fostering individual empowerment. This unorthodox rendering of agency allows the traumatized exile to negotiate the world as it is, not as it could be, as a potential ‘safe’ citizen.

Relationships between morphological types of plaque in Alzheimer’s disease as revealed in silver and immunostained preparations

The objective of this study was to determine the possible relationships between the morphological types of plaque revealed in silver and immunostained sections of Alzheimer’s disease (AD) tissue. The density of cored and uncored senile plaques in Glees and Marsland preparations, and of diffuse, primitive, classic and compact beta/A4 deposits in immunostained preparations were estimated. A principal components analysis (PCA) of the data suggested that three uncorrelated principal components accounted for 80% of the variation in lesion density in the tissues. This suggested that thee processes lead independently to the formation of: (1) the uncored Glees plaques; (2) the primitive beta/A4 deposits and most of the classic beta/A4 deposits and (3) the compact beta/A4 deposits and the remaining classic deposits. Hence, the uncored plaques revealed by the Glees stain and the primitive beta/A4 deposits represented distinct plaque populations. In addition, the classic beta/A4 deposits did not appear to represent a uniform plaque population but to originate from at least two pathological processes. The uncored Glees plaques appeared to the only plaque population closely related to the diffuse beta/A4 deposits.

The usefulness of spatial pattern analysis in understanding the pathogenesis of neurodegenerative disorders, with particular reference to plaque formation in Alzheimer's disease

Discrete, microscopic lesions are developed in the brain in a number of neurodegenerative diseases. These lesions may not be randomly distributed in the tissue but exhibit a spatial pattern, i.e., a departure from randomness towards regularlity or clustering. The spatial pattern of a lesion may reflect its development in relation to other brain lesions or to neuroanatomical structures. Hence, a study of spatial pattern may help to elucidate the pathogenesis of a lesion. A number of statistical methods can be used to study the spatial patterns of brain lesions. They range from simple tests of whether the distribution of a lesion departs from random to more complex methods which can detect clustering and the size, distribution and spacing of clusters. This paper reviews the uses and limitations of these methods as applied to neurodegenerative disorders, and in particular to senile plaque formation in Alzheimer's disease.

Abnormal left and right amygdala-orbitofrontal cortical functional connectivity to emotional faces:state versus trait vulnerability markers of depression in bipolar disorder

Background - Amygdala-orbitofrontal cortical (OFC) functional connectivity (FC) to emotional stimuli and relationships with white matter remain little examined in bipolar disorder individuals (BD). Methods - Thirty-one BD (type I; n = 17 remitted; n = 14 depressed) and 24 age- and gender-ratio-matched healthy individuals (HC) viewed neutral, mild, and intense happy or sad emotional faces in two experiments. The FC was computed as linear and nonlinear dependence measures between amygdala and OFC time series. Effects of group, laterality, and emotion intensity upon amygdala-OFC FC and amygdala-OFC FC white matter fractional anisotropy (FA) relationships were examined. Results - The BD versus HC showed significantly greater right amygdala-OFC FC (p = .001) in the sad experiment and significantly reduced bilateral amygdala-OFC FC (p = .007) in the happy experiment. Depressed but not remitted female BD versus female HC showed significantly greater left amygdala-OFC FC (p = .001) to all faces in the sad experiment and reduced bilateral amygdala-OFC FC to intense happy faces (p = .01). There was a significant nonlinear relationship (p = .001) between left amygdala-OFC FC to sad faces and FA in HC. In BD, antidepressants were associated with significantly reduced left amygdala-OFC FC to mild sad faces (p = .001). Conclusions - In BD, abnormally elevated right amygdala-OFC FC to sad stimuli might represent a trait vulnerability for depression, whereas abnormally elevated left amygdala-OFC FC to sad stimuli and abnormally reduced amygdala-OFC FC to intense happy stimuli might represent a depression state marker. Abnormal FC measures might normalize with antidepressant medications in BD. Nonlinear amygdala-OFC FC–FA relationships in BD and HC require further study.